Putting the body into ketosis and controlling blood glucose levels may prove to be effective therapy against certain cancers. This real case reveals one aggressive self-experimenter who used a combination of the ketogenic diet, fasting and other tools to control his epilepsy and send his brain cancer into remission.

This episode examines the ketogenic diet as a tool to fight against cancer. It is a follow up of the episodes on ketosis and fasting that we have done with Dr. Thomas Seyfried in episode 16, and Gene Fine in episode 36. You definitely should check those out for context before or after you dive into this one to fill in any gaps.

We are talking to someone who has actually used ketosis by a combination of ketogenic dieting and fasting as a therapy to fight his brain tumor. Our guest has gone through a variety of extreme approaches to ensure he remains in a high state of ketosis. In his case, his life depended on it. This episode is not just for those with cancer or epilepsy, but also for those interested in the benefits of the ketogenic diet. You can take some of the tools he used to improve your own state of ketosis if you are having trouble maintaining it.

[W]hen I have my blood tests . . . and [test] a number of markers for potential tumor progression, internally, I am actually much healthier than before I had cancer . . .
– Andrew Scarborough

I met Andrew Scarborough at a conference where he spoke about his experience with ketosis and its effect on his brain tumor. After being diagnosed with a type of malignant tumor called an Anaplastic Astrocytoma, Andrew underwent several months of unsuccessful chemo treatment. He decided to take his cancer treatment and management of his epilepsy into his own hands and to go the ketosis route. This decision was based in a small part on researching Thomas Seyfried’s work, which we will also discuss in the episode.

Fortunately, this decision has yielded very positive results for him, and his tumor has shrunk. In fact, it has disappeared from scans (seen below) and his doctors are now giving him the all clear. Andrew is now working with London-based hospitals to develop clinical trials for treating brain cancer patients using an optimized ketogenic diet.


Andrew's brain tumor before and after being on the ketogenic diet.

Andrew’s brain tumor before and after being on the ketogenic diet.


There are a lot of details in this podcast on how Andrew went about using the ketogenic diet, including the types of foods he ate, how he optimized the diet for his situation, the extreme measures he has taken, and how he has been able to keep up physical activity. We will talk about everything on his journey, including things like eating bugs and sheep’s brain, and quitting eating plant-based foods altogether.

The episode highlights, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. Enjoy the show and let me know what you think in the comments!

itunes quantified body

What You’ll Learn

  • The beginning of Andrew’s brain cancer story (4:46).
  • Andrew is diagnosed with a grade 3 Anaplastic Astrocytoma (12:14).
  • After unsuccessful chemo treatment, Andrew devises a treatment using the ketogenic diet (19:19).
  • Using MRIs to visualize changes in the metabolic activity of the tumor due to the ketogenic diet (20:52).
  • Scans show complete remission since using the ketogenic diet (23:40).
  • Optimizing and maintaining the ketogenic diet for brain cancer management (26:40).
  • The biomarkers Andrew tracks to monitor the effects of the ketogenic diet (28:08).
  • The glucose-ketone index (29:13).
  • Andrew’s typical diet (32:58).
  • Maintaining a healthy 1:1 ratio of Omega-6 to Omega-3 (33:35).
  • The ketogenic foods Andrew eats (36:10).
  • Variations on the traditional ketogenic diet (41:30).
  • Supplementing the diet with insects (46:30).
  • Keeping up ketone levels and controlling seizure activity during exercise (50:16).
  • Andrew’s research on an optimized ketogenic diet for brain cancer patients (54:50).
  • More on Omega-6/Omega-3 ratios (59:15).
  • Limiting protein and fasting (1:00:32).
  • Using magnesium to prevent seizures during a fast (1:02:08).
  • Mimicking chemo naturally with diet (1:06:44).
  • The resources Andrew recommends for those facing cancer or epilepsy or interested in the ketogenic diet (1:11:47).
  • Andrew’s advice on what biomarkers to look at and where to start with the ketogenic diet (1:18:34).

Thank Andrew Scarborough on Twitter for this interview.
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Andrew Scarborough

Tools & Tactics

Interventions

  • Hyperbaric Oxygen Therapy (HBOT): A therapy Dr. Seyfried believes may be beneficial to fight cancer but is relatively non-toxic in comparison to current treatment modalities (chemo and immuno-therapies). It exposes the body to higher levels of oxygen via having the person sit in a pressurized tank with higher oxygen concentrations. Andrew is adding this therapy to his current tools. Typically you visit centers that provide sessions inside hyperbaric oxygen tanks, however some new smaller and lower pressure HBOTs are now beginning to appear in the market that you can buy to use at home.

Supplementation

  • Ketosports KetoForce: KetoForce contains the endogenous ketone body beta-hydroxybutyrate (BHB) in sodium and potassium salt form. The compound BHB can be used as an energy source by the brain when blood glucose is low. Ingesting KetoForce raises the levels of blood ketones for 2.5-3.0 hours after ingestion. (Note: A similar product from the same company is Ketosports KetoCaNa). Andrew uses KetoForce to increase his ketone levels during gentle exercise.
  • Ancient Minerals Magnesium Spray: Most people with epilepsy have a magnesium deficiency. Magnesium supplementation has been used to reduce seizure activity in people with epilepsy. Andrew prepares his own magnesium chloride solution that he takes transdermally multiple times every day (about 230 mg per day) and during exercise, which can be a seizure trigger for him.
  • Curcumin BCM95: Curcumin is a derivative of turmeric which is an anti-inflammatory antioxidant and potentially has anti-cancer properties. Andrew takes Curcumin in tablet form with DHA because it increases the uptake of DHA to the brain.

Diet & Nutrition

  • Ketogenic Diets: The ketogenic diet is a low carb diet which raises the level of ketone bodies in the blood. Tumor cells are inefficient at processing ketone bodies for energy. The diet is commonly used to help control epilepsy in children.
  • Paleo Diet: A diet that mimics the nutrition of early hunter-gatherers, and consists of all lean meats and fish, fresh fruits, and non starchy vegetables.
  • Water Fasts: A water-only fast of at least 3 days and preferably 5 days is recommended by Dr. Seyfried as a tool to reduce cancer risk and to lower your glucose – ketone index to 1.0. They are the standard fast protocol used in most of the research studies looking at cancer inhibition or therapy for cancer patients. Learn more from Damien’s experience with a 5-day-water-fast.

Tracking

Biomarkers

  • Blood Glucose: A measure of the level of glucose in the blood at one point in time. Blood glucose is a biomarker for increased cancer risk. Therapies target reduction of blood glucose levels to limit cancer cell growth. Blood glucose levels vary throughout the day. Ideally levels should be kept below 100 mg/dL and below ~85mg/dL for fasting glucose. Andrew maintains his around 60-70 mg/dL.
  • Glucose – Ketone Index (GKI): The ratio between the concentration of glucose in the blood to ketone bodies in the blood. The calculation is Glucose (mmol)/ Ketone (mmol). Dr. Seyfried created the index as a better way to assess metabolic status. Therapeutic efficacy is considered best with index values approaching 1.0 or below. Patients with chronic disease like cancer have index values of 50 or more. Check out the episode with Thomas Seyfried here.
  • Cholesterol-HDL and LDL: The cholesterol biomarkers include lipoproteins and triglycerides which are found in the blood. There are standard markers that all doctors and labs will run, and some newer specialist labs that are more specific and accurate. There are two main types of lipoproteins, HDL and LDL. We covered these markers extensively in episode 7.
  • Omega-6/Omega-3 Ratio: Many Western diets are deficient in Omega-3 fatty acids, such as DHA, and have excess Omega-6 fatty acids. A high Omega-6/Omega-3 ratio promotes inflammation and the pathogenesis of many diseases, including cancer, whereas increased levels of Omega-3 (a low Omega-6/Omega-3 ratio of about 1) exert suppressive effects.
  • hs-CRP (high sensitivity C-reactive Protein): a marker for systematic inflammation that can be measured over a period of time to determine effectiveness of treatments such as the ketogenic diet. Ideally CRP levels should be <1 mg/L. High levels are associated with chronic inflammation, which is common in cancer and other chronic diseases.

Lab Tests, Devices and Apps

  • Glucometer: is a device used to measure the level of glucose in the blood. Andrew and Damien use the Freestyle Optium Neo Glucose/ Ketone meter. Andrew’s ketones and blood glucose levels hover around 65 mg/dl, which puts him somewhere around 0.6-0.8 on the Seyfried index. Check out episode 16 to learn more about the Seyfried Index.
  • Omega Blood Count: Measures the levels of Omega-6 and Omega-3 fatty acids in your blood. (Note: This test is only purchasable via offline retail stores such as pharmacies and health shops in the UK – an alternative test that Andrew recommends that you can buy online in US or UK is OmegaQuant.com)
  • Complete Lipid Panel: measures total cholesterol, triglyceride levels, HDL and LDL cholesterol, which are all found in the blood. High blood lipoprotein levels are associated with cancer.
  • Complete Blood Count: is a blood panel that measures the levels of the different cells in the blood. Numbers of the different types of cells vary depending on disease status and even between people. The test is often used to monitor cancer progression and treatment.
  • Magnetic Resonance Imaging (MRI): MRI scans use pulses of magnetic energy to visualize internal organs and structures. It can be used on almost any area of the body and provides information on tumors, bleeding, injuries, blood vessels, or infection. MRIs were used to monitor Andrew’s brain tumor.
  • Positron Emission Tomography (PET) scan: A PET scan is a functional imaging technique used to image body processes. A PET scan can be used to identify cancer presence and severity. A radioactive tracer, fluorodeoxyglucose, is used to tag cancerous cells so they can be visualized. Check out episode 36: Quantifying Cancer and Reexamining Which Cancers May be Inhibited by Fasts with Gene Fine to learn more about PET scans and cancer.

Other People, Books & Resources

People

  • Dr. Thomas N. Seyfried, PhD: University of Illinois, Urbana-Champaign. Dr. Seyfried’s research focuses on the mechanisms by which metabolic therapies manage chronic diseases like cancer, epilepsy, and neurodegenerative lipid storage dysfunctions. Check out Dr. Seyfried’s episode on “Water Fasts as Potential Tactic to Beat Cancer.”
  • Dr. Dominic D’Agostino, PhD: Assistant Professor in the Department of Molecular Pharmacology and Physiology at the University of South Florida Morsani College of Medicine, and a Senior Research Scientist at the Institute of Human and Machine Cognition. His research focuses on developing and testing nutritional and metabolic therapies for neurological disorders and cancer. His own website is Keto Nutrition
  • Dr. Colin Champ, MD: A board-certified radiation oncologist and Assistant Professor at the University of Pittsburgh Cancer Institute and University of Pittsburgh Medical Center. He is also board-certified in integrative medicine by the American Board of Integrative and Holistic Medicine. His focus is the role and effect diet and nutrition may have in cancer treatment.
  • Dr. Adrienne Scheck, PhD: An Associate Professor of Neurobiology at Barrow Neurological Institute. Her expertise is in neuro-oncology and her lab has been involved in investigating the effects of the ketogenic diet on brain cancer.

Organizations

Books

Other

  • Ketogenic Diet Resource: Andrew says this website has answers to just about all the questions you could have.
  • Clinicaltrials.gov: This site can provide you with information on clinical trials that are currently being done relating to the ketogenic diet and different cancers.

Full Interview Transcript

Click Here to Read Transcript

[Damien Blenkinsopp]: Andrew, welcome. Thank you so much for coming on the show.

[Andrew Scarborough]: Thank you for having me.

(04:39) [Damien Blenkinsopp]: Yes. You have quite an amazing story that a lot of people are very interested in hearing about. It’s always good to get the context of how this happened to you, and where it all started? Could you go into the beginning, how you made the discovery that you had this condition? How did it start?

[Andrew Scarborough]: Yes. I was studying a Master’s in Nutritional Therapy at the University of Westminster. This is before my diagnosis, and I was suffering from migraine headaches for a few months. Until suddenly I had lost my speech in February 2013, this was nearly 3 years ago now.

What I didn’t know at the time, that was my first partial seizure, and just being a man I carried on.

[Damien Blenkinsopp]: So to describe that, did you have difficulty saying words, or what exactly happened?

[Andrew Scarborough]: I went very dizzy, and then lost my speech completely for about five to six minutes, I was with a friend and we laughed about it because it was a bit strange. Because it was quite a cold day, it was February, I was just thinking when you get cold and shivering. You just stutter and loose — you struggle to speak, but it was a lot more serious than that.

I didn’t do anything about it. A couple of months later, I was experiencing very similar symptoms with pins and needles in my tongue and throat. To cut a long story short, I went on the train after a heavy gym workout. And, I felt like I actually have a lot of energy after the workout, even though I really struggled through it.

I just felt completely wiped out, even though it wasn’t the most difficult workout. I suffered more seizure activity afterwards, when I was getting on the train, very busy train actually in London to go home. And I devastatingly had a crushing headache, like my head was in a nutcracker.

The pressure was constantly building up, then I suffered a quite a traumatic brain hemorrhage, and grand mal seizure on the train, which wasn’t too pleasant, and the whole train stopped. I was rushed to hospital. There was so much blood in my brain that they didn’t know what to say, what actually was the cause.

As I was in hospital not knowing — feeling very confused not able to speak or walk at this point. I was given a CT scan and all that was shown was this massive blood in my brain. It looked like an explosion had gone off. I was still experiencing horrific grand mal seizures at this time, so I had things explained to me, and at the time, they were going in one ear and out the other, because I was so out of it.

That was quite a tough time from my family, and my first diagnosis was an AVM, which is an arteriovenous malformation. Because it looks so poor on the scans — because CT scans are quite ambiguous. All we could really see was just a tangle of blood vessels and arteries.

[Damien Blenkinsopp]: So, they thought it was an artery that had grown the wrong way, or you’d been born . . .

[Andrew Scarborough]: They saw it as being an unusual tangle of mess.

[Damien Blenkinsopp]: Okay, the arteries growing in the wrong way.

[Andrew Scarborough]: Yeah. They said, “No it’s not probably like that, it’s probably a Cavernous Hemangioma instead, which is a tangle of abnormal blood vessels, not tangled in the arteries.” Which is better because it was a bit less life-threatening, but I was given a number of misdiagnoses before. Eventually, I had an operation, because I was continually having these grand mal seizures that were starting to cause me cognitive difficulties, and my speech was getting worse, so I wasn’t able to speak at all at this stage.

(09:11) [Damien Blenkinsopp]: So, going back to the hemorrhage is that a stroke, is it the same as a stroke, or is it slightly different?

[Andrew Scarborough]: It’s very similar to a stroke, it was caused by the pressure of the tumor. Pushing against the side of my skull, and also it was between the speech movement area invading into the motor cortex, that’s why I had lost my speech completely. I had an operation not long after, in May 2013, to try and remove as much as possible, if this very vascular and invasive tumor, which was slightly larger than a size of a golf ball — but invading into the motor cortex area of my brain.

They couldn’t remove all of it because otherwise I would be completely paralyzed or dead. Because I was misdiagnosed, I should’ve had the operation awake but I was unconscious during it. The neurosurgeons said after, “Yeah we probably.”

If he has to do it again, he would have it awake so he could potentially get more out of it, but he couldn’t remove all of it because of where it was in the brain.

[Damien Blenkinsopp]: That’s interesting, what is the difference between you being unconscious and awake, are they able to get some feedback from you?

[Andrew Scarborough]: Yeah. You’re kept awake so they can monitor your responses, while they’re poking around in there to see what can be removed and what can’t, and what healthy brain tissue and what isn’t. One of the main issues with the brain surgery is it’s very difficult to distinguish what’s healthy tissue, and what’s the tumor.

[Damien Blenkinsopp]: So, this is what date now that you’ve had your surgery, and you’ve been given a clear diagnosis?

[Andrew Scarborough]: This point now? It’s two and a half years coming up to three.

[Damien Blenkinsopp]: Okay, it was a few months after your hemorrhage.

[Andrew Scarborough]: That was two months after that I’ve had the operation because they didn’t know what to do with me. There was a lot of blood in my brain, and if you think about a malignant brain tumor, it’s not a great thing if you’ve got a constant blood supply there — and it’s not a fantastic thing if you’ve had this thing that looks like an explosion in the brain, scattering around the cells, and blood everywhere. So, it just makes it more migratory, I guess if that’s the word.

More likely to spread into other areas, which is not ideal. I then had my pathology, finally, and it showed that the tumor was indeed extremely vascular. And there was still some significant scar tissue, as well as some slight enhancement there, but we didn’t know exactly what that was.

[Andrew Scarborough]: So you’re saying, is that a scan?

[Andrew Scarborough]: Yes, sorry.

[Damien Blenkinsopp]: Okay.

[Andrew Scarborough]: — This was the MRI scan after my operation.

[Damien Blenkinsopp]: Is that a straight MRI?

[Andrew Scarborough]: Yes, this was just a standard MRI, but I also had my pathology report from the amount of tumor that was able to be removed, and that came back as an Anaplastic Astrocytoma, which is a Grade 3 Astrocytoma — affecting the glial cells, the astrocytes in the brain, and quite important components of the brain. It’s not a great thing to have, particularly a high grade glioma, which is what mine was.

Brain tumors come in different gradings, so it’s like we’re staging how — with the brain it’s Grades 3 and 4 are highly malignant, and Grades 1 and 2 are slow growing. Grade 1 is typically a solid mass, that you can — if you can operate it can be curable. Even Grade 2s are known to come back, and do grow, but grow at a slower rate. But Grade 3 and 4 are the fastest growing, they grow quite fast. Mine was showing to be heterogeneous, it had quite a few Grade 3 cells in there.

[Damien Blenkinsopp]: Does that mean that it has different types of cancer cells there when you say heterogeneous?

[Andrew Scarborough]: Well, yeah. It showed numerous mutations. It’s very difficult to explain, but it showed that it wouldn’t be chemosensitive, it was negative for IDH1 which is a predictor of longest survival and chemosensitivity. It was also unmethylated for MGMT, which is a repair gene.

And that’s also — it’s not a good thing that it was unmethylated, so it was one of these gene mutations that they say is good to have for longer term survival. I also had tumor suppressor genes missing which again, with these Grade 3 tumors the timescale for survival is variable until it comes back. But in my case, I had just about the worse. It’s scenario terms with the pathology.

(14:33) [Damien Blenkinsopp]: So, did they give you a rough timeline, I guess at that point?

[Andrew Scarborough]: They said it was difficult to tell because of my age and the location of the tumor. Typically in that scenario, it’s around two years when it comes back, and that’s one of the best cases in that particular scenario. It’s a strange type of tumor because in a different scenario with different kind of pathology it can be up to five years or sometimes seven that it comes back.

It’s quite variable, but in my case it didn’t look so good, and I still had some scar tissue where there was lots of — healthy blood supply that could’ve had any enhancement that was present at the time, not great.

[Damien Blenkinsopp]: Must have been a shock, must have been a pretty big shock for you when that one came about.

[Andrew Scarborough]: Yeah, most definitely. I was told that even though my tumor was not chemosensitive that I should probably go ahead and have chemotherapy and radiotherapy, which I did for a short period because I was quite ignorant about it. I thought that it would potentially give me a bit more time.

But then once I’d looked into it I realized that it was only going to cause further mutations for me personally, and I didn’t want to see that. I started to learn my carbohydrate intake and go on a restrictive ketogenic diet after I’ve learned about it prior to my diagnosis, when I was studying a Master’s in Nutritional Therapy.

(16:17) [Damien Blenkinsopp]: Right, what was your lifestyle like before this all happened to you, and how old were you when this happened?

[Andrew Scarborough]: 27, 28. It’s difficult now thinking back, because my birthday’s at September 1, so I was 27 going on 28. It was two and half years ago and I’m 30 now.

[Damien Blenkinsopp]: So roughly 28 or 27.

[Andrew Scarborough]: Yeah. I was on a diet that I thought was healthy, so I was on a low fat, high carb with a complex carb diet, all whole foods, so I thought I was doing a good job, no processed food. I actually had quite a low body fat percentage and quite a high lean body mass. I thought I was very healthy, and I was very athletic.

I’d worked as a personal trainer for a few years. I was studying my Master’s in Nutritional Therapy and it was a shock to me that what I was learning in my undergraduate degree in Nutrition was completely useless, because I was learning all these new information that contradicted all the older information, but I was just learning about it. I thought it was interesting but it seemed to go against most of what I’ve studied for the past few years before that.

I thought I was healthy.

(17:44) [Damien Blenkinsopp]: When they gave you the diagnosis for the cancer —people at home are probably thinking, “Well is this one of those — metastasized, so it would spread to other parts of the body, or does it tend to stay concentrated?”

[Andrew Scarborough]: Yeah, well primary brain tumors typically just spread into the brain, which isn’t great because your brain is very useful. Apart from medulloblastoma, which can spread down the spinal fluid and into the central nervous system. It’s the central nervous system that can spread down the spine, and other also spread into the brain.

Mine is an astrocytoma, it would’ve just spread into the brain, and there can also be secondary tumors that come about as a response in the brain. It’s not a great type of tumor to have.

[Damien Blenkinsopp]: No, tumors are good ones to have, but it’s one of the nastier ones.

[Andrew Scarborough]: It’s the step down from glioblastoma, which is the most common type of brain cancer.

[Damien Blenkinsopp]: That always the worst, is the Type 4. . .

[Andrew Scarborough]: Yeah. I thought with my approach, with my own treatment strategy — I thought I have a little bit more time to play around with things and adjust to strict ketogenic diet. If I had a glioblastoma I would’ve pushed things a lot quicker. I did push things quite a lot, and I go to extremes with this diet and this approach.

(19:19) [Damien Blenkinsopp]: Yeah. Did you consider any other options? You said you took a little bit of chemo and radiotherapy —radiation, and pretty quickly you stopped, was that a couple of months?

[Andrew Scarborough]: I stopped after four months because I was proposed to have it for up to two years which is a long time, and I said no after a few months experiencing how horrible that was, and still having these horrible seizures. I thought, “Well, I want my quality of life to be good at least.” I stopped it, because my scans were still showing this enhancement.

I thought, “Well, we don’t know if that’s necrotic tissue or scar tissue, or if it’s the tumor activity.” But I thought that, because my tumor looked so glowing on the scan that it was potentially very responsive to carbohydrate restriction. So you do get some cancers that seem to use more glucose for energy, and you get some that actually use glutamine more for energy than glucose.

More or less they use both for energy, but because mine was so glowing up — lighting up like a Christmas tree I’d like to say, it showed that it was potentially more efficacious to just really cut down on the glucose, and see what was going to happen from that.

[Damien Blenkinsopp]: So these were all MRIs they were giving you?

[Andrew Scarborough]: Yeah, and interestingly even though it’s different from other cancers where you get a PET scan, and you can still see the enhancement there, on an MRI, that was interesting to me.

[Damien Blenkinsopp]: Do you know why that was? We spoke recently to Gene Fine who is talking about the PET scan, in the use of cancers. Do you know why you were able to see it quite clearly on the MRI in your case? Is that specific to brain cancers?

[Andrew Scarborough]: Yeah, I think from what I’ve seen in the literature it is, I don’t know exactly why that is. I guess it’s just you’re able to see the metabolic activity even with — I think it’s an iodine solution, not the good kind, the more radioactive iodine that they give you, rather than the supplemental iodine which you can get which is actually really good for hormonal control and certain cancers.

[Damien Blenkinsopp]: So, they give you an IV of that when you go to your MRI, so they can see more?

[Andrew Scarborough]: Yeah, that’s the contrast injection that they give you. Sometimes with PET scans, they do give you the — that shows up quite nicely with the contrast dye. I view my scan straight after I have them, so it’s interesting to view that.

[Damien Blenkinsopp]: Yeah. So I think its gadolinium, is that the contrast dye you’re talking about?

[Andrew Scarborough]: That’s one of them, but I don’t have that one from my scan, I have something else. I can’t remember exactly what it’s called, but I’ve had a few different kinds of scans. I’ve also had MRI spectroscopy which is a fascinating type of scan.

It works with lights, allowing you to see the microenvironment in the brain. And we’re looking at how the ketogenic diet is changing that environment within those biomarkers within the brain as I’m progressing. That’s really interesting to see.

(23:02) [Damien Blenkinsopp]: Yeah, so great. What kind of scans have you been having over time, and how frequently? And how have you seen the ketogenic diet impact that over time?

[Andrew Scarborough]: Well initially I had a standard MRI scans which were quite boring. The cancer cells, [unclear 23:19] was that wasn’t the best for brain cancer, even though it’s world-renowned for other cancers. At that time, I had the enhancement and significant scar tissue, and I had Hemosiderin, which is a blood staining, that was quite a lot of that showing on my scan.

Since then I’ve had progression in a way that I’ve been given a statement saying that I have a response, that I’ve achieved complete remission, and the enhancement is no longer present. I’ve also had significant healing of the scar tissue, and I’ve had vast improvement of my symptoms. So, I am completely off medication for epilepsy which I was told by five different neurologists — that I’d be crazy to even reduce the medication, and I should increase it because my seizure activity was so bad.

I’ve just had a linear progression of improvement in that respect, so I’m completely off medication for the epilepsy, and for that, I do a number of things which controls my seizure activity. And if I forget to do those things I instantly have seizures — it’s like being on a tightrope you have to keep up with doing all these things, I haven’t had a seizure in a long time. When I start to stop doing these things, or I slip up even a little bit I get an aura, which is a warning for me that I’m going to have a seizure.

I have emergency measures to reverse that, which I’ve devised myself largely. It’s interesting.

(25:07) [Damien Blenkinsopp]: Yeah, sounds very interesting, we’ll jump into that. So the epilepsy is a symptom, it’s driven by the hemorrhage that you had and some damage?

[Andrew Scarborough]: Yeah, and also it can provide these for an indicator of where you are with cancer with the brain. Particular with the temporal lobe epilepsy which is a typical response from a temporal lobe brain tumor. My tumor was between the temporal and frontal lobe, so I have three different types of seizures, which is fun.

Monitoring my symptoms and my seizure triggers, and my theories on what would resolve the seizures, not just the ketogenic diet but things I could do with the ketogenic diet to optimize it specifically for brain cancer management. I was able to work out what worked out most effectively for me personally and relate that to the literature as well. I was then able to go to my neurologist and say, “Well what do you think of this?”. And then when they said, “I think it’s absolutely ridiculous, there’re no science behind it.”

I was able to show the science behind it and my results. And then they could say, “Well that’s very interesting.” I’ve had success that they didn’t expect.

(26:42) [Damien Blenkinsopp]: That’s great. So when were you given the sign off, when they say, “Okay your scans are clear.” Did they say it’s in remission or do they say it’s clear?

[Andrew Scarborough]: With that kind of cancer it’s never deemed as curable and I don’t think it can be curable, but personally I think you can achieve and maintain complete remission, and maintain that status indefinitely. From close observation of the animal studies, when they come off the diet after they’ve achieved complete remission, same kind of cancers, that it comes back almost instantaneously. The unpublished human studies I know the same thing, the same occurrence.

I am very keen to stay on this very strict ketogenic diet, and I actually feel quite good on this. Internally, when I have my blood tests which I have a myriad of different blood tests just to see how I’m doing in terms of my general health. A number of markers for potential tumor progression. Internally I am actually much healthier than before I had cancer, which I find that kind of funny.

(28:08)[Damien Blenkinsopp]: So what kind of improvements have you seen, what are the biomarkers that stand out for you, the test results that have come back, and been useful?

[Andrew Scarborough]: The first thing I looked at was my vitamin D. When I was first diagnosed it was in a severely deficient range, and now it’s in the suboptimal range. People would say it’s too high now, it’s 200, and previously was 20.

I also have my triglycerides tested, I have my cholesterol done, and all those fun markers. I have a full blood count, my white blood cell count was pretty good, I can’t remember the exact figures. It’s actually better than before I had cancer, which is not typical even years after you had cancer, immunity can be compromised, so your white blood cell count is typically quite low, and I found that quite interesting.

(29:13) [Damien Blenkinsopp]: It’s great to hear about that progression. Let’s talk about the actual things that you’ve done in terms of where you started in your ketogenic diet, because I know that people said they’re ketogenic. Have you been tracking your blood ketones and blood glucose since the start? And have you seen how that’s changed as you’ve changed your diet?

[Andrew Scarborough]: Yeah. The first thing I did I went out and got a glucometer to measure my blood ketones and blood glucose, and I was comparing that to book cancerous [unclear 29:45] disease, and the glucose-ketone index that Thomas Seyfried devised and came up with, with his colleagues. I had a number of conversations with him about it, just over email, and I was amazed that he got back to me.

I found it very interesting, I started with trying to do the fast, to start with, to get me in ketosis quite quickly. But I realized with epilepsy that’s not a great idea. I had quite a few bad breakthrough seizures attempting that.

I decided not to try it that way, I decided to do it gradually and over time I managed to get into the therapeutic range within just a few weeks.

[Damien Blenkinsopp]: When you say therapeutic range what is that?

[Andrew Scarborough]: I was using the glucose-ketone index, which you use a ratio where you divide your blood ketones by the blood glucose, and you come up with a number, and you try and make sure that number is — I think it’s above one. I don’t measure it anymore in that way because I’m consistently in very deep ketosis with very low blood glucose, so I don’t have to do it anymore.

[Damien Blenkinsopp]: Yeah, we actually covered the index with Thomas Seyfried before. I think it’s a glucose divided by ketones, and there’s a couple of other little things you have to do in there, it’s not super straight forward. I put a spreadsheet up for some people who are asking, when he was talking to us he said it was under one.

So I guess that’s what you are aiming for and you seem to be saying you’ve gone…

[Andrew Scarborough]: Yeah at that time, that’s what I was aiming for, but now I’m consistently above 3.5, so I don’t have to worry about that so much.

[Damien Blenkinsopp]: Oh, in the glucose-ketone index?

[Andrew Scarborough]: Well my ketones are typically above 3.5, and the blood glucose is typically hovering around 3.5 — at the very least one to one.

[Damien Blenkinsopp]: Okay, so for the people at home, because in the US the blood glucose measurement isn’t millimolar. So you’re talking around in between 54 and 72 mg/dl, like 3-4 millimolar. I’m guessing you’re hovering around with the Seyfried Index somewhere around 0.6, 0.8.

So it’s well below one that’s what you’re saying because your ketones are so high.

[Andrew Scarborough]: Yeah. In the evenings it goes sky high, well the ketones go sky high, the glucose goes really low.

[Damien Blenkinsopp]: Do you mean from 5 o’clock onwards — it’s interesting because I saw that in some of my fast and some of my earlier experiments also.

[Andrew Scarborough]: Yeah. I guess it’s a hormonal thing that happens, and also because there’s that period of time where I only have typically two meals a day, that’s the in-between period, I guess where it goes that high. So that’s where I’ve unintentionally fasted for that period of time even though the diet’s mimicking fasting itself.

(32:58) [Damien Blenkinsopp]: What is a typical day look? What are you doing now, what is your typical day look like? I’m assuming at the moment you’ve got the most extreme version of your own program for this, is that correct?

[Andrew Scarborough]: Yeah. Typically I have 85% of fat and 15% protein in my diet, but over the last few days, I’ve experimented with 90% fat and 10% protein, and negligible carbs. Typically on my 85% and 15% protocol that I follow which is very similar to the animal studies, and quite similar to very strict ketogenic diet for children with epilepsy.

I restrict my calorie intake to 1,600 calories — calorie restriction is extremely important for brain cancer management. You probably discussed that with other people I’m guessing. What’s also important I think is the other things that I’m doing.

Personally, I think it’s very important to make sure you have correct therapeutic ratio — I like to call it of omega 3 and 6 in the blood, and I have at home testing kit for that which I send off to the lab every few months.

[Damien Blenkinsopp]: Okay, that’s interesting, is that a dry spot test?

[Andrew Scarborough]: Yeah, it is. You just have to collect quite a significant amount of blood, and it gives you a report back just saying what you’re ratios of omega 3 and 6 are in your blood.

[Damien Blenkinsopp]: Which lab are you using for that?

[Andrew Scarborough]: Well, the testing kit is by — if you go on Omegasense.com it comes up. There’s a center called the NutriCentre in London, and I just get it from there. It’s a pretty good test, very accurate.

[Damien Blenkinsopp]: Have you seen that change? This is actually the current levels ratio, it’s not like it’s your diet of the day like we were talking about — the blood glucose and the ketones which are changing all the time. It’s a more stable marker which is evolving over time, so you’re choosing for a range you want to keep it within.

[Andrew Scarborough]: I’m just trying to get us close to 1:1 ratio as possible, and I’ve experimented with a 2:1 and a 3:1 ratio in favor of omega 3 which is quite hard to do, but it’s very interesting. We know that omega 3 fatty acids exhibit neuroprotective properties and can represent a potential treatment for a variety of neurodegenerative diseases. It’s really interesting, we know that they are shown to be cytotoxic to tumor cells themselves.

Ideally, an optimal ketogenic diet for brain cancer should have, in my view a better ratio than omega 3 and 6. I think the standard ketogenic diets that are applied to humans at the moment are way to high in omega 6 which is inflammatory. I struggled when I was doing a standard ketogenic diet because of that.

[Damien Blenkinsopp]: What are you taking in order to raise your omega 3 levels? What are you doing in diet specifically?

[Andrew Scarborough]: Well, initially I was eating lots of brains because they are the best source of omega 3 that you could get, and that’s high in DHA, and one of the main fatty acids in the brain is DHA. The brain is 70% fat, and the rest is mostly water, it just makes sense to me to have in my diet mostly fat and water, that was my main reason for doing that.

We also know that the fatty acid composition of gliomas differs from that founding non-malignant brain tissue quite significantly. The reduction of glioma DHA content is really interesting to view — we know that in gliomas which is what my tumor was, and what a glioblastoma is as well. We know that they have significantly less DHA in and around them.

If we can increase that — the literature shows that it can have a very potent effect, particularly when on a ketogenic diet, in shrinking these tumors.

[Damien Blenkinsopp]: That’s great so you’re still eating brains today, is this a large part of your diet? What types of brains?

[Andrew Scarborough]: I was eating lamb’s brains, but, unfortunately, I’ve stopped eating them because of the very, very low risk of Scrapie which is like a CJD, a Mad Cow disease but the lamb form. Even though it’s a very small risk, and you probably have that same risk if you were to eat any infected tissue of that same animal, I just thought it would be a good idea to avoid it, which is a shame because it’s my favorite type of food on the ketogenic diet.

It’s a perfect ketogenic food, but my second most therapeutic ketogenic food that I found is sweetbreads which is the pancreas and the thymus gland of — in my case I get them from lambs again. I’ve done an experiment which is on YouTube, on my YouTube channel, just look at Andrew Scarborough, and look at my sweetbreads experiment, I’m testing the myoglobin of sweetbreads and it comes up very high on the glucometer for ketones.

When I test my blood after my postprandial blood glucose and my blood ketones after eating, my ketones shoot up very high, and the blood glucose stays more or less the same as before I started eating.

[Damien Blenkinsopp]: That’s interesting. Out of interest, how much do sweetbreads cost? Are they relatively cheap or expensive?

[Andrew Scarborough]: Well I mostly get them for free, sometimes I have to pay a pound for them.

[Damien Blenkinsopp]: Okay, so they are very cheap.

[Andrew Scarborough]: Yeah, because no one wants them.

[Damien Blenkinsopp]: Right that’s what I was thinking.

[Andrew Scarborough]: They’re incredibly nutrient dense, rich in trace minerals such as zinc and selenium, and they’re rich in protein, and omega 3 fatty acids. Like the brain, and like all the fish — the great source of omega 3. They also raise ketones very high.

[Damien Blenkinsopp]: Yeah, that’s very surprising. I don’t know if you’ve heard new supplement ranges which I’ve been playing around with it, exogenous ketones.

[Andrew Scarborough]: Yeah, I take those as well. I take KetoForce, mostly when I’m trying to do exercise because exercise is a huge seizure trigger for me. So yeah I play around with that.

[Damien Blenkinsopp]: It sounds like the sweetbreads are more effective than the KetoForce, KetoCaNa and the other ones.

[Andrew Scarborough]: Yeah. I actually made a supplement, a sludgy juice that the sweetbreads come in because I have them completely fresh straight after the animals are being slaughtered, well not straight after, but not long after, because they have to do a number of things just to make sure they are safe to eat. I made a supplement out of that and tested it, and it was very interesting the results, but it tasted absolutely foul.

[Damien Blenkinsopp]: Is that a downside of sweetbreads, they’re really awesome except they taste bad.

[Andrew Scarborough]: Yeah.

[Damien Blenkinsopp]: Okay.

[Andrew Scarborough]: It’s not the best tasting, you have to boil them for a long period of time, but they’re very nutrient dense and very effective.

[Damien Blenkinsopp]: How do you eat them? Have you got a quick recipe for the people at home, and they’re like, “Oh like a great thing to try out.” But if it tastes horrible is there some way to mask it.

[Andrew Scarborough]: The best thing to do is boil them for about an hour, that’s actually a short period of time typically for sweetbreads. Normally, it’s a lot longer. And then if you add tarragon to it, it actually compliments the flavor, and it actually tastes a lot nicer.

That’s one of the things I do, it goes well with tarragon. I just consume every bit of the animal, and I don’t have any carbohydrate so that’s how I get around possible nutrient deficiencies from not having any fruits and vegetables. And it allows me to not count carbohydrates, so it’s a Paleo-Ketogenic diet.

[Damien Blenkinsopp]: It’s a pure meat diet, right? Basically a pure carnivore?

[Andrew Scarborough]: Meat and fish, and fat, and that’s it.

(41:37) [Damien Blenkinsopp]: I do know there’s a little bit of story behind the reason — first you were on a ketogenic diet and you were doing more of a straight forward one with the coconut oil, and all of these kinds of things, what happened?

[Andrew Scarborough]: I noticed that with certain people with certain types of brain injury, your brain can be more sensitive to salicylates which are found in coconut oil, various vegetables and fruits, especially ones that have seeds. I wasn’t able to have avocados or any of the staple ketogenic foods that you have. I also couldn’t have dairy because I had a reaction to that, and I wouldn’t advise dairy anyway on a ketogenic diet for anyone with cancer let alone — brain cancer, because of IGF-1.

It just doesn’t make sense to me that there’re so many ketogenic diets for cancer management that have been based around dairy.

[Damien Blenkinsopp]: Right. There’s a lot of cheese, cheese is pushed quite hard…

[Andrew Scarborough]: Yeah, loads of cheese and double cream, and it’s not efficacious for me, even though I’m astounded that they get any results with these trans fat. And they do get some results, that’s encouraging for me on my — what I would call a more beneficial and effective ketogenic diet for this circumstance.

(43:06)[Damien Blenkinsopp]: Could you explain quickly the IGF-1, because there are people at home that are not quite up to speed on the IGF-1 and the dairy aspect of it. What’s the problem there?

[Andrew Scarborough]: It activates insulin-like growth factor and that can cause cancer cells to proliferate faster. One of the ways I get around that — I used to eat lots of butter, but because it’s more insulinogenic and it has milk proteins and casein. What I do is I have Ghee, which is clarified butter so the milk solids and the casein have been removed, and it’s much less insulinogenic and I actually get a much better blood ketone readings as a result as well compared to butter.

I find that interesting in itself, and we also know that compared to coconut oil, Ghee has much more omega 3 fatty acids, and coconut oil only has omega 6. If you’re basing a ketogenic diet around — just loads and loads of coconut oil which is just omega 6. Even though coconut oil is fantastic for achieving ketosis, I would advise it in moderate amounts if you can tolerate it because it’s really good.

I would say that making sure that you have enough omega 3 by having more animal fats is more beneficial in terms of the overall nutrient profile than just consuming tons of coconut oil.

(44:44) [Damien Blenkinsopp]: Right. You mentioned you eat all the parts of the animal, I’m guessing you mean all of the organs…

[Andrew Scarborough]: Yep.

[Damien Blenkinsopp]: Do you consume what you would call a variety of these? Do you try to cycle them, and the widest spectrum possible? So what other organs are you eating, are you literally eating all of the different organs on a rotation each week?

[Andrew Scarborough]: Yeah. Literally everything but mostly heart, because it’s very very cheap, it would cost me 60 pence at a time, and you get quite a substantial portion— because lamb hearts are quite fatty, there’s a huge chunk of fat on them. I can just eat them as they are, and I don’t need to add extra fat.

It’s a fantastic source of iron, zinc, selenium, B vitamins, folate, and it’s the best food source of coenzyme Q10. It’s funny how people pay an absolute fortune to get pills that have a coenzyme Q10, and I just get the best source that you could possibly get for 60 pence at a time.

[Damien Blenkinsopp]: There’s a psychological barrier about the taste, and it’s just what we’ve become used to really. I’m definitely nowhere near as far as you — I’ve been eating more organ meats and I’m trying to push it up, I just made another order today from a new company actually. I’m slowly building my way up, and it’s a taste I’m struggling with, recipes I think help with that, learning how to cook and deal with the different tastes, and just getting used to them.

[Andrew Scarborough]: Yeah. I actually did quite well to start with brains, they’re actually the most tolerable in terms of tastes because they just taste like creamy eggs.

[Damien Blenkinsopp]: Oh, I would’ve never thought that.

[Andrew Scarborough]: They taste like creamy salty eggs.

[Damien Blenkinsopp]: You just don’t look at them while you’re eating them.

[Andrew Scarborough]: No. And a number of things I do are just for entertainment, to keep the diet interesting, to make sure I have enough trace minerals. That’s why I added insects to my diet quite early on because anytime you eat the whole animal you’re getting a variety of nutrients. When you eat insects you’re consuming the whole animal — it just makes sense that it would be a beneficial thing to have.

[Damien Blenkinsopp]: How do you consume those? Because I know there are cricket bars out there in the US, how are you consuming insects?

[Andrew Scarborough]: What I do is I get the fattiest insects that are ketogenic, I get waxworms and super worms. Mostly insects that reptiles eat, I get them from a pet shop that sells them for reptiles now, I used to get them online.

[Damien Blenkinsopp]: Oh, man. Okay did you used to buy from [check 47:31 – Bug Grow], was that the specific brand — was that the only place you bought from?

[Andrew Scarborough]: Yeah, I tried a few, I tried silk worm, pupa as well — a few different insects have different medicinal properties, they’re in Chinese medicine. They’re really interesting in terms of the properties that they have. But we largely ignore that, mainly what I do now is I get them from the pet shop.

I just stick them in the freezer to kill them, and then I’ll give them a gentle wash and eat them …

[Damien Blenkinsopp]: You just eat them straight?

[Andrew Scarborough]: The problem, if you get them online is that they’ve been dehydrated and cooked so much that the nutrient profile isn’t as good as if you have them fresh after they’ve been wiggling about. I also grind them up and make my own flour after I’ve frozen them. That makes quite nice breads, I make a zero carb ketogenic bread which is very useful. People actually think it’s proper bread…

[Damien Blenkinsopp]: You don’t tell them right?

[Andrew Scarborough]: I’ve actually offered it to people without telling them, and they quite like it, and then I tell them what it is, and they want to punch me. But it’s actually surprisingly quite nice.

[Damien Blenkinsopp]: A quick story here, I was in Mexico 15 years ago and I went to Taxco. Anyway you go up into the mountains, into this old city and they were selling plastic bags full of live insects for eating. It’s something that we used to do — we don’t do in modern society. . .

[Andrew Scarborough]: If you look at anthropology, and how we evolved, it’s largely ignored especially with these Paleo diets — we evolved primarily eating a variety of insects, and in quite a large amount. It suggested that the man would go out and go hunting — would only about a 20% success rate catching these larger animals.

The woman would be mainly collecting insects for food. Seasonally they would collect nuts and berries, but it’s a fact in anthropological studies that we did consume a large amount of insects before we moved closer to the coast to eat fish, and that’s how our brains developed more. It’s an ignored fact.

(50:16)[Damien Blenkinsopp]: It’s really interesting, we’ll get there. There’ll be people writing books — maybe you, about the missing parts of the Paleo diet, Paleo upgraded. You did mention that, when you exercise you’re taking exogenous ketones, because of your epilepsy, why is that?

[Andrew Scarborough]: When I exercise my blood ketones go down, lower than my individual therapeutic reading for seizure control for me personally. I have to do that, and I also have to take another experimental treatment of mine which is proved effective, which I learned from the literature on epilepsy. It’s a magnesium chloride solution that I mix into water, and I have a specific amount that reverses auras.

An aura for me is when you have all symptoms that you’re about to have a more serious type of seizure. An aura is a partial seizure in itself.

[Damien Blenkinsopp]: Okay. Maybe you would loose your words a little bit?

[Andrew Scarborough]: I would get pins and needles in my mouth and throat, and I would feel very dizzy, and faint. I have this horrible feeling like I’m going to collapse and have a tonic-clonic seizure. When I take the magnesium solution that I take three times a day, it actually reverses that aura, it is a potent preventative measure that I found to control seizure activity extremely effectively.

People with any kind of epilepsy, their levels of magnesium drop very low, and there are certain types of the day that magnesium is at its lowest, and typically that’s when seizure threshold is also at its lowest. If we can control that, we can control seizures very effectively. Also, on a ketogenic diet, supplemental magnesium — particularly magnesium chloride are found most effective.

It acts as a natural statin, it has a beneficial effect not only on cholesterol, in a natural way not like a typical statin where it’s actually destroying that process, it’s working with your body to do it naturally. I find that it also controls blood glucose — it regulates blood glucose very effectively too. I see it as my replacement for my medication that I was on previously, and the medication interestingly actually causes magnesium deficiency as well as calcium deficiency, deficiency in vitamin B-12 and vitamin D.

[Damien Blenkinsopp]: Which medication where you on?

[Andrew Scarborough]: I was on the maximum dose of Levetiracetam, which the brand name is Keppra and Sodium Valproate the brand name for that is, Epilim. I was both on those and the highest possible amount that you could be on. You can imagine the side effects of that, and the nutrient deficiencies that caused were just quite substantial.

When you’re withdrawing from those drugs you could actually get breakthrough seizures if you don’t address those nutritional deficiencies, and those seizures can actually cause SUDEP — it’s shorthand for sudden unexpected death in epilepsy. I was told consistently that I was highly likely to have that if I was to — not only come off my medication which is what I eventually did but reduced the medication. I have to reduce that medication for a period of almost two years.

I had to do it very slowly, and adding these nutrients and trace elements so that I was not having these breakthrough seizures that were life-threatening. It was a difficult balance, but I achieved it.

(54:50) [Damien Blenkinsopp]: It makes it easier when you titrate down slowly, but still you’ve been courageous in pushing for all of these things when you’re getting this pushback which is saying it’s really dangerous. Just in terms of the exercise, how do you bump your ketones up – is it the KetoForce?

[Andrew Scarborough]: Yeah. I consume that throughout my workout but I tend to mostly just do quite a light bodyweight exercise because I don’t want to stress my body too much. Thomas Seyfried himself recommends that cancer patients don’t push themselves too much with exercise, because it just puts too much stress on the body and on the brain. Mostly I just go for long walks, in an area with lots of oxygen, and I’m actually going to start having hyperbaric oxygen therapy fairly soon.

I’m in discussions with a number of facilities about that, and I’m going to start doing case studies on patients. I’m actually working part-time at the moment with Imperial College London in Charing Cross Hospital, to start-up clinical trials hopefully next year with brain cancer patients using — what I would call an optimal ketogenic diet.

We’re looking at magnesium for these brain cancer patients, we’re looking at the omega 3 and 6 ratios in the blood, we’re looking at C-reactive protein as a marker for a systemic inflammation, and we’re able to measure that for over a period of time to see how that changes while on a ketogenic diet.

[Damien Blenkinsopp]: With cancer is that typically high the hs-CRP because of the inflammation, or is that just a. . .

[Andrew Scarborough]: Yeah. It’s typically higher than normal, but one of the main ideas of measuring that is to have a marker that you can measure over time. I’m a huge fan of testing and I know that even if these things have no effect on cancer, they have an effect on epilepsy and blood glucose management.

We know that these are prognostic factors and they’re also effective at managing epilepsy which many brain cancer patients have as a result. I’m very keen to start doing this in patients more, and I’m working very hard to do that.

[Damien Blenkinsopp]: It’s very exciting that you’re able to work in hospitals. This is starting next year you said, potentially?

[Andrew Scarborough]: Yes. It would also be featured in, New Scientist magazine early next year. My story and my approach will be featured, and that’s very exciting as well because it’s getting the message out there and we can then have the actual data on humans which is missing. It would be — as I’ve said before it will be efficacious.

We’ll be able to not just translate the diets that have been used for children with epilepsy which I don’t believe …

[Damien Blenkinsopp]: As good, as they could be?

[Andrew Scarborough]: I don’t think that they’re translatable for brain cancer patients because I think it’s just very different. For example, when I was on the standard type of ketogenic diet, they did include those ingredients. I developed symptoms that were similar to Temporal Arteritis, where my temporal arteries became so inflamed that I nearly went blind and I was prescribed steroids for it.

But instead of taking the steroids what I did is I looked at how much omega 6 I was taking in my diet, and even though my blood glucose and ketones looked fantastic, and the ketogenic diet is anti-inflammatory in itself. I was having these inflammatory responses which were only controlled and reversed when I re-addressed the balance of omega 3 and 6 ratios. That in itself is quite powerful.

(59:15)[Damien Blenkinsopp]: Interesting. Where did your omega 6 ratio start? We read studies where the standard American diet, for example, is you can get ratios of 20:1, 10:1 — quite far off.

[Andrew Scarborough]: I’ve read up to 40:1.

[Damien Blenkinsopp]: Were you not so bad because you said you had a reasonable — you were trying to have a reasonably healthy diet before. I wouldn’t expect you’d have the sad numbers.

[Andrew Scarborough]: Yes, prior to initiation of the diet, I would say I was most likely about a 10:1 ratio. But, on the ketogenic diet, it was probably quite similar actually because it was including lots of nuts, coconut oil, coconut milk, coconut cream, lots of vegetables that were high in omega 6. I just thought it could be done better — then I transferred on to what I like to call a, fishogenic diet.

I was consuming a lot more fish, and I felt instantly much better and then as I cut down on the vegetables – cut them out completely. I had an instant response where I can’t even remember the last time I had a headache, even a mild headache.

(60:32)[Damien Blenkinsopp]: Great to hear. I’m conscious of your time I know that you’re really busy currently. But there’re a couple of things — I do want to make sure we cover before you go. We didn’t speak about glutamine and I know that an important part you mentioned up front that’s something you had to restrict quite sharply. But how did you do that practically?

[Andrew Scarborough]: Well, the first thing I did was limit protein quite significantly, and I did a number of therapeutic fasts, and it wasn’t until then that I actually saw the greatest response in my MRI scans, in terms of the complete remission. One of the other things that’s quite effective is with the magnesium it has an effect on that as well. I need to find the study for that, but I can send it to you if you’re interested in reading it.

Another thing that I’m actually looking into for the long term is Metformin, because Metformin on a ketogenic diet has quite a potent effect. It has a number of mechanisms which I can’t remember all of them off the top of my head, but that’s one thing that I’m playing around at the moment. It gets an effect on MAMP and a few other things.

It’s quite hard to explain, it’s quite technical.

[Damien Blenkinsopp]: In terms of the fast, you said that’s when you really started seeing the effects, so that would mirror — we had Thomas Seyfried on here and he was talking about the importance of the fast. How many days — was that a pure water fast? Was it a seven or five day fast?

[Andrew Scarborough]: It’s interesting because I think that — when these researchers are talking about fasting for brain cancer patients particularly if they have epilepsy, what they fail to note is that there’s ionic changes that are happening in the brain when you’re doing these fasts. A patient with epilepsy can’t — especially if they have brain cancer in my opinion shouldn’t just do water-only fast.

I think that they need to do what I call, a ’magnesium fast’. When I fast I have my magnesium water solution that I make up myself, and that prevents me from having breakthrough seizures while I’m fasting because I have such low body fat percentage. My longest fast has only been nine days. I aimed for 10 but I couldn’t do more, I’ve done that a few times but I need to have my magnesium-chloride solution or I instantly have breakthrough seizures, not the good kind either.

I found out the hard way initially, but now it’s just the easiest thing that I do.

[Damien Blenkinsopp]: You’re taking specifically magnesium chloride, is that because it’s a spray kind or is it actually the magnesium chloride specifically — there’s something about the chloride which is helping?

[Andrew Scarborough]: It has something to do with hydrochloric acid and how you digest it. I’d say it’s more bioavailable and it seems to me to be just in my personal experiences that it seems to get the brain very quickly. The literature doesn’t actually say that, but personally, I found that — even though there is not much in the literature about that.

[Damien Blenkinsopp]: Are you buying a specific brand? We’ve talked about using magnesium spray transdermally, but I’m just wondering if you’re using one of those sprays? How much you’re taking of it?

[Andrew Scarborough]: It’s designed to be primarily used transdermally this particular type, and I just get it from a health food shop, it’s mainly people who do sports who take it, which is interesting and funny. I typically take about five sprays three times a day. I can’t remember exactly how much that is, for 10 sprays it’s 150 milligrams of magnesium.

It’s variable depending on how mixed up the solution is — typically around 230 milligrams in a day that I would take. If you consider our water is too high in calcium and not high enough in magnesium. It’s addressing that imbalance that we have, we know that we should have at least a 2:1 ratio of magnesium to calcium, that addresses that imbalance.

We know that in the mornings after we wake up, magnesium levels are lowest. Primarily take it in the morning, after waking up in the afternoon, and before I go to bed.

[Damien Blenkinsopp]: Have you checked your RBC magnesium levels?

[Andrew Scarborough]: I haven’t because I don’t think it’s an accurate measure. I just go by how I feel, and sometimes — I see the epilepsy as a blessing because everything to do with epilepsy with brain cancer is typically very similar to what would work for treating the cancer. If something is working for the epilepsy, you’ve got a pretty good idea that it’s beneficial for the cancer, and most of the things that I actually research about what helps in terms of my epilepsy, experimentally and otherwise.

I found incidentally that it has quite potent anti-cancer benefits as well. It’s really interesting the relationship. It’s quite empowering as well. What I would call spectacular results because I still can’t believe I’m not having these horrific seizures all the time without medication. It’s quite empowering to know that it’s potentially having the same benefit on the cancer.

(1:06:44)[Damien Blenkinsopp]: Yes, it’s pretty amazing your journey. I don’t know if you’ve come into contact with other people with similar stories to tell — I know that some other people who had cancer, you said, unfortunately, they’ve passed away — the ones you were relating to. But if you come across any other people who have been experimenting like yourself.

[Andrew Scarborough]: Yeah. I actually have a group of friends now who I came into contact with just through seeking out long-term survivors, and I have a group of long-term survivor friends who had glioblastoma many years ago, and now have no sign of disease. I have a group of friends with various other cancers who are still here now. They’ve mostly done a drug cocktail treatment on themselves, which is very interesting.

Personally, I wanted to try and copy that drug cocktail treatment but do it in a natural way just using diet.

[Damien Blenkinsopp]: When you say drug cocktail, is that chemo or is that more Metformin and things like that?

[Andrew Scarborough]: It’s more Metformin and statins, and phosphates, and various other DCA, and other very interesting drugs. Personally, the only one I’m considering is Metformin, and potentially a few others, but mainly Metformin and Curcumin which I take in tablet form with DHA because they work synergistically. Curcumin actually increases uptake of DHA to the brain.

Because we know that around these tumors, or where the tumor was – DHA is very low. We know that if you have Curcumin and DHA that’s a powerful combination. Curcumin is cytotoxic to the cells. We know that DHA is, and is essential for brain functioning.

[Damien Blenkinsopp]: You really have built a whole lot of armory against this — it sounds like you’re doing really well. On the Curcumin – there’s many forms available on the market today, you’re taking one of the bioavailable forms…

[Andrew Scarborough]: Yeah, it has piperine in it as well.

[Damien Blenkinsopp]: Okay.

[Andrew Scarborough]: It’s a component of black pepper. I have a number of strategies that I use, and I’m constantly optimizing my metabolic formula.

(1:09:14)[Damien Blenkinsopp]: Do you feel constant improvement? I don’t know if there are any symptoms because it seems like you’ve got most of it under control. Do you think you’re going to be able to repair your body, do you feel any signs of that in terms of potentially resolving the epilepsy?

Do you think this is more likely something that you’re just going to optimize and maintain so that it never bothers you, so you never get the actual symptoms?

[Andrew Scarborough]: As my brain has been visibly healing at a very fast rate on these scans while I’ve been utilizing this protocol, I’ve also found my symptoms have improved with that quite substantially as well. I had facial paresthesia constantly all throughout the day, everyday, and a number of other debilitating symptoms I couldn’t even go out and walk a few steps. The fatigue was horrendous as well.

Being able to do what I am now and this non-stop activity, and just doing so many different things, and having my seizure activity controlled in such a great way that’s much better than before — even before when I was doing all these things I was still getting more activity. I haven’t actually done that many more things if I compare to even just a few months ago. Definitely improving in quite a dramatic way, despite having to keep up with all these things.

It’s getting easier to control, to the point where I have days now that I have no symptoms at all, but if I get overconfident and I forget to have my magnesium drink or do something that’s just out of my routine, I’d definitely have more seizure activity coming. Even though it’s not to the degree that I used to have.

[Damien Blenkinsopp]: I guess really say why you’re saying epilepsy is a bit of a bonus for you because it’s early warning detection system for you…

[Andrew Scarborough]: Yeah.

[Damien Blenkinsopp]: — Whereas cancers can creep up on you and you won’t know unless you’re watching the scans and even the scans aren’t showing a small progression. So right now you can still have a small amount of cancer left, but you can’t see it. It does seem like a pretty nice little tool, even though it’s not nice to have it, in the longer term it sounds like it’s a beneficial thing for you.

[Andrew Scarborough]: Yeah, I can see it as beneficial now, I couldn’t before but it definitely is.

(1:11:47) [Damien Blenkinsopp]: Well Andrew this has been an amazing — it’s very inspiring episode today. I can really say that — I’m totally going to take some of the things that you have been trying and start testing them out myself. I would like to ask you — where to look first if they would like to learn about this topic if they’re facing cancer or epilepsy?

Are there good books or presentations on the subject, the first places to go to, to start learning themselves about this?

[Andrew Scarborough]: I would thoroughly recommend the book, Cancer as a Metabolic Disease by Thomas Seyfried. I think that’s a great starting point. For anyone starting a ketogenic diet I would recommend, Keto Clarity, that’s a good resource to use. I would also go to www.ketogenic-diet-resource.com — that has answers to just about all the questions that you could have.

For help to a dietician, if you live in the UK I would recommend the charity, Matthew’s Friends. In the US, I would recommend the Charlie Foundation which is the sister organization of Matthew’s Friends in the UK. It has recently started to see — it’s mainly brain cancer patients that they see because they get around with that by saying that they’re treating the epilepsy.

I would also go on Clinicaltrials.gov to see what clinical trials are happening globally to do with the ketogenic diet and different cancers.

[Damien Blenkinsopp]: Right, so if they’ll just search for a ketogenic diet on there…

[Andrew Scarborough]: Yeah, if they search for ketogenic diet and cancer on Clinicaltrials.gov they can see all of the clinical trials that are currently happening in terms of ketogenic diets for different cancers. It’s very exciting that more and more of these are popping up, and I hope to — I have a meeting on Thursday to discuss having proper official ketogenic diets, using the right approach in this country, and that’s really exciting new development.

[Damien Blenkinsopp]: Is that with the government, NHS or some other body that’s going to help promote it.

[Andrew Scarborough]: This is in conjunction with brain tumor research, they’re one of the very few cancer charities that actually are going all at it with this metabolic research, and they’re doing that with Imperial College London. It’s a small charity that’s doing this, it’s quite incredible what they are able to do being such a small organization.

[Damien Blenkinsopp]: It’s great they’re starting to be – some grounds building from the bottom and up.

[Andrew Scarborough]: Yeah, and I’m going to start-up my own individual research with a few of my lecturers at my university because I want to get these things happening much faster than if it’s going through clinical trial protocol. I want to do this myself with lower grade gliomas, so that we can see a long-term response to try and shrink these tumors hopefully, because they are not as aggressive, but, they still are incurable.

I want to see what effect that we can have on them rather than having to go through all the standard treatment to go through clinical trials. I think that’s very exciting going forward.

(1:15:25) [Damien Blenkinsopp]: That sounds really exciting, and I’m sure anyone who – maybe affected would be very interested to know more. What are the best ways for people to connect with you and learn about you, and keep up with you when you’re doing these things, they can stay up to date on them. Are you on Twitter, you mentioned you had a YouTube channel?

[Andrew Scarborough]: Yeah, my Twitter name is @ascarbs, and I’m on Facebook if people want to add me on there, Andrew Scarborough. I also am working on a website at the moment which is www.metabolictherapy.co.uk, and that has a holding page at the moment, but it should be live shortly. I have a YouTube channel, Andrew Scarborough, and I have a blog, My Brain Cancer Story that’s the title of it.

People search for Andrew Scarborough and My Brain Cancer Story, they should find it.

[Damien Blenkinsopp]: Excellent. We’ll put all those links on the show notes of course also, make sure all of that is there. Is there anyone besides yourself you’d recommend to learn more about the stuff that you mentioned, Thomas Seyfried, is there anyone else that people should look to?

[Andrew Scarborough]: I would look at the research by Dominic D’Agostino, also I would recommend Dr. Colin Champ, I’ve had various discussions with him online which are very interesting. He’s very interested in my approach and he is very unique, he’s a radiation oncologist who is very supportive of this metabolic treatment. Very similar to my oncologist who – it’s quite a rare thing to find – but it’s very encouraging.

There’s Dr. Adrienne Scheck, who I’m having a meeting with on Thursday she’s coming overseas from the Barrow Neurological Institute in the US, and she’s the one that does the rodent studies using the ketogenic diet. It’s great to be able to discuss with her.

(1:17:29) [Damien Blenkinsopp]: Great, great, thank you for those. Some quick items on your – just a personal approach on what you would advise people to get started with – are you still tracking any biomarkers, on a routine basis?

[Andrew Scarborough]: Only occasionally with MRI spectroscopy but we’ve stopped doing that now just because it looks a bit boring and nothing’s really changing. It all looks really good, that’s why we’re not monitoring it anymore.

[Damien Blenkinsopp]: So maybe once in every six months or once a year?

[Andrew Scarborough]: Yeah, just to keep an eye on it, but everything that you would expect to be elevated but would be a bad thing isn’t showing up – it sounds like a good thing. It’s very new research, we don’t know too much about it, but it’s very promising for the future.

Because if we can see these things before they show on the scan, in terms of enhancement or just showing in an obvious way then it’s – that can only be good for the patient really. Then we can intervene in a non-toxic way.

[Damien Blenkinsopp]: So if you were to recommend one experiment, basically you’ve done many experiments to get to this point – they’re not proven recommendations by doctors and so on. What would you recommend that someone with brain cancer or potential other cancer – what would be the first thing they should try, the biggest payoff from all of the things that you’ve mentioned, what should their first step be?

[Andrew Scarborough]: The first step should definitely be reducing carbohydrate intake. The second step would be reducing protein intake to maintenance levels, and therapeutic fasts are very important. But the main thing, I would say is the omega 3 to 6 ratio, I believe that they should be an omega 3 to 6 index, just like with the glucose-ketone index, and they should work together, as a synergistic therapy.

Because you could even argue the ratio of omega 3 to 6 is even more important than the ketones. I would also say, the magnesium is very important with that too, those three things. Therapeutic ketosis, the omega 3 to 6 ratio and the magnesium I would say are very important for brain cancer patients.

[Damien Blenkinsopp]: Great, thank you, that’s some great takeaways for people at home. Andrew, I’ve got to say this has been really amazing interview – it’s amazing all of the different avenues you’ve run-down and all of these different aspects that you found to improve your situation. I know it’s going to be an inspiring story for the audience.

Thank you very much for being on the show.

[Andrew Scarborough]: No problem, we did cover a lot but we got there in the end.

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Part 3 in our series of Fasting Self-Experiments. In this longer 10 day water fast I tracked results with a broad set of biomarkers (ketones, glucose, weight, hormones and cognitive performance panels).

This is a long post – if that scares you, jump directly to what you’re looking for:

  1. Why Do a 10 Day Water Fast? (The health benefits that we’re optimizing for)
  2. 10 Day Water Fast Results (Weight, metabolism, cognitive performance, hormones)
  3. 10 Day Water Fast Experience (Anecdotal thoughts, symptoms, and my post-fast rookie mistake)
  4. The Tracking (Details on all the biomarkers tracked and lab tests used)
  5. Tools & Tactics (Details on the exact fasting protocol I used, and some supplements taken)

Video Recorded on Day 10 of Fast Just Before Refeed

Note: I was yet to realize the post-fast rookie mistake I was making!

I’ve been fasting once per month for 5 days since my first water fast experiment in June 2015. If you are new to fasting, you can get all the why and how basic details in that post.

The results from my 5 day fast cycles have been so positive that I couldn’t help but wonder if More is Better when it comes to fasting.

This led me to ask:

“Will I benefit from a 10 day fast programmed into my life once per quarter or twice per year?”

To get an answer to that I broke that down into the following questions I was going to try to answer with this first 10 day fast:

  1. Can I remain productive during a 10 day fast?
    (10 days is a big chunk of time to strike off from work and life – far too big for my taste! Let’s be sure I’m not throwing away the equivalent of 40 productive days a year with this habit)

    • Would my mental performance suffer? Perhaps leading subtly to worse decisions, or perhaps just slower thinking?
    • Would my energy levels remain the same or decrease? Would there be a change in how many hours I could comfortably work per day?
    • How about concentration, focus and drive?
  2. Is “10 day fasting” every quarter sustainable? Specifically, where I’m doing monthly cycles of 5 day fasts in between?
    • Would I double the weight loss of a 5 day fast? And thus make it difficult to recover the weight within the following month? (The question here: Does weight loss follow a linear path based on number of days fasted?)
    • Would a 10 day water fast be as easy, psychologically and physiologically, as the 5 day water fasts? Or would I hate it? (Nothing we hate is going to get done repeatedly)
    • Is there any downside impact on “adrenal health” or cortisol regulation from fasting? (this is a question I’ve been attempting to answer since I started long duration fasting)

itunes quantified body

To try to answer these questions I tracked cognitive performance, hormones, metabolism and weight throughout the fast.

I also committed to following a normal rhythm of life and work during the fast this time. I would run life as usual, and let the chips fall where they may – I would see if the fast got in the way.

(Note: Please do not take this as advice to do this at home yourself – I’m not a doctor, and would be extremely upset if you hurt yourself – please be cautious with fasting.)

The outcome we’ll get to in the results in a second, but but first “the Why”…

Why Do a 10 Day Fast?

We’ve covered the benefits and whys of fasting well in previous episodes, however, as a quick reminder here’s the list:

  • Anti-Cancer: Leveraging the metabolic theory of cancer and Dr. Thomas Seyfried’s work, fasting may be an effective tactic to reduce our future risk of cancer.
  • Immune System Effectiveness: Cyclic fasting has been shown to regenerate immune system cells which deteriorate ‘naturally’ as we age or via environmental or other insults. Thus, it may reduce or stave off some of this natural deterioration and keep us healthier.
  • A Stronger Body: Lean body mass gains including bone density increase and muscle mass increase have also been tracked in studies and myself.
  • Body Fat Removal: Fasting or cycles of fasting can be a useful tactic for removing unwanted excess body fat.

The 10 Day Water Fast Results

Metabolism on 10 Day Fast Looks Similar to 5 Day Fast

In 5 day fasts I consistently see glucose drop to between 50 and 60 mg/dL and ketones rise to between 5 and 7 mmol/L. In the additional 5 days it seems you shouldn’t expect any big change. My numbers came back largely the same.

My ‘switch time’ from glucose to ketone metabolism continues to edge forward to happen slightly earlier with each fast I do. This time just past the 48 hour mark the switch took place – my blood ketones jumped up and glucose dropped down to their fasting equilibrium levels. My metabolism had switched to ketone burning.

10 day waterfast ketones glucose
A few interesting points:

  • There was a slight glucose upwards blip on days 6 and 7 where it rose back up to between 60 and 70 mg/dL. This was most likely caused by the sleep disruption I experienced from day 5 (see sleep details). Low quality sleep tends to impair glucose regulation – thus higher (but still low) glucose.
  • On day 7 and 9 I got several “HI” errors for my ketone readings, meaning that my ketones were over 8 mmol/L, the upper limit of the ketone meter’s range.
  • For the first 3 days post fast, days 10 to 13, my ketones were still spiking high in the evenings and quite erratic – this was most likely an anomaly this time around due to my Post-Fast Rookie Mistake.

Despite the glucose uptick on day 5, I stayed well within the therapeutic range to provide anti-cancer benefits outlined by Dr Thomas Seyfried (see explanation via my interview with him in Episode 16).

So long as you remain under a Glucose Ketone Index of 1, you are assumed to be within the therapeutic range as per chart below where I’m shown to have had a complete 8 days of therapeutic anti-cancer action.
10 day water fast glucose ketone index

Weight Loss: How Much & How Long to Gain it Back?

Over the 10 days I lost a total of 5kg (ll lbs) of weight. The weight loss was at a consistent daily rate as usual, except for Days 8 and 9 where it stalled at a weight loss plateau, before a further drop on the morning of the last day.

I regained all the lost weight by the 18th day after the end of the fast – and this was despite some digestion re-startup issues for the first 3 days post fast (see the post-fast rookie mistake for the details). So the weight was really recovered via 15 days of normal eating.

Weight Loss 10 Day Water Fast

Testosterone on a Fast: Big Drop & Libido Changes

It makes sense that you shouldn’t expect to be on top of your ‘libido’ game while fasting. When food is scarce we should have evolutionarily had more important things on our mind – like finding food to survive.

This was certainly part of my experience. The longer the fast, the less interest I had in women or sex. By day 5 my testosterone levels (DUTCH Test – see in labs) had dropped below the 20 to 40 year old male reference range.

A couple of studies I found corroborated this with testosterone dropping significantly during fasts (and then rebounding strongly with refeeding)1,2.

The Takeaway: NOT a good idea to fast on honeymoons or dates. The day after ending the fast – great idea.

Testosterone: 10 day fast

Is it OK to Fast with Adrenal Fatigue?

In previous fasting episodes I’ve noted that I’m working on “low free cortisol” levels that I’ve been tracking for a couple of years. A situation that I expect, based on symptoms I now understand dates back to as much as 10 years ago.

One of my concerns with repeated fasting (considered a stressor) was that it may not necessarily help with this situation – when you look at it through the lens of “Adrenal Fatigue”.

Specifically, I was referring to the idea that Low Free Cortisol = “Adrenal Fatigue”. Thus adding more stress could exacerbate the issue, reasoning that the adrenal glands are already overstretched in a normal everyday scenario without that added stressor.

In this fast I learned that there’s less reason for concern than I’d initially considered. You need a bit of background to understand why.

Historically, people from the functional medicine realm have referred to “adrenal fatigue” as a state of fatigue of the adrenal glands, whereby you typically have low energy in the afternoons. This can happen to me at times. It is documented and diagnosed via 4-point free cortisol salivary tests like the one from Biohealth that I’ve done previously (See the results from previous adrenal labs in this episode).

However that name doesn’t have a very accurate definition or explanation. The term is used quite vaguely for the most part. We can’t scan an adrenal gland and see it in a withered state for example. We don’t have a specific test that can show the state of ‘adrenal gland fatigue’ that ties it back to the adrenal gland itself.

So a new term that is surfacing for the situation of low free cortisol is “cortisol dysregulation” as a result. It provides at least a ‘less wrong’ definition. Cortisol isn’t normal, it’s lower than it should be – and thus is driving some fatigue symptoms. It’s dysregulated. Another term you may have heard is HPA Axis dysregulation.

The DUTCH test I used to track my hormones is useful where it comes to investigating and better understanding cortisol metabolism as it looks at both free and metabolized cortisol. Metabolized cortisol is a proxy for total cortisol output. The traditional salivary tests used look only at free cortisol levels. Thus, DUTCH enables you to assess whether your total levels of cortisol are low (the adrenal output is lower, or if it’s just free cortisol that is low, and total cortisol is normal).

As you can see below my total cortisol (metabolized cortisol) is right in the middle of the normal reference range.

Metabolized Cortisol Levels (Baseline and Fasted)

10 Day Fast Total Cortisol (Metabolized Cortisol)

So in my case, it turns out that I have above average metabolized cortisol levels – so in fact total cortisol output is well within the normal range. It’s just my free cortisol levels that continue to come back below the reference range (now cross-checked with two labs, DUTCH test + Biohealth #201).

I don’t have reduced adrenal output, I have normal adrenal output – which would fit the old definition “adrenal fatigue”.

That’s good news.

Nonetheless, the low free cortisol has to be troubleshot. The most likely explanation behind this is that I’ve been subjected to a long term stressor and my body has compensated to lower free cortisol levels. That maps to other information – that underlying stress, is most likely high ongoing inflammation levels that I have documented over several years now.

24 Hour Free Cortisol Levels (Baseline and Fasted)

10 day fast 24hr free cortisol

The Takeaway: Rather than just relying on propping up my adrenals with adaptogens, it’s pretty clear that the end game is to continue to explore and resolve all causes of stress. Inflammation is my obvious first target, although it’s another reminder to keep up my lifestyle stress management practices (adaptogens, meditation, circadian rhythm and sleep).

Note: For those who like to dig into the data – here’s an explanation of the cortisol results from the DUTCH test.

Did Mental Performance Keep Up During the Fast?

Although I’ve always “felt productive” when fasting, I wasn’t as sure that my mental performance was the same. This time round I planned to try to capture this information properly. Unfortunately the results weren’t very clear.

I used Quantified Mind, the tool we covered in Episode 33 to track my cognitive performance in terms of Working Memory and Attention Control.

The main issue I was advised to eliminate by Yoni Donner, founder of Quantified Mind was the practice effect. As we perform any mental test repeatedly we get better – to understand if a fast was impacting me cognitively, I needed to try to eliminate that. To do this I used the same test repeatedly during the few months before the fast, due to travel this wasn’t as consistent as I would have liked. The idea is that eventually you peak out, and any practice based improvements will have dried up or be minimal.

10 Day Fast Mental Performance

As you can see in the data above it looks like there were some pretty strong practice effects taking place throughout and after the fast. The fasting period is shaded out in blue.

As a result, I’ll be continuing to use the same test panel in future fasts, and in between, to see if I can separate these out. With continued repetition I should be able to isolate any fasting effects.

The 10-Day Fast Experience

With repeated cycles of fasting I have become a lot more comfortable with “how it feels” – both body and mind do feel different on the water fast – the first experience I was cautious due to this – not knowing if I had new limitations that I shouldn’t cross.

Now that I have got used to fasting, I basically run life as usual. I don’t restrict my activity level or my schedule, or need to plan for it. In this fast of course I committed to making this a goal in itself to understand if fasting limits me.

As a result, during the 10 day fast, I was out meeting friends, business contacts – and even went on a date to an art exhibition.

Nonetheless there are things to note…

Physical Weakness

I experienced less of the feeling of physical weakness than in previous fasts – a heaviness or lack of refined motor control of the arms and legs.

I tested this a bit further on day 2 with one set of 55 push ups (my current 1 set max). This didn’t feel much different to doing it in a non-fasted state.

During this fast as I was going about my days I had times when I actually felt ‘physically strong’ and was naturally walking around at a rapid pace. This was more so on the last 5 days of the fast, so that difference may simply be related to the fast being longer. In many ways the last 10 days were more physically comfortable than the first 5 days.

Sleep – My Next Challenge

On most of my fasts the biggest downside is sleep disruption. After a few days on the fast I tend to start to have interrupted sleep.

This fast was no exception. From day 5 I began to get night wakings as early as a couple of hours after going to sleep. After some of these I wouldn’t be able to get back to sleep for hours. The exception was the last night – on day 10 – I had perfect sleep, longer duration, and deeper than usual judging by the drowsy feeling combined with how refreshed I felt in the morning.

Sleep disruption and night wakings are shown to impair glucose metabolism. So it’s the likely cause of the slight rise in glucose I experienced on day 5 and 6 also.

For future fasts I’ll be making sleep a priority to investigate, track and optimize.

The Mind Retreat

The mental experience of fasting for 10 days allowed me to appreciate more clearly aspects that I’d noticed in shorter fasts. Fasting promotes a less rushed, more practical and more bigger picture thinking state of mind for me.

The contrast of this with the typical more frenetic ‘getting things done’ focus of life is very attractive. In my mind it presents a great counter balance to keep your decisions in check once a month. It enables you to look at life, work from this other perspective once per month (if you’re doing the cyclic fasting) and that strikes me as a good thing for decision making.

This was far more noticeable on the 10 day fast. Some of this may be related to the drop in testosterone (and libido!) I tracked.

The Post-Fast Rookie Mistake

If you’re thinking of undertaking a 10 day water fast yourself. This is possibly the most important section – pay attention – I made the mistake and paid for it.

For 3 days after the fast I suffered from gut and toilet problems. Severe pain the first night to discomfort and the inability to keep anything actually inside me for the 3 following days.

It was a simple mistake. I assumed that what works post-fast for 5 days, should be okay for 10 days despite having spoken with people having done 10 or more day fasts that advised caution.

The biggest difference between the 5 and 10 day fast is how you start to refeed. I prepare and eat a couple of bowls of bone broth after my 5 day fasts without issue. I’ve found it to be a great high micronutrient way to ease back into eating.

However, with the 10 day fast, this turned out to be a disaster. My body simply was not able to deal with high levels of fat found in bone broth. My appetite didn’t return as a result either, so I was having to push myself to squeeze in small meals. After 3 days of failing to get my digestion back to normality with a variety of food combinations I thought would work (vegetable soup, scrambled eggs, etc) I had to rethink my strategy.

I resorted to drinking exclusively blended green vegetable smoothies.

The turnaround was amazing. All my digestion issues disappeared literally with the first couple of glasses, and my digestion issues were completely resolved within the next 24 hours. I kept that program up for a few more days nonetheless, to make sure I was past the issues.

So my strong recommendation to anyone trying this – and myself for future long duration fasts – will be to start with exclusively vegetable smoothies for the first 24 hours as a minimum (better 48 hours). That should lay the digestive foundation to be able to move back to your usual eating patterns.

Symptoms – The Back Rash

I’ve experienced some slight rashes during fasts before. With this longer fast it was a lot more extreme.

By day 10 my whole back was covered with a rash of spots – just the back. It was quite stunning – it made me think back to the time I caught chicken pox.

This rash disappeared just as quick within a couple of few days of refeeding it was completely gone again.

The Takeaways

So coming back to the questions we want to answer:

  1. Can I remain productive during a 10 day fast?
    • Would my mental performance suffer? Perhaps leading subtly to worse decisions, or perhaps just slower thinking?
      Answer: It’s not clear as yet. It doesn’t look like there was any drastic mental performance impact on working memory or attention control. Future testing will need to be done with future fasts to further validate
    • Would my energy levels remain the same or decrease? Would there be a change in how many hours I could comfortably work per day?
      Answer: There was no noticeable big change in energy levels or hours worked during the fast. If anything I felt a little more wired, and thus had to reduce my intake of caffeine.
    • How about concentration, focus and drive?
      Answer: Testosterone is often associated with these attributes in men. Low testosterone tends to reduce these attributes, however while my testosterone dropped during the fast, that’s not something I experienced. In a future 10 day fast I’ll track testosterone on the last day (day 10) to see if the hormonal impact is greater than the mid fast impact (day 5).
  2. Is “10 day fasting” every quarter sustainable? Specifically, where I’m doing monthly cycles of 5 day fasts in between?
    • Would I double the weight loss of a 5 day fast? And thus make it difficult to recover the weight within the following month?
      Answer: Weight loss wasn’t exactly linear – there was a leveling off at one point so weight loss per day was slightly less than with that I’ve experienced with the 5 day fast. The weight was easily regained within 15 days – so there doesn’t look to be an issue with not being able to maintain my equilibrium weight when I introduce 10 day fasts every quarter in between the monthly cyclic 5 day fasts.
    • Would a 10 day water fast be as easy, psychologically and physiologically, as the 5 day water fasts? Or would I hate it?
      Answer: If anything the 10 day fast was easier and got easier as I got into it. This could be due to my growing experience with fasting – “practice effects”, or that fasts do get easier the longer you’re on them. I think it’s probably a bit of both of these.
    • Is there any downside impact on “adrenal health” or cortisol regulation from fasting? (this is a question I’ve been attempting to answer since I started long duration fasting)
      Answer: My total cortisol and 24hr free cortisol were slightly lower on day 5 of the fast compared with baseline. Despite having done many fasts my 24hr free cortisol levels have not dropped from the original values I tracked a year previously – they’re stable. My total cortisol is also well within normal output ranges. So my inclination is to say no. I’d like to check in a future 10 day fast the cortisol metabolism on day 10 to see if there is a ‘declining slide’ in cortisol output over longer duration fasts.

Episode Question: Are you convinced about the rewards of water fasting to try it yourself yet? If not, what else would you need to know to get you there? Let me know in the comments.

Tracking

Biomarkers

  • Blood Ketones (Beta-Hydroxybutyrate / β-hydroxybutyrate): Blood ketones are the gold standard for measuring your state of ketosis. During the fast, ketones are expected to peak in the range of between 6 and 8 mmol/L. Dominic D’Agostino mentions that metabolic acidosis with values over 5 mmol/L place an additional burden of processing on your body, so in non fasting states keeping values between 1 and 5 mmol/L may be optimum.
  • Blood Glucose (mg/dl): A measure of the level of glucose in the blood at one point in time. Values of between 50mg/dL and 60mg/dL are standard for fasts. Non-fasting values should be below 80mg/dL ideally, and at least 92mg/dL.
  • Glucose-Ketone Index (GKI): The ratio between the concentration of glucose in the blood to ketone bodies in the blood. The calculation is Glucose (mmol)/ Ketone (mmol). Dr. Seyfried created the index as a better way to assess metabolic status. Therapeutic efficacy is considered best with index values approaching 1.0 or below. Patients with chronic disease like cancer have consistent index values of 50 or more.
  • Weight (lbs): Standard scales measurement of weight in morning without clothes (to avoid biases).

Lab Tests, Devices and Apps

  • Blood Ketone/ Glucose Monitors: The Precision Xtra in the U.S. or Freestyle Optium Neo in the UK are the current recommended monitors. You’ll need lancets, ketone strips and glucose strips also.
  • DUTCH (Dried Urine Test for Comprehensive Hormones): This advanced hormone test panel from Precision Analytical is currently the most comprehensive and convenient test looking at cortisol metabolism and sex hormones. I used it to track baseline and fasting hormones. You can download my complete lab test results here: Baseline test results / Day 5 of fast test results.
  • Quantified Mind: The free online tool used to track cognitive performance during the fast – you can learn more about using the tool in this episode with its creator Yoni Donner. I used two short tests Yoni recommended to use for a mental performance check-in requiring a minimum of time (~5 minutes):
    • Color Word Inhibition: A test that measures attention control via the stroop effect.
    • Self-Paced 2-Back: A version of the N-Back game used to assess working memory.
  • Muse Calm: Mentioned as one of the better return on effort items discovered through the Quantified Body’s exploration so far. Interview with the founder, Ariel Garten, in previous episode here.

Tools & Tactics

Fasting Protocols

  • Water Fast: “Water fasts” are the standard fast protocol used in most of the research studies, including those looking at cancer inhibition or therapy for cancer patients. People are more or less extreme with the definition of what a water fast consists of. I personally am looking for the ‘biological effects’ or results. I’m not concerned with sticking to purely water unless that’s what is required to gain those results. So my version in this fast includes some supplement support which should not interfere with the beneficial fasting mechanisms – see below in Supplements for details.
    • 5 Day Water Fast: A minimum of 3 days is required to flip most people’s metabolic switch between glucose and ketone metabolism, and attain the benefits of the fast. For this reason a good place to start with water fasting is 5 days, which incorporates 2 days of therapy time (i.e. after the 3 day lead time to switch the metabolism). You can see this effect taking place in my first 5-day water fast self-experiment. The 5 day fast is also manageable on a cyclic monthly basis: 25 days of normal life, and 5 days of fasting per month.
    • 10 Day Water Fast: To provide a deeper dose of therapy (i.e. 7 days) people are extending their fasting times to 10 days, or beyond. As per my interview with Dr. Thomas Seyfried this may be more effective with respect to the anti-cancer effects. Depending on your risk profile, this may be something you consider doing from time to time.
  • Fast Mimicking Diet (FMD): A diet designed by researcher Valter Longo to maximize activation of the beneficial fasting mechanisms while still allowing you to eat to an extent. The details of this type of fast were covered in my FMD self-experiment in episode 31.

Supplements

My goal with this fast was to support my body without interfering with the beneficial fasting mechanisms, and to stay productive throughout (work wise and socially). So this is actually what I did:

  1. Mineral supports: This was the main supplementation I took covering a broad spectrum of minerals.
    • Real Salt: I sprinkled real salt into the filtered water I was drinking throughout the fast.
    • Quinton Hypertonic: A seawater electrolytes solution with a broad spectrum of minerals.
    • Pure Encapsulations Minerals 650: Capsules containing a broad spectrum of minerals.
    • (Both of the above recommended to me by Chris Shade from this episode)

    • Ancient Minerals Magnesium Spray: Typically I apply this to my skin daily after showers for absorption via that route. However, I’ve also started to spray it into my drinking water along with the Real Salt, and continued this during the fast (Note: Spraying the oil in drinking water was a tip from Andrew Scarborough in an upcoming interview – Episode 44).
  2. Drinks: Besides water I also consumed some other drinks during the fast, primarily for productivity purposes. My usual routine is to have a coffee in the morning, with the obvious caffeine jolt – so I kept to that usual routine, just keeping it to simple no calorie versions.
    • Black Coffee: For the first 5 days I took a black coffee in the morning, however I typically found that I naturally didn’t finish it. As the first continued I increasingly felt the caffeine from this single coffee was too much of a stimulant, the effect seemed to be magnified. So half way through I switched to…
    • Teas: Mostly Green Tea, also some Rooibos and Camomile tea. I found the green tea didn’t over-stimulate as much although I was still maxed out on 1 or 2 cups. More than that and I got the jitters.

Personal Note: Background on Using Minerals in Fast

There was another, more personal, reason I included a good amount of mineral supplementation during the fast. Since the episode with Chris Shade I’ve been following his mercury and heavy metals removal protocol.

Part of that protocol requires that you take a break from time to time to halt the process and remineralize the body since a side effect of the protocol is removing needed minerals along with the heavy metals.

I wasn’t going to be following the Shade protocol during the 10 day water fast (I stop all other experiments and protocols while fasting), so it made sense for efficiency to use that time for remineralization.

Other People, Books & Resources

People

  • Dr. Thomas Seyfried: See episode 16 for a discussion of his theories and work.
  • Dominic D’Agostino: Dominic has led some of the research into the benefits of ketone bodies and metabolic therapies, he is now turning much of his research effort towards cancer similarly to Thomas Seyfried.
  • Chris Kresser: Damien first learned about the benefits of the DUTCH test at Chris’ recent seminar in London.

References:

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Heart disease affects 50% of the U.S. population in their lifetime. Learn how to accurately quantify your personal heart disease status and risk, and if necessary, take clear actions to reduce that risk by eliminating plaque in the arteries.

This episode presents an in depth look at heart disease because this is one of the most likely things to shorten our lifespan. We focus on the key topic of quantifying your real heart disease risk.

One in three deaths in the United States are caused by cardiovascular disease. Even worse, one of out two Americans will suffer some form of heart issues, meaning that one half of the population is at risk. The total costs for dealing with heart disease are larger than any other disease by far, estimated at 650 billion dollars in the US.

While heart disease is a big risk which is worthwhile taking a look at, it is not a big risk for everyone. For some people there are other health risks they should look at and assess. Thus it is important to know if heart disease is something you personally need to act on – in a proactive way which reduces the risk for it. Are there specific factors you need to be concerned about?

The way to approach this issue is by quantifying our risk for cardiovascular disease. Naturally, understanding of risk goes beyond the typical cholesterol numbers. We discussed some of the problems with cholesterol biomarkers in Episode Seven with Jimmy Moore which is a useful preamble to this episode. In this show we go deeper into details, looking at metrics which give you a real accurate view of your heart disease status and risk.

There is a way to be very accurate, both [by] blood work and by imaging. To really nail down your personal risk of experiencing the number one killer in the Western world, heart disease.

– Dr. Joel Kahn


DrJoelKahnNew
Dr. Joel Kahn
University Professor & Heart Prevention Doctor

Joel Kahn has focused his career on preempting cardiovascular and heart disease. His goal is to reduce risks as well as to avoid surgery and cholesterol – lowering drugs. He takes a proactive approach by using information and interventions to ensure that heart disease does not become a problem in patients.

He is a clinical professor of medicine at Wayne State University School of Medicine, and Director of Cardiac Wellness, Michigan Healthcare Professionals P.C. He is a Summa Cum Laude graduate of the University of Michigan School of Medicine and author of two books, The Whole Heart Solution and Dead Execs Don’t Get Bonuses: The Ultimate Guide to Survive Your Career With a Healthy Heart.

Joel has also recently set up the Kahn Center for Cardiac Longevity. In their institution they emphasize early imaging of arteries and extensive laboratory evaluation for the correctable root causes of heart disease. So Joel and his clinic have a very quantified and longevity focused approach to this whole area, which is great to see.

I think this is an episode everyone should listen to, because absolutely everyone is going to have to deal with these issues in their life. Inevitably everyone comes into contact with heart disease, whether it be through themselves, their family, or their friends.


The episode highlights, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. I’d love to hear what you think of the episode – and if it has helped you – let me know in the comments!

itunes quantified body

What You’ll Learn

  • What led Dr. Kahn to choose a career in cardiology (4:30) .
  • A holistic view of the true causes behind developing heart disease (6:17) .
  • The causes behind heart attacks and strokes are tightly related and how both conditions are preventable (9:05).
  • How the condition of the endothelium (inner wall of blood vessels) and mitochondria affect cardiac health (10:26).
  • The biomarkers Dr. Kahn uses in his practice and ways to personalize medical and lifestyle advice (15:08).
  • Infrared Sauna treatment is proven to have positive effects on cardiovascular disease treatment (23:27).
  • Using chelation in treating disease to lower toxins levels – including heavy metals (26:03).
  • Early detection of coronary artery plaque using a CAT-scan for coronary artery calcium (30:47).
  • Because CAT scans are radioactive an ultrasound-based carotid IMT test is used for following disease progression (37:09).
  • How to get informed and decide whether to get a coronary calcium test (39:24).
  • Understanding genetic testing results in conjunction with imaging of arteries (41:04).
  • The Liposcience NMR technology platform offers the most accurate measurement of LDL cholesterol particle density (43:35).
  • Familial genetics and lifestyle when tracking lipoprotein levels as a biomarker for cardiovascular disease risk (44:07).
  • Using C- Reactive Protein (CRP) as a biomarker for cardiovascular disease risk (46:36).
  • Measuring blood vessels inflammation as part of a comprehensive heart health assessment (48:04).
  • Diet recommendations for preventing heart disease and examples of successful programs (50:00).
  • Replacing dairy products with healthy hydration is beneficial but strict ketogenic diets exhibit negative health effects by causing adrenal stress (54:19).
  • Why dark coffee is generally a health drink and the caveats to consider when consuming coffee (59:00).
  • Scientific and medical practice sources for discovering topics in this episode (1:01:32).
  • The biomarkers Dr. Joel Kahn tracks on a routine basis to monitor and improve his health, longevity and performance (1:03:50).

Thank Dr. Joel Kahn on Twitter for this interview.
Click Here to let him know you enjoyed the show!

 Dr. Joel Kahn & The Kahn Center for Cardiac Longevity

Books by Dr. Kahn

Tools & Tactics

Interventions

  • Far Infrared Sauna: Sauna treatment improves heart health, especially in patients who have suffered heart attacks or have blocked arteries. As Dr. Kahn claims, repeated treatment consisting of 15 minutes infra-red sauna followed by 30 min rest helps the body sweat-out toxins and improves cardiovascular system function (See study looking at use of infrared sauna therapy for heart patients).
  • Chelation: Chelation therapy has been scientifically proven to rid the body of excess of toxic metals and is approved by the FDA for this purpose. This published study summarizes the findings of the US National Institute of Health clinical trial – specifically on using intravenous EDTA chelation therapy for coronary heart disease. We covered chelation and removing metals in greater depth in past episodes: episode 13 with Chris Shade (Mercury) and episode 19 with Garry Gordon.

Supplementation

  • EDTA: EthyleneDiamineTetraacetic Acid is the main chelating supplement discussed in this episode, and which is supported by the studies, in particular to chelate lead.
  • Niacin: Also known as vitamin B3 – is an essential human micronutrient. Supplemental niacin is primarily used to treat high cholesterol. Dr. Kahn claims that niacin is particularly good at lowering lipoprotein(a) levels – a proven risk factor for cardiovascular disease.
  • Proline / Lysine: Dr. Kahn claims that intake of these amino acids may prevent the damage that lipoprotein(a) otherwise imposes on the cardiovascular system.
  • Coenzyme Q10 (CoQ10): Helps support healthy mitochondria in cells. In turn, this maintains a robust cardiovascular system. Dr. Kahn encourages most of his patients to take this supplement.
  • Vitamin CLiposomal Vitamin C: Proponents of the Pauling Therapy from Linus Pauling argue that heart disease can be treated, and even cured, by substantially increasing Vitamin C intake.

Diet & Nutrition

  • Nitric Oxide (NO) Supporting Foods (Watermelon, Hemp Seeds, Pine Nuts etc.): Nitric Oxide (NO) is synthesized by the inner walls of blood vessels – known as the endothelium. It prevents arteries from constricting or spasming. NO prevents heart attacks in both an immediate and a long term time frame. Dr. Kahn suggests foods which support NO synthesis including watermelon, hemp seeds and pine nuts.
  • Coffee: As a drink, coffee is a rich source of beneficial antioxidants. However, it’s positive effects may depend in part on what type of caffeine metabolizer you are. If you metabolize caffeine slowly then you have a tendency to feel jittery or racing heart and there is some evidence that it may be less heart healthy than for fast metabolizers of caffeine. However, overall caffeine is considered a health food in most studies, and Dr. Kahn recommends 1 cup of black coffee per day to his heart patients.
  • Tea: The intake of tea is also an advisable health practice including green tea, herbal tea, hibiscus tea, or chamomile tea before bed – which is a source of sleep support.
  • Vegetarian / Vegan Diets: A vegetarian diet excludes meat by focusing on plants for food, but may include animal products such as milk and eggs. In addition to excluding all meat products, a vegan diet also excludes all animal products. Dr. Kahn argues that in world areas where people live the longest, and with the greatest freedom from heart disease, the populations are not completely vegan.
  • Paleo: This diet is based on the foods that paleolithic humans might likely have eaten. It includes meat, nuts, and berries, and excludes relatively – recently developed food products including animal products such as milk. Dr. Kahn described his view that there is a lack of scientific evidence to support this diet for cardiac health.
  • Ketogenic: A ketogenic diet is a diet that induces a state of ketosis in the body where the body uses ketones instead of glucose for fuel. Typically this involves a diet with low carb and low to moderate protein intake with high fat intake. Previously, we discussed measuring ketones and ketogenic dieting in Episode 7 with Jimmy Moore.

Tracking

Biomarkers

Cholesterol Based

  • High – Density Lipoprotein (HDL): The traditional measure of ‘good cholesterol’ used by doctors and healthcare. Levels above 60 mg/dL are considered protective of cardiovascular disease. Dr. Kahn stresses the importance of checking your cholesterol, even at around the age 18 or 20.
  • Low Density Lipoprotein (LDL): The traditional measure of ‘bad cholesterol’ – the type which causes heart disease. Less than 100 mg/dL is considered an optimal level, while levels between 160-189 mg/dL increase the risk for cardiovascular disease. Research has shown that LDL alone is not the best predictor for cardiovascular risk. Actually, LDL particles with the smallest sizes are most damaging to the cardiovascular system. Dr. Kahn puts more emphasis on using the LDL particle number and LDL particle size metrics.
  • Lipoprotein(a): Lipoprotein molecules carry cholesterol and similar substances through the blood. A test can be done to measure a specific type of lipoprotein called lipoprotein-a. Higher levels of this marker are associated with risk of artery damage. Dr. Kahn states that in most labs normal reference ranges for lipoprotein(a) should be under 30 mg/dL.

Blood Sugar Regulation Markers

  • Fasting Glucose Levels: A biomarker used to understand blood sugar regulation. Optimum levels are between 70 and 90 mg/dL. Higher levels indicate some level of blood sugar dysregulation, which increases risk for diabetes II.
  • Hemoglobin A1C: A form of hemoglobin which is measured to identify the average plasma glucose concentration over prolonged periods. Higher levels of hemoglobin (A1C) indicate poorer control of blood glucose levels. In turn, these are associated with diabetes and cardiovascular disease risk. Normal levels are less than 5.7%, pre-diabetes levels range between 5.7 to 6.4%, while higher than 6.4% is indicative of diabetes.

Inflammation Markers

  • High Sensitivity C-Reactive Protein (hs-CRP): Elevated hs-CRP levels indicate inflammation which is damaging to inner artery walls. If your level is below 1 mg/L then you do not have a cardiovascular disease risk. Because of the proven clinical use of this biomarker, Dr. Kahn claims it is high time for cardiovascular patients to start measuring hs-CRP.
  • Homocysteine: Elevated homocysteine blood levels indicate blood vessel inflammation and higher risk for coronary artery disease. This marker has previously been discussed in episode 5 with Ben Lynch and in episode 29 with Dr. Nicolson.
  • Lipoprotein-associated phospholipase A2 (Lp-PLA2): This biomarker gives insight into inflammation of blood vessel walls and is useful as part of a comprehensive assessment. The PLAC test measures the activity of ALp-PLA2 (an enzyme) in a patient’s blood. Individuals with test results showing Lp-PLA2 activity greater than 225 nmol/min/mL are at increased risk for cardiovascular disease.

Other

  • Ferritin: Serum ferritin acts as a buffer against iron deficiency and iron overload. Levels are measured in medical laboratories as part of the workup for detecting iron-deficiency anemia. The ferritin levels measured usually have a direct correlation with the total amount of iron stored in the body. Female normal reference range is 12-150 ng/mL and for males it is 12-300 ng/mL.
  • Myeloperoxidase: A very sensitive biomarker for predicting myocardial infarction in patients with chest pain. It shows added predictive value compared to measuring hs-CRP alone.
  • Vitamin D: A vitamin which is essential for bone development and maturation and prevents osteoporosis. The Vitamin D Council suggests an optimum level of 50 ng/mL. The 25-hydroxy Vitamin D Blood Test is the most accurate way to measure how much vitamin D is bioavailable to be used by your body.
  • Free Testosterone: A steroid sex hormone. Physiological effects include muscle growth, increased bone density, and development of male sex characteristics. Free Testosterone is a small portion of this hormone which is bioavailable, because it remains unbound by carrier proteins in the bloodstream. Free testosterone reference ranges for females are 1.0-8.5 pg/mL and 50 – 210.3 pg/mL for males.
  • Estradiol: This is the primary female sex hormone. For females, the levels of this hormone vary greatly because of its key role in regulating menstrual cycles. In the normal reproductive cycle, estradiol levels measure typically <50 pg/ml at menstruation, rise with follicular development (peak: 200 pg/ml), drop briefly at ovulation, and rise again during the luteal phase for a second peak. At the end of the luteal phase, estradiol levels drop to menstrual levels unless there is a pregnancy. The reference range for healthy adult males is 14-55 pg/mL.

Lab Tests, Devices and Apps

  • Coronary Artery Calcium Score (CASC) Test: This test is a type of CAT scan which determines whether your arteries contain clotting plagues by quantifying calcium presence. By measuring calcium scores, the extent of blocking can be determined. This test lasts very short (under a minute), does not require injections, and is not claustrophobic. CASC tests have been shown to predict mortality.
  • Carotid Intima-Media Thickness (IMT) TestThis test measures the thickness of the walls of your arteries and helps determine whether you have a higher risk for cardiovascular disease. Individuals with unwanted CASC Test scores should undergo IMT ultrasound as a follow up for disease progression or risk. This is because the CASC test is based on a x-ray CAT scan, as opposed to the harmless ultrasound waves used in the IMT test.
  • WellnessFX Cardio Lipoprotein Profile: This test panel includes a number of lab tests, including the comprehensive analysis of lipoprotein particle numbers and sizes. It uses the accurate direct-measurement laboratory method (NMR (Nuclear Magentic Resonance) lipoprofile). Individuals with patterns of higher counts of smaller particles have a more concerning lipoprotein profile than those with less particles with greater size.
  • Life Extension Company Blood Testing: Joel mentioned LEF as one of the organizations that provides direct to consumer blood testing that he trusts.
  • Caffeine Metabolism Genetics: Whether you metabolize caffeine more rapidly or slowly depends on the presence of a Single Nucleotide Polymorphism (SNP) genetic variation in the liver enzyme responsible for metabolizing caffeine. The company 23andMe offers a genetic test for identifying slow metabolizes who may be at increased risk for cardiac attack due to coffee consumption.
  • Toxin Concentrations: These can be measured using blood or urine tests available in specialized labs. We’ve covered this subject extensively in previous episodes – see episode 13 with Chris Shade (Mercury), episode 19 with Garry Gordon (Lead) and episode 23 with Kara Fitzgerald (other metals and chemicals).

Other People, Books & Resources

People

  • Dr. David Katz: Founding director of Yale University’s Yale-Griffin Prevention Research Center and current President of the American College of Lifestyle Medicine.
  • Tim Russert and James Gandolfini: Both men were prominent individuals in American culture, whose lives were shortened by sudden unexpected cardiac attacks.
  • Linus Pauling: An American biochemist, author, and educator as well as one of only four individuals to have won the Nobel Prize twice. During the 1990s Pauling put forward a plan for the treatment of heart disease using vitamin C.
  • Stormie Jones: Was the world’s first recipient of a successful simultaneous heart and liver organ transplant at the age of sixShe suffered from an inherited genetic condition named Heterozygous Familial Hyperlipidemia which made her liver unable to remove cholesterol from her bloodstream. In turn, this was also causing her serious heart problems.
  • Nathan Pritikin: An American inventor, nutritionist and longevity researcher. His program features the Pritikin Diet which is focused on a variety of whole (unprocessed) or minimally processed foods.
  • Dr. Dean Ornish:  A cardiologist and the founder of the non-profit Preventive Medicine Research Institute. He coaches patients towards a vegetarian diet but not a strict vegan diet. His program is defined in four specific elements of lifestyle. It is the first scientifically proven program to “undo” (reverse) heart disease by optimizing stress, diet, physical activity, and social support.
  • Dr. Caldwell Esselstyn: His proposed diet for cardiac health is strictly vegan with under 10 percent of calories coming from fats. His program for patients includes walking, meditation, stress management, yoga, and other lifestyle choices to decrease cardiovascular disease burden.
  • Dr. Neal Barnard An associate professor of medicine at the George Washington University School of Medicine. He has led numerous research studies investigating the effects of diet on diabetes, body weight, and chronic pain.
  • Dr. Garth Davis: Among the leading researchers in the field of bariatric medicine – a branch which deals with the causes, prevention, and treatment of obesity.
  • Dr. William Davis: A cardiologist and author of the Wheat Belly blog.
  • Dr. David Perlmutter: A Board-Certified Neurologist and Fellow of the American College of Nutrition.
  • Dr. Alessio Fasano: An Italian researcher who sees pediatric and adult patients in the Center for Celiac Research and Treatment at the Massachusetts General Hospital. He is carrying out important research on the health impact of eating grains.

Organizations

Books and Video

Full Interview Transcript

Click Here to Read Transcript

[04:30][Damien Blenkinsopp]: Joel, thank you so much for coming on the show.

[Joel Kahn]: My complete pleasure.

[Damien Blenkinsopp]: So, I’d like to start with a quick story about how you became a cardiologist; why did you get into, specifically, holistic cardiology?

[Joel Kahn]: Sure.

I knew really from a very young age that I wanted to be a cardiologist. I actually had a very small issue as a young child with a tiny hole in my heart. It healed, but I had the pleasure of seeing a very fine heart doctor until I was about 18 years old.

It had a very good impression on me; [there were] a few scary moments being in a big hospital as a little kid, but overall it was actually very positive. And kind of pursued a fast tract to making this my career. I’ve been doing it now for almost 26 years after training.

Holistic? I just always felt people are more than a pill. Doctors are wonderful people, nurses are wonderful people; I don’t have a chip on any shoulder. But I was exposed to some really good people. I got very involved in nutrition, nutrition lead to Mind Body, nutrition lead to Standard and Alternative Fitness, nutrition lead to supplements, Yoga, meditations.

So I just poured my heart and soul into studying and learning, and expanding my tool box for patients. And then I said, I’m going to start writing about it, because I don’t know if [they] are practicing it. So it’s all been a wonderful journey that’s far from over.

[Damien Blenkinsopp]: I didn’t realize you’d had that heart issue. Is it completely resolved now?

[Joel Kahn]: Yeah. Yeah. It’s very common, a little worrisome to the parents — god bless my mother and father. But it’s another example of if you don’t get in the way of things, the body can often heal itself. And this was a relatively minor thing, so good for that.

[Damien Blenkinsopp]: Great to hear. And it gave you the motivation to get started in all of this. It’s kind of funny who life always does that; it kind of steers us in the direction we end up going.

[06:17] I was wondering, because you’ve been looking at this holistically — and a lot of people focus on the heart, cholesterol, and things like this — could you explain what a formula to get heart disease would be, in terms of a holistic view? Because when you read through your book, it gives you a much more global view of how heart disease comes about than we’re typically used to.

[Joel Kahn]: Yes. And you know, we don’t want to throw away the basics. In essence, there’s two ways to approach this.

Our government, the United States government, has been publishing for a while, every 10 years, major causes of death. And unfortunately heart disease is at the top of that list, every list, every 10 years. But that’s not really the true causes, and starting in 1993 some very open-minded researchers said, “Let’s talk about the true causes.”

And the true causes for 80 to 85 percent of premature deaths were three activities: smoking, poor fitness, and poor diet. And those true causes dwarfed everything else. And it always dwarfed genetics. It’s a lifestyle world, baby, in terms of developing or preventing heart disease.

So, heart disease develops because we smoke too much; fortunately, under 20 percent of the population, and it used to be 40 to 50, so major inroads, it’s falling. Heart disease develops because we don’t move enough, and we’ve gone from farming and active community 150 years ago to everything being tech based, and we’re blessed with all of that. But we are paying a price.

And we now have to use, I have an app on my phone that reminds me to stand 5 minutes every hour. So we’ve come full circle, where technology was the problem and now technology will provide solutions. And desks that go up and down so you can stand at work and such.

And then heart disease develops because of the change in our diet since the Golden Arches hit California in the 50s, and all that’s followed with giant companies and processed food, and our crazy lifestyle where we don’t have time to make meals from whole foods anymore. Those are the big three by far.

A good friend at Yale, head of Preventative Medicine Dr. David Katz says, “Forks, fingers, feet.” Fork, what you do with it will determine your life; fingers what you do in terms of smoking, and feet whether you move and exercise that body. And really that accounts for the majority of it.

Sleep, stress, and love would be the other three. Adequate sleep, managing stress, and including yourself in a community to be surrounded by loving, like-minded people would round out the top six. And that’s a pretty holistic view, but it’s not very difficult, and it’s not very sophisticated.

[Damien Blenkinsopp]: Yeah, great, thank you very much for that.

[09:05] And I think when we think about heart diseases we often think about heart attacks, but is stroke related to heart disease as well? Is that one of the outcomes from the same kind of mechanism?

[Joel Kahn]: Yes. Stroke is a little bit more diffuse or widespread in terms of trying to nail down the cause. The number one listed cause of death in the United States is heart disease, such as heart attack. And number three is stroke, with cancer between the two. Therefore, if you lump heart disease and stroke, cardiovascular disease is the number one cause of death in every segment of the population over age 30, men and women.

But stroke has a shared cause to heart attacks; that is you can get clogged arteries from the lifestyle measures, and in part genetics that I just ran through. But there are other causes of stroke: bleeding disorders, heart rhythm disorders.

So the data is you can prevent about 80-90 percent of heart attacks through adopting a healthy lifestyle that’s neither expensive nor difficult, just rarely done. And you probably can prevent about 60 percent of strokes. It’s not as high because the cause is more commonly something other than atherosclerosis, or hardening of the arteries.

[Damien Blenkinsopp]: Great, thank you for that. Yeah, because I wasn’t really aware that they were so tightly related and preventable as well.

[10:26] In terms of stressors and some of the other mechanisms, could you talk a bit about the actual mechanisms behind heart disease? How this takes place? Without getting, obviously, into crazy detail, because it can get pretty detailed.

But in your book you talk about a variety of factors that we don’t often think about, such as mitochondria, and the gut, and other areas. And we don’t think about those leading to heart disease. So could you give us some kind of overview to show us how these mechanics are working to create a condition.

[Joel Kahn]: Well certainly, and one term that readers and listeners may not be familiar with but is important to grasp is something called your endothelium. And that is, essentially, inside every artery in your body — miles and miles of arteries carrying blood to your brain, your pelvis, your heart, your organs, your toes — is a one cell layer thin lining, like wallpaper on a wall.

And until about the 1980s we thought it was simply just a cell barrier between blood on the inside and the structure of the wall on the outside. But now we know that the endothelium makes many chemicals, the most important of which, or perhaps the most crucial, is nitric oxide, a little simple gas that in a healthy artery is created in abundance.

Arteries making nitric oxide because of a health endothelium will resist the clotting of blood; you want the clotting of blood when you cut your finger, you don’t want the clotting of blood when you’re on the verge of a heart attack. The nitric oxide will prevent; arteries from constricting, or spasming, which again can trigger a heart attack; the Raynaud’s blue-white-red fingers some people struggle with in the cold; leg pain on walking; and also the actual plaque, the actual build up of debris in arteries is resisted by a healthy endothelium with healthy production of nitric oxide.

So, that’s one physiology, and the good news is things that we would associate with a healthy lifestyle –eating a lot of produce, fresh fruits and vegetables, exercising your body, adequate sleep, good blood pressure, good blood sugar, good cholesterol numbers from a healthy lifestyle — are all associated with a healthy endothelium. And if you have a sick endothelium, you can make it healthier though a healthy lifestyle.

All of these things resoundingly shown scientifically. For example, eating watermelon, [it’s] very rich in chemicals that support nitric oxide. Hemp seed [is] very rich in chemicals that support nitric oxide. Other seeds and nuts similarly: pine nuts.

The other one [is] as you mentioned; inside every cell are little organelles, or little structures inside our cells. We have trillions of cells —- brain, heart, muscle, everywhere — and their powerhouse to generate function is called your mitochondria. We don’t think about them, we don’t give our mitochondria a kind of shout-out, we don’t wake up in the morning and say, “Thank you mitochondria for taking care of me while I slept seven and a half hours.”

But indeed, aging is a stress on our mitochondria where they won’t function to make energy so well. And unfortunately we now know not only bad lifestyle, which is way too common — sedentary lifestyle, food-based poor lifestyle, smoking poor lifestyle — but environmental toxins clearly affect our mitochondria: pesticides, herbicides. There’s data that genetically modified products and the herbicide roundup affects our mitochondria. Nutritional deficiency like low magnesium from not eating enough produce affects your mitochondria.

And our cells will age quicker and won’t function as well, and may produce fatigue, may produce congestive heart failure, shortness of breath. But again [it is] an area of science that is very hopeful, because lifestyle can cause our mitochondria to be much more efficient, and, probably most strongly, exercise. The actual number and health of your mitochondria in your muscles goes up when you exercise. You actually, you can be in your 40s and 50s and you can create more mitochondria by regularly exercising to a fairly vigorous degree for a while.

So yeah, those are concepts that I think are important to share. And there’s ways to boost the function of both our endothelium and our mitochondria, both by lifestyle, and not — I’m a fan of selected supplements. The supplement Co-enzymeQ10, CoQ10, which is more commonly used in Europe than the United States, helps support healthy mitochondria and [it’s] something I encourage most of my patients to be on.

[15:08][Damien Blenkinsopp]: Great. So, on this show we talk about a lot of biomarkers, and I know you have preferences for different biomarkers from the standard.

Could you, first of all, walk us through some of the very typical. I mean, when most people go to their doctor they are given the standard cholesterol markers. So could you talk through the LDL, the HDL, the total cholesterol, and if you use those, and how useful you find them.

[Joel Kahn]: First step, and I always like basics, is get your cholesterol checked, even at around age 18 or 20. Because one out of every 400 people may have an inherited disorder called Heterozygous Familial Hyperlipidemia, or FH, and you may be 18 years old with a cholesterol 450.

One out of every 400 is not all that rare. In a typical high school in this state that might be six kids. And it’s better to know it at age 18 or 17 than to find out in an emergency room at age 45 with a heart problem.

But in my practice, I do advanced cholesterol lab values. There’s a variety of different ways. For example I can see two people with a cholesterol of 220 and the LDL cholesterol of 120, and they may be at very different risk for artery damage because we can break down the size of their LDL, the number of particles in their LDL. Usually it’s a technology called NMR spectroscopy, but it’s become a very low cost lab that’s much more accurate.

So I can have two people and I can speak to them differently; that’s called personalized medicine. And say, “Nancy, your LDL is actually very favorable. You don’t have much. They’re large particles, and I think we can leave you alone and continue your good lifestyle. And Joe, your LDL of 120 is constructed largely of small, dense particles, and you’ve got way too many of them. And we’ve got to really kick that lifestyle in gear, and your nutrition in gear, and we’ve got to get that belly a little thinner.”

You know, it can help me define a more guided approach. But when we’re talking population, a standard finger prick or church-based or work-based cholesterol is a good starting point.

[Damien Blenkinsopp]: Right. It’s just a screen to see if it’s worth digging further. So basically, if LDL comes up high, you’d be like, okay I’ll look at the particle number and size to see if this is a problem.

[Joel Kahn]: It can. Yes, that’s one of the things we can do to refine if, everybody needs encouragement about lifestyle, but if they need beyond that consideration of medication or more intense lifestyle.

[Damien Blenkinsopp]: Great. So is it possible for someone to have a high LDL number, which is over the standard reference range, and it not be a problem because the size of their particles is large and small number of particles, basically?

[Joel Kahn]: Yeah. We broke up a little, but cholesterol is associated with developing heart disease. And it is causative, there’s no doubt. I mean, I reflect back when I was in cardiology training in Dallas, Texas.

I took care of a little girl, 11 years old, who was known around the world, Stormie Jones was her name, sweet girl. And she was born with a genetic disorder where she had both genes defective, that was called Homozygous FH. It’s very rare, it’s about one person in a million. But that little girl had had a heart attack, a bypass, a balloon, by the age of 12. And to argue that cholesterol doesn’t have a direct role in damaging arteries has many pieces of science behind it, animal and human, but I always reflect back on Stormie Jones.

So cholesterol is important, but there’s so much variability in human physiology. So when I’m dealing with one person, I try to find if their arteries are healthy or not. There are ways to determine if there’s any early plaque, if there’s any early endothelial damage.

And if I see somebody with a fairly high cholesterol at age 60, for example, but they have no evidence of plaque, no evidence of endothelial damage I’d have a very hard case to put them on a prescription drug, in my mind, because there must be other factors that are protecting them. And yes, they may have an additional 30 or 40 years to worry about, but I’m really going to stress to that person lifestyle — healthy diet, exercise, weight management, blood pressure management — and not necessarily write a prescription drug.

And, you know, there’s always the opposite too. There are people that have had a heart attack, or a bypass, and relatively moderate risk factors, and then we really have to go on a search. We have to go on a search for other biomarkers, like something called Homocystine, lipoprotien(a), Ferritin.

There’s a lot of people that are prediabetic that fall through the cracks, and are suffering artery damage from their prediabetes, but it’s really not been offered as a diagnosis, and that’s kind of a very common one, for example.

[Damien Blenkinsopp]: Right. With the Homocystine, for example, are you looking for the causes? Or are you trying to look a bit further back?

So if you get some high cholesterol numbers and some particle numbers that are indicative, is homocystine more indicative of a cause, so you can refine your prescription, the treatment you recommend? Or is that just a basic filter for your assessment?

[Joel Kahn]: No, I think the ultimate joy is trying to get back to the root cause. And the root cause, certainly the majority of it, is lifestyle. And we’ve talked about that, food choices, which I’ll go over carefully with patients: processed versus unprocessed, high in saturated fat versus low, high in added sugar versus low. [And also] body movement, body fitness, body exercise, adequate sleep, methods of managing stress.

For example, it’s been shown that meditation can have a significant effect on lowering your cholesterol. Kind of pieces of scientific data that are published that aren’t talked about much. When you’re stressed out your cortisol level goes up, your blood sugar goes up, your blood cholesterol goes up, your blood pressure goes up. And a practice of breathing or yoga or meditation can fairly dramatically lower blood cholesterol.

So then getting at the root cause, now the question is after those basics, which need to be addressed every visit, over and over — sleep, stress, nutrition, fitness — do we go further? We do know that there are environmental toxins, and we do know that heavy metals we’re exposed to through cosmetics, through industrial exposure, through dental fillings. We often carry a burden of mercury and lead and cadmium.

Smokers not only are ingesting all kinds of toxic carcinogens, but the ground in Virginia is said to be quite rich in cadmium, which is fine if you have it in the battery that’s powering your radio but you don’t really want cadmium in your blood stream in your body. So you can use blood analysis, hair analysis — take a little snip of hair — or urine analysis and determine if a person has greatly elevated levels of some of the pesticides, herbicides, pollutants like heavy metals.

And sometimes the course directed at identifying and removing those can really restore a person’s health to a much higher level. It’s a slow process because you accumulate those things slowly, and any plan to exit them by avoiding; if it’s an industrial exposure taking more care or changing jobs, don’t walk on your lawn the day that they spray the pesticides or look for more natural organic way to treat your lawn. Consider whether your mercury in your mouth might be a problem or not, you can get tested for that, for example. All those things.

But then there are strategies to remove some of these toxins. And of course considering eating organic versus non-organic to lower our input of pesticides. These are all strategies; and then there are more advanced strategies.

I’m a big fan based on some very fascinating and rich scientific data of the health benefits of sauna on our overall health, and specifically our heart health. And the amount of data that supports it is surprisingly rich, but very rarely taught in the annuls of medicine, of course.

[23:37][Damien Blenkinsopp]: Is that any type of sauna, or is that the infra-red version?

[Joel Kahn]: Well the infra-red is the hottest and most widely mentioned, because in Japan, starting about 20 years ago, heart patients have been treated, heart patients who’ve had a heart attack, heart patients who’ve had blocked arteries or even the very serious problem called congestive heart failure, have been treated with 15 minutes of infra-red sauna followed by 30 minutes of rest and it has been shown that they can enjoy dramatic improvements in health.

And these are all actually published studies; scientific journals, some of them involving up to about 200 patients, which is getting to be respectable size for a research project at all. So that’s infra-red sauna, which is a special kind of deeply penetrating heated dry sauna; not that common in this country at this point. People can consider buying one for their home for under $1000 up to a few thousand, or finding a spa that might have an infra-red sauna, which is growing interest in this country.

But recently, as you may be aware, out of thin [24:50 unclear] came a large research study with 2000 people that were asked how often do you get in a sauna, how long do you sit in a sauna, and all that tracked with actually survival and heart health. And the number of days a week that people used sauna, and the number of minutes per sessions were kind of linearly related to overall health, which was large, and shocking, and made the news. And that’s a slightly different form of sauna. It was dry sauna but not infra-red.

So I think there’s much hope in perusing that. And the theory is that it may have something to do with detoxification. There’s no doubt that the sweat that is generated in such a thing as infra-red sauna is rich in heavy metals, richer than your urine or richer than your blood. You’re actually exiting these toxins from your body in your sweat.

So I’m a big fan of that. Then you can get into other approaches, so called oral chelation, juicing, using green vegetables like broccoli, sprouts, oregano, parsley and other greens to accelerate the exit of some of these toxins from your body in a fairly easy and natural way.

[26:03][Damien Blenkinsopp]: So it sounds like heavy metals in particular sound like something that you think they are quite relevant and important to heart risk issues.

Did you see, I believe there’s some studies with EDTA and heart disease more specifically and the impacts on it with some of the plaque and things on it. Am I correct in that, have you seen those studies?

[Joel Kahn]: Yeah. I was not a fan of recommending chelation. And so let me just take a step back, because not everybody is going to be familiar with chelation.

But because of industrial exposures to heavy metals in the 40s and the 50s — for example a worker exposed to arsenic in an explosion, or lead — there was an interest in trying to treat those acute toxicities. And various medicines like EDTA have been shown in those kinds of exposures to be quite helpful. And they’re, in fact, approved by the FDA for use in these industrial exposures to heavy metals: heavy lead, cadmium, mercury and such.

But in the process of some of those treatments, there were reports that people with heart disease were describing that they were having less symptoms. And some sharp clinicians were observing this and started to specifically treat some people with clogged arteries of their heart and their legs with chelation. And that, to this day in the United States, is not an FDA approved treatment; you won’t get paid for it, and in your charting you could be subject to some exposure for saying that’s why you’re treating them. Using i.v. EDTA for the reversal of atherosclerosis as opposed to heavy metal toxicity.

So, all of that was kind of subject to derision from the standard medical community, including myself. If you would have asked me four years ago, can we talk about the science behind chelation — I know there’s people that say they feel better, but do we have much science? You would have been very hard put.

So again, very forward thinking people about 10 years ago approached the National Institute of Health and said we need to resolve this; is this witchcraft, is this good care, and let’s do a study. And surprisingly the United States government came up with about 30 million dollars and designed a trial using kind of standard i.v. chelation protocols in, ultimately, 700 people that had survived a heart attack — that’s what was required to be entered in — and they were supposed to show up for about 40 weeks.

Some of them got EDTA based intravenous infusions, some of them got some vitamins, but there was no EDTA in there. And at the end of that study, which took a little longer to complete than hoped, was a little bit more difficult to recruit patients, but the overall trend of the study favored an improvement in outcome, like the combination of being alive, freedom from a heart attack, freedom from needing a bypass and hospitalization in those that got the active chelation.

And specifically two groups, if any of those 1700 people were diabetic or any of those 1700 people had actually experienced a fairly large heart attack in the background in their history, they had a dramatic improvement. It was a 40 percent reduced chance of having a bad outcome. And if you had a pill that within about four to five years reduced those bad events by 40 percent, you’d have a blockbuster new pill.

So chelation looked good, actually, and the combination of i.v. chelation plus potent multivitamins — because that was another aspect of the trial, it’s called the TACT trial, Trial to Assess Chelation Therapy — that the combination of i.v. chelation once a week and potent twice a day multivitamins had the biggest impact. But that was announced, I think it was around November 2012, so more than two years ago.

And there’s really been no movement since to seek out reimbursement, or FDA approval. Most doctors clearly are not set about to offer intravenous therapy. There’s a very small chance of harm. You can lower blood calcium levels because it’s going to chelate minerals, and calcium is one of those so very often the mixture has to have some nutrients and mineral support in it. But I have referred patients to colleagues of mine in the area that are experienced and certified in chelation.

[Damien Blenkinsopp]: Great, great, thank you for that, because the connection is appreciated by a lot of us.

[30:47] So I wanted to look at some of the, because I know you recommend some more accurate tests. For someone who really wants to know for sure their heart disease risk and where it’s at, if the status of their plaques, what do you use to accurately and directly see what the picture is looking like?

[Joel Kahn]: Yeah, well thank you for asking that question, because that’s really my passion. My passion is to teach people that there is a way to be very accurate, both by their blood work — and we talked about that — and by imaging, which we’re going to talk about right now. To really nail down your personal risk of experiencing the number one killer in the Western world, heart disease which can come on suddenly, without warning, and the next day there’s a funeral tragically leaving spouses and children and parents wondering how did nobody pick up that there was a burden of disease.

I’ll just give you a quick example. Sadly a friend of mine lost her husband, who was a prominent businessman in my town, who was a very fit person [who] ate healthy, looked good, wasn’t overweight, enjoyed athletics, and a little over two years ago went out for a bike ride on vacation and never came back. And was found at the side of the road and shown by autopsy to have a 99 percent blocked Widow-maker artery. And that shouldn’t happen.

My passion is to say, that’s tragic and we need to circle around that family with a lot of love, but let’s not let the next family and the next family and the next family, you know the Tim Russerts and James Gandolfini from Sopranos and such. We just had a bank president in my town, about three or four weeks ago, who experienced the same tragic end to his life, a man I’m sure was getting good medical care, absolutely.

So, there is the most accurate way right now to [if] you’re 45, 50, 55 years old, you’re concerned that this this number one killer in America could be creeping up inside silently; And you should be concerned, particularly if you’re overweight or sedentary, or [have] blood pressure, cholesterol, blood sugar issues, smoked in the past, [have a] brother, sister, mom, dad with heart disease.

There’s a CAT scan that takes 10 seconds, 20 seconds. You lie down, you’re pushed into a tube, a CAT scanner. It’s not around your head, it’s not claustrophobic. No i.v., no injection of medication. The CAT scan is done, you go home, you get a report. It’s called a coronary artery calcium scan, or coronary artery calcium score, CACS.

You can see the three heart arteries on the CAT scan without any injection of contrast material. Your arteries should contain no calcium; calcium should be in your bones and your teeth. If your heart arteries have calcium, your heart arteries have plaque. And you’re going to have that way before you ever need to have your bypass, your stint, or your heart attack therapy. So you can find out.

And there’s a number associated with it. If your score comes back zero, you have youthful arteries that are free of calcium, and your 10 to 15 year risk of a heart event are extremely low. Keep living healthy, but you can take a sigh of relief.

And if your arteries are prematurely calcified, you’ve got plaque. You may not be 80 percent blocked, you’re probably not going to need a stint or a bypass, but you need to see somebody about it. So that number could be 20, or 100, or 200.

I get people that show up, I saw one yesterday, totally good looking guy 61 years decent lifestyle, his calcium score was 1,100, mainly in the one artery we call the widow-maker. That’s a ton of burden of abnormal artery that we need to deal with by identifying why, and we’ve talked about some of that search.

He had already had a stress test that was normal, so he doesn’t need an angiogram, stint, or bypass, but now he needs a cardiologist who cares about lifestyle and all of the things we’ve talked about. We talked about yesterday about sauna, and heavy metal assessment, and advanced lipid blood work, and a daily aspirin. He’s a heart patient now, so I plead with people now.

[Damien Blenkinsopp]: Right. Yeah, I guess in that situation you would kind of throw everything at it, because it does sound like you were pointing out the worst case scenario, the worst score you’re likely to see.

Would you kind of throw everything at that case? Should he be really worried, and say, “Whoa, I’ve got to really change my lifestyle. Heavy metal chelation, everything I can.”

[Joel Kahn]: Yeah, that person needs to become a good student of the disease, reading my book, reading a book by Dr. Dean Ornish, a book by Dr. Caldwell Esselstyn. Many many good resources: Dr. Neal Barnard, Dr. David Katz. There’s plenty of good resources online for free, or books, or watch the DVD Forks Over Knives. I mean, many good resources, and I encourage my patients to do all of that.

But we ordered up a pretty in-depth analysis, and we’ll sit down in a few weeks and design a personalized plan. Now on the other hand, I see people all the time, they’re carrying extra weight, their cholesterol is 250, their diet isn’t exactly what I’d called in-line with nutritional goals, and their calcium score is zero at age 65. They’ve gone through six decades of life and are identifying no calcified plaque in their arteries, and their risk is very low.

And I don’t want them going to fast food places and eating their french fries, but I can cut back a bit on their medical treatment and focus on lifestyle with a great sense of joy and relief. And I see that a lot; a brother died at age 44 and the sister is zero and is going to smile for the next few years that she isn’t also carrying a burden of life-threatening plaque.

The oddity about the test is in the United States it’s not covered by insurance in about 48 states; 10 years ago places were charging 700 or 800 dollars. It’s very easy now to find that test under 150 dollars, sometimes under 100 dollars, which makes it very reachable for most people.

[Damien Blenkinsopp]: Is it quite widely available, like a lot of hospitals have these machines?

[Joel Kahn]: It’s just a standard CAT scanner, you do have to have special software to calculate that score, but it’d be very surprising if [in] most medium or large towns at least one of the hospital systems, or all of them, don’t offer it.

[37:09][Damien Blenkinsopp]: Okay. As it’s a CAT scan, is this something you shouldn’t do to often because of the radiation? With your patients, if someone’s got a score of 1000 or above, I guess you’re tracking progress over time to make sure it’s not increasing and you’re reversing some of that damage. But are you concerned at all about radiation, and do you do anything about it?

[Joel Kahn]: Well it’s an excellent question. I am a bit hesitant to repeat the CAT scan to follow their disease for two reasons: every time you do it it is some additional radiation, and number two there is not much data that you can drive that calcium out of the artery.

For example, the TACT trial, the chelation trial didn’t, unfortunately, assess calcium score. It would have been nice if we actually knew. So I don’t know the natural history. I know the natural history tends to go up if you do nothing; there are some studies that your calcium score may go up 30 percent a year. So if your score is 100 this year, it may be 130 next year. That’s just an average; it’ll be less for some, more for some. But I’m not so sure what I’d do with a repeat calcium score, because I fear they all go up.

There is an alternative test, called a Carotid IMT, intima-media thickness. This is an ultrasound. So ultrasound, of course, is no radiation; ultrasound can be repeated. And there’s about 700 medical studies on the value of having a special ultrasound machine with special software, that measures the thickness of the wall of your carotid artery.

And that is something you can track every year, every six months, compared to databases that have thousands of people age matched and sex matched, to make sure your arteries aren’t rapidly getting thicker and more plaque ridden. And hopefully actually seeing some improvement. So, if I have somebody with a bad calcium score, I’m probably going to use an ultrasound technique to follow them so I don’t need to keep exposing them to radiation.

That’s kind of a high level approach, but we’ve got the disease that’s the number one killer in America. So we’re throwing all kinds of high pollutant, expensive technology at other issues, it’s about time and way overdue that we try and prevent a million heart attacks in the next couple of years in this country so families don’t get ripped apart.

[39:24][Damien Blenkinsopp]: Who would you recommend takes the calcium scoring test?

[Joel Kahn]: Thank you for asking that. Not people who know they have heart disease. So if you’ve had a stint, a bypass, if you’ve had a previous angiogram that showed you’ve got 40 percent blockages, you already know you have a problem and you need to be working on it with somebody that can direct you.

However, it would be somebody aged 40 to 45 and up who has risk factors; brother, sister, mom, dad with early heart disease; high blood sugar; high blood pressure; smoker. Or maybe around age 50 to 55 just because you’re halfway through life and you’ve got the number one killer in America lurking around.

The American College of Cardiology, a fairly conservative group, gave very high endorsement of this coronary artery calcium score for people with risk factors. So if you’re 50 years old and you’ve got high blood pressure, boom: American College of Cardiology endorsed, and unfortunately not covered by insurance. They would leave it in a gray zone.

If you’re perfectly healthy 50 year old, do you need it? Well, I think that’s a personal decision between you and your doctor. I tend to favor getting one because it’s a very low dose of radiation and we still are dealing with the biggest silent killer in America.

There’s a very interesting documentary that came out two months ago called The Widowmaker. And it’s available online, about 90 minutes. I’d encourage anybody to watch it. It’s all about this topic of coronary artery calcium scoring and why is it not more available to make inroads into the health of Americans and identify those at risk.

[Damien Blenkinsopp]: Great, great, thank you for that.

[41:04]There are actually a lot of other blood markers. If you look at WellnessFX — I don’t know if you know the WellnessFX lab for consumers?

[Joel Kahn]: Which blood test is that, sir?

[Damien Blenkinsopp]: It’s not a specific blood test, it’s a lab which is directed at consumers. So it’s a company called WellnessFX, and some people are using those for blood panels.

[Joel Kahn]: Right.

[Damien Blenkinsopp]: So they have a large array. There’s a few companies like this, but WellnessFX is the best known at the moment. So it’s direct to consumer. They have a cardiovascular panel, which is why I bring it up. And there’s quite a few things on it.

So I wonder if you could just comment on some of the values that they include in their panel, if you find them useful. Because it seems like to me that there are so many markers linking to cardiovascular disease it makes it more complicated.

Because we have all these markers, and I’m sure someone like you could maybe get more data and get a better picture, but for the majority of us, it builds up this kind of complex mass of data. And maybe some of them would be out of range, some of them aren’t out of range, and we’re like, “Okay, so where does this put me? I’m not really sure.”

[Joel Kahn]: Yeah, I agree. I am familiar with WellnessFX. There are some others — I have no financial ties to any of these. There’s an organization that I very much like called LifeExtension.org. They’ve been in Fort Lauderdale for 35 plus years, and you can directly get a kit and blood work — a male panel, a female panel — and they’ve got hundreds of thousands of data points built up over the decades.

So you’re right, I think it is worth [it]. I have not seen the advanced lab test we talk about, the particle number, particle size. I have not seen that available in a direct consumer way; I’m not absolutely certain if that’s at WellnessFX. But you’re going to get a good screen, and you can learn quite a bit.

But I do go back to the idea that imaging arteries remains the kind of litmus test. You can have a lot of abnormalities in your blood stream, but you really need to know if you’ve either got thickened carotid arteries by the ultrasound, or if you have calcified, hard arteries by the CAT scan. You need to know that at least once to make sense of the blood work.

These biomarkers are all associations, where the imaging studies are direct imaging. So I favor the coronary artery calcium scan. In some places [it] requires a prescription, but since it doesn’t involve insurance, not everywhere, you can often arrange it on your own.

I encourage people to pursue these direct blood tests, like you said.

[Damien Blenkinsopp]: Yeah.

[43:35] I just wanted to go through a couple of them. You mentioned the NMR, which is, as I understand it, the most advanced blood test if you really want to understand your heart disease risk. Is that kind of the best one you find, in terms of accuracy and getting the closest to the same bar as the calcium score, if you’re just looking at blood?

[Joel Kahn]: Yes, in terms of blood, that LDL particle number which is most commonly obtained through the Liposcience NMR technology, is at the present, I believe, still the most accurate particle in the blood you can measure.

[Damien Blenkinsopp]: Yeah, Great.

[44:07] So WellnessFX, they have something called LPa, or lipoprotein(a). Are you up to speed on that one? Do you find that one useful? Because it’s a little bit similar in that it’s looking specifically at low density lipoprotein, I understand.

[Joel Kahn]: Yeah. Lipoprotein(a) is a cholesterol particle that a smaller number of the public has heard about. A very large amount of science saying it’s a blood test, the higher your level, the higher your risk of artery damage. It seems to be a highly inherited abnormality.

So I get it basically in pretty much everybody once, but I’m particularly aggressive in people that have a family history of early heart disease in their relatives, because that may be the factor. Usually in most labs lipoprotein(a) should be under 30, and in some patients of mine it’s over 200; it’s seven, eight, or nine times elevated above normal.

What is still lacking a bit is an absolutely clear cut trial that shows that lowering it — we can talk about lowering it in a minute — but lowering it makes a long term difference, just because there hasn’t been such a trial designed and carried out long term. Lifestyle can lower lipoprotein(a), hormonal balance of female and male hormones can lower lipoprotein(a), Niacin is particularly good at lowering lipoprotein(a).

And there’s some work going back all the way to Linus Pauling that you can minimize the effects of an elevated lipoprotein(a) by taking Vitamin C, strengthening the wall of your artery, taking some amino acids called Lysine and Proline, and that they may prevent the damage that lipoprotein(a) may do otherwise.

So there is, finally, there actually is a very strange therapy where, much like dialysis, you can get your blood cleansed through a filter. And this is an FDA approved treatment of people like that little girl I mentioned, Stormie Jones, if she were still alive today. That’s a therapy that would be used for somebody with a familial super high cholesterol.

But that filter also takes out lipoprotein(a), so if somebody has a very high level and vascular disease, that’s an option. So, it’s important, I believe, for people to measure their lipoprotein(a). And again it’s genetic, but I mentioned some things you can do.

[Damien Blenkinsopp]: Great, great.

[46:36] So one that I’ve been using for a long time is high sensitive TCRP. Is that something you find useful?

[Joel Kahn]: I do. We’ve been measuring C-reactive protein for decades, because we were measuring it to assess rheumatic fever, so it has a history going back literally decades and decades. But then along came a patented test, the high sensitivity test, and that seems to be more reflective of artery wall inflammation.

And inflamed arteries are more prone to suffer heart attack, stroke, clot and the rest. So you do not want an elevated high sensitivity C-reactive protein. And you want to measure it. And it is highly correlated with increased risk.

So then I’d get on a search for why it might be elevated, and most common would be abdominal obesity, poor nutrition, a lack of exercise, poor sleep or sleep apnea. But you can also look for occult causes like gum disease, periodontal disease and such, unsuspected prostate disease, prostatitis, and probably a diseased gut. Our Western processed foods, high in salt, sugar, and fat causing gut disorders. Lack of adequate microbiome health probably causes inflammation.

So you’ve got to work on the entire patient in a holistic way.

[48:04][Damien Blenkinsopp]: And so I don’t think we’ve really covered this properly, but inflammation is directly related to heart disease as well? Or is it a bit more of a wavy line?

[Joel Kahn]: Yeah no it’s prime time to measure inflammation and high sensitivity C-reactive protein. There’s also a number of other markers out now, like myeloperoxidase, and a test called the plaque test that give insight into inflammation in vessel walls and can be quite useful in a comprehensive assessment.

[Damien Blenkinsopp]: Great, great.

So in terms of some of these indicators, like CRP, the lipoprotein(a) , they’ve got others like alpolic protein, the HDL, the LDL, none of these are binary, as I understand them.

So if someone has a high CRP score, say it’s four or something like that, is that a sure thing that they have some kind of heart disease risk as well? Or could it just be related to some inflammation, or something like that.

You’re really using these as indirect indicators and you can’t trust the picture from that, but it’s just kind of a notice [that] I should go see a physician and investigate maybe if it’s calcium score.

[Joel Kahn]: Yeah. If it’s elevated, it should prompt a search into lifestyle, it should prompt a search into, as I say, gut health, gum health, prostate health, any other. Even though it’s felt to be largely a vascular marker, it’s a marker of the disease and it participates in, actually, vessel damage. But sometimes it can be very frustrating and unclear. I’ve had people with very high C-reative proteins: 40, 50, 60, 70, 80.

There’s a very limited experience with using a shotgun approach, after searching for every possible cause, an antibiotics like minocycline in the tetracycline family. I have been taught that, and I’ve had rare experience to do that with patients after a very thorough evaluation for every other kind of cause of elevated C-reactive protein. And it came down dramatically and stayed down.

[Damien Blenkinsopp]: Great, great.

[50:00] I wanted to tackle one thing. Could you go over the diet you recommend? As background, I’m Paleo and we’ve often talked about ketogenic diets and high-fat diets on here with people like Jimmy Moore and so on.

So could you give your perspective, where you come from with respect to heart disease; what kind of diet and lifestyle are you recommending?

[Joel Kahn]: I like to stay, in every aspect where I can, grounded in the science that’s available. And in terms of artery health, heart disease, survival and heart disease, the weight of the data is not in the ketogenic or Paleo world, the weight of the data like by 100 to 1 in terms of science at least, is in the world of nearly or completely plant based diet.

[Damien Blenkinsopp]: Okay, so is that a vegan diet?

[Joel Kahn]: Yeah. Well vegan, I’ll distinguish those very briefly.

But you can look at epidemiological studies like the Blue Zones, five areas in the world where people live the longest with the greatest freedom from heart disease, none of them are completely vegan. Except actually Loma Linda, California is one of those five Blue Zones, the longest lived community in American, and ten percent of that community is strictly vegan, the other 40 percent are vegetarian, and the remainder are omnivores. They are the longest lived people in the United States and they have the highest percentage of vegans in the United States of any community, because of the Seventh-day Adventist Church there.

So you can look at epidemiological studies like that, or you can look at the data on heart disease reversal, which is a concept that is scientifically sound. Two centers started studying [that], actually three, Nathan Pritikin in what’s called the Pritikin Longevity Center in Florida. He was an engineer, not a physician.

But Dr. Dean Ornish, a cardiologist, began in the early 1980s a lifestyle that is a largely vegan diet. If you really read between the lines its a very low oil, no added oil diet; so less than 10 percent of calories are from fat. He does allow his patients to have some non-dairy fats and some egg whites. So by strict definition it’s vegetarian not vegan.

And he has now pursued that dietary research for more than 30 years. It’s actually approved by Medicare, because the data is so strong that for heart patients it can halt and reverse their symptoms and disease, and minimize their need for medical care.

Dr. Caldwell Esselstyn began the same research project at the Cleveland Clinic in the 1980s, and has similarly shown [with] follow up catheterizations [and] follow up on patients’ health, dramatic reversal of heart disease without stint, without bypass. And his diet is strictly vegan and again under 10 percent of calories are from fats. Kind of the opposite approach to many ketogenic diets.

And, very compelling, Dr. Ornish has taken his program, which is more than diet —- Dr. Ornish emphasizes 30 to 60 minutes of walking, an hour of stress management by meditation or yoga, and group support — and has shown that in prostate cancer you can halt and reverse prostate cancer with his program. And he’s embarking now on a program in breast cancer, which I suspect, but we’ll have to wait, the results will be positive.

So it’s dramatic research, it’s not out of date. I hear some of my colleagues say, “Oh, Dr. Ornish’s data is aged, it’s old.” Well, he’s working with Nobel Prize winning scientists and continuing to put out some of the most cutting edge data on nutrigenomics and epigenetics. And his diet is one that if all of America were to follow to a large part we’d have a tremendous drop in the burden of chronic diseases like dementia, diabetes, cancer and heart disease. Without question; it’s been scientifically proven.

So my recommendation, I lead in Detroit a patient’s support group for people striving to stick to Dr. Ornish, Dr. Esselstyn, the Pritikin program, the Dr. Neal Barnard, you know, reversing diabetes program. And we have about 1000 volunteer people in the area that get together for meetings and group sessions, and it’s been profoundly effective in improving their health at very low costs, very grass roots.

[54:19][Damien Blenkinsopp]: Yeah. So what do you think of the Paleo principles of dairy and grain avoidance? Would you include those in your recommendations, or are those not relevant?

[Joel Kahn]: Sorry, the question was about grains?

[Damien Blenkinsopp]: Yeah, grains and dairy, in general.

[Joel Kahn]: I’d love everybody to stop eating dairy. I don’t view it as a health food in any setting, and it’s a tremendous burden on animals and the environment. And if somebody is not willing to eliminate animal products from their diet but would be willing to eliminate dairy, it’s one of the most frequent food allergens that people react to. It may be involved in the pathogenesis of Type 1 diabetes in children and young adults.

I wish we could legislate a dairy free world. Even the Harvard School of Public Health has advised greatly minimizing your dairy intake and replacing it with healthy hydration, like water, teas, and coffee, unsweetened; even alcoholic drinks, to a limited degree.

But grains, I know it’s contentious. I have had the pleasure of spending time with Dr. Bill Davis of Wheat Belly, Dr. David Perlmutter of Grain Brain, and I think also a name that’s not as well known, Dr. Alessio Fasano, who’s an Italian scientist now at Harvard who’s really doing amazing research on what grains do to Celiac patients and what’s the actual molecular pathways.

And I tend to favor Dr. Fasano, who I think I’m fairly quoting that one percent of the population is showing signs of Celiac disease, six to seven percent of the population if tested shows signs of gluten sensitivity. And that leaves over 90 percent of the population that neither has Celiac nor documented gluten insensitivity and if they’re reacting to grains, they’re reacting very briefly in a way that’s not a big deal.

And they should be part of a healthy diet. If you look at the scientific data, which I just reviewed and published a blog on in the past six weeks, even just in the last two years the data on whole grains and health is an amazingly strong body of data for survival, for freedom from heart disease, freedom from diabetes, freedom from cancer.

And it’s always a question, what’s it substituting? If you’re eating whole wheat pasta, whole wheat bread or wheat germ you’re probably not eating donuts and fried food and vending machine food because you’re exhibiting an intelligence in a selection on the healthier part of the spectrum.

So, I always encourage my patients that are having problems, take a four week elimination diet from gluten. If you’re having runny noses, rashes, if you’re having unexplained headaches, maybe even for an unexplained cholesterol elevation it could be that it’s inflaming your gut, and four weeks would give us some input on how you’d feel and biological markers.

But I eat whole grains consistently and recommend to my patients they do the same if they’re not in that small percentage.

[Damien Blenkinsopp]: Great, thank you for that clarification.

So if someone is on a Paleo diet or ketogenic high-fat diet, is there a test they could take? Would it be the calcium score, would you recommend that they take that if they want to assess if it’s having some impacts?

[Joel Kahn]: Yeah, well my comment and advice for those that are following a ketogenic diet is if you’re doing it for 10 days to fit into a tuxedo for a wedding, it probably will work and you’re probably not going to do yourself any harm. Long term, again I have to go to science, which there were at least two or three major studies saying long term low-carb ketogenic diets are associated with increased risk of death.

These are studies involving tens, and tens, and tens of thousands of people; yes, they’re databases, yes they’re association studies, but they are strong because there is no data that you live longer with a ketogenic diet. And in the last nine months there’s been specifically a study that ketogenic diets after heart attack are associated with the increased risk of dying.

So I strongly advise my patients not to follow ketogenic diets, and if they choose to, yes I think they should have all the biomarkers. If they don’t know of atherosclerosis then they should be having calcium scoring and possibly the carotid ultrasound testing. But I would advise them against it.

I know it’s all the rage, but it is a stress on the body, it’s a stress on the adrenals. And the healthy carbs found in vegetables, even starchy vegetables and whole grains, are adrenal pleasing sources of nutrition.

[Damien Blenkinsopp]: Great, great. Thanks for the clarification.

[59:00] Winding up, this is kind of a thing that affected a lot of my friends in their 20s. People were working very hard and were taking a lot of caffeine and generally very stressed, [and] we were getting a lot of pains around the heart area.

One of my friends went to a doctor and he said it was just stress and caffeine. I don’t know if you’ve come across this before; is this an issue, or is it just a symptom which isn’t really that important? Maybe too much caffeine or something.

[Joel Kahn]: Yeah. Caffeine in general, I mean it’s interesting. There is some genetic variation, and there is even a blood test you can get that’s a SNP, single nucleotide polymorphism, it tells you if you metabolize caffeine rapidly or slowly. If you metabolize it slowly, it’s going to hang around longer and give you more tendency to feel jittery or racing heart. And if you metabolize it rapidly, otherwise.

But with that aside, if it doesn’t bother you, caffeine is, in most studies, a health food. Now of course, like everything, you dump in some manufactured whitener and sugars, and you don’t have coffee anymore you have some modified, processed, anti-health drink. And certainly a frappuccino isn’t a cup of coffee.

But black coffee, dark roasted coffee two or three cups a day is generally a good boost in the morning, a good brain support. I always would cut it off about two in the afternoon so it doesn’t interfere with sleep. It’s a rich source of antioxidants.

There’s a little concern that your readers may know about that some coffees may be contaminated with mycotoxins, fungal toxins. You don’t really know it because it’s not measured and reported on American coffee sources; it is in Europe, and in fact there’s limits in Europe where they can’t be sold. Coffee beans sit outside and they can get moldy, and the mold can get into the coffee beans.

So you can ask around where you buy your coffee; it’s not a topic that a lot of people know about, and it may be a source of some illness for some people that are sensitive or are drinking lower quality coffees that may have mycotoxins.

With those couple of comments aside, I am pro-coffee. My heart patients ask me, I tell them enjoy a cup of black coffee. I certainly also urge them to enjoy green tea, or any of the teas actually; herbal teas, hibiscus tea, chamomile tea before bed [is a] wonderful source of soothing and sleep support.

[Damien Blenkinsopp]: Right. So it doesn’t sound like there’s any specific mechanism there which would be giving people heart pain from just coffee. Maybe something more like stress?

[Joel Kahn]: Right. There should be no heart pain.

[Damien Blenkinsopp]: Okay, great.

[1:01:32] So, where should someone look first to learn more about your topic? Are there any good books, your books, or presentations on some of the subjects you referenced?

[Joel Kahn]: Sure. I [1:01:41 unclear] appreciated that, and I probably do need to get back to some hospital rounds here. But I do have an active website at www.drjoelkahn.com. And all the blogs and TV interviews and podcasts and things I’ve done over the last few years are there. I encourage anybody to take a peek.

I do have two books out. Last year The Whole Heart Solution, published by Reader’s Digest. And this year a self-published book — but they’re both on Amazon — it’s got the title, Dead Execs Don’t Get Bonuses: How to Survive Your Career With a Healthy Heart, which I think is an important topic and the title has caught a lot of people’s attentions. It’s a real plea to not be one of those dead execs, or dead anybodys, for as long as you can.

I would encourage anybody to read anything by Dr. Dean Ornish, Dr. Caldwell Esselstyn, Dr. Neal Barnard, Dr. Garth Davis in Houston. All active scientists, researchers, clinicians that I think are speaking from the heart about overall health and sort of bucking the trend that all fats are good and animal products are benign.

We just don’t speak about the environment enough. We just don’t speak about animal rights enough, and we have to have a holistic approach to our plate; our plate represents an impact on forests and impact on our waterways and impact on our grandchildren’s world. And our plates represent a process that is very often extremely cruel, extremely unfair to beings that feel and sense pain and terror. And it’s as if we can’t talk about that.

We have labels — Paleo, Mediterranean, Ketogenic — but that’s only partial descriptions. I like to eat a kind diet and my plate is filled with kindness. So I hope that spills into my life as much as possible.

[Damien Blenkinsopp]: Thanks so much for all of those references. That’s a lot of material for people to get through. We’ll put all this stuff up on the show notes, of course.

[1:03:50] One last question. In your own personal life, are there biomarkers that you track on a routine basis? What do you do in terms of collecting data for yourself, for optimizing health and performance, or whatever?

[Joel Kahn]: Yes. I mean, I’ll do inflammatory markers like C-reactive protein, advanced lipid tests like LDL particle number and size. I’ll look at my Vitamin D levels. I’ll look at my male sex hormone, estradiol, total and free testosterone; I try and keep those optimal through natural ways, exercise, weight loss, weight lifting and such, healthy diets, toxin free diets that don’t interfere with the process. Blood sugar and insulin sensitivity, fasting glucose, hemoglobin A1C, important markers. So those would round out the majority that I’m doing: homocysteine level

[Damien Blenkinsopp]: Great, thank you very much for that.

Well Joel, it’s been really great to have you on the show. You know, we’ve covered a lot of ground today and a lot of markers, and I’m sure it’s going to clarify a lot for the audience.

[Joel Kahn]: Well there’s so much people can do. They’re in control of their health. And it starts with realizing that, and realizing the power of food, the power of fitness, the power of abstaining from smoking, the power of sleep, the power of friendship, and then getting credible information. And your podcast has done a wonderful job [with that], and I’m very honored to be able to share with your audience.

[Damien Blenkinsopp]: Thank you.

[Joel Kahn]: Have a great day, sir.

[Damien Blenkinsopp]: You too.

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What is genetic testing able to do and not do with current services? We talk with one of the top genetic lab services to understand how technologies differ in accuracy and where it is working, where it is not yet ready and why.

In this episode we look at the impact that genetics has on our health and wellness. With rapid discoveries in epigenetics, the picture isn’t as clear as when we thought genetics was everything. Epigenetic factors regulate which parts of our genetic blueprints are actually active and working for us at a given time.

As previously covered throughout this show, the typical “cookie cutter” approach to genetic testing often doesn’t lead to results. We look at the potential for genetics to give us precision medicine and precision health, where people get targeted advice and care fit for individual needs. You are an individual; you are an n=1 experiment.

In which areas does modern day genetic testing give actionable information? For instance, what drugs should you use? What diet may best fit you? Which health complications are you most at risk for in the long term – so that you can strategically manage these and put the effort in where it’s really going to count for you?

We put a team together to really go after genetics as a solution for patients, and using genetics and genomics as a solution for patients, and also physicians, for risk assessment or to give them insight into personal issues and to try and take some action against it.
– Michael Nova

Today’s guest is Dr. Michael Nova. He is Chief Innovation Officer and Founding Executive at Pathway Genomics. The company is an accredited clinical laboratory that offers genetic testing services from screening for cancer and other disease predispositions – to precision health and medicine advice. These services differ and are broader than those of 23andMe, which you probably know about as you listen to this show – that’s the genetic testing company that most people have heard of and used.

Pathway Genomics is the first company to bridge artificial intelligence and genetics-based precision medicine or a health mobile app to consumers. It does this in partnership with IBM, and notably IBM Watson which is IBM’s artificial intelligence machine learning platform.

Dr. Nova is the inventor of many of Pathway Genomics’ solutions. He has over 30 patents and many studies published in peer-reviewed journals. He is also a winner of the World Economic Forum Technology Pioneer Award. Finally, he’s a serial entrepreneur and is on the board of advisors for IBM, which is a pretty big deal.

I hope you enjoy this interview with Dr. Michael Nova and it helps you to understand how genetics can be valuable to you personally.

The episode highlights, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. Enjoy the show and let me know what you think in the comments!

itunes quantified body

What You’ll Learn

  • Dr. Nova’s roots in genetics and how Pathway Genomics differs from 23andMe in structure, technology, staff, and interpreting testing results (06:12).
  • Why reporting on genetic tests varies between companies; why testing does not produce ‘black and white’ interpretations of tested parameters (15:22).
  • The meaning of personalized / precision medicine; current applicability and future prospects, as numerous testing technologies become cheaper (17:46).
  • How genetic test panels are researched and converted into actionable information for physicians and individuals (20:40).
  • The complexity of genetic and epigenetic tests and why professional guidance is required when making health decisions based on results (29:30).
  • Why epigenetics is more complex than genetics and how genes are switched on / off by interactions with the environment or due to behavior (33:50).
  • Pathway Genomics and IBM’s Watson collaboration – integrating extremely diverse and data-dense medical information into meaningful outputs (36:11).
  • How genetic testing improves pharmacological prescription decisions and why increasingly complex data is even more useful (39:20).
  • Optimizing exercise for individuals using genetic information (46:04).
  • How to access information about personalized medicine and genetic testing (47:33).
  • What information Dr. Nova tracks on himself and why it is crucial to be aware of your genetics (49:46).

Thank Michael Nova on Twitter for this interview.
Click Here to let him know you enjoyed the show!

Michael Nova, Pathway Genomics

Tools & Tactics

Diet & Nutrition

  • Mediterranean Diet: All diet recommendations at Pathway Genomics are generated based on a Mediterranean diet. Based on personal genetic information, diets can be modified towards a low-carbohydrate or low-fat diet.

Tracking

Biomarkers

  • BRCA genes: There are two BRCA genes, BRCA 1 and 2. Certain mutations in these genes are associated with a high risk for developing breast and/or ovarian cancer. Full gene sequencing and results interpretation is offered by the Pathway Genomics BRCATRUE test. Angelina Jolie underwent preventative breast surgery because of her positive BRCA 1&2 status and her family history with breast cancer.
  • Maximal Oxygen Consumption (VO2 max): The maximum rate of oxygen consumption as measured during exercise, usually on a motorized treadmill. VO2 max reflects the aerobic physical fitness of an individual. The Pathway Genomics PathwayFit test includes sequencing of genes which are relevant to VO2 max in individuals.

Lab Tests, Devices and Apps

  • Pathway Panorama (Not Yet Available): This will be a genetics-oriented mobile health application. It is intended to integrate personal genetics with publicly available scientific medical information from trusted sources. Using the IBM Watson engine, the app will compare this information to the standard of care and provide personalized feedback on health and well-being.
  • Fitbit Charge: Fitness watch with automatic monitoring.
  • Pathway Genomics: Genetic Testing Panels

  • BRCATrue: A genetic test that searches for mutations in BRCA1 and BRCA2 genes.
  • PathwayFit: Analyzes over 75 genetic markers known to impact metabolism, exercise, and energy use within the human body. Provides insight into how your body may process sugars, fats, nutrients, and vitamins. This is the most popular test of Pathway Genomics.
  • Healthy Weight DNA Insight: One of the most comprehensive weight-related genetic tests available. Unique combination of nutrigenetic, medication, and general health information.
  • Mental Health DNA Insight: Identifies genetic variants that affect the metabolism and efficacy of psychiatric medications. More than 30 common antidepressants, mood stabilizers and antipsychotic medications included.
  • Pain Medication DNA Insight: Identifies genetic variants that affect how an individual will respond to the analgesic effects of certain types of commonly prescribed pain medications.
  • Cardiac DNA Insight: Tests for the genetic risk of a variety of heart-related health conditions. Examines eight classes of drugs that affect the cardiovascular system.
  • Genetic Testing Technology Platforms

  • Fluidigm Assays: Pathway Genomics uses Fluidigm assays with high precision and whole gene sequencing to detect ALL Single Nucleotide Polymorphisms (SNPs). These are variations in DNA code which are usually associated with predispositions towards health-related conditions. In comparison, the company 23andMe does not use Fluidigm technology.
  • Illumina Chip Seq Assays: In addition to Fluidigm technology, Pathway Genomics uses this technological platform for genetic testing. The company 23andMe also uses this type of genetic testing technology.

Other People, Books & Resources

People

  • Prof. Roger Guillemin: Dr. Nova started his career in genetic at the laboratory of Prof. Guillemin – who was awarded the 1977 Nobel Prize for Physiology or Medicine for his work with hypothalamic hormones.
  • Jim Plante: Founder of Pathway Genomics.
  • Eric Topol: An American cardiologist, geneticist, and digital medicine researcher. Mr. Topol is a leading voice in the field of personalized medicine and putting the consumer in charge of his/her own healthcare.

Organizations

  • IBM Watson Health: Overview of healthcare applicability of the IBM Watson’ artificial intelligence platform.
  • 23andMe genetic testing A popular and accessible genetics testing service company. The 23andMe model is focused on testing for subsets of SNPs (Single Nucleotide Polymorphisms) across various genes.
  • GeneMed: The company provides cancer and infectious disease diagnostic reagents for different instruments and technology platforms. This company also provides development and commercialization services to partners for improving In Vitro Diagnostic (IVD) products.
  • Lab Corp: Laboratory Corporation of America provides lab testing and services, with expertise in esoteric testing, genomics, and clinical and anatomic pathology.

Other


Full Interview Transcript

Click Here to Read Transcript

(06:12)[DAMIEN BLENKINSOPP]: Michael, great to have you on the show.

[MICHAEL NOVA]: Thank you, it’s my pleasure.

[DAMIEN BLENKINSOPP]: How did you first get into the area of genomics, and now it’s personalized medicine, but was there an evolution towards that? When did this first start for you?

[MICHAEL NOVA]: I was a research associate at the Salk institute a while back in a Nobel Prize winner’s laboratory – his name was Roger Guillemin. It was a very large laboratory; it had a lot of different technologies and scientists that were involved with it, as you can imagine.

The overall function of the laboratory was to study growth factors, and so we were studying everything about growth factors. We were studying how the proteins worked, tissue culture, how they interacted with each other, the DNA and RNA genetics of these growth factors, everything you could think of.

[DAMIEN BLENKINSOPP]: When you say growth factors, what exactly would that be for?

[MICHAEL NOVA]: Things like human growth hormone and thyroid releasing hormone and corticotropin-releasing factor, every kind of growth factor.

[DAMIEN BLENKINSOPP]: Okay. Things that stimulate growth in the human body?

[MICHAEL NOVA]: Yeah, in one way or another. He got the Nobel Prize for the first person to isolate TRF, which was a growth factor that was released in the hypothalamus. A signal that is released in the hypothalamus goes to the pituitary and then turns on all these thyroid hormones. That’s what he got it for, and so we were just peeling back the onion on a lot of different growth factors using different technologies.

I got into genetics there and then I started a couple of companies and took one public in the biotech area. We’ve almost used genetics as part of the technology, but it’s only been recently when we started (with Jim Plante, the founder of Pathway Genomics), we put a team together to really go after genetics as a solution for patients, and using genetics and genomics, I guess, as a solution for patients, and also physicians, for risk assessment or to give them insight into personal issues and to try and take some action against it.

I think it’s really been within the last ten years that the technology has been inexpensive enough that we could even try to use it directly for patients.

[DAMIEN BLENKINSOPP]: Great. First of all, I think a lot of people have heard of 23andMe, but they haven’t necessarily heard of Pathway Genomics, so could you give us a comparison of how the technologies compare and how the service is different? I know Pathway Genomics kind of evolved over time, so potentially a bit of that back story would be helpful too.

[MICHAEL NOVA]: Sure. First of all, the major difference is we have our own laboratory; 23andMe doesn’t. We have a big laboratory staff and scientific staff and curators and all that. All the tests come back to our laboratory and we do the DNA isolation and we do the reading of the mutations on different types of machines and then develop a report that goes back to the physician, which is the second difference: we’re only a physician’s ordered test; we’re not direct to consumer. So there has to be a physician in the loop or some kind of health provider in the loop, certainly on the ordering side, but also on the interpretation of the test.

All our tests are covered by insurance in the United States – that’s a third differentiator. We sell our tests in 44 different countries…

[DAMIEN BLENKINSOPP]: So just on the insurance angle; I understand it that you’re targeting a much smaller range of genetics, and basically you’re targeting specific arrays of things that you want to look at, like pharmacogenetics and other areas of the human body, whereas 23andMe is very, very broad in terms of what they look for?

[MICHAEL NOVA]: Yeah that was going to be my fourth!

[DAMIEN BLENKINSOPP]: Oh sorry.

[MICHAEL NOVA]: You took the wind out of my sails with that one, that was going to be the fourth big differentiator. We offer, like you said, panels of genes. We have a test for fit, nutrition and exercise, which only covers those two elements and then some eating behaviors and some metabolism.

Then we have another test for pharmacogenetics, like you mentioned. And one which is specifically for psychiatric, and another one that’s specifically for pain medications. Then we have a cardiovascular test, a cardiovascular risk, which also has some diet and exercise components in it.

So we have about 12 different product lines, 12 different types of tests, including BRCA. We do whole genome sequencing or next generation sequencing for the entire BRCA gene, if you know that gene. It’s the one that is prominent in certain ethnic groups for hereditary breast cancer. It’s the same gene that Angelina Jolie had. So we test for that as well.

We’re the only comprehensive genetic testing company that has health and wellness products all the way to hardcore next generation sequencing products for risk assessment for things like breast cancer.

A new thing that’s coming is we have an alliance with IBM, who’s an equity partner, and we’re building a mobile application that will basically put an artificial intelligence super computer in a handset to help with managing patient information and giving recommendations back directly to the user. That will be a direct to consumer type of product, but at this point we don’t sell any of our genetic tests direct to consumer.

[DAMIEN BLENKINSOPP]: I’d like to take a little step back because 23andMe and you are really very different propositions. There’s also the technology and the accuracy of the tests, and you have a different price point as well. Whereas I think for 23andMe for the whole thing right now, it’s $99; per array, yours is roughly $199 per different panel. So why is that, what’s the difference in the technology and what you’re delivering?

[MICHAEL NOVA]: It depends on the genetic tests. We do Fluidigm assays for our smaller arrays of up to about 80 different genes; 23andMe doesn’t do that. They basically take an Illumina chip that’s got a certain number of markers on it and run that chip for their $99 test. We also have that chip-based technology and then we also have the sequencing technology, which 23andMe doesn’t have.

So we have, the sequencing technology is basically more expensive than the Fluidigm or TaqMan assays, which are probably the least expensive.

We run every different type of genetic testing in here, but some of our reports require more than one platform. Some of them require the Fluidigm platform plus either maybe a sequencing or plus an Illumina chip, so the cost varies on a particular report based number one, on the technology that we’re using – it could be more expensive to run that particular report.

Then the way we do the reports is also different. We have a physician that reviews the results, we have a dietician that reviews the results, we have all those people that are on staff that are patient and can access at any time, so there’s a little bit more cost that’s embedded into the test or tests, depending on which one the clinician orders from us.

[DAMIEN BLENKINSOPP]: Right. Are your tests 100% accurate, so we could run them one time and we’d know for sure which gene SNPs we have?

[MICHAEL NOVA]: Sure. We have our own laboratory and it’s CLIA certified, CAP certified, it’s New York State certified. We’re the only comprehensive genetic testing company that has a health and wellness panel that’s been certified by New York State, which is very difficult to get.

23andMe can’t sell in New York State; they can’t sell in certain countries because direct to consumers is illegal. It’s illegal in places like Brazil and Singapore.

Our accuracy, since we’re licensed by three or four different licensing bodies, they come in here and inspect us all the time, at least once a year on all of them. So, we have to be extremely accurate.

[DAMIEN BLENKINSOPP]: I guess what I’m getting at also is the chip set that 23andMe is using is pretty reliable but it’s not 100% accurate, as I understand it. So in the past when I’ve done tests – I’ve done the 23andMe and I’ve done some other more specific genetics tests – and the answers weren’t the same. As I understood it, it was related to the technology that 23andMe uses, which is very economical to get a lot of data – which is interesting, so look at a variety of risks – but if you want to actually get clinical based information where you’re going to make decisions, you should run with the sequencing technology that you’re using with your panels to be 100% certain. Or am I looking at the wrong things there?

[MICHAEL NOVA]: No, I think you’re right on one aspect or a couple of aspects of what you said. I think that for things like the BRCA test, which is a very serious type of genetic test, 23andMe only reports on a couple of variants on the BRCA mutations, whereas we run the entire sequence. So the doctors come to us for that particular test; they would not necessarily go to 23andMe, even though the mutations that they provide and the way they do it are probably accurate, but they, just by definition, miss stuff.

It doesn’t mean that their technology is bad, which it isn’t; it doesn’t mean that the way they run the Illumina chip is not sufficient. That’s not correct. For what they’re reporting on, it’s perfectly adequate.

[DAMIEN BLENKINSOPP]: So everything you get reported should be correct with their technology as well – the Illumina chip?

[MICHAEL NOVA]: Yeah and I think it’s a good company. 23andMe is a good company. There are good companies like us and 23andMe and some of the other ones – we’ve been at this for eight years or seven years; we know what we’re doing. We just happen to have our own laboratory and so we’re under a lot of different kinds of governance that 23andMe isn’t under.

(15:22)[DAMIEN BLENKINSOPP]: Do you use blood samples as well, or is it saliva samples?

[MICHAEL NOVA]: Sure, we can use blood, saliva…

[DAMIEN BLENKINSOPP]: Is there a difference in the quality, or is it exactly the same, it doesn’t really matter which one you use?

[MICHAEL NOVA]: Both samples have different pluses and minuses, but trying to get to the same endpoint you still have to conform to what the governing bodies and what the licensing groups want us to report on. So we don’t have any choice but to make them equal in the end – if you gave us a blood sample or a saliva sample. But the way we do each one… in some respects it’s harder to do saliva because there are more contaminants in it and whatever, but then it’s a much easier test. People don’t necessarily want to get needle stick all the time.

[DAMIEN BLENKINSOPP]: I guess I’m trying to understand like I had a blood test run through DNA sequencing and a couple of the SNPs were different compared to my 23andMe. What would be the cause of that or is it a mystery?

[MICHAEL NOVA]: We can’t do that necessarily. We would certainly have to report on the same SNPs in the report in the same way so I don’t know. It could be a number of different things.

23andMe, again, has been around for a long time and so I think the accuracy of their reports and what they’re reporting on is really good. It’s hard for me to make a kind of black or white decision on something like that.

[DAMIEN BLENKINSOPP]: No, no, I’m not talking black or white, I’m just curious if there was a technological basis or something like that.

[MICHAEL NOVA]: There might be.

[DAMIEN BLENKINSOPP]: Yeah, I just figured it was the slightly different configuration of the technology.

[MICHAEL NOVA]: I’ll give you a really good example here and I think people don’t realize it: If you went and got a SMAT panel or a CAM panel from one company, like LabCorp, or you went and got one and put in the same sample to Quest, there’s no question that there will be a little bit of difference in what each one of these things reported on, but just a tiny bit of difference. That doesn’t mean that they’re wrong – either of them.

People think that genetics is black and white and the laboratory results are exactly 100% supposed to be the same all the time; that’s not necessarily true. And then we don’t know a lot more about the genetics either: There are 25,000 different genes, and we probably know what about 10,000 of them actually really do, but then they have to work with each other and all this kind of stuff.

I think getting the information on the particular SNPs is not necessarily the hard part; the hard part is interpreting what it means and giving that information back to the patient.

[DAMIEN BLENKINSOPP]: So it may be just a different reporting basis, that’s what it sounds like.

[MICHAEL NOVA]: Yeah, it could be.

(17:46)[DAMIEN BLENKINSOPP]: Taking a little step back, because I know this is basically your area, what does a shift to personalized or precision medicine and health mean versus where we are currently in the world?

[MICHAEL NOVA]: As a physician, we’ve always kind of practiced personalized medicine. When somebody comes in and they’ve got some condition they’re worried about, we give them their medications or help based on them as a person. But now, we’ve got a lot more tools. There’s a lot more granularity in what we can actually see that might be affecting this individual or even preventing things from happening.

Genetics is just one of those tools. So there’s genetics, there’s epigenetics, there’s transcriptomics, there’s all these different types of technologies now that are becoming less and less expensive. They’re kind of getting weaved into the management, if you will, of patients, and that’s what doctors are doing, basically, with our reports.

Precision medicine is just another name for personalized medicine, but I think one of the reasons there’s a much bigger push for it now is that we’re really seeing some major advances in cancer-targeted therapies using genetics, we know cancer is a genetic disease, a molecular disease. We’re now starting to target individual mutations in these cancers to give better results.

We’re now getting a clearer understanding of things like obesity – there are 97 genes that are related to obesity – they’re all different metabolites. It’s not necessarily going to be one size fits all and now we just have technologies that are getting less and less expensive to weave in information for the physicians to make decisions on. That’s where it’s at right now.

This is going to be an ongoing process forever; there’s going to be some sort of genetics or -omics or precision medicine technology that we’ll be able to use to really personalize individual therapies or prevention regimes or whatever you want to call it.

b>[DAMIEN BLENKINSOPP]: I guess one of the things about personalized is, if we take a comparison: If you have a cough today, you’re given the same drug no matter who you are; but in the future – and you have a panel which is pharmacokinetics – you could look at the impact of the drug on you – depending on your genes, drugs have a different impact. So it’s taking it up to a much more personalized level than what is possible today by just looking at someone.

In some cases, maybe you’ll see they’re different and maybe have got some blood test that is slightly different, but the genetics adds another layer of personalization.

[MICHAEL NOVA]: This is standard knowledge in the industry that anywhere between 40 and 50% of all drugs that are prescribed fail for the user, and especially the first time around. That’s a huge number.
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If we can add some way of tailoring those drugs – maybe you take this antidepressant instead of that antidepressant or you take this cough drug versus some other cough drug because your liver is metabolizing it different based on your genetics – you’re more likely to get a much better result.

Again, that is certainly where everything is headed in this whole precision medicine area.

(20:40)[DAMIEN BLENKINSOPP]: Great. So I also just wanted to talk to you – your tests are insured compared to the other ones, so I guess that the extent of research done on the specific panels is quite deep to get to that level where now tests can be insured.

[MICHAEL NOVA]: Yeah it depends. I’ll just take Medicare as an example because they’re kind of the gatekeeper for insurance coverage and our tests are covered by Medicare. The way that Medicare does it now in the United States, it looks at a panel on a gene by gene basis, and some genes have more clearly defined outcomes and predictability than others. So, on a panel of 80 genes, they might only cover three or four of them, but that’s enough to cover the entire cost of the panel.

There are three big levels of gene coverage in America. There’s a) genes that are covered automatically, like methylenetetrahydrofolate and some of the genes for warfarin metabolism. These are covered automatically, it’s an automatic payment, and since the technology on the panel is cheap enough, at least for us, to get over the cost of doing just that one gene, whatever Medicare decides to pay us, we make enough money to cover the panel. That goes for all the other insurance companies too, whether it’s United Healthcare pays on certain things, Aetna pays on certain things. Some insurance companies don’t pay at all on genetics, one way or another, so it really is not just based on whether the data is good enough, but it’s also based on whether a certain insurance company thinks it’s relevant enough to pay for it.

[DAMIEN BLENKINSOPP]: Right, right. As you’re saying, only part of your panel will necessarily be covered by that, and then there’s other things you’ve added, which you feel are relevant too. How’d you make those decisions? What kind of level of research has to be done?

[MICHAEL NOVA]: Yeah. We have a very strong curation. We have, I think, 15 PhD level geneticists and genetic counselors, and myself and a number of MDs, and we basically go and we grind through the literature. We look for human clinical studies and see if the data is relevant enough or there’s enough human clinical studies to put the gene into the panel and then report on it. We can only report on what the human clinical studies tell us.

There are plenty of genes and plenty of studies out there that we never would report on because we don’t think it’s relative; we don’t think that the data is strong enough. So to give you an example, in our healthy weight and fit test – which is our most popular test by far – we rate the science level in the test.

A really good clinical scientific study, let’s say on thousands of patients, and it has to be replicated in the same ethnic group, showed the same results and hopefully over multiple times, then that gets four stars.

Then there are other studies that aren’t quite as well validated but we think that there’s relevance because it might only have been done in two or three clinical studies of 500 patients each, which isn’t necessary a thousand patients but it’s 500 and it does show the same phenotype or it does show the same direction for what the genetics is reporting on. That’s a pretty good study so that gets put in the test too.

[DAMIEN BLENKINSOPP]: Great. I was going to actually ask you which was your most popular test but you’ve already brought it up.

So in terms of what that test gives people, who’s asking for the test and in what conditions are physicians looking for this kind of test? Is it someone who’s had a recurrent obesity problem for a very long time? What are the kinds of conditions and what’s actionable about that information for the physician once he gets it?

[MICHAEL NOVA]: For that particular test, we have a lot of different types of physicians that order it. Some are obviously looking for weight management, weight control in their population. But we also have people that are diabetics that are trying to use it to control their sugar levels or hemoglobin A1c levels, so we have a whole group of anti-diabetic groups that are using the test.

We have cardiovascular groups: many cardiologists think that most cardiovascular disease can be prevented by diet and exercise changing, so we have a lot of cardiologists that order the test and try to put people on more balanced types of diets, more personalized types of diets. Not necessarily to lose weight but to cut down lipid levels and other things that cardiologists worry about.

Then we have performance groups: we have performance athletes, we have gyms like Equinox health clubs that order our tests for a lot of their gym members to either increase performance or put on muscle mass, depending on what exercise.

So basically we have a lot of different types of groups, not just one type of clinician or group that orders the test.

[DAMIEN BLENKINSOPP]: Great. Is there an example you could walk us through of one of the most actionable genes in that area which people look at?

[MICHAEL NOVA]: Well, on that particular test… or do you mean all our tests?

[DAMIEN BLENKINSOPP]: The most popular one, because you said this was the most popular, if there’s one specific gene that people watch out for more than others.

[MICHAEL NOVA]: I don’t think it’s one particular gene. There are about 80 genes that we report on and we chop up the test into basically seven different sections. One section has to do with what is the best diet for you if you’re trying to lose weight and we have four different diets. That’s based on 50 different genes and how they interact with each other. Then we give you a diet recommendation, whether it’s low-carb, low-fat, standard Mediterranean or balanced diet. All of our diets are based on Mediterranean, but some have lower carbohydrates than others; some have lower fats.

Then we also give diet plans along with. So that’s a very popular part of the test, that section.

Another popular part of the test is we have a behavioral section, which looks at things like eating disinhibition – “I can’t stop eating.” Those genes around “When I start eating, I can’t stop eating.” Those genes in your dopamine pathway. We look at sugars – “Do I have a sweet tooth? Do I tend to like sugars more?” So this whole behavioral section is a very popular chunk of the test as well.

Then we have a standard metabolism section – we look at things like do you have a tendency to have increased insulin? Do you have a tendency to have increased lipid levels? Those types of genes, and there are multiple genes in that section – 20 or 30 genes in that section, so that’s also a popular part of the test.

[DAMIEN BLENKINSOPP]: Right. One of the interesting scenarios I think is the diet, the high fat versus the low-carb and the low-fat. Because a lot of the dietary recommendations today, it’s basically which crowd do you want to go with? I’m with the low-carb crowd; I’m with the high fat crowd, high protein…

Some of the genes can be pretty significant in that area, like the APOE gene. Could you talk a little bit about that and how that influences your diet and whether fats are going to be good for you or are basically going to be problematic.

[MICHAEL NOVA]: Let’s go back and look at diets in general. Most people, if they got on a diet and it was less calories than they usually intake and they stayed on that diet for years, they would probably lose weight. But it’s very difficult to get people to do that for a number of reasons.

So what we try to do is we try to look at particular genetics around fat metabolism – and APOE is one of them, and PPARgamma, and even FTO and some of these other genes – and not only how you process fats but also how you taste things. You have bitter taste receptors that we look at.

People don’t eat things that they don’t like, so we try to tailor the diet based on a number of these big subsets, whether it’s how you metabolize lipids – and people that have two copies of the FTO gene, there’s no question that they have trouble metabolizing fat in a low carbohydrate diet than somebody that doesn’t have those. That gene has been very well characterized and is a known obesogenic gene along with MCR4. If you put those two genes together, people that have those two genes tend to be about ten pounds overweight than people that don’t have them.

So we take that information, then we go back and we design a diet that’s based around not only what your metabolism is but also what you potentially would like to eat and make it a diet that isn’t too rigorous, that you’ll never stay on, and then try to give you direct diet plans – basically what to eat, literally, on a daily basis: Breakfast, lunch and dinner, this is what you should eat.

Then we have diet specialists and nutritionists and exercise physiologists and all that stuff, that if you really need help with that kind of stuff, we have ways to get you that as well.

I guess what I’m getting at is we don’t like to look at genetics in a vacuum. It’s one part of a big puzzle, and the more pieces of the puzzle we can put together, the more success we have for personalizing things for the user. That seems to really work.

We have other 20,000 physicians in the US that are ordering our tests and they keep ordering it over and over again, along with our diet plans and whatever information we give them, and the results speak for themselves – they’ve shown that what they get out for their patients is really working.

(29:30)[DAMIEN BLENKINSOPP]: Can we just go back to a distinction that you made was that you’re not doing genetics, you’re more doing genomics, right – the interaction of all of the genes together? Is that what you mean by you were saying?

[MICHAEL NOVA]: That’s a little bit of a slicing that onion really thin.

[DAMIEN BLENKINSOPP]: So what is the approach? You’re saying that it’s not a good idea to look at just one specific gene on its own?

[MICHAEL NOVA]: Yeah, very few things are one gene and then you have something bad happen. Even then, even for things like BRCA, it’s still only a relative statistic. Even if you have BRCA and you’re Ashkenazi Jewish and have the mutations that are relevant, there is still only a 80% probability that you’ll end up having breast cancer. So that means there’s 20% that you wouldn’t have breast cancer.

So very few things are one gene, one bad outcome, fortunately. It’s usually multiple genes. Again, we talked about obesity – there’s at least 80 or 90 different genes that have something to do with making somebody obese. And how they all work together? That’s the gold nugget in all this business is how to figure out how they all work together.

[DAMIEN BLENKINSOPP]: The BRCA gene is interesting because they’re pretty extreme decisions, or as you say, very rational decisions, but a lot of people see it as an extreme decision that Angelina Jolie has taken and it’s been in the press and everything.

One factor into that is that there’s genetics versus epigenetics and how we approach genetics in practice when there’s potential for some epigenetic influence and where the gene’s not actually turned on or off, right? You don’t know which one it is – is it turned on or is it turned off? Were Angelina Jolie’s BRCA genes – were they turned on and, therefore, they did represent the risk?

So, just based on what you said there, you said there was an 80% chance – I don’t know if that was a real statistic with a certain BRCA gene, but would it be in that kind of order that they were looking at BRCA?

If you took your BRCA panel, even not looking at the epigenetic influence, is there an 80% chance that that risk really exists, without taking into account the epigenetic influences?

[MICHAEL NOVA]: Correct. And remember, BRCA was first isolated in the Ashkenazi Jewish population – that’s where it’s most relevant. Angelina Jolie had family members who had breast cancer. So her decision to have surgery was based not only that she was BRCA1 and BRCA2 positive but also the fact that her mother, I think, died of breast cancer, and she’s half Ashkenazi Jewish.

So there were a number of factors that went into her decision to have surgery, not only to have her mammaries resected but also to have her ovaries taken out. I think she went down that path as well because there’s an increased risk, potentially, for ovarian cancer, which is still a very serious disease.

So you have to take all the information in total. If there was no breast cancer in her family and she wasn’t part Ashkenazi Jewish, then there might be a reason to not potentially go down that path. But that’s up to her and her clinician to work that out.

That’s why we don’t think a test like that, which is a very serious test, should ever be direct to consumer. That, for us, is something that really needs some guidance along with trying to make decisions about that.

[DAMIEN BLENKINSOPP]: Right. Excellent. I think the epigenetics area – how do you approach working with your physicians and advising them?

Do you ask them to look at factors like you were just talking about hereditary? – what’s the situation with your parents, your grandparents; other things you can look at in conjunction with some of your tests in order to capture the epigenetics? – whether something’s actually taking place or not: Do you say, “You should run these blood tests if you get these genes, and thus you could make a better decision based on that,” or do you tend to keep it to the genetics themselves?

[MICHAEL NOVA]: We tend to keep it to the genetics at this point because epigenetics is fairly new. There’s not enough data – although I do totally believe in it – in a lot of respects for us to weave that in to the process of, “You’ve got this gene but it’s not turned off.” We can do that from a technology stand point, but there’s not enough clinical data to make really informed decisions around that.

[DAMIEN BLENKINSOPP]: Right. I was talking more, at this point, as you say, epigenetics is relatively new and it’s probably quite expensive at this point for you to be integrating that type of service.

[MICHAEL NOVA]: Those kinds of expression assays – although Illumina has a methylone chip, but I don’t think it’s a clinical grade thing – it’s definitely more expensive than the genetics.

(33:50)[DAMIEN BLENKINSOPP]: I was thinking more about metabolites and lipids and things like that. So for example, we were talking about the APOE, so if your cholesterol markers are off, that would be an indicator that that gene is switched on – correct?

[MICHAEL NOVA]: Yeah, something is definitely not working correctly or you’ve got something in your diet, also, that’s not the correct diet. Maybe you’re eating too much of X, you should be eating more of Y. So there’s, again, a number of different factors – genetics, epigenetics, proteomics, metabolomics.

The metabolomics and the proteomics and looking at lipid panels, those give you a snapshot, an immediate time of day, this is what your lipid level showed. What genetics does is give you a tendency towards where potentially the lipid levels in the long run will go if you don’t take certain actions doing certain things.

[DAMIEN BLENKINSOPP]: Yeah it does. I think the area of epigenetics is potentially very confusing to people because there is this aspect of genes potentially staying switched off. Say, for instance, exercise is an important mechanism for turning off – I’m not saying this is true – but the APOE gene, right?

[MICHAEL NOVA]: There’s been data that’s shown that FTO gene for obesity can be mitigated with certain exercise and diet regimes; those are known facts. There are starting to be really hardcore data around using the environment, and epigenetics is all around using the environment – what you do in your environment to turn genes on and off – and there is data around that.

That would be one example of something that in the near future we might end up reporting on. You can change how genes are expressed by something in the environment.

[DAMIEN BLENKINSOPP]: I’m sure at this stage it’s just at a discussion level with you and colleagues and other people that you know, but how far out do you think these kinds of things are, like being able to take the next step and understanding the epigenetic aspect of it and making decisions based on that as well as just the genetics?

[MICHAEL NOVA]: Epigenetics in some respects is even more complicated than the genetics because there are so many different things that can turn genes on and off: there are methylation patterns, there are acetylation patterns, there are phosphorylation patterns, which means molecules that actually bind the DNA, or histones or whatever, and modify things and turn genes on and off.

And then there are all the microRNAs. There’s thousands of different microRNAs, the junk matter in DNA that will turn genes on and off if they’re expressed or not. So it’s extraordinarily complicated!

(36:11)[DAMIEN BLENKINSOPP]: IBM is an equity partner in Pathway Genomics?

[MICHAEL NOVA]: Yes.

[DAMIEN BLENKINSOPP]: Right. I wanted to talk about Pathway [unclear 36:16] but I think it’s also relevant to what we’re discussing right now, it being so complex and everything. Are you looking at bioinformatics and things like that potentially in the future?

[MICHAEL NOVA]: See that’s what computers are really good at. They’re good at taking noise, basically. Whereas we would look at it and not come up with any pattern; a computer’s really good at making patterns out of things. They’re not necessarily sentient, but they’re really good at taking databases and huge amounts of information and then telling you that these two things are linked together – that’s what the information is. That’s basically what we’re starting to build with IBM.

We have a very strong bioinformatics group and engineering group, and this is an artificial intelligence. Basically, it’s the Watson artificial intelligence that can play chess and was on “Jeopardy!” the show in the United States. So we have to train it.

We like to say it’s a little bit like a dog: you train the dog by lobbing it a question and seeing what answer you get back and seeing if it’s relevant. 99% of the time to start with it’s not relevant, then you have to tell it why it’s no, and go back “It should be this instead of that.”

It’s a huge process to train, especially around health care, because there’s nothing that’s more data dense than health care data. It’s not just genetic data we’re interested in; we’re interested in your electronic health record, your lab results, your wearables – your Fitbit data and all that other stuff. We want to take all that information and then compare it to the standard of care that’s what’s going to be in the Watson engine, and then give you back a recommendation that’s really personalized.

If you asked a question like, “I’ve got a nose bleed” – if you have our mobile app Panorama – “I’ve got a nose bleed, what should I do?” you would get a different answer potentially than what I would because I’ve scanned all this different information about you and compared it to what is the standard of care, and since you’re a little bit different in this gene and your latest lab result is a little bit different over there and maybe you went for a run and fell on your face, all of those bits of information are really important in order to give you a decision or some sort of recommendation about what to do.

[DAMIEN BLENKINSOPP]: Right. That sounds incredibly ambitious.

[MICHAEL NOVA]: Sure.

[DAMIEN BLENKINSOPP]: But you are going to release something relatively soon, aren’t you, so what will that be when it comes out?

[MICHAEL NOVA]: We will have public beta, sometime September to October time frame this year. We’re going through trials right now with the alpha version.

Like you said, it’s a very complicated problem because it deals with a lot of different types of data, and then getting that data so Watson can understand it, which is a whole engineering task on its own, and then getting the right information into Watson – or IBM, the super computer, the artificial intelligence – and then getting the right and curated information in there so it has the state of art in what people are thinking in terms of health care.

So you’re right, it’s extremely ambitious, and we’re really, really excited about it.

[DAMIEN BLENKINSOPP]: Yeah I can imagine. It will be fun to use it when it comes out. Is it going to be sold through iTunes or something, how’s it going to work?

[MICHAEL NOVA]: Yeah, we’ll go through the iStore and all that, and whatever Android is.

(39:20) [DAMIEN BLENKINSOPP]: Okay great. One of the other things we touched on that I wanted to get a bit deeper into because I think a lot of people don’t realize how varied this is, is pharmacogenomics.

You have several panels; it’s quite extensive the number of panels, it seems, under that area, because you have mental health areas and other areas. Is it extremely varied the impact a drug can have on each and every person? Is this very common that drugs have very different impacts per person?

[MICHAEL NOVA]: I’ll start with the panel. We have two or three different panels for pharmacogenomics. One is what you mentioned, it’s a mental health panel that has things like anti-depressants, antipsychotics, mood elevators, 30 or 40 different drugs and they each are metabolized in your liver a little bit differently.

One drug is metabolized differently to another drug, and we look at those mutations in your liver enzymes – they’re called cytochromes.

Then there are also transport proteins that have variance in how the drug is transported from the blood into the cells. There are a couple of drugs in there that have different transport kinetics. Then there are some of them also that get excreted by your kidneys, and they have a little bit different kinetics.

So we put that whole panel together on mental health based on a lot of this genetic information, or the best that we could find. Doctors use it to try and start somebody out on a drug rather than guessing what this person should have, or they’ll change a drug based on the genetics because they’ll understand why this potential drug isn’t necessarily working.

Then we have other panels. We have a pain panel, which does the same kind of thing but around pain medications – the codeines, oxycodone, morphine, tramadol, things like that – they get metabolized differently.

[DAMIEN BLENKINSOPP]: When you say metabolized, it means processed by the liver?

[MICHAEL NOVA]: Yeah, processed by the liver. There’s also transporters and uptake and excretion that are a little bit different for some of these drugs. Again, we use that information on a broad panel of different genes to tailor what potentially would be better for somebody than something else.

That kind of data is getting better. The good thing about genetics in general is that the data just gets better and better; it doesn’t get worse. It’s not like cold fusion – it’s not going to go away. It’s just going to be integrated more and more into the practice and pharmacogenetics and, obviously, drug metabolism is a huge deal.

To give you a good example: in the Asian population, there’s a drug called carbamazepine and it’s used as an anticonvulsant. There are genes involved around the metabolism of carbamazepine that if you have these particular genes, you will probably have a very high likelihood of going into Stevens-Johnson Syndrome if you take carbamazepine, and that’s a very serious disease.

[DAMIEN BLENKINSOPP]: Stevens-Johnson Syndrome; could you just describe the effects of that because I don’t think it’s very common but it’s pretty horrific, right?

[MICHAEL NOVA]: Yeah, it’s an allergic reaction basically, an immune reaction against this particular drug and you can basically end up dying from it – you go into anaphylactic shock and your skin starts to slough off. It’s a really nasty way to go if you want to call it that way. But again, it’s not very common.

But it is common more in Asians, and so screening for carbamazepine is 100% done in South-East Asia, Taiwan, places like that that are still using the drug as part of an anticonvulsant regime. They won’t put anybody on it if that person comes up with that particular variant.

That’s a really good example of how using a genetic test will really literally dial out a lot of drugs or dial in a drug based on your genetics.

[DAMIEN BLENKINSOPP]: Right. Currently though today, it’s a little bit of a trial and error process if you see a physician. Even with antibiotics sometimes, unless you’ve had tests done, it’s trial and error. We’re working hopefully towards a place where there won’t be any of that trial and error, it will be eliminated over time by these kinds of tests.

With the caveat that epigenetics sometimes will have some influence, so it’s not 100% fallible. In terms of the pharmacogenomics, there’s still some potential that basically says “This drugs better than this one for you”. It’s not 100% fallible, correct?

[MICHAEL NOVA]: No. Again, what we try to do in the genetics business is report on what the literature tells us – period; that’s the bottom line – and is that result valid.

We know, in pharmacogenetics, that across all drugs, 40 to 50% of them fail when they’re first given, so that’s a huge problem. So, dialing in the right drug, even though it might not be 100% correct… although the Stevens-Johnson issue, with this particular gene and carbamazepine, is almost 100%, so there’s nobody in their right mind if they knew that that patient had those particular genes would put somebody on carbamazepine because that’s one of those issues that is almost really one gene, one effect – you just don’t do it!

[DAMIEN BLENKINSOPP]: Yeah, right, when the risk is so high. What other high risk ones are there? Is warfarin a big one?

[MICHAEL NOVA]: Yeah warfarin potentially could be a big one for a couple of reasons. A dosing of warfarin to begin with is a little bit difficult, you have to have really strong expertise in doing that. The way it’s done is it’s done over a period of time to figure out what your INR is and how you’re metabolizing it and then getting the right dose.

Warfarin is a serious compound; you don’t want to mess around with it. It’s basically rat poison and it’s a very serious anticoagulant, as are some of the other ones like Plavix. But if you can figure out initially which dose of warfarin is better for that individual based on its genetics, that’s a good thing.

Warfarin tends to be used when a problem arises, like potentially a stent or you’ve got some sort of other issue that needs anticoagulation so you need to put them on warfarin immediately. I think that having a point of care warfarin test for pharmacogenetics is probably the way that that is going to go. Nobody wants to sit around and wait for a day for some sort of genetic test to come back before they put them on a drug like warfarin if they need it immediately, if they’ve got an embolic stroke or something like that; you’re just going to do it anyway.

[DAMIEN BLENKINSOPP]: Right. That kind of information is helpful to have it already pre-done. That is why – it’s pre-empting the need for genetic data on you. In some cases it’s worthwhile doing, right? Cancer…

[MICHAEL NOVA]: Yeah, and then the holy grail in a certain period of time it will be 500 dollars or a thousand dollars to get a whole genome sequence of all your genes, all your DNA. Then everybody gets it done, insurance will probably pay for it, and it just gets put in your record at birth. That’s probably where it’s going.

If you look at the long-term goal of getting everybody genetically tested, that’s probably where it’s going to end up. Then you’ll just pull down the information when you need it – it’s already in your file, it’s in your electronic health record. Does this patient respond to carbamazepine? Does he respond badly to warfarin? You’ll just know that because you’ll just drop down the information electronically.

(46:04)[DAMIEN BLENKINSOPP]: Great, thanks for that. One other thing you mentioned, which I’m sure is going to be interesting to some people, is the athletics aspect and the performance there. Have you got any specific examples of genes you’re looking at and reporting that are useful for training or changing/optimizing there?

[MICHAEL NOVA]: Yeah, there’s a lot of genetics on VO2 max. Some people tend to have a tendency to have a higher VO2 max than other people based on their genetics. How do you use that information in order to tailor your workouts? Maybe you’re one of these people that has a low VO2 max, maybe you need to do more X exercise than somebody that has a tendency to have a higher VO2 max. So there are genes around that.

There are genes around power and endurance: some people tend to be more power people, which means that they respond better to power athletics or power sports than people that are endurance runners. There are some pretty famous genes in that power area – actin is one of them and ACE and some other genes.

Then there are genes around exercise and insulin response, exercise and sugar response. Our panel covers a lot of these and gives you a broad snapshot of what potentially would be a better type of exercise for you than somebody else.

[DAMIEN BLENKINSOPP]: Right. so the type suggestions would be resistance training versus endurance aerobics, cardiovascular kind of work – these kinds of recommendations?

[MICHAEL NOVA]: Yeah, and then a sophisticated personal coach – we use an Equinox personal coach – uses that information to tailor what types of exercise regimes, along with their diet, potentially would be better, you’d get more response around than something else.

(47:43)[DAMIEN BLENKINSOPP]: Great, thank you. Where would you recommend someone look to learn more about personalized genomics? Are there specific books or presentations of the subject that you know are good resources to learn more about this?

[MICHAEL NOVA]: I think we have a couple of them on our website, pathway.com. There’s a lot of them out there. The University of Utah has a very comprehensive genetics database.

If you really want to get down to hardcore genetics, all the genes are listed in certain databases such as GeneMed and NIH has a database of all the genetics and all the genes, all the variants and what they mean.

You can Google in “Genetics textbook” and there’ll be 50 of them that come up. Hospital groups like the Mayo Clinic has a really good genetics site, Harvard’s got a good one, Stanford and UCSF, they’ve all got really good information on those websites about genetics.

[DAMIEN BLENKINSOPP]: Great, great, great, thanks. How could people best connect with you and learn more about you and your work? Are you on Twitter or are you active anywhere else?

[MICHAEL NOVA]: Yeah, people lob in stuff to me all the time. I figure my email is usually the best way to get hold of me, or Twitter – we have a Twitter account from Pathway Genomics. A lot of information gets disseminated through the usual media outlets.

[DAMIEN BLENKINSOPP]: Alright, great. Is there anyone besides yourself you would recommend to learn more about this, for personalized approaches, whether it be pharmacogenomics or anything else?

[MICHAEL NOVA]: There’s a lot of academic groups, every major university has somebody that’s doing it. I could certainly give you a list of…

[DAMIEN BLENKINSOPP]: It sounds pretty broad. I don’t know if there’s anyone more in the populous base, potentially working with big companies like IBM or doing some similar work, potentially different in some areas to you that would be of interest?

[MICHAEL NOVA]: One person that’s been pounding the genetics drum bag for a long time has been Eric Topol, you’re probably familiar with him. He’s one of the leaders in personalized and putting the consumer in charge of his own health care. That’s basically what we’re trying to do here from a number of different angles.

(49:46)[DAMIEN BLENKINSOPP]: Great, excellent. A couple of questions now just on your own personal approach and view of body data; what kind of things have you had tracked for yourself, whether it’s genes or other biomarkers or fitness activity trackers? What kind of things do you track on your own biology?

[MICHAEL NOVA]: I’ve had my genome completely sequenced, so I know as much about my own genome as probably is available. So in that respect, I know what’s good for me. Then I’ve certainly changed around my diet a little bit and the types of exercise that I do based on what my genetics have shown me.

I do wear one of these Fitbit tracking gadgets, and there’s a lot of them; there’s a lot of different types. Then I’m going to for sure use Panorama, this health care app that we’re going to come out with, because it will be integrated into your cell phone. You type in “What shall I do for my exercise today?” and it will tell you, “Based on your genetics or lab results X, Y, Z, you should do this. You’ve already done a thousand steps, you should do this now. You can eat this. There’s a store around the corner, you can buy it there.”

There’s a whole bunch of different parameters that I think will be very, very useful in terms of tracking where you won’t know what’s really happening. I think that’s another thing that users will like about Panorama is there’s not going to be a lot of input; you don’t have to do a food log.

Users don’t want to do that kind of thing. We live in 140 character world!

[DAMIEN BLENKINSOPP]: Yeah, there’s a burden to collecting information.

[MICHAEL NOVA]: There’s a total burden. That’s a very good word to use. There’s a total burden and we’re trying to make it very easy for it to be done automatically, so you feel as though you almost have a guardian angel on your shoulder, in some respects.

[DAMIEN BLENKINSOPP]: Are you integrating it with existing sources of information or are you just making the app very easy to integrate? A bit like Evernote, which you can upload all sorts of things into it.

[MICHAEL NOVA]: Yeah, it will be both. You’ll be able to take what you want, or we’ll go out and find it. We’ll go get your Fitbit data, we’ll go get your electronic health record, we’ll go get whatever lab result, provided we get permission from you to do it, obviously. There’s consent that’s going to be involved in this whole thing.

We’ll try and make that, as you said, that burden or that bar really low. We’ll make it very easy for you to get a very inexpensive genetic test through the application.

[DAMIEN BLENKINSOPP]: So you’ll be able to buy a Pathway genetic test through the app and it will get integrated automatically?

[MICHAEL NOVA]: Yeah, or anybody else’s genetic test. Whether you’ve got 23andMe’s; we’ll integrate that information in there.

[DAMIEN BLENKINSOPP]: Great, great. Okay last question – I always ask this of everyone – what would be your recommendation to someone trying to use some data, any kind of data, to make better decisions about their health?

[MICHAEL NOVA]: Knowledge when it comes to preventing things from happening and to changing your behavior when it’s based on real science is a very powerful thing. We hear that all the time – “Oh, that’s why I didn’t like X or Y. Now I know it’s not all my fault. Now I can change it and stick to some potential diet regime with a lot more confidence and I’m going to get a better outcome.”

So for us, knowledge is power in order to change behavior, and that’s the name of the game for a lot of us is trying to change your behavior. Because you have a lot of power to be able to do that. Giving the consumer more information about themselves is a very powerful thing.

[DAMIEN BLENKINSOPP]: Right. It’s like once someone understands something more clearly, it gives them more clarity, it gives them more confidence; it makes it a lot easier to keep that behavior on board.

[MICHAEL NOVA]: Right.

[DAMIEN BLENKINSOPP]: Well Michael, thank you so much for your time today. I really enjoyed the chat.

[MICHAEL NOVA]: My pleasure.

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Water fasting or ketogenic therapies may be effective with some cancers, and not with others. Learn about the PET scan and how it can provide insights into whether a cancer is likely to be responsive or not to the water fast tactic we’ve covered in previous episodes.

In this episode, we return to look at ketosis and water fasts as a tool to help treat cancer. This builds on the previous episodes looking at Ketosis with Jimmy Moore and the impact of water fasts on cancer with Dr. Thomas Seyfried.

In this episode, we dig deeper into the cancer topic looking at how ketogenic or low-carb diets may contribute via mechanisms related to insulin and ketones to inhibit cancer growth. We look at why only some types of cancers may benefit from these types of ketogenic treatments, and the data behind it. The data backing up this episode, is that of the PET scan — Positron Emission Tomography. PET Scans can be used to understand what type of cancer a person is dealing with and more importantly, whether it is likely to respond to ketogenic therapies or not.

For cancers that are dependent on glutamine more than glucose… They can be aggressive… and they may not show up on a PET scan, and they also may not be responsive to a low carbohydrate diet.
– Dr. Eugene Fine

Our guest is Dr. Eugene Fine. He’s currently a professor of Clinical Nuclear Medicine at the Albert Einstein College of Medicine. Most recently, in 2012, he published a study in the scientific journal of Nutrition on 10 cancer patients treated with a low-carb diet. He’s currently expanding his research by working on the use of low-carbohydrate diets combined with chemotherapy in animals.

This is all linked through his area of specialism, which is PET scans — positron emission tomography — where he has been identifying and monitoring cancers for the use of this type of scan. We’ll also touch on some of his studies looking at the impact of ketones, in vivo, on normal cells and malignant cells, and how that differs compared to glucose.

The episode highlights, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. Enjoy the show and let me know what you think in the comments!

itunes quantified body

What You’ll Learn

  • Reducing carbohydrates in diet and reducing insulin secretion in the body may inhibit cancer growth (4:06).
  • How ketones inhibit cancer cells (10:06).
  • Why are cancer cells over-expressing uncoupling protein 2 and reactive oxygen species (12:35)?
  • Dr. Fine explains how he uses PET scans to identify many different types of cancerous cells and severity by using fluorodeoxyglucose, or FDG (17:32).
  • If the cancer does not show up on the PET scan (as is the case with prostate cancer and glutamine dependent cancers) it may not respond to a low carbohydrate diet (23:57).
  • Dr. Fine discusses quantitating the PET scans (30:50).
  • Any inflamed area might also show up on the PET scan associated with the FDG (32:36).
  • This research is in the beginning phase and needs to be studied on a larger scale as the next step (34:11).
  • Dr. Fine describes his “recharge trial” where cancer patients were put on a low carbohydrate diet to observe the effects of the diet (35:00).
  • During the trial the patient’s blood levels were measured to determine whether they were ketotic (37:42).
  • Dr. Fine discusses the results of this recharge trial by identifying that inhibiting insulin may have effects on cancer progression/remission (40:31).
  • Cancer may adapt to the environment where it “grew up”. So if you develop cancer already on an low carb diet, will not be affected by a low carb diet as an intervention (45:05).
  • Damien and Dr. Fine discuss other ways to change ketone/insulin levels (49:44).
  • High calorie versus low calorie diets are discussed (53:13).
  • The biomarkers Gene Fine tracks on a routine basis to monitor and improve his health, longevity and performance (1:03:29).
  • Gene Fine’s one biggest recommendation on using body data to improve your health, longevity and performance (1:09:14).

Eugene J. Fine, MD

Tools & Tactics

Drugs & Supplements

  • Metformin: A drug which is used to improve blood sugar regulation in diabetes. Researchers are looking at its wider applications with cancer treatment as it has been found to inhibit insulin secretion.
  • Ketone esters and salts: A new range of supplements making ketone bodies directly available to the body and thus inducing ketosis. There are various forms including Beta Hydroxybutyrate Monoesters (BHB monoesters), and Beta Hydroxybutyrate mineral salts (BHB combined with Na+, K+, and Ca2+). One available for purchase is Ketosports KetoForce and Ketosports KetoCaNa.

Diet & Nutrition

  • Low-carbohydrate diet: this programme limits carbohydrate consumption to increase ketosis. This was the main discussion point for this episode.
  • Ketogenic diet: The ketogenic diet is a low carb diet which also raises the level of ketone bodies in the blood.

Tracking

Biomarkers

  • Beta-Hydroxybutyrate/β-hydroxybutyrate (Blood ketones): Ketone bodies can be used as a source of energy, similarly to glucose, for most cells in the body. However, now it is recognized that ketone bodies might inhibit the growth of cancer cells instead of fueling them. Some information about testing ketone levels can be found here. Normally, there should be little to no ketone bodies in the blood or urine. However, ketone bodies increase during a low-carb diet. The most accurate way to measure ketone bodies is through a blood draw but urine tests are also available. More information on ketones and ketogenic diets can be found in episode 7.
  • Insulin: Insulin is a hormone produced in the pancreas and released in response to blood sugar levels and metabolism of carbohydrates and fats. This hormone controls the glucose blood levels to attempt to maintain normal levels. Fasting insulin levels are normally less than 25 mlU/L. After a spike of glucose in the system (after eating) insulin levels will rise but should normally not reach levels higher than 275 mlU/L. Glucose production in the body is inhibited when more insulin is released. Hyperinsulinemia occurs when there is too much insulin circulating in the body.
  • Hemoglobin A1c (HbA1c): Measure of glycated hemoglobin, or hemoglobin to which glucose has become attached – a process that occurs when blood sugar levels become excessively elevated. A proxy measure used to assess your average blood sugar over time. Since hemoglobin is part of the red blood cells it is exposed to blood sugar over the lifetime of the red blood cell, thus giving a measure of exposure over the cells average lifetime (approx. 3 months). As such this measure is used to identify blood sugar control issues. Standard lab reference ranges show anything below 6% as fine, however this already represents blood sugar dysregulation. Optimum HbA1c levels are below 5%. HbA1c has been well researched.
  • Blood Glucose Levels (mg/dL): A measure of the level of glucose in the blood at one point in time. Fasting blood glucose levels are specifically taken when you have not eaten for at least 8 hours and optimally would be between 75 and 85 mg/dL. Health concerns with blood sugar regulation such as diabetes risk start to rise over 92 mg/dL. Levels can be measured at home using a glucose monitor and glucose testing strips (an explanation for the use of glucose monitors can be found in this episode).
  • Cholesterol-HDL and LDL: The cholesterol biomarkers include lipoproteins and triglycerides which are found in the blood. There are standard markers that all doctors and labs will run, and some newer specialist labs that are more specific and accurate. There are two main types of lipoproteins, HDL and LDL. We covered these markers extensively in episode 7.

Lab Tests, Devices and Apps

  • Positron Emission Tomogrophy (PET) scan: A PET scan is a functional imaging technique used to image body processes. As described in this podcast, a PET scan can be used to identify cancer presence and severity. A radioactive tracer, fluorodeoxyglucose, is used to tag these cancerous cells. As discussed by Dr. Fine, the cancerous cells identified in this way may be treated using a low-carb diet as a supplement.

Other People, Books & Resources

People

  • Steve Phinney, MD, PhD: Dr. Phinney has completed research regarding low carb diets.
  • Jeff Volek, PhD: Dr. Volek has also participated in research about low carb lifestyles. Together, Dr. Phinney and Dr. Volek wrote a book called The Art and Science of Low Carbohydrate Living.
  • Douglas Spitz, PhD: Dr. Spitz is a radiation oncologist who has studied the ketogenic diet as an additional treatment for cancer. His research can be read here.
  • The Caveman Doctor: Colin Champ, MD is a radiation oncologist who has researched the role diet plays as a supplemental treatment for cancer.
  • Otto Warburg: Warburg hypothesized in the early 1900’s that aggressive cancer growth is due to energy generated by the breakdown of glucose.
  • Thomas Seyfried, PhD: Dr. Seyfried is interested in fasting and diets used to treat cancer. More information can be found in The Quantified Body podcast.
  • Valter Longo, PhD: Dr. Longo has published many articles regarding fasting benefits for cancer patients.
  • Dominic D’Agostino, PhD: Dr. D’Agostino is well known for his research with ketogenic diets and performance. More information can be found here.
  • Richard Feinman, PhD: Dr. Feinman is a professor at the State University of New York. He has collaborated multiple times with Dr. Fine. Dr. Fine wrote two blog posts on Dr. Feinman’s site: Part 1 and Part 2.


Full Interview Transcript

Click Here to Read Transcript

[Damien Blenkinsopp]: Gene, thanks so much for joining us on a call today.

[Gene Fine]: Oh sure. Good to be here.

[Damien Blenkinsopp]: To give a better background, we spoke to Dr. Seyfried about his ideas and his work on ketogenic diets, fasting, and cancer. And what I found interesting about your work is you’ve dug into different areas, and you’ve differentiated cancers and I wanted to get up to speed about what you’ve been up to. And potentially, also, you’ve got some slightly different views on the whole thing.

So, first of all I wanted to talk about what do you see as the mechanisms of effect behind, if we’re inducing ketosis to inhibit the cell growth of some cancers. How is that working from your perspective?

[Gene Fine]: There really are three linked mechanisms, I believe, that have the potential to inhibit cancer growth. And two of them — well actually all three of them — one is that by reducing carbohydrates in a diet. And we have to realize that most of the carbohydrates we consume are sugars and starches, which digest the sugars — about 90 percent of them.

[And] that if we strictly limit carbohydrate to very low values, we’re inhibiting insulin secretion. And insulin alone is a stimulus to cancer growth. So, if you inhibit insulin you’re reducing one of the important stimuli to cancer growth through that alone. The insulin receptors on cancer cells will be inhibited, and so the growth signals will be inhibited.

[Damien Blenkinsopp]: Is that differentiated? Normal cells have uptake of insulin and they respond to insulin also. Is it that the cancer cells respond to a greater degree? Or what’s the difference there, if there’s any?

[Gene Fine]: No, not at all. In fact, I think the concern would be that the cancer cells may respond to a lesser degree. However, the important thing is that as adults we need some insulin. Without any insulin, we’re Type One Diabetics, but we don’t need much insulin at all.

We need insulin when we’re kids, because kids grow up when they have carbohydrates and protein and insulin helps them grow. When you’re an adult and you eat too much carbohydrates it tends to make you grow sideways. So excess insulin in an adult is not such a good thing; it contributes to obesity and to diabetes.

[Damien Blenkinsopp]: I guess we would throw in body builders in there as well, because they’re always trying to stimulate insulin to stimulate greater muscle growth.

[Gene Fine]: Yeah, well I mean if you’re extremely physically active, you probably can eat whatever you want. I’m not talking about recommendations for body builders; I haven’t studied that. I know that others have. Jeff Volek and Steve Phinney have looked at athletes, and they recommend low-carb diets for them as well.

But the main group that I’m really talking about is the average person who is, unfortunately, a little bit more sedentary than they used to be. And in this group we really don’t need very much insulin to go about our normal activities. And so carbohydrate restriction is probably safe.

[Damien Blenkinsopp]: Right. So would you put protein in there as well? Because protein also can stimulate insulin.

[Gene Fine]: Yeah, that I think is an interesting and maybe more controversial area.

Protein certainly can stimulate insulin. And the question about how much protein to consume in a diet is really an important one, but an independent question which I think has not been answered. I mean, if you look in the literature recommendations for protein in the diet are all over the page; they vary from 20 grams a day to 150 grams a day.

So I don’t know that I’m really in a good position to comment on that because it hasn’t really been adequately studied by anyone, including us. In our own study we didn’t limit protein, so we might have done better than we did if we had.

But nonetheless, our human study did show that the patients that had the highest level of ketosis were the ones who did the best in terms of stable disease or partial remission of their cancers. And those who had the lowest levels of ketosis had progressive disease.

[Damien Blenkinsopp]: So you’re talking about how insulin inhibition mechanism, are they basically opposite correlates? So when insulin goes down [it is] in response to ketosis going up? Is that basically the rough mechanism, so that you could map those to each other? That’s why with a low carbohydrate diet, ketosis goes up and insulin goes down.

[Gene Fine]: Yes. I didn’t actually clarify that. I was saying, yes, that’s the general idea.

I didn’t quite complete the thought that really there are three mechanisms by which a very low carbohydrate diet could inhibit cancer growth, and one of them is, as I say, by reducing carbohydrates in the diet and reducing insulin secretion.

Insulin by itself is a stimulus to cancer growth, but very low insulin will at least have the potential to slow that. So insulin by itself would slow the cancer growth. And there are two cellular mechanisms, so I could insulin twice.

But in addition, there are systemic effects in the whole body, and very low insulin causes mobilization from fat cells — in fact, that’s how you end up losing weight — and the fat gets broken down in the liver. And increased breakdown of fat in the liver leads to production of ketone bodies and ketosis. And ketosis independently, we’ve shown at least in metabolic studies in cell culture, that ketosis itself can cause inhibition of cancer cells. So it can inhibit cancer cells; it leaves normal cells alone. And as I say, we also showed that in our human study.

[Damien Blenkinsopp]: Yes. Yes, thank you. So there’s three mechanisms.

[Gene Fine]: Yeah. Well two of them I consider to be insulin, because there are two different insulin pathways that could be inhibited. And the third mechanism is the systemic effect of low insulin causing ketosis in the liver.

Increased fat mobilization causes ketosis in the liver, and the ketone bodies circulate in the body. Normal tissues tolerate it very well and can use ketone bodies as a fuel, but the cancer cells — at least that we’ve shown in vitro — can be inhibited by them.

[Damien Blenkinsopp]: Great. It’s interesting to look at the mechanisms, just in case later on people discover different tactics for modifying insulin, for example. I mean, like there’s drugs and stuff. Or, for introducing additional ketones or something.

So, we were talking just before the call about the study where you were actually looking at how ketones inhibit some of the cancer cells. Could you talk a bit about that? Because I know there was some glucose and ketones involved, and it was interesting how it’s done.

[Gene Fine]: Yeah. In cell culture studies, when we started this a few years ago, we studied three different normal tissue lines that were fibroblasts, which are normal connective tissue that we have in our body. And we also studied seven different cancer lines. Five colorectal cancer line variants and two breast cancer lines.

And what we found was that all seven of the cancer lines — well we grew all of the tissues for four days in a cell culture in glucose medium. And we saw how much they grew. But in parallel with that, we also grew the same cells in glucose medium but with added ketone bodies.

And, as I mentioned before, ketone bodies are a nutrient for normal cells, so we didn’t expect there to be any problems in the fibroblasts, and in fact the fibroblasts continued to grow normally when we added another nutrient.

However, all seven cancer lines showed growth inhibition. And they had differing degrees of growth inhibition when we added the ketone bodies. And we found that the degree of inhibition of the cancer lines was proportional to how much they over-expressed a particular protein called uncoupling protein 2, which actually reduces the efficiency of the cell in producing ATP.

So it turns out that the cancer cells were producing less ATP than they ordinarily would when we added ketone bodies. So the ketone bodies were metabolically inhibiting ATP production, and in proportion to their over expression of this interesting protein.

And the degree of ATP inhibition was exactly proportional to the degree of growth inhibition, which makes a lot of sense. That it requires ATP to grow. So that seemed to be pretty good evidence that we had at that point that it could be metabolic inhibition of cancer cells by these ketone bodies.

[Damien Blenkinsopp]:Yeah, that’s interesting, because, like you said, you’re actually adding something, you didn’t change [anything else]. You’ve got the same amount of glucose, so theoretically, even if cancers couldn’t process the ketone bodies very efficiently, they have the same amount of glucose there. So, in theory they could have been okay. But you’ve actually shown that somehow the ketone bodies are inhibiting that.

Would it be fair to say that the cancer cells are trying? It’s like they’re taking in the glucose and the ketone, and that they’re trying to process that. But because of the inefficiency, they’re not able to. Because it’s kind of interesting that it’s got this inhibitory mechanism there. It’s like they’re trying to, but they’re not very successful at it.

[Gene Fine]: Right, and one of the big questions is, of course, why are the cancer cells expressing uncoupling protein 2. And this has been observed that cancer cells were expressing uncoupling protein 2, for at least 10 or 15 years. There were studies in the early 2000s that I first saw that got me clued into the fact that they were doing this. And I thought well what could uncoupling protein 2 do to a cancer cell, and why would they do that?

The general explanation that I’ve adopted is that cancer cells also overproduce, what are called reactive oxygen species. And reactive oxygen species are chemically active molecules that are produced in all tissues, normal cells as well. But they’re higher in cancer cells than they are in normal cells.

And the thing about reactive oxygen species is that they actually act as sort of a two edged sword. They’re required for normal cell signaling. They’re a signaling molecule that helps cells grow, and develop, and proliferate, and so forth. However, they also are very chemically active and can cause mutations.

And mutations are also somehow the life-blood of cancer cells. Cancer cells become cancerous on the basis of mutations, and in fact they’re sort of evolutionary masterpieces in that they continue to evolve because of mutations. If a particular cancer mutation kills a singular cancer cell, well that’s fine, that cancer cell dies. But if another mutation that happens to be caused in another cancer cell makes that cancer cell even more aggressive, well then the cancer becomes more aggressive.

So, reactive oxygen species when over-expressed in cancer cells actually provide a mechanism for continued growth and continued development as an aggressive cancer. The problem, of course, is much too high reactive oxygen species will kill a cancer cell, as they will kill any cell. In fact, it’s very high levels of reactive oxygen species that are caused by chemotherapy, and are caused by radiation therapy.

So there has to be a limit on how much reactive oxygen species a cancer cell can actually produce. And what I believe, and I can’t say that I’ve proven this at all, is that the increased expression of uncoupling protein 2 — uncoupling protein is in fact, or believed, to limit reactive oxygen species. So it makes sense to me, but without proof, that the reason — quote unquote reason — for the increased production of uncoupling protein 2 is to provide a natural limit. A higher limit than a normal cell, but a limit on the amount of reactive oxygen species that the cancer cells produce.

So that’s my my overall belief. UCP2 is there for a reason. But it happens, it just happens, that that reason, which is important for the cancer cell, may actually be exploitable in terms of diet, because it also reduces the efficiency of production of ATP. I don’t know if that exactly adds up, but that’s what I believe.

[Damien Blenkinsopp]: Yeah, my understanding is — I’m just trying to re-summarize from what I understand and how it fits in — mitochondria create reactive oxygen species, and they tend to do that more with glucose fuel than with ketone fuel at a higher rate. And also when they get damaged they tend to create more reactive oxygen species, so they’re not as efficient. Does that fit in with what you just said?

[Gene Fine]: Yes.

[Damien Blenkinsopp]: Okay, great. So, somehow it seems like when the ketone bodies are being used though, in this scenario it’s potentially creating more reactive oxygen species via ketones, because of the protein change there?

[Gene Fine]: I think that’s not really clear. I don’t believe the ketone bodies… Other people who have looked into this a little bit, I think, are somewhat ambiguous about it as well.

I don’t believe that ketone bodies cause increased reactive oxygen species, but I can’t say that I know that for certain. I do believe, from at least the mechanisms that we’ve explored, that ketone bodies provide a complementary way of inhibiting cancer growth metabolically. If they also produce increased reactive oxygen species, and therefore contribute to higher levels of reactive oxygen species that are cell killing, that would be interesting.

But I don’t have direct proof of that. I believe that’s been suggested by others. Possibly Doug Spitz who’s a radiation oncologist, and I don’t know but Colin Champ, who is also a radiation oncologist. He’s written about this, but I’m not sure he’s described increased reactive oxygen species production through ketone bodies. It’s possible.

[Damien Blenkinsopp]:Alright, so great. There are some mechanisms you’ve been looking at there.

And another that’s been interesting about your work is that you’ve been looking at the differences between the different cancers in your studies with PET scans, which is of course your background and your area. Could you talk a little bit about the PET scan and how you use it to assess the cancer?

[Gene Fine]: Yeah, sure.

Most cancers — most aggressive cancers I should say — end up becoming, well first of all they begin to outstrip their blood supply. Their blood supply becomes erratic, and instead of having blood vessels well supplying nutrients to the cancer cells, the cancer cells become relatively hypoxic; they don’t usually have enough oxygen. And hypoxia will interfere with the ability of a cell to use the Krebs cycle as a means of developing energy.

So most cancer cells actually depend on glycolysis, which is anaerobic glucose metabolism, in order to develop their ATP. Now, because they’re using so much glucose and they over express glucose transporters and glycolytic enzymes, because they’re using so much glucose, if you inject a glucose like tracer — a radio tracer — whether it’s carbon-11 glucose, or another one that we liked to use in general nuclear medicine, fluorine 18, fluorodeoxyglucose.

This is a glucose analog, and it gets taken up very avidly by cancer cells that are aggressive. These aggressive hypoxic cancer cells take up FDG very avidly. There’s also something called the Warburg effect, which Otto Warburg, famous biochemist, demonstrated 100 years ago that aggressive cancers, in fact, they may be hypoxic but that even if you expose them to normal oxygen conditions, they still retain this glucose and glycolytic dependence.

In any event, the result is the same that aggressive cancers light up on a PET scan if you inject a patient with FDG, with fluorodeoxyglucose. And a PET scan is basically a nuclear medicine study. These radioactive tracers give off emissions, which allow you to see where the radio tracer goes.

So FDG distributes through the body. Glucose is used by a lot of tissues, so you can also see the heart, you can see the brain because these are often glucose utilizing structures. However, you don’t expect to see FDG in locations where it shouldn’t be. But if you have metastatic disease, which these kinds of hypoxic glucose dependent cancers, FDG will go to those sites as well.

And in fact this one image can be used, or a total body PET scan using FDG can be thought of as a one step metastatic workup, because you can actually see the full distribution of cancer cells throughout the body.

[Damien Blenkinsopp]: So is this the gold standard for assessing the severity of cancer? Could you give us an idea of when you would use this kind of scan?

[Gene Fine]: Yeah, everything in medicine really is very empiric. So if it works, it works. And certain cancers are particularly avid for this kind of tracer, where they do become hypoxic glycolytic cancers. And it’s turned out to be useful in management of cancers in one way or another.

For example, in a solitary pulmonary nodule, you’re trying to determine if this is likely to be a cancer or not or if it’s a benign module. Benign nodules don’t tend to take up glucose that avidly, but the malignant ones do. So an FDG scan can be very useful in just a diagnosis of whether a lung nodule is in fact cancerous.

But PET scans are useful in the management and decision making processes of breast cancers, of uterine cancers, actually a variety of lymphomas, in particular, are usually quite avid and PET scans can be quite helpful. Esophageal cancers, gallbladder cancer, colorectal cancers, PET scans can be quite useful because they light up, and they show you not only where the tumor is, but where the metastases are.

[Damien Blenkinsopp]: And the other thing, I guess it would simply appear bigger if it’s getting worse? So on your PET scan, if you did one every three months with a cancer patient and it was getting worse, you’d see it getting bigger and potentially spreading to other areas of the body. Is that how it comes back?

[Gene Fine]: Yes, you can definitely see how it spreads.

And nowadays I should actually say that most PET scan devices are actually two devices in one. They’re PET and CT, CAT scans. So you actually can get even better information, because the CT scan is really a computerized three-dimensional x-ray. So you’re actually able to see exactly where in the body.

The PET scan doesn’t have a road map of the anatomy, it’s just where the fluorodeoxyglucose goes. But on the CT scan, it gives you the underlying anatomy, so you get the anatomy as well as the functional arrangement at the same time and in the same locations. So you can identify exactly where you’re seeing it. And that’s very helpful.

I should actually mention that there are certain cancers that PET scans are not useful for. For example, pretty notoriously, prostate cancer is an unusual cancer. It’s unusual in a lot of ways.

Actually 80 percent of prostate cancers are rather slow growing and indolent. And probably for at least that reason, that may be one expression of the reason why they don’t actually take up glucose that avidly. It’s usually the aggressive [cancers] that take up FDG.

But also some other cancers, such as mucinous cancers that are filled with so much mucin that you lose out the effect of what you see on a PET scan. So mucinous cancers of the colon and the of the lung often don’t take up much fluorodeoxyglucose.

Squamous cell carcinomas of the lungs of course are very avid, but these mucinous ones are not. And endocrine tumors, very functional, they’re often not as glycolytic. They often operate on oxygen and they can have a normal Krebs cycle and normal metabolism. So thyroid cancers, unless they’re extremely aggressive, are not this slow growing, and they take up much less FDG. So PET scans with FDG are not as useful for certain kinds of cancers, such as these.

[Damien Blenkinsopp]: That’s important because — tell me if this is over simplifying — anything that doesn’t show up in a PET scan, would it be less likely that any type of low carbohydrate diet or inhibition of insulin and up-regulation of ketone is going to have an impact on it, as we’ve been talking before?

[Gene Fine]: Yes, true.

In fact that’s very interesting because — I was mentioning prostate cancer before — prostate cancer actually, it’s not even approved for PET scan use, I should mention. Because they say 80 percent of prostate cancers don’t take up FDG. But in fact prostate cancer is also not associated with obesity. It’s not associated with hyperinsulinemia. It’s not associated with high glucose levels in the blood.

In fact, interestingly, there’s an inverse association of diabetes with prostate cancer. Patients with diabetes — it’s a little bit odd to use the word, because I’m not sure that it’s accurate, it may not be cause and effect, but it’s at least an association — are so called protected with diabetes against prostate cancer.

Now I don’t want to recommend getting Type 2 Diabetes to protect yourself against prostate cancer, but the point is that not all cancers would respond to a low-carb diet either. It doesn’t seem to have anything to do with the mechanism of that particular kind of cancer.

[Damien Blenkinsopp]: Right. The mechanism you described earlier was higher insulin would lead to more aggressive cancers, but in this case you’ve described, Diabetes 2 you’d have higher insulin, but it’s actually reducing the likeliness of getting prostate cancer. Is that correct?

[Gene Fine]: Yeah, it appears to be. As I say, at least epidemiologically, it fits the mechanism of the — I should also mention that 20 percent of prostate cancers are actually very aggressive.

So this is a distinct minority of prostate cancers. I don’t know that anyone has done much study of whether these aggressive prostate cancers, this subvariant, which grow much more rapidly, actually are glucose dependent. They may well be, but I don’t know that they’ve been studied this way. So I can’t comment on those. But they might be FDG avid.

The other thing though is that actually aggressive cancers, very aggressive ones, not uncommonly develop a taste for, not glucose, or not just glucose, but also an abundant amino acid that circulates in the blood called glutamine.

For cancers that are dependent on glutamine more than glucose, they might have even bypassed. They can be aggressive, and they may be glutamine dependent, so they may not show up on a PET scan, and they also may not be responsive to a low carbohydrate diet. So there are other subtleties here that have to be explored before knowing exactly what to do in these kinds of situations.

[Damien Blenkinsopp]: Well I’m guessing potentially restricting glutamine might have a kind of impact there. I guess there’s no studies that have been done on that.

[Gene Fine]: That’s hard. It’s hard to do that, because glutamine is synthesized by the body, and it just comes out of ordinary metabolism.

Glutamine and Glutamate are products of protein metabolism. Glutamine can actually be synthesized, glutamate can be synthesized from alpha ketoglutarate, which is a product of ordinary metabolism. So it can actually be synthesized, and is, and then circulates in the blood steam in high concentrations. And you can’t really restrict glutamine in a diet and expect glutamine to go away; it won’t happen.

I think there are approaches that are trying to figure out how to limit glutamine in the blood, but I’m not sure how successful they are. It seems to be an important metabolite and substrate for a lot of different mechanisms. It’s actually used by the brain, indirectly at least. And so, there really are glutamine restrictions, I think, is something still for the future.

[Damien Blenkinsopp]: In summary out of everything you’ve been saying, that the fasting approach or the low carbohydrate approach is, in your view, only applicable to some types of cancers, and typically the most aggressive ones.

[Gene Fine]: Yes, I would agree with that.

The other thing I should mention is that the fact that there are plausible mechanisms where cancers could be inhibited by a low carbohydrate diet, cancers of the types that we’ve been discussing, doesn’t guarantee that it would be inhibited.

And I should also mention about the PET scan, that a PET scan in the way we used it in our clinical pilot study in 2012 with 10 patients was that the PET scan indicates that we can at least identify a cancer that is glucose dependent. We can do that on a PET scan. So those, from the perspective of our hypothesis are carbohydrate, or at least have the potential to be carbohydrate restriction sensitive.

It doesn’t guarantee it, because we don’t actually know which cancers will have the appropriate characteristics and qualities. Maybe not all cancers will express uncoupling protein 2, or whatever other mechanism we were describing earlier. So we can’t guarantee it.

And in fact, if I would describe the hypothesis that I believe, it’s that — I actually have this on a slide in front of me because I like getting the wording exactly right — that large cohorts of individuals with cancer in the developed world do not experience sustained ketosis, or other features common to the insulin inhibited very low prone state. We’d expect many cancers to express a range of plausible vulnerabilities, and accidental adaptations to this unfamiliar metabolic microenvironment.

So, I think that’s the broadest statement that I feel comfortable making, that we can’t guarantee that an individual cancer is going to be responsive to this, even if it has a positive PET scan, because we don’t yet know all of the characteristics that are required. But we do believe that those kinds of cancers are at least eligible for that possibility.

[Damien Blenkinsopp]: Right. Well so it sounds like at the moment there’s nothing really concrete on this, but we think there’s a higher probability of some types of cancers, so that the most likely cancers to respond to this would be ones which tend to be more glucose dependent.

[Gene Fine]: The ones that show up on PET scans would be the ones that would have eligibility. So, we actually treated in our 10 patient study a range of patients, and there were several with lung cancers, there were several with breast, several with colorectal. There were a couple with esophageal [cancer]. So those were the ones that we actually treated.

This was a very small study, so it’s a little hard to generalize from them. But in addition, as I say, the ones that are associated with hyperinsulinemia and hyperglycemia could also be eligible, I would say; endometrial, uterine cancers, perhaps pancreatic cancers, and others have actually begun studying that as well. Possibly kidney cancers, and maybe gallbladder cancers as well.

So these are the ones that I would consider to be at least potentially eligible for this, depending on what else we learn.

[Damien Blenkinsopp]: Great, great.

Particularly in those cases, if I have cancer I’d probably want to get a PET scan to see if it lights up.

I don’t know if you have an index there or if it’s just something visual you use. Do you have any kind of index you use with PET scans to understand the severity, like how much is lit up?

[Gene Fine]: Yeah, there are ways of quantitating PET scans, and you can eyeball the uptake, which is often done for purposes of saying whether the cancer has spread to a location or not. If you have a primary.

But if you have a, I like using the solitary pulmonary nodule because so many of them are benign and others are also malignant. And so people have attempted to develop quantitation, and there are a variety of different ways. One of the common ones is called the standardized uptake value.

And you compare the uptake there, essentially, to the average uptake in the whole body. And a value has been assigned by a number of investigators as a cut off that can be useful, and that’s an SUV of 2.5. That’s two and a half times the average value in the body is assigned as being a cutoff for cancers.

Now all these cutoff values have overlaps, and some of them turn out to be benign, but the frequency tends to be much higher. And the higher the SUV the higher the likelihood for cancer.

The reason that there can be uncertainty in this is that the uptake of fluorodeoxyglucose can also be seen in inflammatory tissues, and inflammatory situations, for example even in pneumonia. You can see pneumonias take up FDG. You can see benign granulomas take up FDG, although they usually take up less. But in fact you can get false positives.

[Damien Blenkinsopp]: Oh, so could this be any type of inflammation in the body? Basically where white blood cells are active?

[Gene Fine]: Yes.

[Damien Blenkinsopp]: And there’s a lot of inflammatory conditions in the gut these days. Is that something that would potentially influence it?

[Gene Fine]: Yes. You do in fact. With the colon there are also patterns of uptakes, so the thing is inflammatory conditions in the intestines and the colons, for example, usually there are patterns of uptake, and you actually see an outline of the colon with FDG distributing itself throughout the colon and basically showing the shape of the colon.

Whereas cancers usually have a site of origin and they can be somewhat irregular. But they generally have a round or a spherical type of initiation and shape. And come in clumps. So there is usually quite a big difference between what you see intestines and that as well.

But these are non-invasive diagnostic tests, which are absolutely marvelous because things used to be much more invasive. But they do have false positives. Your goal in a non-invasive test is to be able to screen well, and therefore identify those patients who may have this condition.

And if it’s negative it can be extremely helpful because then the patient doesn’t have it. But if you do have it you may still have to, in some cases, go on and do a invasive biopsy in order to determine what’s actually there.

[Damien Blenkinsopp]: So I guess, just to be practical for anyone at home that might be related to some cancer case or perhaps working with cancer patients. So if it does come up a positive PET scan, it may be worth using a ketogenic diet, a low carbohydrate diet as one of the tools. Could you just confirm more, and tell me that that’s not correct. And then talk a little bit about your recharge trial, where you were actually looking at this.

[Gene Fine]: Sure, okay. I think that it’s hard to generalize. I have spoken, patients have found me on the internet and have called me and discussed their particular cancer situation. And I don’t consider myself explicitly an advocate for this, simply because a 10 patient study — which I’ll talk about in a minute, our recharge trial — is a very small study, and it’s pretty hard to generalize from a study of 10 patients.

But it’s not appropriate to make a scientific conclusion when generally the standard of evidence is that you have to do large, randomized controlled trials. However, that would be the direction I’d like to go to find out more information. And also the fact that it certainly is uncertain whether this works in all patients with PET positive cancers.

But I can talk a little bit about the recharge trial, as preliminary as it is. And what we did was we studied 10 patients with advanced cancers, which is to say they all had PET positive studies and they all had failed several rounds of chemotherapy and were still progressing. So they had had chemotherapy, they were therefore eligible for an experimental trial of the diet, because nothing really was working anyway.

And these patients signed informed consent and they were told that we didn’t know what the outcome was going to be, but we were going to put them on a 28 day trial diet of very low carbohydrate. And so the patients agreed to this, and for 28 days under nutritionist and dietitian guidance they were taught to change their diet.

They had a two to three day trial diet, just to see if they hated it, to make sure. If they didn’t hate it then they could go ahead, but we didn’t want to have people who were clearly not going to be able to complete the diet. We limited it to 28 days because change in diet is hard for anybody. It’s not easy. However, just about anyone can stay on a diet for a month.

So we figured that this would give all the patients a chance to succeed. And principally, the first goal we had to have was safety and feasibility. Was this actually safe? There wasn’t really a lot of reason to believe that it wasn’t safe, but you still have to try that out before you can do anything else.

And it was, there were no unsafe adverse effects. The worst effects that sometimes were reported in this, that we did see were some patients had some reversible constipation — as I say reversible — and reversible fatigue within a couple of weeks. And that’s generally the worst that happened.

So the patients were able to span the diet. Half the patients stopped a little short of 28 days, like 26 or 27 days. We considered that really a successful completion. They didn’t stop because of the diet, they stopped because these were patients with advanced cancers who had planned before they had heard about this trial to go on vacation.

They had bought tickets and thought this might be the last vacation they would be taking. So we weren’t going to interfere with that, and we got the PET scan two days earlier than we had expected and they then left the next day for vacation. So really everyone completed the trial without any adverse effects.

Now, what we did see was that, and we measured ketosis as the standard for how compliant they were. Patients would report their food intake and they would tell us what they ate, and the dietitians would record that. But food recall can be inaccurate.

The most reliable way we could determine whether they were on a ketogenic low-carb diet would be to measure ketone bodies in the blood. And we did find that all of the patients were ketotic. In fact all of them became ketotic — and we measured this weekly for four weeks, a baseline and then four weeks — patients became ketotic really by the end of the first week. So we know that they were ketotic for the period of the four week trial.

[Damien Blenkinsopp]: Were you measuring blood levels?

[Gene Fine]: Yes, these were blood levels. We felt that that was going to be a more accurate measure because urine levels can be influenced by hydration state. If you’re very hydrated you’ll dilute your urine, if you’re dehydrated you’ll concentrate it. So this is more accurate.

[Damien Blenkinsopp]: Yeah, absolutely. We discussed this with Jimmy Moore, who you know well, in a previous episode.

[Gene Fine]: Oh yeah, that’s right. And he actually interviewed me one time as well. That’s right.

So the goal, as I say, was the 28 day diet. And what we did find was that, one patient we actually had to exclude from analysis because, it took us four years to recruit 10 patients. Most patients are on chemo and they don’t really have this opportunity.

And we also didn’t want patients who were too thin because that would have trouble getting past the investigational review board. These are thought of as weight loss diets and you don’t want a cancer patient to lose too much weight. So we had to restrict our patients to patients who were normal weight or above.

Now finding patients with advanced cancer who had not lost too much weight took a long time to get this group of patients together. It took four years to recruit them, there was a lot of time in that.

So beggars can’t be choosers, and we didn’t notice that one patient had had advanced breast cancer with chest wall invasion, but she’d had it for 14 years. And this was different from all the other nine patients, who had failed multiple chemotherapies. She’d had this for 14 years and had never sought any treatment for it at all. She had no surgery, she had no radiation therapy and she’d had no chemo.

So in retrospect we realized, oh my gosh, this patient clearly has much more indolent disease. Even though it’s advanced, it’s progressing so slowly we would have to exclude this patient from analysis because in one month she wouldn’t show change.

She was stable from that point of view, so we couldn’t show progression of disease in this patient in a one month diet. And it turns out she wasn’t very compliant with the diet anyway, and she showed very little change. So the reality was we had to exclude this patient. So we really only evaluated nine patients.

Anyway, getting to the gist of that, of the nine patients the results on the face of it were really not terribly impressive; five patients showed, well four patients showed stable disease, one patient showed a partial remission on the PET scans. We had a baseline PET scan indicate the patients had glucose dependent cancers, and we had a follow up PET scan to monitor the change in the PET scan as an index of whether these patients responded in some way.

But four patients had continued progressive disease. So on the face of it, this is really not that impressive. However, the interesting thing about the difference between these patients is that the patients who had the stable disease or partial remission had three times the levels of ketosis compared to those who didn’t.

So the fact was that whether this was an issue of compliance or metabolic effect, whatever that was with the level of compliance they achieved, the reality was that the patients who showed the best responses were those who had the most ketosis. So that was also consistent with our hypothesis that the ketone bodies and the effect of low insulin levels, which would include ketosis, would have some varying on the outcome.

[Damien Blenkinsopp]: So did the same thing show up? The higher the inhibition of insulin the better the result?

[Gene Fine]: Yes,that’s essentially what we’re saying. That the more it was inhibited, it’s effects were best measured by measuring ketone bodies. Insulin itself varies so rapidly that unless you time it exclusively the same way, timing after a meal and so forth, you have to be very careful. So we use ketone bodies as a more robust measure of the effects on insulin inhibition.

[Damien Blenkinsopp]: So is that pretty concrete then? That there will always be an inverse correlation? That that’s been established very well in science?

[Gene Fine]: An inverse correlation between ketone bodies…

[Damien Blenkinsopp]: Because as you say, insulin can go up and down very quickly so it’s kind of difficult to know where it is. But in scientific studies it’s been pretty well established that insulin is inverse to ketone bodies, so then it’s okay to assume that.

[Gene Fine]: Right, but they act on different time scales. Insulin spikes very rapidly after a meal, and ketone bodies gradually build up over a period of days after chronic low insulin levels.

So you can go out of ketosis fairly quickly, but not as quickly as you can spike. You can spike an insulin level pretty level and the ketone bodies will decrease over a period of hours, the insulin levels change rapidly over a period of minutes. It’s a little bit different time scales, but yes there is a general inverse relationship for chronic insulin levels and ketosis.

The other thing I wanted to mention about this is that the patients who did show progressive disease also showed evidence of, which we weren’t really looking at, we wanted patients who did haven’t coincident other diseases, particularly diabetes because we didn’t want to be treating two conditions at the same time. So we basically made sure that the patients were not diabetics and were not taking diabetic medications.

However, in retrospect we did notice that the patients who showed progressive disease had evidence of pre-diabetes. That these were patients who were the four heaviest, they actually were the four heaviest of the group of 10 patients. They also had baseline glucose levels 100 and above.

There was more evidence of pre-diabetes in this group than there was in the group that showed a response. And there were lower levels of ketosis. So, overall, we don’t know for a fact that this is the way to screen patients, whether this is actually a biomarker. I would suggest that it makes sense that in patients who have pre-diabetes, pre-diabetes is marked by high insulin levels, and it takes quite some [time].

So that in this group, a low-carb diet didn’t seem to have much benefit. In fact, it didn’t have any benefit at all, they had progressive disease.

Now of course the way you want to treat, at least the way I like to treat patients with pre-diabetes, is put them on a low-carb diet. But I think that that would take several months to improve their insulin insensitivity, and if they already have cancer that’s probably not what you want to do in this particular group. If they have cancer and they have pre-diabetes, you’d probably have to treat the cancer as a separate entity.

[Damien Blenkinsopp]: Right, because it’s going to take a longer time to have the metabolic impact that you want.

[Gene Fine]: Right, and you don’t want the cancer to be progressing during that time, so you probably have to make your choices in that case.

[Damien Blenkinsopp]: So, from your study I remember one thing you were doing was in order to assess the better performers was you were looking at the relative ketone change.

[Gene Fine]: That’s right. And we actually, we used relative ketosis, interestingly, rather than absolute. Now, the absolute ketosis was not very different in the two groups. But I actually believe the relative ketosis is more important, mainly because — let’s see if I can describe that succinctly.

When you looked at the baseline ketosis, baseline levels of ketone bodies, absolute values.

[Damien Blenkinsopp]:: So this is before you start the low-carb diet?

[Gene Fine]: Fasting levels, right.

There were some patients who had issues of values, who had like 0.04 millimolar. And then there were others who had 0.4 millimolar. So that’s factor of 10.

Now, the absolute levels of ketosis rose in most patients to about 1.0 millimolar. A patient that only went from 0.4 to 1.0 went up by a factor of just two and a half. A patient that went from 0.04 to 1.0 went up by a factor of 25. So there is a much bigger change in the overall metabolism, and the change of the metabolism in a patient that started at a lower value.

I would propose — and this is what I actually believe — is that the patients who were living with a baseline ketone body level of 0.4 were actually acclimating their cancers to a higher level of ketosis during the period of the cancer’s growth, initiation, and development. And in fact that these cancers may be well acclimated, in other words adapted to, that they grew up in a level in which they were used to these levels.

And so that you can’t expect — well, put it this way. Whereas I do believe that people who live in environments where they eat mostly meat and fat during the year — let’s just say Inuits for example that haven’t been exposed to McDonalds and Laps living in northern Finland and live on reindeer meat all day long — that people who live under those conditions I would suggest, and I don’t know what the evidence is exactly, that they will have lower incidences of cancer.

However, should a person under those circumstances develop cancer, you know you sure as heck would not put them on a low-carb diet, because you know that they developed cancer already on a low-carb diet.

So that’s what I’m basically saying. If you have somebody who already is in a state of higher levels of ketone bodies and cancer develops in a person like that, then you certainly wouldn’t expect that patient to be as responsive to a low-carb diet.

[Damien Blenkinsopp]: It’s interesting because there’s a lot of things in biology, like somatic signals, where, like if you think about the treatment of antibiotics, right, you basically have to pulse it. You have to pulse it and do it one go has to be done effectively. If you get chronic antibiotics for a while then it stops having it’s impact, and you don’t get the benefits, and so on.

So it’s interesting that you identified this mechanism where a body could be a lot more beneficial to, let’s say do something. I mean I’m sure you’re aware that Dr. Seyfried recommends a five day fast, which is a more extreme version of what you did in your study, and potentially may be more beneficial because it is more extreme. As you said, and maybe there will be a higher therapeutic value.

[Gene Fine]: Yeah, that’s right. And Dr. Seyfried is one, also Valter Longo in California has recommended calorie restriction and fasting as well. And I think that those methods may have some other unique benefits that carb restriction may not have. They also may not be as easy to implement, but I think that they’re all in the ballpark, and there may be values for all of them.

[Damien Blenkinsopp]: So one thing I did want to bring up is when we were talking to Dr. Seyfried he mentioned he’s using an index now, which is called the glucose ketone index. I don’t know if you’ve spoken to him about that, or come across it.

It’s simply glucose divided by ketones in millimolars. And he’s been using that to look at his approach to metabolic therapy and see if it’s effective. I’m just wondering if you could compare that to the relative ketones. Would that make sense for you, or you haven’t looked at this?

[Gene Fine]: I haven’t done that, so I really don’t feel up enough to comment on it. I didn’t do that. I actually might want to go back and calculate that as well in these patients to see if I can get those numbers and make some correlations. But I haven’t actually done that yet.

[Damien Blenkinsopp]: Yeah, it strikes me it just might be interesting because, as you said, some of the diabetic patients went up, potentially high glucose. So you might see something similar there. Based on it.

[Gene Fine]: Yeah, that’s right. I was just thinking about that.

[Damien Blenkinsopp]: Great, great.

There’s a few things I wanted to bring up here in terms of the other tactics people might use. Which I don’t know, you may not have an opinion on these. But there are other things that can change the levels of ketones in our body. You can use MCT oil, or ketone esters, exogenous ketones basically, or a high fat diet.

My personal experience with these, for instance, is I’ve been on a high fat diet for a while and in my fasting insulin tests, my insulin is pretty low compared to the average. And I understand that that’s pretty standard. So I was just wondering what you thought of these kind of approaches. Also, if you’ve seen anything that might say there would be similar impact. Because they’re basically mimicking the effects of a low carbohydrate diet.

[Gene Fine]: Well yeah, I actually don’t know what way a high fat diet is distinguished from a low-carb diet. There are three macro nutrients, and basically a low-carb diet is a high fat diet. I don’t know if a high fat diet necessarily is also a low-carb, but it must be lower in carbs because you don’t really make up the difference in protein.

[Damien Blenkinsopp]: Right, you’re right. The question is the protein. That’s the missing…

[Gene Fine]: Right. And as I say, I haven’t tested the protein values. We didn’t restrict protein in our group. I think we could have.

We were dealing with patients who, as I say, had advanced cancers, and we were getting them as through referrals from their oncologists as volunteers, and we really didn’t want to give them something too complicated to do, so we just tried to [simplify it]. But yes, protein, certainly restriction might have had further benefit.

But as far as inducing ketosis with medium chain triglycerides, coconut oils and the like, ketone esters, I think these are interesting approaches. They can certainly, possibly offer more convenience, rather than going through a low-carb diet. And that I think has value.

The other thing to note is that they don’t actually mimic the full effects of a low-carb diet because they don’t inhibit insulin. So, there is that aspect of it. While there may be value, I’m not sure that they’ll produce the full effect.

[Damien Blenkinsopp]: Great, great. Thanks for the commentary.

Now the other thing I wanted to just bring up was metformin, I don’t know if you’ve looked at all at that.

[Gene Fine]: Well, yeah. I mean, I’m aware that this is being used, at least in trials, as another potential mimicker. And it has it’s own value. I think what it does for me is it illustrates the value of low-carb diets, because what it really does, metformin, is it limits glucose and thereby insulin secretion. So, it’s fine. To me it’s major mechanism is the same mechanism as a low-carb diet.

It has some independent mechanisms. It seems to up-regulate AMP kinase, which happens also to be done by low-carb diets. So metformin may have some advantages. It’s a drug. It’s a very well tolerated drug, but it’s not a universally well tolerated drug.

There are some side effects that have been reported. Not frequently, but some patients develop lactic acidosis, which can be very serious. And some patients develop hypoglycemia. So, I think overall it would be considered a very safe approach, it just has to be tested, like everything else.

[Damien Blenkinsopp]: Great. Thank you.

I was wondering if you had any opinion on calorie deficit versus high intake of calories. I could be on a high fat diet, or a low carbohydrate diet, and still have a surplus of calories versus a deficit. Do you think that’s anything that could be either affecting your results, or something to look at?

[Gene Fine]: Yes, it is something, definitely, to look at. The calorie restricted approach has been advocated…well, it’s just been advocated. I can’t say exactly whether the mechanism is the same, overlapping, or somewhat different.

But I can just say this, that in our study we actually wanted patients to not lose weight. We encouraged them to overeat. Overeat a low-carb diet, but overeat. So to eat as many calories as they needed to sustain their weight.

So the only comment I can make about this is that all the patients lost weight. We did not intend for them to lose weight, that was not our goal. We encouraged them, we would be weighing them weekly and we’d tell them, “Eat more, eat more. You’re making these shakes, add more cream to it. Add more oil to your foods. Put butter on everything.”

Well anyway, whatever it is that we encouraged them to do, all 10 of them lost weight. They lost on average about four percent of their initial body weight. The interesting thing about that, I just suppose that this is why these diets are effective as weight loss diets.

No one knows exactly why they work, but you certainly can speculate some pretty plausible mechanisms. One is that ketosis may inhibit appetite. Another is that your inhibiting insulin, and insulin, as I say, under the influence of carbohydrate makes you fat and keeps you fat. The absence of insulin does the opposite. It releases lipids from your fat cells, and metabolizes them in the liver. So the fact is that low-carb diets intrinsically may be weight loss diets.

We believed in our study that it’s possibly to defeat this. That there’s such a thing as overfeeding, and maybe if one is particularly conscious about this, one can do this. But the other interesting factor is that seven out of the 10 patients were above a body mass index of 25, which is to say they were overweight. Only three of them were in the normal weight range, between 20 and 25.

And as it happens, the patients who lost the most weight were the heaviest. Frankly they were delighted with their weight loss, even though we were trying to maintain weight just for the principles of our study.

The patients who were in the normal weight range, the two who were the higher two in the normal weight range — I should say, the heaviest patients lost about five to six percent of their body weight. The patients who were in the normal weight range, the two heavier of them — 25 BMI and 23 — lost about three percent of their body weight. And the patient who was 20 lost no body weight at all.

So what this tells us is something we all know also, which is that the closer we approach our ideal body weight, the harder it is to lose weight. I don’t know whether you’ve observed that yourself, whether you have gained, lost or are stable in terms of your body weight, but I believe that high fat diets do not necessarily cause weight loss, particularly in people who are approaching their ideal lean body weight.

[Damien Blenkinsopp]: I’ve been on this diet for many years, just as an n=1 experiment. I think I lost a bit of weight when it first started, but ever since I’ve been really stable, ever since. And I’ve never paid attention to the number of calories. Sometimes I’m sure I’m eating a lot of calories, and sometime I’m not eating so many, for whatever it’s worth.

[Gene Fine]: I should also mention one other thing, which is that in our study, when we calculated what the calorie intake was on the basis this is of course on the patients self-reports, that all the patients reduced their calorie intake as well. Now, we didn’t want them to, but the measured calorie intake on the basis of their self reports was reduced, in fact by about one third.

The other interesting thing though is that the stable disease effect and partial remission, those patients who showed stable disease or partial remission had three times the ketosis. But the degree of weight loss in the two groups was the same. They both lost about four percent. So although there was weight loss in all the patients, weight loss, or calorie deficit, did not appear to correlate with the effects that we saw.

[Damien Blenkinsopp]: Well that’s a great point then.

I think the other point you illustrated, if we’re talking about your studies, is how difficult it is to set a good cancer study up, given the situation with the patients and you’re trying to control for a lot of things. So, as you say, it took you four years to recruit the patients for the last study. So I think it gives us a much better appreciation of how difficult it is to do these types of studies.

[Gene Fine]: Yeah. I think it is the fact that physicians are trained to treat with drugs and that’s very understandable. Drugs generally work well. And in cancer, it would be naive to start off with the assumption that diet is going to be a successful therapy. It has to be tested.

And so, whereas there was some reluctance, there wasn’t entirely, and many of the oncologists were very helpful and cooperative and referred patients when they were on a chemo holiday, or chemo break. That’s what was needed to get this study done. And also the fact that I didn’t want patients who were too thin and too sick.

But I think going forward, I think that we can count on, perhaps, some additional support. And we are actually aiming for human studies going forward as well. Right now, as I say, we’re also trying to couple diet with drugs in animal studies. So this combination, we hope, will lead us somewhere.

[Damien Blenkinsopp]: Yeah, Great. So is it the first time someone’s been trying to couple chemotherapy with diet? Or are there existing studies that you’re basing your current work on?

[Gene Fine]: Coupling a low carbohydrate diet with other therapies has been done. I know that Colin Champ and Doug Spitz, I believe, have coupled low-carb diets with radiation therapy. As far as coupling with drugs, I’m not actually immediately aware that anyone has done that. I think that we may be the ones who are looking at that right now.

[Damien Blenkinsopp]: Great. Wrapping up a bit, thanks so much for your time today.

Where could we learn more about this subject? Are there other people you would look to to learn more about this? Perhaps people you’ve worked for who are doing a lot of studies in this area. You mentioned Valter Longo, of course who was mentioned in Dr. Seyfried’s as well. Or are there any books or presentations on the subject that are good?

[Gene Fine]: I’m trying to think, other presentations. I know that there are some other people working in the area that I know have been doing good work.

Dominic D’Agostino in Florida. I think he has a website, and it would be interesting to look at some of the work that he’s done. A somewhat, I hope, accessible discussion of what we’ve talked about.

I have a couple of guest blog posts that I wrote. My colleague Richard Feinman has a generalized biochemistry and metabolism web blog, and he invited me to write some guest blog posts for his web blog. So I wrote two.

One which is on the general hypothesis, which I didn’t even discuss today. I mean, I discussed it in the broadest forms, but I didn’t discuss some of the details. And the other one is more on the clinical trial, on the recharge trial. So it gives more detail on that.

And I think Colin Champ has an interesting website as well, Caveman Doctor. I think I’d look at that. These are other resources. I think I’ve mentioned most of those that I know.

[Damien Blenkinsopp]: Great, great. So, we’ll put links to all of that in the show notes, thank for those.

Well how about you? What are the best ways for people to connect with you? I mean you mentioned the blog posts, which we’ll put in. Is there anything else? Do you have a website, or are you on Twitter? Is there anywhere you are active where people could learn more about what you’re up to?

[Gene Fine]: Let’s see. The website that I have is my website at Albert Einstein. You can also, through the blog posts that I mentioned it gives other links to papers that I’ve written as well as to my website. So I think that probably the most complete portal, you can look me up just at Albert Einstein and find my website there. And that will also link me to the dietary studies and the blog posts and the papers. They all connect to each other.

[Damien Blenkinsopp]: Great, great. We’ll put those on the show notes.

Something we spoke about just before the interview, your perspectives are a little bit different to Dr. Thomas Seyfried that we’ve already had on the show. Could you briefly summarize where you think you might have a different opinion?

[Gene Fine]: Well, I just think that we really are in the same camp. I think that we both believe in metabolic therapy, as do the other people that I’ve mentioned. I think that he believes that when he describes cancer as a metabolic disease, he believes that the fundamental problem is it starts as a metabolic disease in abnormal mitochondria. That may be true.

The only thing that I think that I would differ is that that abnormality in the mitochondria, I believe, is a genetic abnormality, even in the mitochondria. That you still have, what’s happening in the mitochondria is that, to me the fundamental problem in cancer is actually a genetic mutation that leads the cells to increased proliferation and growth and unlimited growth and immortality, and so forth.

The source of these mutations, I believe, could certainly be in the mitochondria, but in fact if it is, and that would make sense to me, it would be increased reactive oxygen species. And increased reactive oxygen species can cause mutations in the genetic portions of the mitochondria, and that would cause abnormal mitochondria. Or it could cause mutations in the DNA of the cell. Certainly hydrogen peroxide, peroxide can migrate over distances and can migrate into the nucleus.

So, I actually believe that the fundamental problem that leads to the cancer may initiate in the mitochondria with reactive oxygen species, but nonetheless results in the fundamental change of cancer is in a mutation. So I think that [in a] certain sense we’re describing the same phenomenon, but we have a different emphasis on which syllable we’re emphasizing.

[Damien Blenkinsopp]: Right. Potentially where it starts and where it finishes, and so on.

[Gene Fine]: Yeah, yeah.

[Damien Blenkinsopp]: Great. Great, thanks for that clarification.

Before you go, I just wanted to look at a bit of what you do on a personal level with your body data. I was just wondering if you track any metrics at all for your own health, biomarkers, or anything like that on a routine basis. Maybe yearly, or more so?

[Gene Fine]: When I started studying this in, around 2003, and I got interested in it, by the way, from my friend and colleague Richard Feinman. He’s a biochemist, and he’s been interested in this principally from the point of view of the effects on metabolic syndrome, diabetes, lipid disorders, and so forth.

However, I came in from the nuclear medicine background, and PET scanning and Warburg effect, and hypoxic cells. For me it was attractive for the possibility that this may have some effect, low-carb diets in inhibiting glycolosis, and as I mentioned earlier through the uncoupling protein 2 having a unique inhibitory effect on cancers while sparing normal cells.

So in 2003 when I got interested in this, and I decided that — you know, I never really had a weight problem, but I had gradually put on a few pounds over the years. And I have a small frame, so I’m about five foot nine, and 165 pounds. For me that was carrying excess fat.

So I figured well, you know, if I’m going to study this in others I might as well experience what it’s like for myself. And maybe I’ll even have some benefit in terms of overall body composition.

To make a long story short, I’ve been on a low-carb diet of various degrees of strictness over the years. In some cases I’ve been ketogenic, I’ve been very strict. In other cases, I’ve just been low-carb, but not likely ketogenic. I haven’t been under 50 grams a day, I’m not quite sure.

But the short story is that over a period of now, what 2003, really 2004, about 11 to 12 years, I’ve lost 33 pounds. Sometimes it’s been in fits and starts, but I’m very, very happy and comfortable with my weight right now. I like myself at 132. I have a small frame. I feel that for me I am lean and fit, and that’s a good thing.

There’s that aspect of it. In terms of other biomarkers, the numbers that I like to look at, in particular, are those that have risk profiles for, well my glucose and my hemoglobin A1C has dropped. In addition, my fasting blood glucose.

[Damien Blenkinsopp]: So if you remember, where did they start and where are you at now? And are you happy with the numbers now?

[Gene Fine]: Well yeah. I mean, I think I’ve been stricter lately and more consistent, so I’ve only been monitoring them really. I don’t think I’ve really been taking very close watch of them.

But I think over the past year or two my blood glucose, a couple of years ago had actually been at 100, and my hemoglobin A1C I think at one time was around 5.7. I’m sorry, this was only about one year ago.

The hemoglobin A1C changes slowly, but in two successive measurements, I’m about to come up with a third, it’s dropped to 5.7 to 5.6 now to 5.5, and I’m expecting it will continue to be going down because I’m doing this. And my fasting blood glucose is now about 94. So it’s dropping, and I’m satisfied with that.

I used to eat what was recommended. I used to eat a low fat diet, which of course means a high-carb diet, and I think I suffered the consequences. But little by little that has been reversing.

From the point of view of my lipid profile, the things that I’m most interested in are those that are atherogenic, that contribute to risk of cardiovascular disease. And I think the current thinking, which makes some sense to me, is that it’s not so much LDL which is targeted by the cardiologist, because LDL is a mixed bag.

Low density lipoproteins really consist of two major fractions. One of the light, buoyant LDL, which is really not harmful, and the other is the small dense LDL, which is. And what happens on a low-carb diet is you reverse the ratio. You reduce the amount of small dense LDL.

And the good measure of that, because it’s hard to get that measurement directly. There are only a few labs in the world that actually measure small dense LDL directly. You have to send away to specialized testing for them. However, there’s a good index of it and it’s the ratio of your triglycerides over your HDL.

[Damien Blenkinsopp]: So there’s a proxy?

[Gene Fine]: There’s a proxy for small dense LDL, yeah.

[Damien Blenkinsopp]: Oh, great.

[Gene Fine]: And so when I started, I guess when I first measured my triglycerides to small dense LDL when I had been not very compliant at all, my triglycerides at one point were about 150, and my HDL was about 50. So the ratio was about three. And since going on a low-carb diet, my triglycerides fell in half, to 74, and my HDL went from 50 to 75. So basically my ratio is now one.

[Damien Blenkinsopp]: That’s pretty high.

[Gene Fine]: So all the things went in the right direction. I’m very pleased that the HDL went up, without any major increase in exercise, just the diet alone. And my triglycerides fell in half. So those are both just exactly what you would expect on a low-carb diet, and what you want.

[Damien Blenkinsopp]: Great, thanks for those.

They’re very useful, especially the triglyceride HDL ratio. Because it is difficult to get the, I guess you were talking about the NMR, nuclear magnetic resonance. We spoke about that in a previous episode. And then there’s the LDLP to get the number of particles. But as you say, there’s only a few specialized labs, so it’s not as accessible. So it’s great to know that there’s a proxy to use also.

Last question here. What would be your number one recommendation to someone trying to use some kind of data to track, whether it’s biomarkers or something else, to make better decisions about their own health?

[Gene Fine]: Yes, well I mean it depends on what aspect of the health you’re talking about. But I don’t know if ketosis is necessary.

As I mentioned, any change of diet can be difficult to sustain over the long term. I don’t even know what it takes. Willpower is something that, what is it. So, it’s hard to know how to do that.

And by and large the reason I would say it’s hard to change diet is people eat what they like. And you want to eat what you like, and so changing your diet means you’re, by definition, changing it to something that you didn’t prefer. So it seems as though there’s a fundamental issue there.

On the other hand, I think that if you have a weight issue that you’re not happy with, or your doctor reports blood lipid markers or glucose markers that you’re not happy with and evidence of pre-diabetes or diabetes, and you’re on meds, so forth — let’s not consider meds yet. Let’s just talk about without being on meds. Because low-carb diets, if you can actually go on them and you’re also on meds, you have to do that under supervision because you might actually become hypoglycemic, and you have to be careful about that.

But without considering meds if you just want to, say, improve your health in terms of obesity or aspects of metabolic syndrome, lipid disorders, blood glucose levels, pre-diabetes. Without going on a strict low-carb ketogenic diet it’s not as hard, I think anyway, to reduce the quantity of carbohydrates that you eat.

You can have a breakfast where, you can cut out, well cut in half the size of the desserts that you eat. You can cut in half the amount of mashed potatoes that you eat. You can eat one slice of bread instead of two, or you can not eat bread. Although that sometimes is hard for people, but if you eat the bread and don’t eat the mashed potatoes, you’ve reduced the number of carbs that you eat.

So if you just start by reducing certain portions of carbohydrates. And I actually found I still have carbohydrates a little bit now. I have a sort of modified Atkins Plus, I call it, or South Beach Plus. I have a little ice cream at night. It’s my treat.

Overall, I probably eat about 60 grams of carbs a day. But, I treat myself to a little bit of ice cream at night. I’ll find out what that’s done to my lipid profile, by the way. But I don’t think it’s going to have a major effect. I think that overall it’s going to be still pretty good.

So the idea of reducing the overall quantity of carbs, I think, is actually important. I think that with the average American diet, I don’t know if the same is true in UK but probably, that overall consumption of carbs is 300 to 400 grams a day. And that’s really quite a lot. And if that could be cut in half to 150, that would be a big improvement.

So, I think that that would be lower stimulation of insulin secretion. Yeah, I think that that would be my principle recommendation in terms of health.

Now as far as exercise is concerned, exercise is also something that many people do but can’t stick to an exercise regime. And overall, I think that even if you look at the overall impact on insulin sensitivity and improving metabolic profile, there’s no question that exercise helps. But it really comes a distant second to diet in terms of having a dramatic impact on insulin sensitivity and these other biomarkers of lipids and glucose and so forth.

So that, while you’ll never hear me discourage anyone from wanting to do exercise, I think that if you want to have an immediate and more dramatic effect, the thing to do would be to reduce carbohydrates in the diet somehow.

And that’s probably the best I can say at the present time, because as I say, I don’t think anyone has a magic bullet as to how to help someone go on a diet. It’s never easy, but if you can find a way to reduce carbohydrates, you’re off to a start.

And if you feel encouraged by the results that you see, you tend to continue it.

[Damien Blenkinsopp]: Absolutely. Thank you for bringing that up, because we’re introducing changes here, new habits. And as you say, it’s super difficult.

I feel one of the things that helps people is making it clearer how helpful it can be in different areas of their life. Once you’ve heard it 10, 20 times from different people who are studying these things, like yourself, in different areas. I think it makes it easier for people, just because of the repetition, for the clarity in their heads.

I think part of the problem is the mystery and the misunderstanding, especially in the media and the press. The more times you’ve heard five different stories, the less you feel like taking action against any one of them, because you’re just not sure, you’re hesitant.

So thank you for your time today, because it’s certainly helping with these type of things.

[Gene Fine]: Thank you. I’m glad that you have this program, really, to spread the word through interviewing people who are active in the field.

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A look at a collection of high impact endurance tools and tactics – and the top biomarkers to watch for optimization. Vetted by an endurance athlete with years of experiments and competitions behind him.

Today’s episode is about endurance training and using high-impact tools to get the most out of it. We look at self-tracking in diet and exercise when aiming to optimize your body to perform at peak capacity.

We discuss factors playing a role in improving endurance through a healthy progression. What self-quantifying strategies are useful for tracking overall performance and health?

This episode features actionable takeaways on dealing with a variety of obstacles commonly experienced by endurance athletes.

How to make use of ketogenic dieting in maximizing fat-burning efficiency during physically demanding exercise? Which biomarkers are important for tracking individual organ-systems functionality in the body? How to maintain a healthy hormonal status?

Overall, we look to beneficial and practical tactics for athletes wishing to upgrade their performance and discuss common pitfalls to avoid in cultivating endurance.

On this full-on ketosis diet… the endurance payoff was huge. The amount of focus that I had for long periods of time. My ability to just hop on a bike and ride for hours with no fuel at all, with just water. It was pretty profound, because you produce all these ketones as a bi-product of fatty acid oxidation, and they’re used as the preferred fuel… while you’re out exercising. And that’s a huge boon to an endurance athlete.
– Ben Greenfield

Today’s guest is Ben Greenfield who is a professional competitor in endurance-demanding events, including triathlon and Ironman races. Ben has 11 years experience coaching athletes and fitness professionals.

Throughout his athletic career, he has researched physiology of upgrading endurance using a quantified approach. He has performed numerous self-experiments targeted towards understanding his performance parameters, and towards optimizing his diet and exercise.

Ben is the author of a New York Time’s best-selling book titled “Beyond Training: Mastering Endurance, Health, and Life”, which was published in 2014. His top-ranked iTunes podcast is called BenGreenFieldFitness.

The episode highlights, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. Enjoy the show and let me know what you think in the comments!

itunes quantified body

What You’ll Learn

  • Ben uses his biohacking experience to coach people on living healthy and attempting on-the-edge extreme exercise (4:46).
  • Ben’s interests in endurance training and research developed over time. No big eureka moments, just meaningful experiences (7:12).
  • Important biomarkers in endurance training specifically, and practical reasons for these picks in exercise self-tracking (11:24)
  • Why regulation of sex-hormones and cortisol (the stress hormone) are important to track in endurance training (15:50).
  • Why standard reference ranges for free testosterone are often not applicable to endurance athletes (16:48).
  • Liver enzymes, kidney parameters, Vitamin D, and digestive track inspections are also key biomarkers for healthy endurance training (18:20).
  • The digestive track plays an upstream role in multiple athlete pains and discomforts (21:18).
  • How to fight thyroid system dysfunction in endurance training (24:17).
  • The key lessons Ben learned from his 12 months ketosis dieting experiment (26:10).
  • The biomarkers for detecting adrenal fatigue symptoms (27:22).
  • Biomarkers and tests for autonomic nervous system functionality and distinguishing adrenal fatigue from thyroid system dysfunction (28:03).
  • Incorporating Heart Rate Variability (HRV) tracking in endurance training (31:39).
  • HRV is Ben’s ultimate marker for optimizing endurance training and quantifying overall health (33:23).
  • Success in endurance training requires optimization between high-volume achievements and short-duration precisely aimed tasks (34:29).
  • Dealing with negative effects of endurance exercise and ketogenic dieting (39:01).
  • Maximizing ketogenic dieting benefits and potentially useful supplements (44:34).
  • Breath ketones are an easy way to test for purposeful ketosis (46:20).
  • Tracking important biomarkers and avoiding excessive ketosis (47:20).
  • Why oxaloacetate can be used as a supplement with ketogenic dieting (48:25).
  • Why cold thermogenesis works for athletes’ bodies, for recovery and for overall performance (50:27).
  • The portal outlining Ben’s work and relevant people recommended by Ben (53:17).
  • Ben’s most-important advice on living healthy is being grateful several times per day (54:48).

Thank Ben Greenfield on Twitter for this interview.
Click Here to let him know you enjoyed the show!

Ben Greenfield, Greenfield Fitness Systems

Tools & Tactics

Interventions

  • Cold Thermogenesis: Can be achieved through a variety of cold exposure methods such as cold showers or dipping into cold water streams . In cold thermogenesis hormesis is used to promote positive adaptations in the body as we saw in episode 8. Amongst other improvements it can help to burn fat more efficiently and improve blood vessel functionality in part by promoting development of your Brown Adipose Tissue (BAT). BAT is a type of fat which is active tissue and able to generate heat.

Tech

  • Heart Math Gratitude exercises: The Institute of Heart Math promotes using specific gratitude exercises to optimize the HeartMath Heart Rate Variability (HRV) score. We’ve discussed the HeartMath form of HRV previously in episode 6. This exercise can be done with one of either of their two HRV feedback devices: Inner Balance for iOS or emwave2.

Supplementation

  • Thyro-Gold: Thyroid glandular extract produced by the New Zealand company Natural Thyroid Solutions. This supplement is used as a biohack to correct thyroid-system dysfunction, sometimes caused by ketogenic dieting – especially with very low carbohydrate intake and endurance exercise.
  • AndroGel: Although the use of testosterone hormone-containing products is illegal in professionally-sanctioned sports events, this supplement is sometimes used because free-testosterone levels often drop in a ketosis state.
  • Ketosports KetoForce: KetoForce contains the endogenous ketone body beta-hydroxybutyrate (BHB) in sodium and potassium salt form. The compound BHB can be used as an energy source by the brain when blood glucose is low. Ingesting KetoForce raises the levels of blood ketones for 2.5-3.0 hours after ingestion. (Note: A similar product from same company is Ketosports KetoCaNa).
  • benaGene: This supplement, oxaloacetate, was previously covered in depth in episode 30 in an interview with its creator Alan Cash.
    Greenfield uses this specifically to increase the rate at which his liver synthesizes new glucose molecules, during a low-carbohydrate ketogenic diet including exercise. The goal is to take advantage of its ‘glycogen sparing’ effect, since glycogen is less available in ketogenic diets, and thus get more intensity out of workouts.

Diet & Nutrition

  • Ketogenic Diet: A ketogenic diet is low in carbohydrates intake and high in fat intake. As such, it induces a state of ketosis in the body – the condition in which the body burns fats and uses ketones instead of glucose for fuel. Previously, we discussed measuring ketones and ketogenic dieting in Episode 7 with Jimmy Moore.
    To provide scientific support in favor of ketogenic dieting for endurance, Ben suggests the research of a University of Connecticut team investigating athletic training and human performance. For more information, see this recent scientific review authored by them on using fat as fuel for endurance exercise.
  • Cyclic-Ketogenic Diet: In some people, full ketogenic diets can lead to hormonal or organ dysfunction (e.g. thyroid). The cyclic-ketogenic diet is the solution often used to avoid these downsides. This is a low-carbohydrate diet with intermittent periods of high or moderate carbohydrate consumption (e.g. a refeed with carbohydrates every weekend). It is used as a way to maximize fat loss while maintaining the ability to perform intense exercise during a ketosis state.
  • Based on his 12 month ketosis self-experiment, Ben has concluded that eating anti-inflammatory food, as well as increasing intake of food containing medium-chain triglycerides (MTCs) and resistant starches, are all beneficial in reducing the potential negative side effects of ketogenic dieting.

Exercise

  • Polarized Training: Polarized Training is scientific terminology for the concept of easy-hard training. Researchers from the University of Stirling in Scotland have concluded that using an approach which excludes medium-intensity training is more beneficial for building endurance compared to an approach that includes medium-intensity training. The polarized training model (80% low-intensity; 0% medium-intensity; 20% high-intensity training) produces more positive results in endurance athletes, compared to the competitor threshold model (57% low-intensity; 43% medium-intensity; 0% high-intensity training).
  • Murph Workout: “Murph” is a CrossFit workout named after Navy Lieutenant Michael Murphy, who was killed in Afghanistan June 28th, 2005. He was awarded the Congressional Medal of Honor after his death. It first appeared on the CrossFit site 18 August 2005. This workout consists of (in order): 1 mile run, 100 pull-ups, 200 push-ups, 300 squats, and a 1 mile run at the end.

Tracking

Biomarkers

  • Heart Rate Variability (HRV): HRV is the measure of the change in the heart’s rhythm over time based on changes between sympathetic and parasympathetic activation. HRV was previously covered in the context of optimizing training workouts using HRV in Episode 1 with Andrew Flatt and using HRV as a biomarker for longevity in Episode 20 with Dr. Joon Yun.
  • Triglyceride to High Density Lipoprotein (HDL) ratio: Researchers have shown that using the triglyceride to HDL ratio is a better predictor of coronary disease risk factors, compared to tracking total cholesterol (which includes HDL and other lipoprotiens). A ratio of 2 : 1 or less is considered optimal.
  • High-Sensitivity C-reactive protein (hs-CRP): CRP is a protein that increases in the blood with inflammation and is used as a marker for cardiovascular health (high levels over 1 mg/l are indicative of higher cardiovascular risk). Both diet choices and overtraining can lead to high levels of hs-CRP (over 1).
  • Ketones: Ketone concentrations can be tested in blood, breath and urine samples to determine if you are in ketosis (burning ketones for fuel) and to what extent. We covered these markers extensively in episode 7 – how to measure ketones.
  • Creatinine and Blood Urea Nitrogen: These two biomarkers are often elevated above normal levels in endurance athletes, without being indicative of a health risk. In endurance training, creatinine levels lower than about 1.1 mg/dl do not pose a health risk. It is also relatively normal to have BUN levels over 20mg/dL.
  • Liver Function Tests: When excessive exercise is present, the blood levels of liver enzymes Alanine Transaminase (ALT), Aspartate Transaminase (AST), and Alkaline Phosphatase (ALP) are elevated above normal.
  • The 25-hydroxy Vitamin D Blood Test: The most accurate way to measure how much vitamin D is bioavailable to be used by your body is the 25-hydroxy vitamin D blood test. Optimum vitamin D levels range between 50-70 ng/ml.
  • Salivary cortisol to Dehydroepiandrosterone (DHEA) ratio: An increase in DHEA levels is highly suggestive of adrenal dysfunction because DHEA is produced exclusively by the adrenal glands. Excessive exercise stresses the body to produce very high levels of cortisol, which causes a depletion of endogenous DHEA. This results in an elevated cortisol to DHEA ratio. Testing for this ratio several times per day provides a more complete image of adrenal function, compared to a snapshot provided by simple monitoring of blood cortisol levels. A normal cortisol : DHEA ratio is approximately 5:1 to 6:1.
  • Thyroid Functional Test Panel: A TFT panel typically includes thyroid hormones such as Thyroid Stimulating Hormone as well as the thyroid hormones triiodothyronine (T3) and thyroxine (T4). Excessive exercise can stress the body to produce high-levels of cortisol (the stress hormone) which inhibits the conversion of thyroid hormone from inactive (T4) to biologically active (T3). This can result in lower levels of active thyroid hormone despite normal or up-regulated levels of TSH. Thus, testing for (active) T3 hormone concentrations is more relevant for endurance athletes self-tracking. Optimal reference ranges for TSH are 0.4 – 2.5 milliunits per liter (mU/L). Optimal reference ranges for free (bioavailable) T3 range between 350 – 780 pg/dL.
  • Sex Hormone Binding Globulin (SHBG) and free testosterone: The standard reference ranges for SHBG are 0.2-1.6 mg/dL for non-pregnant adult females and 0.1-0.6 mg/dL for adult males. Changes in SHBG levels affect the amount of free hormone that is available to be used by tissues, including the levels of free testosterone. In case SHBG levels are in abnormal ranges, then free (bioavailable) testosterone should be tested (reference ranges 1.0-8.5 pg/mL for females and 50.2-210.3 pg/mL for males).
  • Tests for detecting adrenal fatigue and thyroid system insufficiency

  • Iris Contraction Test: This test consists of you looking at the pupil of your eye in a mirror while shining a bright light at your eye. The light should cause the pupil (center black spot of your eye) to contract or become more narrow. The contraction should be sustained for longer than 20 seconds before the pupil starts to flicker or dilate. Otherwise, if the pupil starts to flicker immediately upon shining light, this is a good indication that you have adrenal fatigue – mainly because your adrenal gland is functioning properly in managing blood pressure.
  • Dizziness Test: If you lay down or you sit down and you stand up quickly and you get dizzy, then this is a sign of blood pressure mismanagement. Importantly, problems with blood pressure often accompany adrenal fatigue because one of the main functions of the kidneys is to regulate blood pressure via production of hormones in the adrenal gland.
  • Broda Barnes, MD Temperature Test: This test was developed by Dr. Broda Otto Barnes, who was best known for developing novel perspectives on hypothyroidism – a type of thyroid system disease. In essence, you do oral and armpit measurements every morning in bed upon waking up and keep a graph of the results. If your temperature is consistently low, then this is an indication that your thyroid system is dysfunctional even in the absence of a blood thyroid test.

Lab Tests, Devices and Apps

Other People, Books & Resources

People

  • Dr. Terry Wahls: Dr. Terry Wahls is a a clinical professor of medicine at the University of Iowa. Previously, Dr. Wahls was kind to participate in the third episode of our show, where we focused on linking mitochondrial health to autoimmune and chronic disease.
  • Alan Cash: Alan Cash is the CEO of Terra Biological. Previously, he has been a guest on our podcast in Episode 30, where we discussed the potential for using oxaloacetate as an anti-aging supplement.
  • Joe Friel: Joe Friel holds a masters degree in exercise science and is a USA Triathlon and USA Cycling certified elite-level coach. For Joe’s blog click here. For his Twitter click here.
  • Sami Inkinen: Sami Inkinen is a balanced person. He is a successful businessman and a top-age Ironman competitor. For his Twitter click here.
  • Dr. Peter Attia: Dr. Peter Attia is a scientist who is knowledgeable in healthy endurance exercise and self-quantification. For Dr. Attia’s Eating Academy Blog click here. For his Twitter click here.

Books

Other


Full Interview Transcript

Click Here to Read Transcript
[04:46] [Damien Blenkinsopp]: Ben, welcome to the podcast.

[Ben Greenfield]: Hey, thanks for having me on man. And I’ve got to ask you, is it Damien, or Damion? Or Dami-something else?

[Damien Blenkinsopp]: Or Damian? It depends where you come from, I guess.

[Ben Greenfield]: Okay. Just checking. I don’t want to stick my foot in my mouth.

[Damien Blenkinsopp]: Yeah. You can call me Dam. I tell people to call me Dam, just to avoid all those questions.

[Ben Greenfield]: There we go. I want to sound like I’m cursing the entire episode.

[Damien Blenkinsopp]: Yeah. But it even works in Asia, tried and tested.

[Ben Greenfield]: Nice.

[Damien Blenkinsopp]: I mean you’ve got a three letter name. That works well.

[Ben Greenfield]: Yeah, totally. Ben.

(05:12) [Damien Blenkinsopp]: So, Ben, you’re into triathletes, Ironman, and basically the way I look at you is you go around searching for tactics and tools to give you an edge in these areas that you’re interested in. Is that a fair kind of back story to who you are and what you’re doing?

[Ben Greenfield]: Yeah, I do a lot of that I guess n=1 guinea-piging myself. Going out and doing crazy things like training with the Navy SEALS or doing these Spartan Races or Ironman triathlons, things like that.

But then I also think I learn just as much via a lot of the coaching and consulting that I do, just because people typically come to me for one of two reasons.

They either want to do some crazy feat that’s completely unnatural for the human body to do, like they want to go run 100 miles in the wilderness or something like that, and figure out how to do it without destroying themselves. So my job is to figure out how to do that from a nutrition and a physiology and an exercise standpoint.

Or they come to me because they basically want to live as long as freaking humanly possible, and want me to manage how do you sleep when you want to do something like that, how do you exercise, what do you measure, what do you pay attention to in your blood and your gut. And so there’s that kind of biohackiness that I get into.

And I’ve got to admit, for me personally it’s a little bit of both, really. I certainly do want to live as long as possible. I also want to do as many crazy events as I can during the process, see as much of the world as I can at the fastest pace possible. And so for myself, personally, I’m doing a little bit of both.

But sometimes people come to me and want to do something that I know nothing about, so I’ve got to go and learn it. So part of it is that, too. That, or if it’s not coaching someone it’s writing about that. Because I’ve done a lot of writing recently. This morning [I] published a big article on my website about how to use marijuana to get performance enhancing gains.

And I never really would have delved into that if I hadn’t been asked by so many people, especially here in the US with the growing legality. It’s like, can I use this while I’m exercising? That type of thing. So it’s a little bit of everything.

[07:12] [Damien Blenkinsopp]:Yeah, great. So [what was] the event that started the whole Ben Greenfield fitness podcast, and the blog and everything? How’d you get involved in that? Because you’re obviously very passionate about it.

[Ben Greenfield]: Yeah. Well there’s, I mean I get that question a lot, and frankly – nothing against you – but it annoys me, because I hate when people go, “When did you decide to do this? When did you decide to do that?” I never make decisions. I don’t have a 10 year business plan. I don’t have some ‘Come to Jesus’ moment where I said, “Oh hey, I want to learn how to exercise.”

It’s just that I live my life. I do things that I’m passionate about, or that other people who I’m helping are passionate about and tend to fall into whatever I might fall into based on that. I’m getting into hunting right now – well specifically bow hunting and hunting competitions – before that obstacle racing, before that Ironman Triathlon, before that water polo, before that body-building, before that I was a collegiate tennis player.

It’s just like life is a series of chapters and moving targets. It’s never just like one commitment to do one thing. But I would say, to give you a rough answer to your question, the very first time I decided to something a little bit more endurance orientated – which I would define as something that has a nutrition rate.

You don’t see people dropping out of baseball or cricket games because of fatigue and heat stroke and lack of nutrition. That’s very rare, but you see it all the time in marathons and Ironman triathlons and things like that. So I would say the first time I started to get into that side of sports would have been my first Ironman Triathlon that I did back in the city of Portalane, Idaho in 2007.

And up until that point I’d been primarily an explosive power athlete. Like body-building and tennis and stuff like that. But my girlfriend, who is now my wife, was a runner. She ran cross-country for University of Idaho. So I kind of had to take up running, to a certain extent, just to be able to woo her.

And she dragged me to a triathlon one day and she actually had me run the running leg of the triathlon, which hurt like hell. I was a body builder; my boobs were bouncing up and down and my lower back was locking up and it was horrible. But it kind of got me interested in this high that you can get from endurance sports.

And so I wound up doing a few triathlons and doing, what I would say, is the biggest mistake for anyone who wants to avoid getting into endurance, that is I went and watched an Ironman Triathlon. And after watching Ironman and watching these intense feats of physical performance and the huge feeling of satisfaction and self-completion that these people were experiencing as they threw up their arms when they crossed the finish line I was like, I want that. I want to experience that.

And so I signed up for an Ironman and began taking everything I had been studying. At that point I had a Master’s Degree in Exercise Physiology and Nutrition and I was able to start applying that stuff to my training, and experimenting with a lot of what I was finding in research and sports science and seeing what worked and what doesn’t.

For example, all laboratory studies, or most of them, done by the white coats in their little labs will tell you that the body can take on about 200 to 250 calories of fuel during exercise. You can oxidize 200, 250 calories of carbohydrates while you are exercising. But for anyone, especially anyone who’s above about 150 pounds who has tried to go out and do an Ironman Triathlon, you completely bonk after about five hours on that number of calories, and you technically need about twice that in order to be able to get by in an Ironman race in most cases.

So, it’s a situation where what they’re saying in the lab and textbooks actually doesn’t work once you get out in real life and you try this stuff in the streets, in the trenches. So, that’s been kind of fun too, figuring out from research what works, and what doesn’t.

[Damien Blenkinsopp]: Right. Yeah, we often talk on here about n=1 experiments are often going to be different to the research, for a variety of reasons like the ones you brought up, and the use of averages, and other things like that.

[11:24] So, anyway, in terms of endurance training, since we’re there, what kind of biomarkers have you found to be the most useful to track your performance? Or what do you track around your capabilities for endurance training, and see as important?

[Ben Greenfield]: Oh, for endurance specifically?

[Damien Blenkinsopp]: Yeah.

[Ben Greenfield]: So for endurance specifically, that’s a great question. So one would be your level of HSCRP, which really that’s just for exercise in general. Or high sensitivity C-reative protein, just to make sure that your levels aren’t straying too high above 0.5. And the reason for that…

[Damien Blenkinsopp]: So that’s kind of your benchmark? You try to keep them under there? Where do yours tend to hover around?

[Ben Greenfield]: I actually fall below 0.2 now for HSCRP, probably because I eat a very anti-inflammatory diet, very clean. And I won’t insult your listeners’ intelligence by defining what a clean diet or an anti-inflammatory diet is, because it’s pretty easy to go out and figure that out with Dr. Google.

But I eat very clean. I also use a lot of anti-inflammatories. Like I make ginger tea, and I use a ton of turmeric, usually combined with black pepper to increase the efficacy of it, and I use percumin and I consume a lot of very dark and colorful vegetables with very limited amounts of dark and colorful fruits, and wild caught fish, and fats, and things that really help with inflammation.

And I’m also very careful with my training, where I do extremely focused and intense, but short, bouts of training with a specific purpose. I never go out and just pound the pavement for the hell of it, which is a great way to build up a lot of voluminous training based inflammation.

And so I have a very precise, dialed in training program that also includes things that help to mitigate inflammation, like foam rolling, and cold soaking, and these things that can help to remove a lot of these byproducts of metabolism that can create inflammation. So, inflammation is a biggie. Honestly, it doesn’t take a rocket scientist to figure out that if you keep your inflammation controlled, it’s a good thing.

So, a few others that I’ll pay attention to for endurance. When we’re talking about labs, as far as blood goes, TSH, preferably a full thyroid panel, is pretty prudent to pay attention to simply because high level endurance training can inhibit conversion of inactive to active thyroid hormone.

And because of the high amounts of cortisol that can potentially be produced through an improper training program can stress the body out enough to where you experience some hypothalamic pituitary adrenal axis insufficiencies, particularly high cortisol, creating a feedback loop that reduces the conversion of inactive to active thyroid hormone and thus an increase in thyroid stimulating hormone. So your body turns out a bunch more thyroid stimulating hormone to try and get more T4 present, even though a lot of that T4 isn’’t getting converted into T3.

And by monitoring TSH, if you see a pattern or a rise in TSH many times it’s concomitant with an increase in cortisol and stress, and often also accompanies a not enough eating period. Sometimes not enough carbohydrates is the biggest culprit, but in many cases just not enough damn calories, period. Damn, not referring to your first name but to the curse word. Just so we’re clear.

That’s another one is TSH. Cortisol, I alluded to, but when we’re looking at a hormonal panel, I also like to pay attention to sex hormone binding globulin. Because the body has this interesting mechanism where when it’s stressed out, when it’s in a time of famine, in a time of need, under high amounts of stress, doing a lot of migrating, a lot of moving with low amount of calorie intake, the last thing you want the body to do is produce a bunch of babies at that point.

And so sex hormone binding globulin often rises simultaneous to cortisol to keep total testosterone bound, and keep it from being available as free testosterone. So even if your testes are working just fine, or your pituitary gland is working just fine, –obviously talking about the males more than the females now– and even the leydig cells in your testes are producing testosterone just fine, if sex hormone binding globulin levels are really, really high that’s all for naught. And so that’s another really, really important one to keep an eye on. And that’s typically addressed by addressing cortisol.

[15:50][Damien Blenkinsopp]: Right. So, why would you look at SHBG versus free testosterone, or that marker? The [unclear 15:56]?

[Ben Greenfield]: Well, because if free testosterone is low, but if you look upstream perhaps it’s because total testosterone is low because the leydig cells in your testes are not producing enough hormone because you’ve got low levels of luteinizing hormone. In contrast to that, perhaps your luteinizing hormone production is fine, your leydig cells are producing enough testosterone just fine, your total testosterone is high, but it’s more of a cortisol issue than it is a central nervous system issue or a glandular issue.

So that’s why you test that versus just looking at free testosterone.

[Damien Blenkinsopp]: So basically, free testosterone could be many, there’s more reasons behind it, but the SHBG is more specific to endurance and specific dynamic.

[Ben Greenfield]: Yeah. Really, two reasons behind it. Either you aren’t producing enough total testosterone, or you are producing enough total testosterone but it’s not getting converted. So those are really the two main things to look at.

[16:48] [Damien Blenkinsopp]: So, are you looking at the standard reference ranges for that, or do you look for something a bit more precise?

[Ben Greenfield]: A lot of times you have to look at symptoms synonymous, because standard reference ranges are going to vary widely.

I’ve worked with a lot of endurance athletes who have very high libido levels, show no signs of over-training, have very robust nervous systems, high heart rate variability, low cortisol, and even low sex hormone binding globulin, but their total testosterone is in like the high 300s. Which, for a body builder they would scoff at that and say, oh that’s rock bottom low. Even though a lot of times hypogonadism is levels below 100.

And you’ll get many people who just feel like fricking crap at 300, and some people will be closer to 500, and some people will need levels of 700, 800, or even 1000. So it kind of depends. It varies widely, I suspect based on genetics as a big part of it.

So ultimately it’s really tough to hold things up to reference ranges. I mean, you can ballpark it. You can say well if total testosterone is starting to get below 300, that’s where we would really start to get a little bit concerned. But it really is kind of tough. A lot of times it’s a moving target based off of a cluster of other symptoms.

If someone’s complaining of low libido and low motivation, and lack of energy, etc, and their testosterone is at 400, well that’s a pretty good sign that 400 is not going to be adequate for them. So I know that’s one of those deals where it’s total soft science, but it does really depend. That’s one of those ‘it depends’ answers, but that is definitely a variable that I will look at.

[18:20] Liver enzymes is another one, like alkaline phosphatase, aspartate aminotransferase, the ALT, the AST, some of these liver markers just because a lot of times they can be elevated when excessive exercise is present. And so that’s another one to pay attention to. It doesn’t have to be excessive exercise; sometimes it can be alcohol, pharmaceutical intake, things of that nature. But liver enzymes are the one that I’ll look at.

Kidneys, a lot of people say to look at kidneys, but frankly it’s very rare for me to see an athlete who doesn’t have slightly elevate creatinine and blood urea nitrogen levels, which are two common markers in the kidneys that a physician will get concerned about if they see elevated, but that are very common to see elevated if an athlete is exercising anywhere in the 48 hours leading up to a blood panel.

So, as long as creatinine levels aren’t much higher than about 1.1, and as long as blood urea nitrogen isn’t through the roof and – I apologize, but off the top of my head I don’t remember the lab reference ranges for blood urea nitrogen. The reason being that I do most of my coaching for blood panels with a company called WellnessFX. It’s basically more like a dashboard with graphs, more than it is hard numbers, so occasionally I’m looking at graphs more than I am numbers.

[Damien Blenkinsopp]: And they just have those red zones.

[Ben Greenfield]: Yeah, exactly. They’ve got red, yellow, green, which actually annoys me some of the time. Because they’ll flag high LDL as red when I purposefully try to get my LDL high. So there’s some issues with the whole red yellow green type of quantification. But anyways, blood urea nitrogen and creatinine, even though a lot of people talk about those, they’re not super duper important in my opinion, because they’re always going to be a little bit elevated.

Vitamin D, that’s another one that I’ll look at just because of it’s importance. As you can suspect, a lot of these aren’t just specific to endurance, they’re specific to exercising period. Just as a hormone and a steroid, vitamin D is another important one that I’ll look at.

And then as far as other things, I typically will have most of the athletes I work with or the people I advise do at least once a year a full gut panel. You know, a comprehensive gut panel that includes parasitology, measurement of pancreatic enzyme production, measurement of yeast and fungus and any type of bacterial overgrowth in the digestive tract because I find that, especially when you’re jogging your body up and down for 10 plus hours while racing, having a really, really good gut and GI system and very efficient digestion is incredibly important.

And so I will look at things like presence of yeast or fungus, like Candida Albicans, or the presence of H pylori, or absence of hydrochloric acid, or absence of pancreatic enzymes, or overgrowth of specific bacteria, or lack of short chain fatty acids in the digestive tract, in the colon, and a lot of those things that tend to influence an athlete’s performance or their feelings of well-being. So that’s another thing I’ll pay attention to.

[21:18][Damien Blenkinsopp]: Right. A lot of people wouldn’t think of that as something performance related, more like a chronic issue related.

Have you got any case studies where you saw people, basically not performing but not having any negative symptoms in terms of GI distress or anything that they would have noticed, but when you put through these tests some negative results came?

[Ben Greenfield]: Sure. Now we’re delving a little bit more deeply. And I mean, obviously explosive diarrhea halfway through a marathon can be a good sign of digestive enzyme insufficiency, but so can, for example, vitamin B12 or vitamin D deficiencies, or even if you go more advanced and run like an organic acids profile, or an amino acid profile, severe imbalances of a lot of micro-nutrients.

Well if you’re not digesting your food efficiently, for example, if you’re not producing adequate hydrochloric acid, you’re not activating pepsin to break down proteins, beginning in the stomach an moving on to the small intestine, then you’re going to: a. have undigested protein fragments winding up in the bloodstream causing some auto-immune issues, and that can include fuzzy thinking, which no athlete wants.

But then you also can get amino acid deficiencies, like deficiency in the ability to create neurotransmitters, and also deficiencies in the ability to repair and regenerate skeletal muscle tissue, because you aren’t breaking down the proteins that you’re eating.

And the same could be said for something like inflammation in the digestive tract from wearing down of the microvilli. So perhaps you’re not producing adequate levels of lactase, so you’ve got some lactose issues and bloating and gas. Or you’ve got inflammation that is resulting in malabsorption of fat-soluble vitamins, so vitamins A, D, E, and K aren’t getting absorbed properly, or bacteria aren’t helping you to produce those, and so you experience hormonal deficiencies, or steroid deficiencies.

And so, yeah the gut is incredibly important, and that’s one of the things I’ve been kind of getting on companies like WellnessFX, for example, to do is to not just use the strategy of blood testing but also really pay attention to the gut. I mean, in an ideal scenario, what I would like to see is a done-for-you system.

And for me right now, what I do is just kind of string this together for the athletes who I work with. But a done-for-you system where you get your blood testing, you get your gut testing, and you get your genetic testing so we can look at everything from genetic snips to bacterial imbalances in the gut to all the blood and biomarkers, and have all of that done with either one panel or one service.

That would be really nice, because right now you’ve got to go to typically three different places. You’ve got to go to whatever DNAFit, or 23andMe, and you’ve got to go to DirectLabs, or Metametrix for GI affects, and then you’ve got to go to WellnessFX for whatever else. And then if you want to do food allergy testing, well then you’ve got to throw in a Cyrex panel, or something like that.

So maybe it’s a first world problem to want all this stuff to be available in one central location, but it certainly would be nice.

[Damien Blenkinsopp]: Yeah. It’s so near the early days from that perspective. There’s a lot of specialized, it’s still kind of specialized in terms of the labs. Each is in their little separate box and everything.

[Ben Greenfield]: Yeah.

[24:17] [Damien Blenkinsopp]: So, in terms of the kinds of decisions you’ve made, or you’ve advised a client based on some of these values, some of this data that’s come back, what have been the biggest changes that you’ve implemented to optimize training?

[Ben Greenfield]: You mean as far as training?

[Damien Blenkinsopp]: So, say the TSH came up too high, what would you do about that?

[Ben Greenfield]: Oh okay, so for high TSH, obviously it’s never a shotgun approach. It’s never a multivitamin. So for high TSH it may be looking at your carbohydrate intake. That’s the first thing that I’ll look at.

Even before you look at total amount of calories, you just make sure nobody is on some low, like 40 gram per day carbohydrate diet, because frankly a lot of the ‘low carb’ or ‘ketosis’ based diets that are out there were created for sedentary people. Even the bulletproof diet. I love the whole bulletproof philosophy, but it was written by a computer programmer, not by an athlete.

And so the levels of carbohydrate, and even the levels of calories in that diet, have to be adjusted and modified for a hard-charging athlete, especially an endurance athlete. So, otherwise with caloric depletion and carbohydrate depletion, you basically lose a lot of your ability to convert inactive to active thyroid hormone.

And in the case of calories, as you would deduce through common sense, when you send your body a message that calories are insufficient but you’re still requiring it to move a lot, your body down regulates metabolism. And one of the main ways it does that is by down regulating thyroid.

So, I look at carbohydrates, I look at calories, and then I also look at dietary intake of organ meats and fat soluble vitamins, which can also assist with thyroid health. So in my case, because I did an n=1 experiment about a year and a half ago where I did 12 months of ketosis.

Not cyclic ketosis, not cycling carbohydrates in and out throughout the day, but full on eating only 5-10 percent of my total daily intake from carbohydrates. Very low carbohydrate diet. Too low, in my opinion, for most endurance athletes who want to maintain optimal levels of health elsewhere.

[26:10] [Damien Blenkinsopp]: Did you see negative effects from that over the 12 months?

[Ben Greenfield]: Yeah, and that’s what I’m getting at with the thyroid. I started taking thyroid glandular extract. I took one called Thryo-Gold, which is made from New Zealand cows, that are like an A2 cattle.

A lot of A1 cattle has proteins in it that cause an immune reaction within the human body, but cattle that are breed via A2 are cattle that contain this A2 genetic profile that is more bio-compatible with the human body. And so I basically took a T1, T2, T3, and T4 combo, and that seemed to turn my thyroid around. But that was after I had already done a number on it.

So for thyroid, that would be an example of what I would do with something like thyroid, would be increase calories, increase carbohydrates, increase intake of organ meats and fat soluble vitamins. And then for a really hard-charging athlete who insists upon doing something like restricting carbohydrates to tap into the performance enhancing effects of ketosis, understand that you’ve got to get on extra help from the thyroid.

Since your body isn’t going to make T3, dump it into the body. And preferably get it from a whole source, like levothyroxine or synthroid. But a source that contains other elements of thyroid in addition to just T3, so you’re not creating an imbalance.

[27:22] [Damien Blenkinsopp]: Great. Well, connected with the thyroid issues, I was wondering if you’ve come across adrenal fatigue also. If that’s every come up with you or with anyone else.

[Ben Greenfield]: Absolutely. Adrenal fatigue, gosh. There’s like four chapters of my book on that alone. But adrenal fatigue, well what do you want to know about it?

[Damien Blenkinsopp]: Well first of all, have you looked at some of the tests? I’ve done some of the salivary tests.

[Ben Greenfield]: Oh yeah. Yeah, like an adrenal stress index is kind of gold standard, cortisol DHA. If you look at the cortisol DHA curve, that’s much, much better when you’re addressing something like adrenal fatigue versus a blood cortisol measurement, which is just a snapshot. You want to see a moving target of salivary cortisol levels, preferably matched to salivary DHEA levels, throughout the day.

[28:03][Damien Blenkinsopp]: I was just thinking, based on it’s endurance exercise, and it has this tendency to raise cortisol, that that would be more of an issue and something that you would keep an eye on. Or by monitoring TSH, does that kind of take care of itself? If the TSH is alright then you tend not to have an adrenal issue as well?

[Ben Greenfield]: No, not necessarily.

You can still have adrenal fatigue and have a thyroid that’s managed properly. Because what you would typically see in that case is someone is eating boatloads of calories and taking care of themselves from an energetic standpoint, but simply outputting too much energy. They’re just training way too much. Even though they’re supplying their thyroid with what it needs, there’s just too much training still.

And a lot of times you’ll see inflammation high, but yeah. Cortisol DHEA, and that adrenal stress index can be a good measurement. And there are less quantitative measurements. You could do a pulst test, where you look in a mirror and you shine a bright light at your eyes, and your pupils should stay dilated. But if it stays dilated and then just starts flickering rapidly.

[Damien Blenkinsopp]: Have you tried that one?

[Ben Greenfield]: I have, yeah.

[Damien Blenkinsopp]: Because I was just wondering. I did try it and I find it a little bit difficult to judge.

[Ben Greenfield]: Yeah, it’s certainly not as precise as a salivary measurement, but once you’ve done it a few times you can definitely see the pupil, and whether or not it’s actually flickering versus staying dilated. If you look at if for long enough, it’s just going to start flickering period, but if it starts flickering after just a few seconds, that’s typically a sign that your kidneys are not producing enough aldosterone, which is synonymous, or can accompany, adrenal fatigue.

The other one is just the dizziness test. If you lay down or you sit down and you stand up quickly and you get dizzy, that can be a sign of blood pressure mismanagement that often goes hand-in-hand with adrenal fatigue. And again, these are the super cheapo poor man’s methods, but it can give you clues.

And then there’s temperature tests for thyroid, the Broda Barnes Temperature Test, where you do oral and axillary measurements of your temperature in bed every morning, and keep a running graph. And if it’s consistently low, that can be a pretty good indication that even if you haven’t done a blood thyroid test that your thyroid might be having issues.

So, there are a lot of things. One of the best ones I like though is just pure heart-rate variability. Testing the interplay between your sympathetic and your parasympathetic nervous system by using something like a Bluetooth enabled heart rate monitor and one of these heart rate variability apps, and simply paying attention to whether heart rate variability is high or low on any given day.

And if it’s consistently low, and you see consistent suppression of both sympathetic and parasympathetic nervous system feedback, then that can be a pretty good sign that you’re on the cusp of adrenal fatigue illness or injury, and so that’s another really good one to pay attention to. And I do that one every day myself.

[Damien Blenkinsopp]: Do you do it in the morning as soon as you wake up?

[Ben Greenfield]: Yes, that’s gold standard, because that’s where most of the studies have been done on heart rate variability were five minutes resting in the morning.

[30:45] [Damien Blenkinsopp]: Right, right. I believe you use the HR…what’s the name of the company?

[Ben Greenfield]: SweetBeat?

[Damien Blenkinsopp]: Yeah, SweetBeat.

[Ben Greenfield]: Yeah, but because I want to build up that technology and add some features and stuff like that, I’ve actually white labeled their technology. And so I use the app called NatureBeat now, but it’s the SweetBeat technology.

[Damien Blenkinsopp]: Great, great. Yeah, she’s been on the show.

[Ben Greenfield]: Yeah.

[Damien Blenkinsopp]: So I was using that for a long time, and then I just recently started using iFleet, because I also talked to the guys at iFleet, and it does have this other thing that they just added recently. You might just want to check out.

It’s kind of interesting. It shows how high your energy levels are on a given day, so it kind of does this matrix thing. So it shows you if your in the bottom right corner, it means something a little bit different. So I’ve been checking it out. I’m still trying to understand what it means each day. But I do find that when I’m at the bottom, low energy, those days tend not to be good. Even if I have a high HRV.

[31:39] So anyway, out of interest, what is your HRV levels? Because you think normally endurance athletes have higher HRV, right?

[Ben Greenfield]: Yeah. Usually higher HRV, which isn’’t necessarily a good thing if you’ve got what are called HF to LF ratio imbalances.

You want your HF to LF ratio to be pretty close to one. That’s sympathetic and parasympathetic nervous system feedback. And if parasympathetic nervous system feedback, which would be your high frequency number, if that’s super duper depressed, and your LF is really high that can be an indication of aerobic based over-training, or vice versa.

So ideally you’ve got high HRV and a pretty close to a 1-1 ration between HF and LF. That’s what you want to go to. And you want both HF and LF to be up in the thousands. That’s a sign of a really robust nervous system.

So, my values tend to be between about 92 and 98, with HF and LF values that vary between about 4,000 to 8,000, around in there. Generally with a 1-1 ratio, depending on what my previous day’s training had looked like.

And I would expect, for example, this Tuesday I’ll do a CrossFit’s Murph and I’ll do that with a 20 pound weighted vest on, and just crush myself. And that will take me about an hour to do, and I guarantee my LF value will be tanked the next day. But I also won’t be doing any sympathetic nervous system training for like 48 hours afterward.

[Damien Blenkinsopp]: So you recover within 48 hours?

[Ben Greenfield]: 48 to 72 hours, depending.

[Damien Blenkinsopp]: These scores recover for you pretty quickly?

[Ben Greenfield]: Yeah, but I mean, if I were to do something epic, right? Like, usually something that gets you to the state of glycogen depletion. Or let’s say instead of Murph, I do double Murph, or I do a Murph with a 5k sandwiched on either end rather than just a mile, then it can take me several days to recover, for sure.

[33:23] [Damien Blenkinsopp]: If you had to pick one marker to optimize your endurance training by and make decisions on, which one of the ones we’ve talked about would it be?

[Ben Greenfield]: HRV.

[Damien Blenkinsopp]: Okay, great.

[Ben Greenfield]: Just because it’s easy, right? You don’t have to give blood.

And maybe at some point, once we’ve got the lab and chip technology finalized, and I can put a drop of blood onto a little dongle that will plug into my iPhone and I can measure, let’s say, testosterone cortisol ratios, maybe that will become a more valuable metric for me. But at this point, I would have to say something simple and easy to utilize and relatively inexpensive, the HRV would be the one that I’d choose.

If I had to choose an actual blood biomarker, tough to say. Tough to say. I guess I’d probably have to go with HSCRP, again. Just because inflammation is generally going to be high when cortisol is high. It’s generally going to be high when diet is crappy, it’s going to be high when triglycerides are high, it’s going to be high when omega-3 fatty acids are low. So, that’s a pretty good one to measure.

[Damien Blenkinsopp]: Yeah. So it catches a lot of things. Mainly whenever something starts going wrong.

[Ben Greenfield]: Yeah.

[34:29] [Damien Blenkinsopp]: Well so you’ve referred to over training quite a bit over this as something that you’d have to change. So HRV would be one of the first places you’d see over training.

Are there any other tell-tale markers, and what do you suggest, more to the point, because you mentioned earlier that you do very – is it short, intense kind of endurance exercises. And I think a lot of people when they’re thinking about endurance, they’re thinking about very high-volume, kind of long duration activity.

So how do you approach it, and avoid over training? What are the top things you’ve taken in over time?

[Ben Greenfield]: First of all, one of the common pitfalls that people fall into with endurance training is doing the long voluminous training every weekend. It’s very stereotypical that you’ll see in a lot of athletes these Saturday long bike rides and then Sunday long run, for example. Or in a marathon, the Saturday long run.

I’ve found that in most cases, you can maintain endurance really, really well. Unless you’re a professional athlete trying to perform at the peak of performance, most people can perform just fine. With doing digging into the well like that, really, really, deep for like a death march, a really long ride or something like that, you typically only need to do that one to two times a month. Not every weekend.

I’m a bigger fan of using shorter, very temporal based intervals. So to give you an example, for the Ironman triathletes that I work with, while their peers are out doing a five hour ride followed by an hour long run, my athletes will be doing two hours of 20 minutes at race pace followed by 5 minutes recovery. So a very focused activity with a specific goal in mind. And then they’ll finish that up with a 15 minute tempo run at a cadence of 90 plus.

So it’s all extremely high quality. And then once a month they’ll go out and do something big, something long, something voluminous that builds the mental tolerance to training, but that doesn’t dig so deep into the well as doing it every week.

And the reason for that is based off of the human body’s natural slow twitch muscle fibers. The human body’s ability to cool because we’re upright and not covered in fur and hair. Our ability to sweat, rather than pant, to reduce heat. And a cluster of other factors.

We’re pretty good at going for long periods of time. And when training for endurance, bigger limiters are things like power, speed, cadence, strength, the integrity of the fascia connective tissue, the intelligence to be able to use nutrients and calories properly.

And really pointing in one direction, and going for long periods of time is not that much of a weakness for the human body, but the problem is that it’s easy. And people take pride in it. They’re like, “Oh I persevered today. I did my three hour run.”

And my question to you is well yea, but what did you accomplish side from being on your feet for long periods of time? Which frankly I could stand up at my standing workstation and write an article for three hours and get the same amount of time on my feet as you just did out pounding the pavement. So it would be better in that case to do something with intervals at race pace for a shorter period of time.

Focus on cadence. Allow enough time before and after for a good warmup. Maybe some meditation and breath work. Some good recovery. And so that’s where the more intense, more quality, lower volume approach nine times out of ten trumps the voluminous approach.

The exception to that fact would be the person who has a lot of time on their hands to train: the professional athlete. Professional athletes, assuming they’re using this 80-20 approach, it’s called polarized training. 80 percent of your training is done aerobically, with about 20 percent done high intensity.

That approach works very well, and it is what a lot of the elite cross-country skiers and marathoners and cyclists etc. will use, but what is important to understand about that approach is it requires many, many hours per day.

That approach can require two to four hours per day of training, and even more than that, on weekends, for example. And the majority of folks simply don’t have the luxury of time available to utilize that approach effectively. That in a nut shell is my approach to training.

I’ve got a couple of athletes who I work with who are more, what I would consider to be on the professional level, who have that luxury of time. And I do train them with that aerobic approach, where they’re out doing long voluminous sets of training at a controlled heart rate aerobically, putting lots of time in the saddle or time on the pavement. But its very few and far between that I’ll recommend an athlete to train like that.

[Damien Blenkinsopp]: Great, great, thanks. That’s a great summary of it.

[39:01] I wanted to move on to, because I know you did this 12 months of ketogenic dieting. Could you talk a little bit about that? Give us an overview. What was your approach to that, what were you actually eating, and was there any specific goals to track over the year?

[Ben Greenfield]: Well yeah, for that specific diet, that was for a study at University of Connecticut that was done on, basically, a group of athletes who followed a high-carb/low-fat diet, versus a group of athletes who followed a high-fat/low-carb diet.

And it was basically a measurement of fat oxidation during exercise. And they also did muscle biopsies before and after exercise to see the rate of glycogen use as well as the rate of glycogen replenishment following the post work out meal to just see if the body does a better job at oxidizing fat, or at sparing glycogen during exercise when you’ve eaten a high-fat diet.

And it did turn out in that study that the athletes who followed the high-fat diet were oxidizing a lot of fat. The textbooks tell you that you can burn about 1.0 grams of fat per minute, and the group of athletes who followed the high-fat diet were burning 1.5, 1.6, 1.7 grams of fat per minute. Literally rewriting the textbooks when it comes to how much fat you can burn during exercise.

I haven’t seen the muscle biopsy data yet to see how much glycogen conservation actually took place, or whether or not the body became more glycogen depleted when using primarily fatty acids as a fuel. But ultimately, what that diet consisted of was really controlling carbohydrates.

Whereas I would normally – and this is what I do now – I would carb-cycle, or I would do cyclic-ketogensis or cyclic-ketosis, where I don’t eat carbohydrates all day long and at the very end of the day, typically in the post-workout scenario, with dinner I’ll eat anywhere from 75 to 200 grams of white rice, red wine, sweet potatoes, sourdough bread. You know, safe starches, not like pizza and ice cream, but good carbohydrates. And then the rest of the day just high fat and moderate protein.

Whereas on this full on ketosis diet, it was pretty much just things like bulletproof coffee, and high fat shakes and lots of coconut milk and coconut oil, and heavy cream and MCT oil and seeds and nuts, and just fats, fat, fats. Bone broth and avocados, and olives, and you name it.

And frankly, in my opinion, it wasn’t that enjoyable to have to not have sweet potato fries, and not have, even coconut ice cream has cane sugar in it. So you have to make your own with chocolate stevia. And so it’s a little bit laborious and a little bit tough, but I mean at the same time the endurance payoff was huge.

The amount of focus that I had for long periods of time. My ability to just hop on a bike and ride for hours with no fuel at all, with just water. It was pretty profound, because you produce all these ketones as a bi-product of fatty acid oxidation, and they’re used as the preferred fuel by the brain, by the heart, by the liver, by the diaphragm while you’re out exercising. And that’s a huge boon to an endurance athlete.

And like I mentioned, there’s some blow-back. Like the TSH could take a hit, the testosterone could take a hit. But ultimately, it’s a cool little bio-hack. If I could go back and do it over again, I would definitely start taking thyroid glandular earlier to stave off some of those thyroid issues.

I would,– it’s not legal – but I would really encourage folks to pay attention to testosterone. And I mean like, you can’t use testosterone in a WADA, or a USADA or like an NCAA sanctioned event, but my testosterone dropped so much during that experiment with ketosis, I would say if you’re not competing, use AndroGel or just some kind of testosterone support because your testosterone is going to fall to pieces.

And then the question becomes well is it really worth it to you if you’re doing this thing and you’re not even competing.

[Damien Blenkinsopp]: Yeah. Did you feel different?

[Ben Greenfield]: Oh, yeah.

[Damien Blenkinsopp]: Because we talk about testosterone with things like anxiety, your drive, your libido, of course. And so did you get any kind of low testosterone symptoms?

[Ben Greenfield]: Oh yeah. Absolutely. I mean even something as simple as only having to shave every four or five days, whereas normally I would just shave every one to two days.

[Damien Blenkinsopp]: That’s a benefit.

[Ben Greenfield]: I mean, little things like that, but you notice. Yeah, potentially. You save money on razors.

Yeah, the libido, sex drive, number of times having sex per week, desire to have sex, quality of the erection, all of those kind of things certainly they took a hit during ketosis. They weren’t good. But that was, mind you, ketosis in the presence of high amounts of physical activity. Even doing the ‘low volume approach’ it’s still a massive amount of work, right?

[Damien Blenkinsopp]: Right.

[Ben Greenfield]: You’re still working out 60 to 90 plus minutes every day, and longer than that on the weekends.

And you look at something like Dr. Terry Wahls and her ketosis approach for managing MS. Well sure. I mean, that’s going to work just fine for managing MS. I mean, going on a walk with your dog every morning, and maybe lifting easy weights, three sets of 10 for 20 minutes twice a week.

But once you jump into hard exercise, it’s a whole different type of ketosis.

[Damien Blenkinsopp]: Right, right. Just to be clear, were you getting better times? Did you feel like you were competing better?

[Ben Greenfield]: Oh, I was competing way better. Yeah. Absolutely.

[Damien Blenkinsopp]: Right. But it’s just the downsides to your lifestyle, to all the other things, were too great to do this on a constant basis.

[Ben Greenfield]: In my opinion, yes, because I don’t like being cold all the time, I don’t like not having libido. So again, I’m not saying you can’t do it properly, even though it’s way, way tougher once you get into training, but I think that you basically have to use supplementation pretty intensively.

[44:34] [Damien Blenkinsopp]: Did you kind of see the benefits evolve and get much better as the months passed, or is this something someone could do on a month basis, one month on and one month off?

[Ben Greenfield]: For exercise, you barely even see any benefits until you’ve been doing it consistently for about six months, and the real benefits start to manifest after one to two years.

But the other thing to realize is that right about the time I finished up the experiment, companies like KetoForce started coming out with beta hydroxybutyrate salts that could be consumed to elevate your ketone bodies, even in the presence of a lot of carbohydrates or glucose. And so it’s possible that now, since the experiment that I did, you could get the best of both worlds.

And I actually have some bottles of the beta hydroxybutyrate salts and the resistance starches, and a lot of the things that, if I had to go back and do it all over again, I would try to get the best of both worlds. I would eat more carbohydrates, but then I would also hack myself into ketosis by consuming actual ketones bodies.

The question there becomes a matter of long term health and gut health and how that actually manifests in terms of actual symptoms or the way you felt, or even I would definitely pay close attention to blood and biomarkers.

Were I to delve into that type of bio-hack? I potentially may. I could see myself, and obviously I’m at a point in my athletic career where I’ve still got a good eight years of hardcore performance left in my body, and I could see one of those years being spent utilizing a ketonic approach again, but with the incorporation of beta hydroxybutyrate salts, resistance starches, even higher amounts of MCT oils, particularly like the C8s and the C10s. And a little bit more attention paid to ways to get into ketosis that go above and beyond just carbohydrate restriction and exercise.

[Damien Blenkinsopp]: This is great Ben, this is a wealth of information.

[46:20] In terms of the biomarkers you would track, you said you would track some biomarkers if you were going to do this again what kinds of ones that we haven’t spoken about already would you look at? Did you track your blood ketones?

[Ben Greenfield]: Yeah. Breath ketones. I mean, urinary ketones become, many times, absent after a few weeks in ketosis just because you’re utilizing your ketones. Blood ketones are accurate but expensive and invasive to test, and breath ketones are pretty [easy].

There are breath testing monitors like the Ketonix device that, one breath and you know your ketones, and you’re good. So breath testing is a really good way to go as far as measurement of ketones. You look for values anywhere from 1.0 up to 3.0 millimolars. You’ll finish exercise as high as 7.0 millimolars.

You’ll rarely see ketoacidosis, which would be like 10 plus millimolars. It is a non-issue. I have yet to see any athlete I work with go under ketoacidosis, which would be an actual deleterious biological state. Not something you need to worry about unless you are letting yourself become severely hypoglycemic.

[47:20] [Damien Blenkinsopp]: So again, is that something you saw evolve over the months? Like your ketones ratings would get higher.

[Ben Greenfield]: Yeah. You get to the point where it’s just super duper easy to get into ketosis. Yeah. And your ability to go for long periods of time without eating just goes through the roof.

So ultimately, the biomarker I would say, in addition to what we’ve already talked about, would be breath ketones. And then pay attention to triglycerides too, because they’ve shown that compared to total cholesterol values, a better predictor of your coronary disease risk factors is your triglyceride to HDL ratio, specifically keeping that at one or lower in terms of your number of triglycerides versus HDL.

But I’ve found that some people will switch to a high-fat diet and have such a high intake of vegetable oils, and even an imbalanced high intake of animal based oils, like butter for example, versus olive oil and avocados. Their triglycerides go through the roof.

Pay attention to that HDL ratio. That’s my advice is make sure that that thing isn’t getting much above one, that would be another important thing to pay attention to, especially on a higher fat intake.

[Damien Blenkinsopp]: Great, great. Excellent points.

[48:25] So there are a couple of other things I’ve noticed you’ve done in your experiment. I read your book of course. One of the things that we’ve come across before – I spoke to Alan Cash from benaGene –oxaloacetate, and I was wondering what you’ve done with that and if you’ve tracked anything or learned anything about that.

[Ben Greenfield]: Yeah, obviously if you talked to Alan Cash your listeners can go back and listen to that to learn more about what oxaloacetate is. But in a nutshell, the reason that I used it was because it can increase the turnover rate of lactic acid into pyruvate, and increase the rate at which lactic acid is shuttled back up into the liver to be reconverted into glucose.

And so if you are eating a low-carbohydrate diet anyways, that by nature means you might not be taking as much exogenous glucose in, or might not even have as high a level of glycogen stores, but you can still take the lactic acid that you’re producing as a byproduct of metabolic activity anyways and have that reconverted into usable glucose sources to have a glycogen sparing effect and to get a little bit more intensity. And so the way that would be achieved if you’re going to increase the rate of that cycle, which is called the Cori cycle, would be via the use of oxaloacetate.

And so, I actually did use that. I don’t use it right now. It’s one of those things where it’s just like, I would benefit from it its just one more supplement to remember to take. But I certainly used it through that entire ketotic experiment with the oxaloacetate just to increase the conversion of lactic acid into glucose.

[Damien Blenkinsopp]: Right, it sounds like it would help specifically in that ketogenic diet state when you’re exercising.

[Ben Greenfield]: Exactly.

[Damien Blenkinsopp]: So you designed it that way? You decided to take it before, or was it something you came up with afterward to help?

[Ben Greenfield]: I talked to Alan at one of the Bulletproof bio-hacking conferences. We talked about the physiology of oxaloacetate, and then based on that I just kind of had a little light bulb moment, where I realized that if I was restricting carbohydrates anyway, that this was one more way that I could create endogenous glucose more quickly.

[Damien Blenkinsopp]: Great, great.

[50:27] Cold thermogenesis. Do you still play around with that? Is there anything like, for instance, have you seen your HSCRP any time, potentially when you first started it or did it a bit more intensively, change with that?

[Ben Greenfield]: Yes. I have not done a dedicated experiment with cold water exposure, cold temperature exposure, or the use of ice baths or cold showers to see the direct effects on HSCRP, although reduction of inflammatory cytokines has been observed in literature when it comes to cold thermogenesis and inflammation.

What I use cold thermogenesis for is increased conversion of white adipose tissue to brown adipose tissue. Simply because it’s very difficult to kill fat cells, but you can convert fat cells into energy utilizing and heat producing tissue. And that’s one thing that cold thermogenesis is good for. That would mean cold baths, cold showers, cold soaks, etc.

Also very useful for increased production of endothelial nitric oxide synthase, which can cause your blood vessels to dilate much more readily, which is good for everything from exercise to sex to heating your body when it needs to be heated. And then there’s also increased tolerance to the mammalian dive reflex, which is that activation of our sympathetic fight-or-light nervous system in response to stress.

And when you are able to withstand cold stress without taking that sharp influx of breath, that means that you have become more resilient and more resistant to subconscious activation of that fight-or-flight nervous system. You’re better at controlling stressful events that happen.

And so, what I do is I never take a warm shower. I do a cold shower in the morning, cold shower in the evening. I do once per week a 30 minute cold soak that gets me up to shivering level, typically needing to shiver for one to two hours afterward in order to regain warmth. And those are the ways that I use cold thermogenesis. I also keep my house relatively cold. My office is at about 55 degrees. In my home, typically I’ll sleep at 60 to 65 degrees.

It’s just a really, really good way to make yourself tough, to burn fat, and to increase blood vessel health. And it’s just super simple. And frankly, the other cool thing is when I go hunting or when I have long periods of time outdoors or when I’m at the beach and evening comes and I forgot my coat, I don’t get as bothered, which is just kind of nice. You’re just more tough.

[Damien Blenkinsopp]: It sounds like the only time it was an issue when you were doing you ketogenic thing. What was the issue there? Were you getting a lot colder, or?

[Ben Greenfield]: Yeah, but that was because of the thyroid. If you have hypothyroidism, cold thermogenesis is going to be very uncomfortable. Heck, even normal temperatures you’re colder during. So I was still doing cold thermogenesis then but it was quite unpleasant. It was hard for the body to get warm again.

[Damien Blenkinsopp]: Okay. Right, great.

[53:17] Some quick fly questions that I have just to finish off here.

First of all, if people want to connect with you and learn more about you and what you’re up to, where is the best place? Twitter, your website?

[Ben Greenfield]: Bengreenfieldfitness.com, because if you go there, you’ll find links to my Twitter, Facebook, Instagram, my blog, my podcast, etc. So that’s a good place to go as a portal.

[Damien Blenkinsopp]: Great, great. And who besides yourself would you recommend to learn more about endurance training, or some of the other topics we spoke about today? Ketogenic diets and so on?

[Ben Greenfield]: As far as people who have their head screwed on straight who are paying attention to the research, I’d say three people come to mind.

Number one would be Joe Friel. He’s coached a lot of professional cyclists, but also has just been in the sport a long time and pays attention to the science and the research and has a pretty good unbiased view of things.

Sami Inkinen, who is a top age group for Ironman competitor. He’s a higher fat diet, pays attention to quantified data, and is a smart, well spoken person who performs well.

And then Dr. Peter Attia, who I would not say is on the pointy edge of physical performance, even though he’s in much better shape than the average, general population. He’s not out doing Ironman triathlons or anything. But, as far as the science goes, he probably knows the science better than just about anybody else when it comes to being able to speak to these things, and he also does quite a bit of self-quantification himself.

So, those would be three people that would be good resources for this.

[Damien Blenkinsopp]: Great, thanks so much for that.

[54:48] Beyond everything, like all the biomarkers we’ve spoken about today, are there any other biomarkers you pay specific attention [to] on a routine basis, I don’t know whether it’s monthly –that you feel are important that we haven’t spoken about?

[Ben Greenfield]: I’ll finish with this because it’s important. And many times in our type of circles it’s not talked about, and it’s not quantifiable to a great degree, as far as I know. And that would be simply paying attention to your levels of gratitude every single day, and multiple times per day.

For me, I guess you could kind of quantify it – at least six times per day I’m grateful. Because I’m journaling, and at the beginning of the day I journal three things I’m grateful for, and at the end of the day I journal three amazing things that happened to me that day. So there’s at least six times per day that I’m being grateful for things.

And then I practice quick coherence technique, which is something you can read about at heartmath.org, which increases heart rate variability and decreases stress. And that’s where you simply think of something that you love or someone you hold dear, and you imagine intense feelings of gratefulness washing over your body and going into your heart after you feel those feelings of gratefulness.

Saying thank you to people, saying I love you to people, randomly calling up people and telling them how much you appreciate them. If you listen to my voicemail, I ask people to end their voice message by telling me one thing that they’re grateful for that day.

It’s certainly something that’s not super duper quantifiable, again, but it is one thing, not a biomarker, but certainly something I pay attention to every day is gratefulness for being alive, for the people in my life, for the experiences that I’ve had, and for simply being able to take one more breath.

[Damien Blenkinsopp]: Excellent. Thanks for that, that’s not the typical, but definitely something really important. So I can see how that would be useful. I do a meditation gratitude every morning too, and I find that really, really useful.

So Ben, thanks so much for your time today. It’s been really stock full of biomarkers and hacks and everything, so it’s really been a great episode. Thank you for your time.

[Ben Greenfield]: Awesome. Well thanks for having me on, Dam.

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Is some aspect of mitochondrial damage behind cancer? If so, can this theory help us take control of cancer via tactics such as yearly or more frequent “7 day water fasts”.

When we think about death, cancer is often what we think of first. If you’re like me, most, if not all, of the deaths affecting you personally in your life may have been due to cancer.

Part of what makes a cancer diagnosis so devastating is that it’s mechanisms – how it works, where it comes from, how we can treat it effectively, how we can track it’s development, assess our risk and avoid it – continue to allude us. That makes us feel powerless against it.

Today’s episode is about the theory that mitochondrial damage is behind cancer, and how this theory may let us take control of cancer. We also hear our guest discuss the power of “water fasts” as a potential tactic to beat cancer.

If that’s true then tools that we have today such as ketogenic diets, fasting, lipid replacement therapy and other approaches to mitochondrial repair may help reduce or eliminate the risk of cancer, and even treat it when we have it.

We’ve already seen how important our mitochondria, and keeping them healthy, is in previous episodes, looking at longevity and aging with Aubrey de Grey, and autoimmune diseases with Terry Wahls. Today we add to that list the role they may be playing in the cancer diseases process.

“All cancers can be linked to impaired mitochondrial function and energy metabolism. It’s not a nuclear genetic disease. It’s a mitochondrial metabolic disease… therapeutic ketosis can enhance mitochondrial function for some conditions, and can kill tumor cells.”
– Dr. Thomas Seyfried

Today’s guest, Dr. Thomas Seyfried, is Professor of Biology at Boston College, where he leads a research program focused on the mechanisms by which metabolic therapies such as ketogenic diets and fasting can manage chronic disease and cancer. He sits on the editorial boards of four research journals, and has over 60 published papers on cancer and metabolism.

He is the author of the review paper Cancer as a Metabolic Disease, appearing in the Journal of Nutrition and Metabolism in 2010, and of the textbook in 2012 entitled Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer.

He’s a frequent lecturer and speaker at conferences on the topic of cancer, impaired mitochondrial function, and using ketogenic diets and fasting tactics as therapy to treat and avoid cancer.

This was personally an important episode for me. I hope you feel more in control of your cancer risk after listening to it, as I do having followed Dr. Seyfried’s work.

The show notes, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. Enjoy the show and let me know what you think in the comments!

itunes quantified body

Show Notes

  • How the idea that a change in mitochondrial function is behind cancer started in the 1920s (4:10).
  • The ancient energy mechanism through which cancer cells can bypass the mitochondria through fermentation instead of normal mitochondrial respiration (7:20).
  • The part of mitochondrial function that seems to be compromised in cancer – oxidative phosphorylation (8:15).
  • Different types of cancer cells and tumors have varying damage to their mitochondria. The worst and most aggressive cancers have the least mitochondrial function (9:00).
  • The oncogenic paradox (9:00).
  • Lipids such as Cardiolipins in the inner membrane of mitochondria are the part responsible for respiration (15:10).
  • How Dr. Seyfried pooled research from over 50 years together to develop his conclusions on cancer and the mitochondria (18:00).
  • Therapeutic ketosis and fasting can enhance mitochondria (23:00).
  • Ketone bodies produce cleaner energy, with less oxidative stress (ROS) than glucose molecules, when used for fuel in the mitochondria (27:00).
  • Nuclear genetic mutations prevent cancer cells from adapting to use ketone bodies as their energy source (29:30).
  • Which biomarkers could be indicative of cancer risk? (33:10).
  • Using therapeutic fasting of several days to improve your metabolism (36:00).
  • Using combined blood glucose – ketone meters to take readings and using Dr. Seyfried’s calculator to calculate Glucose – Ketone Indices (38:00).
  • It requires 3 to 4 days of fasting to get into the therapeutic glucose – ketone index zone (42:00).
  • “Autolytic cannibalism” to improve overall mitochondrial function – the mitochondria can either be rescued, enhanced or consumed (47:30).
  • The difficulties with directly measuring mitochondrial respiration vs. anaerobic fermentation and lactic acid to assess cancer status (49:50).
  • Weight loss can come in two types, pathological and therapeutic. The weight loss via fasting is therapeutic and healthy (52:00).
  • Cancer patients do better with chemotherapy, with less symptoms, when they are in a fasted state (52:00).
  • Cancer centers currently do not offer mitochondrial based therapies, only chemo or immuno therapies (57:40).
  • The biomarkers Dr. Thomas Seyfried tracks on a routine basis and his use of the ‘fasting’ tool (101:40).
  • What Dr. Seyfried would do if he had cancer (102:30)
  • Should you remove organs if you discover you have a high genetic risk for cancer? (E.g. BRCA1 as with Angelina Jolie) (103:30)

Dr. Thomas Seyfried

The Tracking

Biomarkers

  • Blood Glucose: A measure of the level of glucose in the blood at one point in time. Dr. Seyfried’s therapies target reduction of blood glucose levels to limit cancer cell growth, and according to his theories high blood glucose is a biomarker of increased cancer risk.
  • Glucose – Ketone Index (GKI): The ratio between the concentration of glucose in the blood to ketone bodies in the blood. The calculation is Glucose (mmol)/ Ketone (mmol). Dr. Seyfried created the index as a better way to assess metabolic status. Therapeutic efficacy is considered best with index values approaching 1.0 or below. Patients with chronic disease like cancer have index values of 50 or more. Thomas’ paper on the use of GKI for cancer patients has just been accepted for publishing: The Glucose Ketone Index Calculator: A Simple Tool to Monitor Therapeutic Efficacy for Metabolic Management of Brain Cancer. It is on Nutrition & Metabolism journal here and you can download an excel sheet to calculate the Glucose Ketone index here.
    Glucose Ketone Index - Thomas Seyfried

    Glucose Ketone Index Tracking of a Water Fast as Therapy for Brain Tumors Trial – Thomas Seyfried

Lab Tests, Devices and Apps

The Tactics

Treatments

  • 3 – 5 Day Water Only Fasts: A water-only fast of at least 3 days and preferably 5 days is recommended by Dr. Seyfried as a tool to reduce cancer risk and to lower your glucose – ketone index to 1.0. He recommends doing this twice yearly. For cancer patients he recommends much more intensive use of the water fast.
  • Ketogenic Diets: The ketogenic diet is a low carb diet which also raises the level of ketone bodies in the blood. We discussed this in depth, as well as the Ketone biomarkers and devices in episode 7 with Jimmy Moore on Ketosis.
  • Intermittent Fasting: An approach to fasting where you fast for part of the day or certain days per week. There are many approaches to this, however in Dr. Seyfried’s research he has found this doesn’t have a significant enough impact on raising ketone bodies to be therapeutic. He has only seen this via the water-fast.
  • Hyperbaric Oxygen Therapy (HBOT): Another therapy Dr. Seyfried believes may be beneficial to fight cancer but is relatively non-toxic in comparison to current treatment modalities (chemo and immunotherapies), and would like to trial in conjunction with fasting protocols.

Supplements

  • Oxaloacetate: A support for the mitochondria, also dubbed as an anti-aging supplement as it has caloric restriction mimicking effects. It is sold by Dave Asprey in his “Upgraded Aging” formula.
  • 3-Bromopyruvate (3BP): Dr. Seyfried would like to incorporate this non-toxic molecule in combination with fasting therapies to treat cancer patients.
  • PQQ (Pyrroloquinoline Quinone): Mentioned by Damien as a potential tool for mitochondrial biogenesis.

Other People, Resources and Books

People

  • Otto Warburg: A well known scientist who worked on cancer in the 1920s and 30s and discovered that cancer cells have different metabolism to normal cells.
  • Albert Szent-Györgyi: The oncogenic paradox was first coined by this nobel prize winner for his work with vitamin C and energy metabolism.
  • Valter Longo PhD.: Dr. Seyfried referred to Valter Longo’s work at the University of Southern California on the impacts of fasting on patients undergoing chemotherapy.
  • Angelina Jolie: The actress recently had her breast’s removed when she discovered she has the BRCA1 genetic mutation, that predisposes women to breast cancer.

Organizations

Books


Full Interview Transcript

Transcript - Click Here to Read

[Damien Blenkinsopp]: Thomas, thank you so much for joining us today.

[Dr. Thomas Seyfried]: Thank you.

[Damien Blenkinsopp]: I’d like to start off with basically kind of an overview, because you are putting for a different theory of cancer compared to that that’s been the reigning theory for a very, very long time now. Could you describe the differences between the two theories, and what is the basis for your new theory?

[Dr. Thomas Seyfried]: Well, it’s not that my theory is new. The theory was initiated in the early part of the last century, in the 1920’s through the 30s and 40s, by Otto Warburg, the distinguished German scientists and biochemist. It was Warburg who found that all tumor cells continue to ferment glucose in the presence of oxygen. Put it this way, lactic acid fermentation.

This is a very unusual condition that usually happens only when oxygen is not present. But to ferment in the presence of oxygen is a very, very unusual biochemical condition. Warburg said, with his extensive amounts of data, that the reason why tumor cells do this is because their respiration is defective. So, in our normal bodies, most of our cells generate energy through respiration, which is oxidative phosphorylation. And we generate ATP this way.

But cancer cells, of all types of tumors and all cells within tumors, generally have a much higher level of fermentation than the normal cells. And this then became the signature biochemical defect in tumor cells. And Warburg wrote extensively on this phenomenon, and presented massive amounts of data – he and a number of other investigators.

But what happened after Watson and Crick’s discovery of the structure of DNA, and the findings that genetic mutations and DNA damage were in tumor cells, and the enormous implications of understanding DNA as the genetic material, this just sent the whole field off into a quest to understand the genetic damage in tumor cells. And it gradually became clear to many people that cancer was a genetic disease, rather than a mitochondrial metabolic disease as Warburg had originally showed.

[Damien Blenkinsopp]: Right, so when you were talking about the energy and respiration of the cells, just a minute ago, that was actually in fact the mitochondrial respiration, and energy generation from mitochondria within cells.

[Dr. Thomas Seyfried]: That’s correct. That’s correct, it’s mitochondrial. It’s an organelle within all of our cells, the majority of our cells – erythrocytes have no mitochondria, so they ferment. But the mitochondria are the organelle that dictates cellular homeostasis and functionality, and provides health and vitality to cells in our organisms, and ultimately our entire body.

And when these organelles become damaged, defective, or insufficient in some way, cells will normally die. But if the damage or insufficiency is a gradual chronic problem, the cells will resort to a primitive form of energy metabolism, which is fermentation. Which is the type of energy that all cells had, all organisms had before oxygen came onto the planet, which was like a billion years ago.

So what these cells are doing then is essentially going back to a very primitive state of energy metabolism, which was linked to rapid proliferation. Cells would divide rapidly and grow widely before oxygen came onto the planet. So what these cancer cells are doing is just falling back on the type of energy metabolism that existed for all organisms before oxygen came on the planet.

[Damien Blenkinsopp]: Does that type of fermentation type of respiration, metabolic activity, is that originating from the mitochondria, or from the cell itself?

[Dr. Thomas Seyfried]: No, there was no mitochondria before oxygen came on the planet. So this was purely a reductive activity within cells. It doesn’t require mitochondria, it’s a purely cytoplasmic form of energy. Glucose is taken in, and rapidly metabolized to pyruvate through cytoplasmic in the cytoplasm, and then the pyruvate is reduced to lactic acid or lactide, which is called lactic acid fermentation.

And this then could drive energy metabolism, and the processes that can emerge from this type of energy metabolism. But it’s a very inefficient form of energy generation, and it’s often associated with rapid proliferation.

[Damien Blenkinsopp]: Right, thank you very much. So, in very simple terms it seems like, basically what you’re saying is, as the mitochondria get damaged they stop functioning, and then the cell goes back to the original form of energy generation, and it’s as if the mitochondria weren’t there any more.

[Dr. Thomas Seyfried]: Well it’s not that they’re not there. They are there, and they can also participate in certain kinds of amino acid fermentations. They still play a role in generating energy and nutrients for the cell, but it’s not through the sophisticated aspect of energy generation through oxidative phosphoryation. That part of their function seems to be compromised, but other parts of their function can take place. But they’re not generating energy through what most cells would generate energy through, which is respiration or oxidative phosphorylation.

And I also want to point out, it’s not a complete shut down of oxidative phosphorylation. Tumor cells, depending on the grade, and how fast they grow, and how aggressive the tumor is. It is true that some very, very aggressive tumors have very few, if any, mitochondria. So these cells are primarily massive fermenters.

But some tumor cells still have some residual function of their respiration, and they grow much more slowly than those tumor cells that have no function, or very little function, of their respiration. So it’s a graded effect, but the bottom line is the cells continue to grow, but they’re dysregulated. Because the mitochondria do more than just provide efficient energy. They are the regulators of the differentiated state of the cell. They control the entire fiber network in the cell. They control the homeostatic state of that cell.

So these organelles play such an important role in maintaining energy efficiency. And when they become defective, the nuclear genome turns on these oncogenes, that are basically transcription factors that drive fermentation pathways. So the cells are able to survive, but they’re dysregulated.

[Damien Blenkinsopp]: Right, which becomes cancer.

So, in what ways are the mitochondria getting damaged. What is the context for this kind of damage that takes place today? Is this a modern phenomenon, because, obviously cancer has become a bigger and bigger target of medicine over the years, and, potentially, it’s been growing. I’d like to hear your view on that.

Is cancer something that’s always been around, or is it something that affects us more today, and how is it that the mitochondria are getting damaged?

[Dr. Thomas Seyfried]: Yeah, what you said there is referred to as the Oncogenic Paradox, which has been discussed by Albert Szent-Gyorgyi, who received a Novel Prize for his work on Vitamin C and energy metabolism and these things, and John Cohn from England. These people had referred to this phenomenon as the called the Onogenic Paradox. How is it possible that so many disparate events in the environment could cause cancer through a common mechanism?

And when we think of what causes cancer, we think of carcinogens. And these are chemical compounds in the environment that are known to be linked to the formation of cancer. So there’s a whole array of these kinds of chemicals that we call carcinogens. Then there’s radiation can cause cancer. Hypoxia, the blocking of oxygen into cells, can be linked to the formation of cancer.

A common phenomenon and finding is inflammation. Chronic inflammation that leads to wounds that don’t heal. This is another provocative agent for the initiation of cancer. Rare germline mutations, such as the mutations in the BRCA1 gene that a lot of people hear about because of Angelina Jolie bringing attention to that area. Viruses, Hepatitis virus, papillomaviruses. And there’s a variety of viruses that can be linked to cancer. Age. The older people get, the greater the risk of cancer.

All these provocative agents all damage respiration. Their common link to the origin of cancer is damage to the mitochondria, and damage to the respiratory capacity of the cell. So the paradox is solved once people realize that these disparate, provocative agents work all through a common mechanism, which is basically damage to the cellular respiration.

Now, but people say, “Well what about all the genome mutations? What about all these mutations?” Which is a major focus in the field right now, is that cancer is a nuclear genetic disease. Now what happens is the integrity of the nucleus and the genetic stability of the nucleus becomes unstable once energy from respiration becomes defective.

Now it’s very interesting. All of the so-called provocative agents that are known to cause cancer through damage to respiration release these toxic reactive oxygen species, which then cause nuclear genetic mutations. And this is what most people are focusing on. The nuclear genetic mutations in the tumor cells are the targets and focal point of the majority of the cancer industry. Now, when you look at the disease as a mitochondrial metabolic disease, the nuclear genetic mutations arise as secondary downstream epiphenomena of damage to the respiration. So what most people are focusing on is the downstream effect, rather than the cause of the disease.

[Damien Blenkinsopp]: You’re saying that because mitochondria are damaged and energy output is damaged, that causes the cell to lose it’s integrity?

[Dr. Thomas Seyfried]: Lose the genomic integrity.

[Damien Blenkinsopp]: Ah, genomic integrity.

[Dr. Thomas Seyfried]: Yeah. Most people you talk to about this, they say “Oh, cancer’s a genetic disease. We’re trying to talk all these genetic mutations. Every kind of tumor has all kinds of mutations. We need personalized therapies because the mutations are different in all the different cells, and the different types of cancer.” And that’s true, but all of that is a downstream effect of the damage to the respiration.

So, people are focusing on red-herrings. They’re not focusing on the core issue of the problem, which is stabilized energy metabolism. And this underlies the reason for why we’re making so little progress in managing the disease.

[Damien Blenkinsopp]: So, I don’t know if you can break it down into a bit more detail. The mitochondria are made up of several parts: the outer membrane, the inner membrane, and so on. Is it certain parts, or is it any part of the mitochondria that’s getting damaged?

[Dr. Thomas Seyfried]: Yeah, it’s very interesting. It seems to be we’ve defined the lipid abnormalities, the lipid components of the inner membrane of the mitochondria. So there’s certain types of lipids that are enriched primarily in the inner membrane of the mitochondria. This lipid called cardiolipin. It’s an ancient lipid that’s present in bacteria and in mitochondria, but it plays a very important role in maintaining the integrity of the inner membrane, which is ultimately the origin of our respiratory energy, which is that inner membrane.

And many of the proteins that participate in the electron transport chain depend, or are dependent under interaction in the lipid environment in which they sit. So, lipids can be changed dramatically from the environment, which then alter the function of the proteins of the electron transport chain, effecting the ability of that organelle now to generate energy.

This is a real issue, and that inner membrane can be effected by all these carcinogens, radiation, hypoxia, viruses. The viruses themselves, or the products of the virus, will enter into the mitochondria and take up residence, thereby altering the energy efficiency of the infected cell.

And most of the cells die. When you interfere with respiration, most cells die. But in some cells of our body that have the capacity to up-regulate fermentation, these primitive energy pathways, they survive, and they go on to become the cells of the tumor.

[Damien Blenkinsopp]: Great, thank you for that. So, this is a very different theory to that which most people have come across, which, of course, you just outlined with the DNA mutations. Which bits of research have you pulled together in your book, and in your presentations, that you feel like present this view of the world the most strongly. Are there key research elements, researchers that have gone on, and maybe it comes down to four pieces that you feel strongly support this versus the other argument?

[Dr. Thomas Seyfried]: I think that’s an extremely important point. What is the strongest evidence to support what I’ve just said? And what I did in my book in evaluating the therapeutic benefits that we’ve seen in managing cancer by targeting fermentation energy. How is it possible that we overlooked this information? It’s very interesting.

Over the last 50 years, various sporadic reports had been published in the literature showing that if the nucleus of the tumor cell is placed in a new cytoplasm, a cytoplasm that has normal mitochondria – and this is cytoplasm either from a newly fertilized egg, or an embryonic stem cell. Because now we have this technology where we can do these kinds of nuclear transplantations. And this ultimately was what lead to the cloning of Dolly the sheep, and these kinds of experiments. These had been done many, many years earlier in frogs, and in mice, before we moved on to the larger mammals and things like this.

But it became clear that when the nucleus of the tumor cell was placed into the normal cytoplasm, sometimes normal cells would form, and sometimes you could clone a frog, or a mouse, from the nucleus of the tumor cell. Now this was quite astonishing. Because people were thinking you would get cancer cells, because the mutations in the nucleus, if the hypothesis is correct that this is a nuclear genetic disease and the gene drivers are in the nucleus, then how is it possible that you could generate normal tissues without abnormal proliferation. In other words, normal, differentiated tissues from the nucleus of a tumor cell.

I was able to pull together a variety of these reports that had been sporadic in the literature over 50 years. And when these reports came out, it was considered kind of an oddball report that didn’t support the gene theory, but most people discounted it, because it was one singular report. But every four or five years, another report. Eight years would go by, another kind of report. And some of these studies were done by the leaders of the field, the key developmental biologists, the best there were. These people were heavy-weights in the field.

And they were coming to the same conclusions. That we were not getting tumors from transplanting the cancer nucleus into a normal cytoplasm. We were cloning mice, we were cloning frogs. We were seeing normal regulated cell grow. Now how can this happen, if the nucleus is supposed to be driving the disease?

So what I did was, I put all these reports together in a singular group. And I distilled it down to what the ultimate results showed. And then when you look at the whole group of papers, together for the first time, and the conclusions are consistent from one study to the other, using totally different organisms, totally different experimental systems, the results are all the same. The nuclear mutations are not driving the cancer disease.

And then if you take the normal nucleus and put it into a tumor cytoplasm, you either get tumor cells or dead cells. You never get normal cells. So this was clear. It became very clear to me, and when people look at these kinds of observations in their group and their totality, it’s a devastating statement on the nature of the disease. It’s not a nuclear genetic disease, it’s a mitochondrial metabolic disease. And the field has not yet come to grips with this new reality.

[Damien Blenkinsopp]: Just on that point, quickly, if you were to predict the future, do you think that this view of cancer metabolism is going to get traction in the near future? Say the next five years, next ten years, and what will it take to make that happen?

[Dr. Thomas Seyfried]: Well, it’s already gaining a lot of traction. People are now coming to realize that metabolism is a major aspect of cancer. But, unfortunately, what the field has done, there’s still links to the gene theory. So, the top papers come out and they say, “Oh, the abnormal metabolism in cancer cells is due to the nuclear gene mutations. Therefore, we still must be on the quest to find out what these mutations do.”

They have not evaluated in the depth of the information that I’ve presented. It becomes clear that this is not a nuclear genetic disease. So the mutations are not driving the disease, they’re the effects of the abnormal metabolism.

Now, there’s a groundswell of new interests in this. Now this opens up a totally different way to approach cancer. Once you realize it’s not a nuclear genetic disease, but it’s a mitochondrial metabolic disease, you have to then target those fuels that the tumor cell is using to stay alive. These amino acids and glucose, which can be fermented. Those molecules that can be fermented through these primitive pathways now become the focal point of stopping the disease.

So it becomes a much, much more manageable and approachable disease once you realize that if you take the fuel away from these tumor cells, they don’t survive. They become very indolent, they stop growing, they die. And now this gives you an opportunity to come in and target and destroy these cells, using more natural, non-toxic approaches.

[Damien Blenkinsopp]: Right. If you could reinforce that a little bit, because as I understand it, the current approach, which is pushed the most, is to target all of the different nuclear genetic mutations – and there’s many, many thousands of them, you can’t really count how many there are, because it’s constantly developing – versus, with mitochondria, as I understand it, mitochondria are all the same. So it’s a completely different problem when you look at it from that respective. Am I summarizing it correctly?

[Dr. Thomas Seyfried]: Yes, I think you’re absolutely right. I mean, it’s a completely different problem. It now becomes a problem of energy metabolism. And the nucleus becomes a secondary peripheral issue.

[Damien Blenkinsopp]: Right. And the fact becomes much simpler, because you’re targeting the same problem versus thousands of different problems.

[Dr. Thomas Seyfried]: Absolutely.

[Damien Blenkinsopp]: And then therapy is… Today we’re developing thousands of hundreds of different drugs to target different types of cancer.

[Dr. Thomas Seyfried]: Yeah, it makes no sense. And the issue is every single cell in the tumor suffers from the same metabolic problem. But every single cell in the tumor has a totally different genetic entity. And we’re focusing on the very different aspects of every cell, rather than the common aspects of every cell.

The problem becomes a much more solvable problem once you target the commonality. The common defect expressed in all cells, rather than the defects that are expressed in only a few of the cells. You would not do that until you came to the realization, and saw the data, that this is a disease of energy metabolism, not nuclear genetic defects. It’s a totally different way of viewing the disease.

[Damien Blenkinsopp]: Right. Thank you.

This may be kind of off subject for you, let me know if it is. But, I understand it, there’s also, more and more people are starting to link other types of diseases – say multiple sclerosis, Parkinson’s, and some of the other chronic diseases that we have and are not very solvable today – to mitochondrial disease. So I’m wondering if in any way you link that to the same origin of cancer, here. That we’re discussing.

[Dr. Thomas Seyfried]: Well, those diseases, that’s true. There are mitochondrial abnormalities in Parkinson’s disease, Alzheimer’s disease, epilepsy, and Type 2 diabetes. I mean, you can go right down the list and find a mitochondrial connection to a lot of these different diseases. But the mitochondria can be damaged, and insufficient, and influenced in many different kinds of ways. So, only cells that can up-regulate, significantly up-regulate fermentation, can go on to form tumor cells.

But many of our cells are not killed outright, and they struggle. For example, the brain. We rarely get tumors of the neurons in the brain, because if you damage the respiration of the neuron, the neuron will die.

Many of the tumors in the brain come from the glial cells. These are supportive cells of the brain, they play an extremely important role in the homeostasis of brain function. But those cells have a greater capacity to ferment than do the neurons. So when mitochondria are damaged in neurons, the neurons usually die. You can never get a tumor cell from a dead cell.

Now Parkinson’s disease and Alzheimer’s disease, these are situations where populations of neurons die from reactive oxygen species. So these reactive oxygen species, which are produced by inefficient mitochondria, kill the cell. And the cells never form tumors, they just die. So you have populations of cells in the Substantia nigra in Parkinson’s disease, or in the hippocampus in Alzheimer’s disease, where the neurons are dying. And they’re dying from mitochondrial energy inefficiencies.

And the idea then, is can we enhance neuronal function by using therapies that will strengthen mitochondrial function. And the answer is, yes. And this is why these ketogenic diets are showing therapeutic benefit for a variety of different ailments, a very broad range of ailments. But the diets and these approaches – what we can therapeutic ketosis – can enhance mitochondrial function for some conditions, and can kill tumor cells in other conditions.

So one now has to appreciate a new approach to managing a variety of diseases that may have a linkage through inefficient mitochondrial metabolism.

[Damien Blenkinsopp]: Could you talk about – we’re coming into treatment here a little bit now, based on your theory. There’s the difference between ketone, or like, fat versus glucose metabolism in the mitochondria. And you were just talking about efficiencies. Could you go over that? What is the difference there? Why is it that glucose metabolism is different that of fats and the production of ketones?

[Dr. Thomas Seyfried]: Yeah, well the body is very flexible. It can burn energy from carbohydrates, which is glucose, or it can burn energy from fatty acids. Or it can burn energy from ketones. And we evolved as a species to survive for considerable periods of time without food. It’s amazing how people don’t understand this. They think if they don’t eat food in a week or less, they’re going to drop dead. This is nonsense.

We evolved as a species to function for long periods of time. As long as we have adequate fluids, water, the human body can sustain functionality for extended periods of time without eating. Now, you say to yourself, well where are we getting our energy. We evolved to store energy in the form of triglycerides, which are fat. And many of our organs store fats to various degree, and we have fat cells that store fat.

Now, when we stop eating, the fats are mobilized out of these storage vacuoles in the cells. And the fats go to the liver, and our liver breaks these fats down, like a wood chipper, to these small little ketone bodies, which now circulate through the bloodstream, and they can serve as an alternative fuel to glucose. So we can sustain, because the brain has a huge demand for glucose, but the human brain can transition to these fat breakdown products called ketone bodies.

So this all comes from storage fat, and our brains can get tremendous energy from these ketones. The energy in food comes from hydrogen carbon bonds that were produced during the production of the food. Ultimately from planets and the sunlight. But the energy in the bonds is ultimately derived from the energy of the sun. Now, our bodies break down these bonds, and recapture that energy. What we’re doing then is just recapturing this energy.

Now ketone bodies, when they’re burned in cells, they have a higher number of carbon oxygen bonds. They produce more intrinsic energy than does a glucose molecule, which is broken down to pyruvate, which is a glucose breakdown product. And when ketones are metabolized, they produce fewer of these reactive oxygen species. They work on the coenzyme Q couple within the mitochondria to produce clean energy, energy without breakdown products. It’s a very efficient form of energy.

[Damien Blenkinsopp]: I like that analogy there, because people could relate to how we had lead gas before, and we cleaned it up a bit, and now we’ve got less waste products in the environment.

[Dr. Thomas Seyfried]: Yeah!

[Damien Blenkinsopp]: It’s a little bit similar.

[Dr. Thomas Seyfried]: It’s the same thing. I mean, our bodies are so super energy efficient when we begin to force them into a situation. In the past, this was done all the time, because in the past the humans almost were extinct a number of geological epochs, for the ice ages, lacks of food and all. And I mean, we have a very energy efficient machine in our bodies that can generate this energy from within. Clean, powerful, efficient energy that allows us to sustain our mental and physiological functions for extended periods of time.

And this comes from the genome. Our genome has a remembrance and a knowledge to do this. It evolved over millions of years to do this. The problem today is that this capability is suppressed by the large amounts of high energy foods that are in our environment. And what happens, this then creates inflammation and the kinds of conditions that allow inefficiencies, and eventually inflammation and the onset of cancer.

So, returning to the more primitive states allows our bodies to reheal themselves. And, as I said, here’s the issue. The nuclear genetic mutations that collect in these cancer cells prevent those cells from making the adaptations to these food restrictive conditions. So, because the mutations are there, the cells are no longer flexible. They can’t move from one energy state to the other, like the normal cells can, which have integrated genomes.

So, the mutations can be used to kill these tumor cells, but by forcing the body into these different energy states in a non-toxic way. It’s not necessary to have to poison people, nuke people, surgically mutilate people to make them healthy. There’s natural ways we can do this, if we understand the differences in metabolism between normal cells and cancer cells.

[Damien Blenkinsopp]: So, from your perspective, anything that would help to repair mitochondria, would that be helpful against cancer?

[Dr. Thomas Seyfried]: Oh, absolutely. Absolutely. You’re not going to get cancer in cells that have very healthy mitochondria. If mitochondrial damage is the origin of cancer, and the cells have very high efficient mitochondria, it’s very unlikely. The risk of developing cancer in those situations is remarkably low.

There are groups of people that we have in the United States, the Calorie Restriction Society of America. It exists in other areas throughout the world. These people have a very low incidence of cancer. They’re in a constant state of ketosis, and the incidence of cancer in these people is very, very low.

Now, I have to admit. This is not an easy lifestyle. People don’t want to be restricting themselves all the time, and doing this stuff. This is the issue. We live in an industrialized society that has come a long way to create an environment that is free of the massive kinds of starvations, and these things that existed in the past. So it’s hard to take your body and go back into these primitive states to do this kind of thing.

[Damien Blenkinsopp]: Right. So, there’s [unclear 31:58] a really big focus on what you’ve been saying on reactive oxygen species, which is kind of like the mini explosion that takes place inside a car when it’s running. And I think people can relate to the fact that all engines are causing damage while they’re running, because they’re producing heat, and so on.

So, with the mitochondria, it’s basically the same. And you’re saying that when we’re on a ketogenic diet, or where we’re fasting and we’re producing this more efficient type of fuel, it reduces our assets [unclear 32:23] causing less damage. And it’s an important type of the damage that is caused to mitochondria.

And this is why eventually it helps with the status of the mitochondria, to heal them and repair them, or to limit the additional damage that goes on which would help to promote the cancer. Is that a good summary, or have I got some things wrong?

[Dr. Thomas Seyfried]: It’s a very close analogy. I would say this is exactly what it is. We damage our body by the kinds of foods we eat, the kinds of environments we’re exposed to. And the mitochondria in certain cells just get damaged, and these cells then revert back to a more primitive form of energy, which is fermentation, which then leads to a total dysregulation of the growth of the cell. Collects these mutations that come as a secondary downstream epiphenomena of this.

And the thing of it is is, how do you target and eliminate those kinds of cells. And cancer, people must realize, this is systemic disease, rather than a focal disease. People say, “Oh, what does he study? He’s a liver cancer, breast cancer.”

These cancers are all the same. They’re metabolically all the same. You need to treat cancer in a singular global systemic way, and this then will marginalize and reduce the growth of these cells. And you have to be able to do it non-toxically.

And these ketogenic diets, or therapeutic ketosis, is just one way to enhance the overall health and well-being of the body while targeting and eliminating these inefficient cells. And this can be done if people do it the right away.

[Damien Blenkinsopp]: Great, great. Thank you very much.

So, based on this theory, what kind of biomarkers would give us insights into someone’s potential to develop cancer? Because today we look at 23andMe data, for example, genetics to kind of asses our risks of future cancer. For instance, on mine it says my highest potential cancer is lung cancer. And that’s pretty much the only markers that we’re given. Are there markers related to mitochondrial function, or damage, that you would feel that would be relevant to estimating a future potential risk of cancer?

[Dr. Thomas Seyfried]: Yeah, well I think one of the risks of cancer is high blood sugar, blood glucose levels. I mean this creates systemic inflammation, which underlies a lot of the so-called chronic diseases that we have, including heart disease, and Type 2 diabetes, and Alzheimer’s disease, and cancer. These are just the predominant number of chronic diseases that we’re confronted with.

So, if we know that high blood sugar is a provocative agent that increases the risk for cancer, then making sure your blood sugar levels are low. And the other thing too is elevation of ketones. So we developed what they call a glucose-keton index that can be used for people to prevent cancer, as well as managing the disease.

So if the glucose-ketone index, which we have defined as the ratio between the concentration of glucose in the blood to the concentration of ketone bodies in the blood. If this index can be maintained as close to 1.0 or below, the body is in a very high state of therapeutic energy efficiency. Which is then going to reduce the risk for all of these different kinds of chronic diseases. So, and if you look at most people with chronic disease, their index is about 50 or 100, rather than 1 or below 1.

We’ve just developed this, and we’re working on a paper. It’s called the Glucose-Ketone Index. It was designed basically for managing cancer, because patients who have cancer, if they want to know what these therapies are doing, how they’re working, you look at your index.

Now, people who don’t have cancer, who would like to do something to reduce their risk, they would do the same thing. And people would say, “What’s your index today?” “My index is 1.2.” You’re in a very good state of health.

And if most people – I can guarantee – people who eat regular foods, their indexes are about 60 or 70, not 1.2 below. Because what you do is when you have a lot of carbohydrate in your bloodstream, the ketones are very, very low. They’re like 0.2, 0.1. And you’re blood sugar is like 4 or 5 millimolar, and your blood ketones are 0.1 millimolar. Well what do you think your index is going to be? It’s going to be huge.

But then if you increase your ketones, if you can bring the ketones bodies up to the same level as glucose, then I have a 1.0.

[Damien Blenkinsopp]: Is this sensitive enough to manage potential? You made a very clear scenario of 60, where that’s a very dangerous situation to be in.

[Dr. Thomas Seyfried]: Oh no, no. I don’t want to say it’s dangerous. I want to say it’s the norm.

[Damien Blenkinsopp]: Oh, okay. Great.

[Dr. Thomas Seyfried]: It’s not dangerous. When you take somebody who has Type 2 diabetes, and his blood sugar is like 300 milligrams per deciliter – and you have to divide that by the number 18 to bring it down to millimolar – and his ketones, you can’t even measure them. I mean, these guys are inflamed. Their bodies are in an inflamed state. And inflammation will cause all kinds of effects.

So, you want to bring people down. How do you get these low numbers? Well, you can either go on these calorie restrictive ketogenic diets, or you can do therapeutic fasting, which is water only fasting, for several days. You’ll bring those numbers right down. You’ll get into an extremely healthy state. Because the ketones go up naturally when you don’t eat, and blood sugar goes down naturally when you don’t eat.

So then you enter into these states, it’s called therapeutic ketosis. The problem is it’s very, very difficult for most people in our society to do this, because our brains are addicted to glucose. If you take somebody who stopped eating for 24, 36 hours, this guy thinks he’s going to go crazy. It’s almost like trying to break the addictions to cigarettes, alcohol, drugs. It’s not easy. It’s very, very difficult to break the glucose addiction.

[Damien Blenkinsopp]: Absolutely. It takes a little bit of time to change your metabolism.

[Dr. Thomas Seyfried]: Yeah.

[Damien Blenkinsopp]: So we spoke to Jimmy Moore before. I don’t know if you connected with him before, and his book…

[Dr. Thomas Seyfried]: Yeah, I know Jimmy.

[Damien Blenkinsopp]: Right, right. So we spoke about some of the different ways to measure ketones. We had the blood test, the blood-prick test with the precision, which is a little bit expensive today. And you have the breath test, the Ketonics, which has just come out. With that index, are you using the blood-prick test, or are you using maybe blood labs, or something a bit more complicated?

[Dr. Thomas Seyfried]: There’s a couple of companies that use the blood test, the most accurate. It’s more accurate than the breath, blowing into a ketosis meter. Or you do urine sticks. So the most important measure, of course, is blood. So you have to take a blood stick. There’s only a few meters that can do both ketones and glucose, using the same meter.

You have to use different sticks. There’s a ketone stick, and a glucose stick. So from the same drop of blood, you can get your blood sugar, and then you can put a new stick into the machine, which is a ketone stick, and then you can take the same drop of blood and get your ketones.

Now what we did was we developed a calculator so that all the person would have to do is to push the button on the meter, and it would calculate already your glucose-ketone index. This would give you a singular number from a drop of blood.

[Damien Blenkinsopp]: So you’ve developed your own device, you’re saying, which does that calculation?

[Dr. Thomas Seyfried]: We developed the calculation. It’s called the Ketone Index Calculator. And because you have to convert everything back to millimolar. Because many of the ketone meters give you blood sugar in milligrams per deciliter, and ketones in millimolar. So we have to convert. You can do all this by hand, you just have to do the divisions and all of this stuff.

[Damien Blenkinsopp]: So you’ve got an online calculator where people can put their values in and it will give them the index?

[Dr. Thomas Seyfried]: Well, we don’t have that yet. What we did was develop the calculator that could be incorporated into these meters.

[Damien Blenkinsopp]: I see.

[Dr. Thomas Seyfried]: This is the thing. So people, regardless of whether you’re a cancer patient and you want to manage your disease, or you’re a person who wants to prevent cancer, or you’re an athlete who wants to know what his physiological status is, or you’re someone who wants to lose weight. All of these issues, you can get a sense, a good solid biomarker sense, by looking at your glucose-ketone index.

And everybody can do that from these meters that are capable. But the meters right now are not designed to give you glucose-ketone indexes. And this is what we’re saying; it’s the index that will tell you your overall status, your health status.

[Damien Blenkinsopp]: Right. So I imagine, right now, you’re approaching the providers of these tools to see if they can incorporate this calculation into their devices?

[Dr. Thomas Seyfried]: Yes. Exactly. They don’t have it yet. They’re not even aware yet of the potential market, or interests, among the general population. Not only for people that are afflicted with various diseases, but people who are healthy and don’t want to get those diseases.

So this is a very simple tool. The only drawback from it is you have to stick your finger with a little prick to get a little bit of a drop of blood. The people with Type 1 diabetes do this regularly. This is not an issue. But for those people who are into this, and they want to do it the right way, and they want to get accurate biomarker measurements, then they would do this. For those people who are interested in this.

This is invasive in the sense that you have to prick your finger to get a drop of blood, but it’s not invasive in the sense that you have to take tissue samples, or any of this kind of thing.

[Damien Blenkinsopp]: And so this is something that people could do on an on-going basis? So I’m guessing for someone with cancer – I don’t know if this would be something you would say – they’d probably want to look at daily, or every few days, or something like that. And someone else, maybe it’s just something they need to do a lot less intensive routine, in terms to just monitor the levels of their general ketogenesis.

[Dr. Thomas Seyfried]: Yes. You’re absolutely right about this. People who are trying to manage their diseases thoroughly might want to do this maybe once or twice a day. Just like someone who might have Type 1 diabetes. They measure their blood sugar several times a day.

The issue right now is the glucose strips are relatively cheap – they’re like 50 cents a piece – but the ketone strips are much more expensive. They can range from anywhere from $2 to $5 a stick.

[Damien Blenkinsopp]: Do you know if that’s due to economies of scale? Or if it’s simply because not enough people are using them yet?

[Dr. Thomas Seyfried]: Yes, it’s an economy of scale, absolutely. Because very few people measure their ketone levels. But now, linking those ketones to your overall general health, a lot of people would be interested in this.

And people in general like numbers. They want to know, and especially a singular number that would dictate your state of health. If you can say to somebody, “Listen. My index is between 1.1 and 0.9,” people would automatically know this guy is in a tremendous state of health.

People like to know that. You say, “Where is your number?” And people like to keep log books. They like to record these numbers. And they also link this to a greater sense of well-being. People who have their numbers down in these ranges, they tell me – and I’ve done it. Some people get into a state of euphoria. It’s like unbelievable.

When your body starts burning these ketones, it’s like you enter a new physiological state. And athletes are doing this sometimes. So it’s a whole new realm of how to monitor your own health with accurate biomarkers that give you an indication of your health status.

[Damien Blenkinsopp]: So do you follow a similar prescription to Jimmy Moore? I believe you understand his approach, where he’s eating a high fat diet, or sometimes he’s fasting. Kind of like intermittent fasting, which has become pretty popular these days.

[Dr. Thomas Seyfried]: Well intermittent fasting is, from what we’ve seen in our work, you don’t get the health benefits, the power of the health benefit, until you’ve gone three to four days without any food. Just drinking water. And then those who can go a week, like a seven day period, this is really when you start to see your blood sugars going down and your ketones going up.

But once you can get into this zone – we call it the zone of therapeutic management – where now you know your in the zone, this is where the health really comes in. And when you say periodic fasting, now there’s a lot of people that I know – numbers of people – who have a rather restrictive diet for the week, and then one day a week they’ll not eat anything. So, it’s one day off on food, like a 24 hour period where they’ll just have maybe a green tea, no calories, or just pure water.

[Damien Blenkinsopp]: Some of the intermittent fasting regimes propose that approach, a 24 hour fast every two days.

[Dr. Thomas Seyfried]: Yeah, but then you’ve got to know, okay what did that do to my index? How effective was the 24 hour fast on my index? And you look down, you say, “Well, I didn’t get my ketones up very far. They went from 0.1 to say, 0.5.” Okay, but if I go four or five days, it goes from 0.1 to 3.0. Oh wow, this is the magnitude difference.

[Damien Blenkinsopp]: Yeah. So have you looked at different people, because when we were talking to Jimmy, he was saying that different people have different responses. It’s based on their current state of metabolism. They’ll have to be more extreme in their approach to get the same level of ketones, and the same impact on an index, depending on, potentially, how damaged their mitochondria are. I don’t know how you look at it.

[Dr. Thomas Seyfried]: Yeah, no, that’s a really important point. It’s certain people. It’s also certain sexes. Women can get into these ketone states much easier than men. And young people can get into these zones much, much easier than can older people.

So it’s an age issue, it’s a gender issue. We’ve seen some of our students get down their blood sugars down into the low 30s, which people would say would be a crisis situation, you’d have to go to the hospital. But their ketones are elevated, and when the ketones are elevated, you have no crisis situation. It’s only when you lower blood sugar and don’t elevate ketones that you have this situation.

Males have a lot more muscle, they tend to burn protein, which can be converted to glucose. So their blood glucose doesn’t go down as sharply as women, the blood glucose of females goes down. Females can get their blood sugars down and their ketones elevated – from all the data that we’ve seen for several years on different gender – and this is what we see.

And older people are simply locked into a much longer lifestyle of high glucose. And for them to get their blood sugar down, it’s a real struggle. And also their muscle mass over the age. They have a lot of other issues that play into this whole thing.

And you’re absolutely right, it’s an individual thing. Some people can’t tolerate this. They get really sick, they get light-headed. Where other people make the adaptations much more quickly. So again, people have to know their own physiology.

But they have to have the biomarkers that let them know. They need to see these numbers, and once they see these numbers they’ll know that they’re on the right path, and they probably can do this if they persist a little bit longer. Rather than throwing their hands up, not knowing what’s going on, being very frustrated. And as I said, once you have this information and knowledge, that these kinds of things become much easier.

[Damien Blenkinsopp]: Yeah. It definitely helps with your confidence in something if you can see that, maybe you don’t feel better, or you don’t feel a difference yet, but if you see the numbers starting to move then it gives you that sense of accountability, and motivation also. I think that’s one of the very helpful aspects of these kind of indexes that you’re talking about.

[Dr. Thomas Seyfried]: Absolutely. This is a very important point, you’re absolutely right about this. Because when you see that you’re killing yourself, and nothing’s happening, or you don’t feel anything, but when you see numbers starting to change in the direction you know your hard work is starting to pay off. And then you get motivated, and you want to see then how far you can push these numbers.

Now this is not going to hurt anybody. You’re just lowering blood sugar and elevating ketones, and your body gets into a new state of health. And people feel it, believe me. You can feel this stuff happening. But there’s a rocky road going from the high glucose state to the high ketone state. And that rocky road can be more rocky for some than others.

[Damien Blenkinsopp]: Absolutely. So there are other aspects to mitochondrial health that certain people are looking at at the moment. I don’t know if you’ve come across any of these, but I thought I’d just throw them out in case you had some comments on them.

Some people are talking about mitochondrial repair, in terms of repairing the membranes with specific lipids, by providing those lipids to help reinforce the mitochondria. Other people talk about things like PQQ to help stimulate biogenesis of new mitochondria. I don’t know if you’ve heard about these things, or have any ideas or opinions on them.

[Dr. Thomas Seyfried]: Well, in my book I called it autolytic cannibalism. And this is basically, the mitochondria can either be rescued, enhanced, or consumed through an autophagy mechanism. And when you stop eating, now every cell in the body must operate at its maximal energy efficiency. That means that the mitochondria in those cells must be operational at their highest level of energetic efficiency. Otherwise the cell will die, and the molecules of that cell will be consumed, and redistributed to the rest of the body.

Now, in cells that have some mitochondria effective, or more efficient than other mitochondria within the same cell, the inefficient mitochondria can be incorporated into the lysosome. The parts of that mitochondria can then be redistributed to the healthy mitochondria within the cell. And this way you eliminate internal energy inefficiencies, but without having to kill the cell, because the cell is able to repair itself.

Whereas those cells that can’t repair themselves die, and their molecules are then consumed by macrophages, excreted back into the blood stream, and the nutrients now are used to support the health and vitality of those cells in the body that have this higher energy efficiency. It’s a remarkable state of efficiency. So it works both with individual cells, and throughout the whole entire physiological system.

[Damien Blenkinsopp]: Great, great. Thank you. I’m just thinking, you’ve spoken about fermentation versus respiration. Is there any way to measure that, that you know of? Is that being done in studies? So are the studies coming out are comparing the state of fermentation versus respiration taking place in people’s bodies, and correlating that to cancers, or anything like that?

[Dr. Thomas Seyfried]: Yeah, that’s kind of hard to do, because we all have lactate in our bloodstream, and the lactate comes from erythrocytes, our blood cells. The blood cells have a shorter half-life than many of the other cells in our body, and those cells have no mitochondria. They have no nucleus. So they’re little cytoplasms that primarily ferment.

But they don’t use a lot of energy, because the role of that cell is simply to exchange gases. So it floats around in our tissues, it deposits it’s oxygen and picks up CO2, as more or less a little mailman running around, picking up this and dropping that off. And they have a shorter half-life. But they have lactate.

Now if you have a tumor, or if you’re under hypoxic stress, lactic acid will go up in your bloodstream. But it’s hard to know if a tumor will do that. Sometimes what tumors will do, they have a phenomena called cachexia. This is where the tumor cells will send out molecules that will digest proteins, or dissolve proteins in our muscles and other proteins. And these proteins then go to the liver, and are broken down into amino acids, and the amino acids are conjugated into glucose.

So the glucose goes now into the tumor cell, and some of the proteins and the amino acids go to the tumor cell after being broken down. So the tumor is essentially causing our body to starve to death. We might be eating, but it looks like we’re not gaining any weight, and we’re becoming moribund and looking like we’re starving to death. This is an effect of the tumor,.

Sometimes you don’t see that. Sometimes lactic acid will go up, and sometimes it won’t. So there’s a lot of ambiguity of looking at a good biomarker to assess the state of what level of tumor growth you might have, other than the fact that you’re losing weight even though you’re eating. Which is the cachexic state; you’re kind of wasting from within. This is the whole thing.

And this is one of the fears that the medical profession has with cancer patients, because they say these poor people are losing weight through this cachexic mechanism, and then you come along with a metabolic therapy, and they say, “Oh, this can’t work.” But the issue, of course, is that there’s two types of weight loss. One is a pathological weight loss, and the other is therapeutic weight loss.

Pathological weight loss is cachexia, and of course if you treat it with toxic chemicals and radiation, you get so sick with fatigue, nausea, diarrhea, vomiting. I mean, this is pathological weight loss. Therapeutic weight loss is you’re losing weight, but your body is getting extremely healthy, and killing cancer cells at the same time.

So weight loss can come in two different varieties: pathological and therapeutic. And people have a tremendous difficulty in understanding the differences between these kinds of weight loss.

[Damien Blenkinsopp]: I think we’ve mentioned on a podcast before that when people are fasting in this state, they actually feel better, even if they have, for instance, chemotherapy. They tend to do better in chemotherapy when they have been fasting.

[Dr. Thomas Seyfried]: Yes, because it reduces inflammation. We published a number of papers showing how therapeutic fasting reduces systemic inflammation. Systemic inflammation contributes to a pathological state, and facilitates tumor growth.

So therapeutic fasting, while at the same time you’re taking a toxic drug, it’s like what are you doing here. But it does take the sting out of that toxic drug. People feel better when they’re therapeutically fasting. I think Longo’s group down at University of Southern California has clearly shown that some of these cancer patients can do a lot better, and feel better, when they’re fasting while they’re taking chemotherapy.

But you’re absolutely right about that.

[Damien Blenkinsopp]: Thank you so much for this interview[unclear 53:08] Thomas. I want to ask you just a few more questions to round off now.

What do you think will happen in the next five or 10 years, or hope? What are your visions for this area, in terms of biomarkers, like testing devices, or change in the way we approach this? Do you think there’s specific opportunities ahead, are there specific questions you’re looking at at the moment to resolve, in research, or so on?

[Dr. Thomas Seyfried]: Yeah, well I think the people themselves are demanding a change. The issue is that they haven’t been shown other alternatives, other than the standards of care, which are conducted by the major medical schools: Dana Farber Cancer Center, MD Anderson, John Hopkins, Yale Cancer Centers, Sloan Kettering, UCSF. The major industries of cancer and academics are closely aligned in how to do this.

And it’s not working. We’re having about 1,600 people a day are dying from cancer in this country. And the statistics in other countries in Europe, and China, and Japan, are not far off of this. And if we had Ebola outbreak in this country, where 1,600 people were dying a day, this would be of the greatest catastrophe that people can imagine.

But for cancer, it seems to be okay. This is the norm. Well it doesn’t have to be this way. It doesn’t have to be this way. And the issue here is that the people see that we have more, and more survivors, and people doing pretty well on these metabolic therapies. Why are we not doing this as more of a general treatment as opposed to these toxic approaches to manage the disease?

So I think the change will come from the grassroots. I don’t see it coming from the top medical schools, because these people are not trained. They’re medical education doesn’t give them the training to identify these approaches to therapy. It’s not part of the medical training.

There are a number of physicians that are recognizing this now, and they want to become part of this new approach to cancer management. Now, you have to realize that we’re just beginning. This is just a new field, it’s a beginning field. Even though the science is well, well established, the implementation of this science for patient health is just at the beginning. It can be refined, it can be modified.

A lot of this now we’re talking about, the potential for managing cancer in a non-toxic way with greater therapeutic efficacy, is just beginning. So, I think that we need more trained people. We have to have people that understand this. Eventually, these kinds of approaches will be more and more recognized, and more and more implemented in the overall society.

The problem is people have not yet found a way to make a large profit on this kind of an approach as you can with certain drugs, and immunotherapies, and these kinds of things. But that will probably come in time, once people understand what the best approaches and techniques are.

[Damien Blenkinsopp]: Another aspect I wanted is there’s more research being undertaken on mitochondria over time. Do you think that will help, in any way?

[Dr. Thomas Seyfried]: Yeah, I think it will help a lot, like you said, with the lipids. And we’re looking into this ourselves. I think there’s ways that we can enhance mitochondrial energy efficiency through various diets and supplements, and things like this.

And there will be a real quantitative measures that can assess this, for people to recognize what works and what doesn’t. So I think it’s just that it’s an area that has been not well appreciated, and not well recognized.

And as long as people think that cancer is a nuclear genetic disease, the focus on the mitochondria hasn’t been there. People have known the importance of mitochondria, and it’s been a very major area of scientific research. But it’s not recognized as the solution to the problem. It’s kind of a side effect.

What we’re looking at is understanding mitochondrial functions, and it’s interaction with the nucleus and other parts of the cell to maintain a healthy cell – a healthy society of cells – and a healthy overall physiology. All linked to the mitochondrial energy metabolism. This is going to be a very exciting new development.

[Damien Blenkinsopp]: Yeah, I agree. There’s not a day that goes past that I don’t think about mitochondria these days. And hear someone talk about it. It happens a lot on this show, also.

If someone wants to learn more about your work, and this theory of cancer, and the index you were talking about, where should they go?

[Dr. Thomas Seyfried]: Well, I wrote the book On Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of the Disease. That’s published by John Wiley Press. Unfortunately, it’s a science book and it’s not cheap, like you’d find most of the Amazon books, but it gives you the literature, it gives you the science. It gives you the hard evidence to support everything that I’ve said.

Another book that’s just appeared is Tripping Over the Truth: The Metabolic Theory of Cancer, by Travis Christofferson, who’s written a book for the layperson, where he actually read my book and went back to test all the things that I was saying, and actually talking and visiting and interviewing those scientists who work in the gene theory, and work in the metabolic theory, and get the word directly from them. It reads like a novel, and it’s much less scientifically intimidating than what I wrote.

I wrote this book to convince my peers, and people in the cancer and scientific field, the evidence that supports what I’m saying. This sometimes can be intimidating to the layperson. Whereas Travis went out and actually interviewed those scientists, and asked them the specific questions. And now it becomes a very intriguing story; I mean, how did this cancer thing get so far out of whack with what we know about it. People like to see this, and read it.

So that is another book that’s generating… If you go on Amazon, you’ll see the reviews. They’re all quite outstanding for Travis’ book. And I’ve been privy to a number of other books that will be coming out over the next year, which are harping on the same general theme, that cancer is a metabolic disease, and it can be beaten by metabolic solutions. Totally different than what’s been going on in the main focus.

And this is kind of shocking, because you go to the top cancer centers, and they don’t speak anything about this. They’re still talking about the standards of care as they have been done, or they’re talking about immunotherapies, which is the new buzzword for the cancer field, where you’re going to identify all the mutations, and then make anti-bodies to the defective proteins, and then treat people. And they show a few survivors on the cover of the Wall Street Journal saying how wonderful this works. But they don’t show you the other evidence showing how many people are dying from this.

All this will change, because the people in this society, the public, is going to be fed up with the lack of progress, and what we have is a new way to approach this problem based on solid scientific fact. It’s just that these facts are not well understood or recognized at this point.

[Damien Blenkinsopp]: Great. Thank you very much, and we’ll put all of this in the show notes, so people will find these links easy. Also the index you spoke about, I’m guessing there’s nothing really published about that. If people go to your website in the future, will you have something on there which will talk about that in more detail?

[Dr. Thomas Seyfried]: Yeah. We have a paper that’s under review right now, where we’ve submitted a paper for the index, and we’re in the process of making some revisions on the index. And the index was, in this paper, was mostly focused on managing brain cancer, but we also noted that this index could have a broad applicability to a whole range of different diseases.

And in the Journal of Lipid Research, which is the top journal in the field of lipid biochemistry, I edited one of the issues that was entitled Ketone Strong: Emerging Evidence for the Role of Ketones and Calorie Restriction for the Management of a Broad Range of Diseases. So, more and more scientists are getting involved in this, and more and more information will be coming out. Both in the professional scientific journals as well as in the public interests articles in journals, and magazines, and radio shows.

More and more people will be coming to know this, and I think the field is going to have to deal with it. And I think in the long run, we’ll emerge into a new way to manage these chronic diseases with a lot less toxicity, and greater efficacy.

[Damien Blenkinsopp]: Great, great. Thank you. Now, just two more questions, personal questions for you.

What data metrics do you track for your own body on a routine basis, if any?

[Dr. Thomas Seyfried]: Well, basically I try to get on a scale and see how much I weigh. Obviously, if you can keep your body weight at a stable level for a period of time, this is certainly one way to maintain homeostasis.

I’ve done the three day fast, but as I said, when you’re older like myself, it’s very uncomfortable, but it’s certainly doable. It’s like training exercise. You’d have to do it probably a couple of times a year to get into the state. I think every time you do this, you become more confident in your ability to do it again.

There is a state of uncertainty and discomfort, like, “Oh my god, I’m not eating any food. How can I go, and I feel uncomfortable, and a little light-headed.” And you try to drink water to say, “Maybe I can fill my stomach up with water and I won’t feel as hungry.” And then you start getting water intoxication. And eventually you realize that you really don’t need to drink a lot of water, and you just have to bite the bullet.

But as I said, as we begin to do this, we realize that it’s not so life-threatening as everybody would think it would be. So I think I try to do that. But as I said to a lot of people, they said, “Oh, you must do this all the time.” No, I don’t do it all the time. But if I had cancer, I’d know exactly what I would do.

[Damien Blenkinsopp]: What would you do? Just to speak it out clearly.

[Dr. Thomas Seyfried]: I would stop eating.

[Damien Blenkinsopp]: Completely?

[Dr. Thomas Seyfried]: I’d get my index down below 1, that’s for sure. And then I would transition off to these high-fat, nutritious kinds of diets, ketogenic diets, and maintain my index. And then of course, we’re investigating – it’s very hard to get funds to do this kind of stuff too, because it’s not considered sexy science – what is the best combinatorial therapy that would work with therapeutic fasting and ketogenic diets, that would put the greatest amount of pressure.

And most of it has to do with what kind of non-toxic drugs would you dovetail in with therapeutic fasting and ketogenic diets? And like hypobaric oxygen therapy, 2-deoxyglucose, 3-bromopyruvate, oxaloacetate. I mean, we can go down these lists. Most of these are non-patentable drugs, but they have tremendous power when used together with these other therapies. And most of this stuff is just trying to figure out the dosages, the timing.

These kinds of issues, it’s just like perfecting the engine. How did the car engine become so efficient today from the way it was in 1900?

[Damien Blenkinsopp]: Right. So the things you just mentioned either stress the cancer cells specifically, like hypobaric oxygen, or they support the mitochondria, oxaloacetate, right?

[Dr. Thomas Seyfried]: Yes! Exactly. What you’re doing is you’re enhancing mitochondrial function in normal cells, and you’re putting maximal metabolic stress on the tumor cells. For the first time, we’re using our normal cells to directly combat and battle the cancer cells, while enhancing their health and efficiency.

[Damien Blenkinsopp]: So for someone who has, say we do a 23andMe test – like a lot of people on this podcast do their 23andMe test – and it comes out with some DNA, and it says, maybe you have a pretty high chance of cancer in your lifetime – and it could be lung cancer or whatever. Lung cancer’s not a good one, because often it’s smoking. So, one of the other more general ones, like breast cancer.

What would you basically say that they should be fasting once per month for three days, or twice per year for seven days, and maybe looking at those therapies you just outlined.

[Dr. Thomas Seyfried]: Yeah. People who have Li-Fraumeni syndrome, which is an inherited germline mutation in the gene for P53 which encodes a protein in the electron transport train, or BRCA1. Product of the BRCA1 gene has been found in mitochondria. We look at a number of these so-called inherited genes that increase your risk for cancer. But as I told you, everything passes through the mitochondria The mitochondria are the origin of the disease.

So, the inherited mutations simply make that organelle slightly less efficient in certain cells of our body. Not all cells, but only certain cells, like the breast, the uterine, or these kinds of things. And we know that there are people, like if you inherit the BRCA1 mutation, your risk of cancer goes up significantly. But not everybody who has BRCA1 mutation develops cancer.

So clearly the environment can play a huge role in determining whether that gene will be expressed or not. You can do prophylactic removal of organs, and things like this, to reduce your risk. But it would be just as effective in my mind to transition the body to a metabolic state that would minimize the problem of that gene influencing the mitochondrial function. It seems a lot less draconian than doing these massive surgical mutilations.

Or you can do both. The idea is some of these inherited mutations, they might have a preferred organ – like a breast, or a uterus, or ovary – but you’re not going to remove all your organs. You’re not going to remove brain. You’re at a higher risk, so what can you do to lower your risk? As I said, if you keep your mitochondria healthy, the risk is going to be significantly reduced.

People need to know this so they can make choices that would be best suitable for them.

[Damien Blenkinsopp]: Thank you so much for the information today. This is really an information packed episode. It’s got this great new take on cancer, which I think is very positive, because it’s talking about something which people can have more control about. So it’s not just that this is a new approach, and the older approach has been struggling for quite a while, it’s become very expensive, and so on, with not so much success, but also that this is an approach which is within people’s own manners, sphere of management.

A lot easier to start having an impact on their own lives. So it’s very positive from that perspective also.

[Dr. Thomas Seyfried]: Yeah, I agree. Absolutely.

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Functional medicine is a framework for tackling health issues and an approach to optimizing health that contrasts sharply with today’s “standard of care” medicine model. In this episode we look at assessing the body via the functional medicine framework and your detoxification system.

Where “standard of care” excels at dealing with acute health crises, like car accidents injuries and deadly pathogens and infections, functional medicine has grown to tackle primarily chronic health issues.

The argument for a future where we turn increasingly to functional medicine is that:

  • where traditional medicine seeks to manage disease (e.g. pharmaceutical therapy or surgery), functional medicine seeks to identify and resolve the causes of disease.
  • Where traditional medicine seeks to place you in a ‘disease category’ (e.g. multiple sclerosis), functional medicine takes a personalized approach.

We’ll get more into what these mean in the episode.

Today’s guest is Jeffrey Bland, PhD who is often referred to as the “Godfather of Functional Medicine“. He has been working for over 25 years in the pursuit of what today is functional medicine, he has over 120 peer reviewed papers on nutritional biochemistry and medicine, is the co-founder of the Institute for Functional Medicine founded in 1991, has served on many boards of health and nutrition companies, a highlight of which was serving as Director of Research at the Linus Pauling Institute where he worked directly with Linus Pauling for a time.

“We are in a health revolution right now that is second to none.”
– Jeffrey Bland, PhD (Godfather of Functional Medicine)

Jeffrey is also the author of “The Disease Delusion: Conquering the Causes of Chronic Illness for a Healthier, Longer, and Happier Life“. This is a book I found to be a great read to understand the functional medicine framework and how it looks at the mechanisms for chronic disease and optimum health. I highly recommend it, in particular if you are a physician or if you personally are plagued by chronic health issues.

The show notes, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. Enjoy the show and let me know what you think in the comments!

itunes quantified body

Show Notes

  • How functional medicine differs from traditional medicine in its approach (5:00).
  • A concrete example of how functional medicine looks at disease: Multiple Sclerosis as a personal disease with many different causes (7:10).
  • What changes when you stop focusing on the effect (the disease) and start looking for the causes (13:00).
  • How people typically get led to the world of functional medicine – and what the root causes of illness are (17:10).
  • Do all headaches have real causes that can be investigated, understood and resolved? (21:10).
  • How the functional medicine framework puts you back in control of your health no matter the cause (23:30).
  • The birth of the functional medicine framework (the 7 core physiological processes), how it was designed and how it has stood the test of time (26:10).
  • In practice: What you can expect from a visit to a functional medicine doctor – what they’ll ask, what they may test, what process they will go through with you to diagnose and resolve your health issues etc. (30:00).
  • Example biomarkers, labs and tests used commonly in the realm of functional medicine. (36:30).
  • Detailed look at the detoxification process within our bodies (one of Jeffrey’s 7 core physiological processes from Functional Medicine) (36:30).
  • Are “Healing Crises” or “Detox Symptoms” necessary in detoxification or during health issue resolution? Or it something we should avoid? (52:00).
  • How ‘fasting’ can be counterproductive to the detoxification process (53:30).
  • The specialized set of labs and tests that are used by functional medicine practitioners (56:00).
  • Jeffrey’s perspective on the future of medicine and what he sees as a “revolution in healthcare” currently taking place including (A) “omics” revolution (genomics, proteonomics), (B) internet and social media and (C) big data analysis (59:00).
Thank Jeffrey on Twitter for the information and insights he shared with us in this episode. Click Here to let him know you enjoyed the show!

Biomarkers and Frameworks

    Frameworks

  • “Antecedents, Triggers, Mediators, Signs and Symptoms”: Functional Medicine framework that starts the process with a questionnaire or enquiry from the physician aiming to identify possible items from this list to look into in more detail with tests.
  • MECE (Mutually Exclusive, Collectively Exhaustive: A framework tool mentioned by Damien that is used extensively in the management consulting world to effectively define and solve problems.
  • Inflammation

  • hs-CRP (high sensitivity C-Reactive Protein): A marker of inflammation from blood labs that Jeffrey remarked as a useful tests as an early step in some cases.
  • Blood Sugar Regulation Measures

  • Hba1c (Glycated Haemoglobin): A proxy measure used to assess your average blood sugar over a period of time. Since haemoglobin is part of the red blood cells it is exposed to blood sugar over the lifetime of the red blood cell, thus giving a measure. As such this measure is used to identify blood sugar control issues. Levels of 5% or higher can be indications of blood sugar disregulation.
  • Triglycerides: A measure commonly reported in lipid panels that provides an indication of the excess calories coming into your body and getting converted into fats. High triglyceride levels indicate blood sugar management issues.
  • Cardiovascular Health

  • HDL (High Density Lipoprotein): Often referred to as the good type of cholesterol, this marker comes with your typical cholesterol panel. Higher levels of HDL are generally better as they are cardioprotective.

Links to Resources

Jeffrey Bland, PhD and the Functional Medicine Movement

Supplements and Treatments

  • N-Acetyl Cysteine: Mentioned as a supplement that helps to support detoxification (note: it does this via helping to increase glutathione levels).
  • Sodium Citrate and Sodium Bicarbonate: Jeffrey mentioned these as approaches to ‘alkalinizing’ the body’s cells and thus helping improve detoxification. Another supplement that works similarly is Potassium Citrate.
  • Coenzyme Q10 (CoQ10): Jeffrey mentioned the role of CoQ10 as a detoxification support.

Other People, Resources and Books Mentioned


Full Interview Transcript

Transcript - Click Here to Read

[Damien Blenkinsopp]: Great, Jeff, thank you so much for joining us on the podcast this morning.

[Jeffrey Bland]: My deep pleasure. Thanks so much, I’m looking forward to the discussion.

[Damien Blenkinsopp]: Yeah, your book is great. I really appreciate it. It really gives a great perspective on a number of things, a different perspective than most people are used to seeing. So the first thing I wanted to go into was functional medicine. What is the difference between functional medicine and contemporary medicine, the medicine we are used to when we are going to hospitals and primary care doctors and so on? How would you define the differences?

[Jeffrey Bland]: Well Damien, I think that’s a very good question and it really asks of us what is the elevator speech if you have only got a couple of floors in an elevator to describe the difference of how you would do it. And we have grappled with this question for some time and I am not sure I have completely gotten it down, but let me give it a try. The medicine that most of us are familiar with is insurance reimbursable kind of traditional hospital based or clinic based health care, that in which I was trained in and most docs today were trained in. It is focused on the disease, the primacy of disease, and so it is all about the diagnosis and then finding the appropriate treatment for that diagnosis.

The diagnosis is really related to a clinical series of presenting signs and symptoms so the patient comes in with whatever their complaints are. The doc reviews those complaints, they do whatever lab tests might be suggested from those complaints, and then from that name a title of a disease is finally given from which then reimbursement can occur and therapy can result, generally pharmacotherapy with some kind of drug or drugs and surgery. That, however, doesn’t ever really address the question of where these things came from, what is the cause of these conditions. so often we end up being able to treat effectively the signs and symptoms of it’s outcome, the disease, without treating its cause.

Functional medicine is all about the cause, it’s not about what you call it. It’s all about how you got there. So the most important thing for a functional medicine provider is to understand what we would call the journey that led to a diagnosis to treat the cause and not the effect, whereas medicine today I think is more involved with calling what the final destination is and treating its effect rather than its cause.

[Damien Blenkinsopp]: Great, and if we could take a concrete example I think that might help to clarify it for some people. One of the diseases that is defined by the world of primary care and so on is multiple sclerosis, right? So that’s a disease condition and there are a number of drugs and things around available to treat that. How would functional medicine look at that? What are the differences in the way you would look at multiple sclerosis?

[Jeffrey Bland]: I think that’s a really excellent example, actually. That fits right into this discussion very nicely and in fact it is actually one of the examples that i use in the book The Disease Delusion to help the reader to kind of understand the difference between the functional medicine approach and a traditional diagnostic pharmacology approach.

So a functional medicine practitioner, when they would see a person who has been diagnosed with MS would first ask the question in their mind – what do we know about MS? We know that multiple sclerosis is a member of the autoimmune family of disease. These are the diseases that are characterized with the body’s immune system attacking itself, attacking the body itself and leaving the collateral damage.

In the case of MS the body’s immune system is attacking the nerves. And specifically the insulation of the nerves, which are the myelin sheaths, the things that coat the nerves that are kind of like insulation on a wire that is plugged into the wall socket. It is the insulation on your nerves and it protects the wire, the nerves, from being damaged or having problems with transmitting electricity like you would have in the socket of a light.

And so when your body’s immune system attacks the insulation of your nerves, the myelin, it starts to lead to kind of a short circuit of the nervous system, just as if if you lost the insulation off the wire and it goes to your lightbulb, you might end up short-circuiting that and maybe sparks would fly out or you would catch the curtains on fire or any number of collateral damage could occur from losing that insulation. And so the treatment of choice is to give an individual who has that diagnosis of MS, drugs that are designed to try to block the effect of that immune reaction against your nerves, so it would be certain kinds of anti-inflammatory drugs or drugs that prevent the insulation of the nerves from being further damaged.

The functional medicine approach, however, would be to ask why is that person having the loss of the insulation on the wires of their nerves? What was the cause of this? And the first kind of assumption that many people have is well, that must be in my genes. Gee whiz, I have family members that have autoimmune disease or I have a family member that might have even have had MS. It must be my genetic inheritance. However, when the data is looked at as it relates to that specific disease, MS, like so many other of the autoimmune diseases, there is a very weak linkage between genetics and MS.

It is not a hardwired genetic disease. So it may have a weak linkage to certain immune relationships that give rise to autoimmunity, but it is not a disease where we can say this is a cause, this is caused by your genetic heritage. Therefore there must be another factor or factors, and this is where the functional medicine detective story emerges, because a functional medicine practitioner would then say let’s look at all the various factors that have been identified in the medical scientific literature that are associated with the cause of an immune system attacking the nerves. And this could be things like toxic chemicals, it could be things like heavy toxic elements like mercury or cadmium.

It could be things like reactions to certain food proteins that your body sees as foreigners, one of which would be gluten. It could be the result of insufficiency of specific vitamin factors, particularly vitamin D, which has been studied extensively by Michael Hollick, Dr. [Heeney 00:11:20], and Dr. [Holub 00:11:22] as it relates to vitamin D insufficiencies. Or it could be associated with situations that relate to the exposure to what you would call xenobiotic chemicals, certain agents that activate the immune system, including certain members of the drug family which certain individuals have immune response to and it becomes seen as a foreigner that the body’s immune system then starts attacking the nerves. So there is a whole laundry list of various agents that might trigger the immune system of a person who is considered normally healthy to now start developing an immune reaction to their nerves.

So rather than just jumping in and giving a person something that blocks the inflammation, the functional medicine provider would start going through as a detective might – the Sherlock Holmes of the etiology of the condition, asking could this person that has this condition have these problems? Could they be suffering from too much mercury? Could they have too much cadmium? Could they be suffering from exposure to certain chemicals? Could they be taking certain pharmaceuticals that activate the immune system? Could they be vitamin E deficient? Do they have certain food allergies like gluten that are inducing this immune response?

Then from that detective approach that the kind of examination, a tailored, personalized program for that individual’s own forum of MS would be developed, rather than just treat them as a person with MS like you would with any other person with that diagnosis, you now design a program based on their specific, unique presentation that is focused on managing the cause and not just the effect. And those results, when you deliver that model in clinical practice, can be extraordinary. It can be miraculous.

We have seen literally hundreds of patients over the years that I have been involved with the clinical research and overseeing clinical research centers and when patients come in with various forms of MS or various forms of autoimmune disease and how there are conditions once you identify the cause and not just the effect can be completely turned back and you go into remission. So that is a different model.

[Damien Blenkinsopp]: Yeah, thank you very much for that. So if I kind of retake it and see if you can say if this is accurate or not. Traditional medicine is looking at the effect and it is trying – the effects, and the symptoms you have. they are trying to categorize a number of diseases that they have on record. They have a hundred different diseases, cancers, multiple sclerosis, Parkinson’s, and all these things which have been categorized according to symptoms, a list of symptoms, whereas when we are coming from the functional medicine side we kind of ignore that for the moment and we say okay, just because they have these symptoms we don’t know what the actual cause is.

So we are going to do a number of different tests and we are not going to make any assumptions about what is actually causing this until we have done some investigation and the idea is that we can find any number of causes and they could end up at the same symptoms due to the mix of genetics, epigenetics, and the other processes going on in our bodies. But they can arrive at the completely different ending, the symptoms, from completely different causes. Is that an accurate representation of what you just said?

[Jeffrey Bland]: Yes, I think very much so and I think for the listener it is important to know that the number of diseases within the diagnostic handbook are literally thousands of different diseases. And often a doc might feel that their job is over once they have got a good diagnosis because then they can dial up a specific pharmacotherapy. But within each of those diagnoses, no matter what the name is, whether they have diabetes or arthritis or MS, every person with that diagnosis, that specific diagnosis, presents slightly differently.

They have a different reason that it gets worse and it has progression. So in the absence of personalizing treatment to the individual need and focusing on the cause and not the effect, you don’t get the optimal outcome. And that is the functional medicine revolution, looking at the person as a unique individual and personalizing their treatment program appropriately.

[Damien Blenkinsopp]: Right, thank you very much. Another aspect I wanted to see and what a value that I see in a functional medicine encounter where I came into contact with it from my personal story is because it is the story of categorization of systems there are many people that fall through the cracks, however, because their symptoms aren’t acute enough so they don’t meet a diagnostic criteria.

For example, an MRI wouldn’t show the white blips used for multiple sclerosis in those kinds of scans, for example. Or they are not meeting those diagnostic criteria which falls neatly into one of those categories and they maybe have some symptoms which are considered that everyone should have these days. For example, everyone complains of headaches and everyone has a bit of fat around their stomach these days and they find it hard to get rid of and they blame it on a number of things.

So my own personal story is that I kind of fell through the cracks because I didn’t fit into any categories and I know there are many people who do that. And we finally end up at functional medicine, and functional medicine seems to say we can try and resolve any condition that you have from a basis of looking at a list of potential causes and it is supposedly a comprehensive list of things that can go wrong in the body and working its way through that.

So is that another way to look at it? I know a lot of people kind of end up at the functional medicine road end of medicine because they have kind of fallen through the cracks or they have some chronic condition which doctors aren’t addressing properly. Is that a fair assumption as that is how most people arrive at functional medicine and also if you are able to in fact pretty much attempt to resolve any kind of symptoms or anything that is not working correctly in the body?

[Jeffrey Bland]: Yes, and again I think you really pointed to a major issue within the way that our healthcare system works right now, which is basically a disease-care system as we know it. It is not so much focused on health as it is the treatment of disease. So when a person has broad ranges of chronic symptoms that cut across many different organ systems, it could be fatigue and pain and low energy and cognitive dysfunction and gastrointestinal problems and alternating constipation and diarrhea and sleep disturbances and depression.

They may come with a whole laundry of different chronic systems and depending on what doctor you see, they are all going to try to drive those symptoms into a specific diagnosis and it is going to be based on their background. So they are going to find the disease that they are most comfortable with to use that as a name that they are going to apply to that cluster of symptoms that the patient presents with because they have to get a disease diagnosis so they can get reimbursed. So they are going to call it something. Well the something they call it may not be nearly as important, as you have said, as how the patient got there. And what were the various factors in their lifestyle and their environment that were really creating this complicated disturbance in the physiology that has caused their chronic illness?

It is not a disease as much as it is a disturbance that is caused by the mismatch between their genetic uniqueness and their environment. And if you don’t start asking those questions then you never really get the answer. What you do is you end up with kind of a round robin of different doctors with different treatments that treat different treatments with different drugs to suppress pain or inflammation or suppress sleep problems or to block stomach acid. What is unique to those is you are basically uncoupling the smoke detector, you are not treating the fire i the room. You are uncoupling the signs and symptoms that were there really to tell you there is something going on that needs to be addressed.

So the functional medicine model often is very attractive to a person who has a history who has a lack of success with the traditional disease diagnostic and treatment model because it just hasn’t been successful in managing the range of their clinical problems because they have never asked the right questions. And it turns out that if you look at the kinds of conditions that are dominant within our society today they are these chronic conditions. In fact, over 75% of healthcare expenditures in our system today are spent for the management of chronic illness – not acute disease, but chronic illness. Yet, when you go to have a chronic illness managed it is often managed with drugs that were used for acute care. They are not really drugs that treat the cause of the chronic illness, they are drugs that are treating the acute symptoms and not treating its cause.

So I think we have a very big mismatch of what patients would like and what the treatment approach that they are getting, where it is being applied. And that is where functional medicine has a big role to play.

[Damien Blenkinsopp]: Yeah, great, thank you. So just to give the audience a bit of an idea about this, would you say that headaches are resolvable? Is that the type of chronic condition that we – I have had some strange headaches when I got ill a few years ago and they sent me to a psychologist. And in the world of functional medicine I know that happens to a lot of people, or they keep getting the answer that everyone kind of has headaches and it is not resolvable. And I think headaches are a very common thing, a common complaint today. And a lot of people are going to pharmacies and taking medications for this.

Do you think this is something that is resolvable, like in 90% of the cases, with the functional medicine approach? Or at least there is a good percentage of those that can find some kind of cause behind that and it is not normal to just have headaches?

[Jeffrey Bland]: Well again, I think that is a wonderful example. You are picking some great examples. Headaches is one of those conditions that is a sign or a symptom and not a disease in itself that has many multiple functional contributions that lead to what we call headaches. So it could be a magnesium deficiency, it could be a vitamin B6 deficiency.

It could be, again, another relationship to a food or environmental sensitivity or toxicity of types. It could be related to a problem with the microbiome, that bacteria are producing toxic secondary byproducts that have an effect on the function that we see ultimately as a headache. It could have to do with the vascular effects that are associated with the lack exercise. It could be due to hypertension because the person is taking the wrong kind things in their diet and lifestyle that are increasing their blood pressure and putting them on a vegetable-based diet and lo and behold their headaches go away.

So a functional medicine provider would look at this list of potentials and start making a differential diagnosis of that individual patient or an assessment as to what their specific causation might be of their headache, and work with them not just giving them a headache treatment remedy and drug to again, uncouple the smoke detector of the headache and to treat the cause of that condition. When, in fact, that occurs, i don’t have a specific percentage I could give you but I would say for sure the vast majority of chronic headache sufferers will be in remission. Their headaches have been demonstrated to go away. So I think this is another great example of a clinical presenting sign and symptom that through a functional medicine systems biology approach it can lead to remediation because you treated the cause not just the effect.

[Damien Blenkinsopp]: Right, and what I love about the philosophy is that it kind of puts control back in our hands because we are saying that there is always some cause of what is happening and it is not just that in conventional medicine they will put it down to genetics or something that is not addressable. Often in functional medicine the locus of control comes back to us and it just says that we have to find the cause. If we can find the cause then we can fix it, no matter what is going on with the human body and causing these symptoms. Is that a fair reiteration?

[Jeffrey Bland]: Yeah, absolutely, exactly. If I was to try to kind of distill down the whole focus of my book The Disease Delusion, that is really what it is all about, returning the power to the individual for the control of their health. I think a lot of people have had their health kind of hijacked from them because they feel it’s either a consequence of their genetic lineage that they had no control over or it’s their doctor that is control their health. In essence what we have learned since the deciphering of the human genome in 2000 is that actually we control, each one of us controls how are genes are expressed. And the way that we think, act, believe, behave, rink, eat, exercise, sleep, have relationships with other people, think of ourselves as valued parts of society.

Those all have direct impact on how our genes are expressed and regulate how we look, act, and feel. So I think this is a hugely empowering age in which we live, in which the individual becomes much more important than they were in the previous period of society when we were all part of massification of society where we just wanted to be part of the average. Now, the power of the individual has become very, very important and we can give people the tools to not become doctors, but to understand themselves well enough that they can start navigating through life in such a way to design their own health program that is contrasted to their own disease treatment program, which comes from the doctor.

[Damien Blenkinsopp]: Excellent. So in a minute I would like to give us a little bit more a practical or quantified focus – we often talk about quantified aspects here – about how to make use of labs and data and functional medicine to identify the causes that you are talking about. But first of I just wanted to look at that basically you have a framework in your book The Disease Delusion, and it is this framework for saying these are all the potential causes of problems. The framework that you describe, is that the basis of functional medicine today? Or is that coming from you? Could you give us a bit of an overview of where that framework is? I think it’s really great, a lot of the aspects of it – I haven’t seen them described in that way before.

I think it seems like what we would say in consulting language – MECE was mutually exclusive and comprehensive, basically, so it covers everything. It is a very nice framework, I can say, from my consulting background. But just from your perspective, where does that come from? Is that something recent or is that something that has been used in functional medicine for a while? Is that something that you are hoping that will be used more and more going forward?

[Jeffrey Bland]: Yes, thank you. The way that this functional medicine concept was actually birthed was through 1989 and 1990 my wife and I hosted meetings about a week long each in Victoria pretty strongly on Vancouver Island where we invited about 30 or 40 of the top opinion leaders that we had met from different fields to kind of sit down quietly over a period of a few days with a whiteboard and address the question – what would be the best possible medical system that you could conceive of with your experience from the different disciplines they represented. Let’s not talk about reimbursement and let’s not talk about fair financing, let’s just talk about theoretically what would this system look like.

And from that to your exploration emerged the concept that we would develop a system that really looked at the individual and how they, over time, had altered function and we had different diagnostic criteria, different assessment tools, and we would be able to, earlier on, be able to understand when a person is heading at a trajectory towards a disease well before they become a cancer patient or a heart disease patient or a diabetic patient or whatever it might be. And that led us into asking what would be then the types of things we would want to know of that person so we would be better able to, early on, understand their trajectory towards not-optimal health.

And we started looking at the scientific and medical literature and this group of people were pretty good and understanding what was going on within the discoveries that were being made and we eventually started putting references and articles together and stacking them in different piles to see if they fit into different kind of what we call ‘buckets.’ And from that eventually emerged the fact that these conditions that lead to altered function that later became diseases as a person progresses towards more severity could be characterized into seven different buckets. And we call those the seven core physiological processes. And over the now-subsequent 25 years since that time lo and behold those buckets were pretty close to the way things have evolved in science and in medicine over the last quarter century. So those buckets included detoxification, they included immune defense, it included hormone signaling, they included gastrointestinal function and included structural relationships that included bioenergetics. Each one of these seven core physiological processes, by the way, I have described in individual chapters in my book.

Then we developed questionnaires for the patient that were associated with presenting clinical symptoms and signs that were associated with the dysfunctions in each of those seven areas. And to help the person to better understand where were their strengths and where were their weaknesses, and that formalism became then the functional medicine assessment program and approach. And obviously over the last 25 years it has become much more sophisticated and much more well-defined and well-understood. But I am quite amazed and what we birthed or germinated in 1989 and 1990 that has really proven out over the last quarter century to actually be very applicable to clinical intervention and to improving outcome in patients with chronic illness.

[Damien Blenkinsopp]: Great. I didn’t realize the structure of the framework had been around that long. I assumed it was actually maybe something that you had come up with pretty recently because as you say, it echos all the current themes of research and everything that is currently going on in it. So in terms of the process that you go through, if you could give us a very high view of what happens when you go to see a functional medicine doctor with some complaints that you are not sure of – is it a very typical process? Like, do you start with the questionnaires, you said, to kind of identify the different parts of that seven piece framework that goes wrong? Can you walk us through the kind of top level of what would happen if someone went to functional medicine?

[Jeffrey Bland]: When you go to kind of your traditional disease-focused practitioner, the whole drive is to try to get a differential diagnosis, try to get a name that you can put on your condition. And that’s different than the functional medicine practitioner. They may obviously be interested in a diagnosis if a person has one, but their approach will be different from the beginning in that the approach is to look at the antecedents, triggers, mediators, signs, and symptoms. Now, what does that mean?

Antecedents are the preceding factors in that person’s life that may have given rise over time to the clinical condition and the problems that they are experiencing. And that has to do with looking at your genetic background, looking at your family history, and looking at various kinds of things that may have happened earlier in life, it could be illnesses, surgeries, and just a really good what I call historical, history and physical, as well as bringing genetic information into the story and other aspects of their environment and lifestyle habits. That is antecedent.

Then the next question is what are the triggers that are triggering your antecedents? Those kinds of signs and symptoms that you are presenting with, the things that brought you to see a healthcare provider. Most patients, when they are most people and they feel perfect, they don’t wake up and say, ‘Oh gee, I ought to go see one of my health care providers because I feel so good today and I ought to find out why.’ But they come because they have a series of complaints. So the triggers could do things like maybe an automobile accident or maybe a severe trauma that you have had, a psychological trauma with a partner, a spouse, or a child. It maybe be an infection. It may be that you just were put on a certain medication, that you are having an adverse response to it. Maybe an environmental exposure so these are the triggering agents that then are the exacerbators, like the straw that broke the camel’s back.

The triggers then produce a series of what we call mediators in the body. Mediators could be different hormones, it could be inflammatory cytokines, it could be different types of things that relate to our body’s immune response that you can measure through laboratory testing. So these mediators are your body’s response to the triggers that laid on top of your antecedents. And then those then produce your signs and symptoms of different severity, duration, and frequency. The evaluation of that whole story that I have just described, antecedents, triggers, mediators, signs, and symptoms, gives rise to an understanding of the patient’s story. And the patient’s story is the most important part of this whole differential assessment that the functional medicine provider uses. Now, maybe that story will ultimately lead you to say that we can call the story diabetes. But it is diabetes of a unique type that is unique to that person, that needs their own type of intervention because of 100 diabetic patients there are 100 different stories with the same diagnosis.

So this is how one would come about developing a relationship with a functional medicine provider versus an individual that might just say, ‘Oh, you have diabetes. Okay, so you’re going to get metformin and you’re going to get Actos. That’s the drugs of choice.’ In this case, we are looking at a much more deep and broader relationship between why your blood sugar and insulin-related glucose problems are presenting based upon your own antecedents, triggers, mediators, signs, and symptoms.

[Damien Blenkinsopp]: And having been through this process myself, I would say that something that comes across very different from the first part is that the question I was put to first when I went through the process was I was asked when was the last time you felt completely well? And I think the answer to that comes back very differently to when you go into a traditional doctor’s office and I had to think back and I was like, ‘Well, actually, this has been going on for over ten years. There were some tiny things that were going wrong many, many years ago.’ So I think that is an interesting question and it really starts the whole discussion on a completely different level. Is that the typical question that would be asked.

[Jeffrey Bland]: Yes, I think you will notice in my book that the first questionnaire in the book asked that very question – do you feel your health has changed significantly within the last year? That is a very, very important question because it helps us to understand the trajectory towards change, the change in health which is related to functional change, which is related to there is something going on that your genes didn’t change in that year. Something happened to how your genes are expressing their function. And then we start asking the questions from there. So yes, that is a very first-level, important question.

[Damien Blenkinsopp]: Great, thank you very much. Now, how does this connect with what we call more quantified aspects of this in terms of lab tests or any other diagnostic tools. Is there a typical first stage in looking at lab tests? Are there kind of favorite areas of testing of functional medicine? What kind of things would you say are important in functional medicine when it comes to the testing aspect?

[Jeffrey Bland]: Well, I think this is a little bit like the layers of an onion. We start off with the easiest and the least expensive things first, which is a good assessment using the antecedents triggers, mediators, signs, and symptoms approach that is unique to functional medicine. You can do that by questionnaires and these are kind of pen and paper pieces of information and many of those questionnaires have been included in my book and also what I call physical assessment. And their functional medicine provider is very skilled in understanding how to assess nutritional inadequacy with presenting signs and symptoms and how to assess different immune-related dysfunctions so you have a good physical and history evaluation and start there. That is the least expensive and the least invasive.

Then the next level would be to say okay, we have identified certain areas, let’s call it a gastrointestinal area, where you have got recurring irritable bowel syndrome or you have got all upper GI dyspepsia where you have reflux disorder or something of that nature, so you have certain kinds of information around a particular area of the body that is experiencing problems and you want to get more information about what is the nature of that functional difficulty. Now, you would go into more detailed testing.

So for GI problems you might do a stool test to evaluate whether there are funny bacteria that are producing what we call dysbiosis and causing inflammation of the of intestinal tract, you might do a certain type of blood test looking at different types of inflammatory agents like high-sensitivity C-reactive protein, which is a marker of inflammation. So you then start to put together a series of questions as a practitioner that would be the questions that you think are most important as you try to decipher that patient’s individual problem, always remembering that you want to keep the cost of your assessment to the lowest level possible so you don’t throw the whole kitchen sink and you start to layer on the testing as you are making your discovery. And you may have if it is a very complicated, sophisticated case, it may require more testing and you may have to do fatty acid testing, amino acid testing, immune testing, and there may be all sorts of heavy metal testing. So there could be a whole range of different things you layer on, depending upon how sophisticated the problem that person is presenting with.

[Damien Blenkinsopp]: Thank you. Are there any particularly, amongst functional medicine providers, any particularly popular areas of testing or specific tests that you may have seen provided more value over time and then are kind of your go-to tests which you tend to find more information there and find them more useful?

[Jeffrey Bland]: Yes, I think there are. I think that you could start with probably the most common and also one of the most informative and that is to test glucose tolerance that person has. And this is how insulin is working in their body. So this would be, starting with a simple blood test of blood glucose and what is called hemoglobin A1c, to see if they have a problem in managing their blood sugar and managing their insulin reactivity in the body, and they probably would also want to measure in their blood what’s called triglycerides and we would want to measure HDL, the so-called good cholesterol. But that portfolio of tests that was specific to insulin would help us to identify whether that person might have an insulin resistance and a glucose intolerance. So if they had an elevated blood sugar, they had an elevated hemoglobin A1c, they had an elevated triglyceride and a low HDL, we would say, ‘Oh, now that is a person that has a form of what is called metabolic syndrome and we would want to start managing their therapeutic approach, the functional approach based upon the fact they are insulin resistant.

For another person, it might be that they are presenting with, as I mentioned, a long history of gastrointestinal-related problems. So in that person we would be more interested in maybe focusing on doing what is called a comprehensive stool analysis to look for things that are going on in the digestive system that are related to dysbiosis, inflammation, and food or toxic response. For another person, it might be that they have headaches and cognitive dysfunction and dysphoria and kind of depression symptoms and low energy. And we might think that sounds like a person that is more likely to be toxic so we would want to do something related to toxicity testing and probably do assessments of their liver’s ability to detoxify foreign chemicals.

All of this, by the way, I have described in the book in different chapters as to how you put this together. But based upon the presenting signs and symptoms that a person has, it helps guide the individual as to what the specific quantified information they would want in order to make their assessment.

[Damien Blenkinsopp]: Thank you very much for that and I would like to take a bit of a case example with detoxification because I think this is an area in which traditional medicine tends to address less and functional medicine tends to consider more strongly and look more at. So it would be nice to, as you say in your book, you go into each of the seven areas in a lot of detail. And you give a lot of good case studies, which is very helpful to connect to what is going on there. So in a detoxification case what kinds of things that you were just talking about, liver tests and so on, what kinds of things would you look at first to understand if someone had a level of toxicity of toxic burden that they had to deal with and that was potentially causing their symptoms?

[Jeffrey Bland]: I think there are two types of testing that are done for toxicity and its relationship to the body’s ability to detoxify. The first is to look at the presence of toxins in the body and there are a variety of different types of testing protocols or tests themselves that actually measure the level of things like [inaudible 00:41:25] or heavy metals like cadmium or mercury or lead or arsenic or aluminum that can induce toxicity. So these would be examining the presence of toxins in the bladder, in the urine, or in the sweat or fatty tissue. And the other type of test is to look at the individual’s ability to detoxify and our detoxifying system is controlled principally by two very unique enzyme systems that are present in our body. One are called the [inaudible 00:42:00] enzymes and the other are called the conjugase enzymes. And they reside to a great extent in the liver but they are found in virtually every other tissue in the body as well, including the gastrointestinal tract where these enzymes sort of clamp on to these foreign substances and to detoxify them and be able to eliminate it in a nontoxic form, even in the urine and the stool, to get them out of the body. And people have a significant difference in their detoxifying abilities from person to person. this has to do with both differences in their genes and their genetic ability to detoxify. One might have what we call a fat detoxifier effect for certain chemicals. Another might have a slow detoxifier effect. And secondly it has to do with how they have treated their detoxifying systems. In other words, have they eaten the right foods with the right nutrients that are necessary for the support of those detoxifying systems? Nutrients like magnesium, the B vitamins, Co-enzyme Q-10, N-acetyl-cysteine – these are nutrients that are known to be very important for support of our detoxification system.

So the detoxifying ability of our body is really related to how much toxin are we exposed to and what is the relative effectiveness of our detoxifying system in the body to get rid of them? And so we can have too much exposure or too little detoxifying ability, both of which leads to a state of chronic toxicity. I call it metabolic poisoning. And this condition is not so obvious that the person is acutely toxic, like you would have from a poison like strychnine, but the symptoms are often seen by what I call chronic both immune and nervous system toxicity. These are the two most sensitive functions of our body to toxicity. One is our immune system and the other is our nervous system. So the signs and symptoms that are seen with chronic metabolic toxicity are focused around neurological symptoms.

So this has to do with depression and sleep disturbances and foggy brain, where a person can’t think clearly – low energy and various forms of cognitive dysfunction where they can’t manipulate numbers or quick ideas as effectively as they used to. With immune toxicity it has to do with an immune system that is kind of working against itself. You have inflammation present and you also have increased rates and various risk to infectious organisms, viruses, and bacteria, so that the combinations of those symptoms often is associated with this cellular toxicity for which then the appropriate detoxification program for that patient that is based upon their own unique case can lead to extraordinary benefit and improve their function.

[Damien Blenkinsopp]: Thank you very much because I think also the area of toxins and detox – if you are working in a health store today – I am in LA and places like [Air One 00:45:14] or Whole Foods, there is a whole range of detoxification supplements. There are aspects of the products in the shops like alkaline water and so on. There are a lot of products now that are focused on helping to detox, but I feel like there is a fair amount of a lack of rigor in a lot of the scientific basis for a lot of these.

One of the areas that I have heard you talk about at the detox summit, which I thought was particularly interesting, is the topic of alkalinity, which comes up a lot. There is a lot of alkaline water that is sold in shops, for instance. And it is said that if we take in more alkaline we make our bodies more alkaline, and it helps us to detox better. What is the scientific basis for that and is it actually true? What kind of things can be done in reality if it is effective to actually make that change?

[Jeffrey Bland]: Alkalinity is related to the balance between acids and bases in the body. And for those individuals that are not necessarily up on their human physiology our body, in its natural state, if you look at the blood it is slightly more basic than it is acidic. It has what is called a pH, which is a measure of acid and base characteristics, and if it was perfectly balanced it would be a pH of 7, that is neutral. A number higher than seven means it is slightly more alkaline and a number lower than seven means it is slightly more acid. The lower the number goes, the more acid, and the higher the number goes, more alkaline. And the body’s pH is around 7.37 in the blood, which is slightly alkaline, slightly higher than neutral, which is seven.

The situation in terms of chronic illness is that often cells or tissues have pH that is lower than 7.37, meaning they are shifted towards a more acid side slightly, not into what we call metabolic acidosis, which is an acute situation that can be life-threatening, but just a slight shift in the alkaline balance. And this is a consequence of a whole series of metabolic effects that shift the pH of cells slightly towards a more acid side. When I say slightly towards a more acid side what I really should say is a less alkaline side.

The detoxification of the process that occurs within cells in the liver and other tissues requires a pH and a balance that is more close to 7.37. It likes that more alkaline state for optimal detoxification function. If a person has a poison in their cells, that poison often shifts their cellular pH to the more acid side, less alkaline. And there are many studies that in poison centers that have shown that if you administer an alkalizing agent to that person, and this could either be done intravenously or orally, meaning given something by mouth like sodium citrate or sodium bicarbonate, these are alkalinizing substances and it will then improve their detoxification ability.

Now, in the case of chronic metabolic toxicity you don’t need to use – and obviously administration into your blood of an alkalizing agent – but an alkalizing diet can be very, very helpful and these are basically vegetable-based diets. Animal-based diets tend to have an acid residue and they tend to be acidifying. Vegetable-based diets rich in plant foods tend to have an alkaline residue and tend to be alkalizing. And so you can use plant foods, a plant food diet and more vegetables and fruits in alkalizing or you can also use supplementary alkalinizing substances like sodium bicarbonate or sodium citrate, other things that will slightly shift your body’s balance more towards the alkaline state. And that will help improve your detoxification ability.

[Damien Blenkinsopp]: Great. So a couple of clarifications on some of the things that you spoke about there. You were talking about the blood pH 7.37 and if we wanted to measure this slight acidity change that you spoke about, is it possible run lab tests on the cell pH and the tissue pH? You were talking about those verses blood, which I believe blood is always kept roughly at 7.37 and it doesn’t actually change and it is just the cells and the tissues that actually change. Is it possible to quantify that and is it a very slight change or are we talking about 7.1, 7.2? So it is kind of like a [inaudible 00:50:02] test to understand that?

[Jeffrey Bland]: Yes it is, and I am talking here about very slight changes. More acute or more dramatic changes are associated with life-threatening conditions because your body needs to stay within a very close range in its pH in order to function, or the muscles can’t work correctly and the brain can’t work correctly. Your heart can’t fire correctly so if you change too much in your pH you can have very, very serious problems. So we are talking about very small shifts in cellular pH. As it relates to technology, yes, there are research technologies and there are probes, cellular probes, that can be used to measure intracellular pH. But these are not standard diagnostic pieces of equipment.

So most of the time an assessment of pH is really built on clinical signs which can be things like muscle cramping or things like in the case of moving acidosis you have people whose breath changes, it becomes sweet and acidotic. You have people who have difficulty with chronic pain that is often associated with a slight shift in pH. You know about lactic acidosis that we call the muscle pain and fatigue-related problem that occurs in the marathon and heavy exercise. There is chronic lactic acidosis that is associated with this as well as chronic muscle pain. So these are more common types of things that I think one uses for assessing pH balance versus using a specific diagnostic laboratory procedure.

[Damien Blenkinsopp]: Great, thank you for that clarification. The other important aspect I have seen about alkalinity is there is a lot alkaline water for sale now in a lot of the shops. From your perspective, does that help to change the cellular pH? Is that beneficial at all or is there no science behind that?

[Jeffrey Bland]: Well, I haven’t seen a lot of good research on it. I mean, a lot of these things that we see that are being sold commercially – I have a theory of interest but in practice there is no real clinical data to support their expense. And when we start looking at some of the cost and benefit relationships, the cost is reasonably high and the benefit is not so obvious. So I am a little bit skeptical of some of these claims that are being made.

[Damien Blenkinsopp]: Thank you very much. Another important topic and one that has always been relatively confusing to me on my journey of getting better is healing crises, or detox crises. Supposedly when we are detoxifying sometimes we have to go through this period of feeling worse in order to feel better. What is your perspective on that?

[Jeffrey Bland]: Yeah, I think that is another very interesting observation, having been involved with this field of metabolic detoxification now for the better part of 30 years and published many papers and seen literally thousands of different patients under controlled studies in detoxification over those 30 years. I have come to the recognition that the concept of a healing crises we ought to drop the term ‘healing’ and just call it ‘crisis.’ There is no such thing as a healing crisis. When you are in crisis if you have acute symptoms that is not a good thing. That is the body saying you are overdoing it.

A properly designed detoxification program does not produce a crisis. It may produce transient symptoms, it may produce a feeling of spaciness on the second or third day, ravenous hunger for a couple of days until you get your body adjusted. It may even have things like joint pains and headaches that occur, but these are not a crisis. They should be easily manageable and if they are not then that program that you are using for detox is inappropriate and it needs to be modified.

[Damien Blenkinsopp]: Thank you very much. What kinds of things could bring this on? Through my journey I was going through a lot of healing crises until actually I came across you talking in the detox summit. I finally got the answer to this question which I had been asking a lot of people for a long time about these healing crises, and if it is necessary or not. It makes it very hard to understand if you are getting better or if you are getting worse, so I think it is very confusing for a lot of people on their journeys, no matter the condition.

So in terms of where this comes from, since I learned about this – I don’t get healing crises anymore and it is really great. It is obviously a great benefit to the patient, and it keeps them more motivated as well. And from your perspective where is the healing crisis coming from? Is it something specifically that hasn’t been addressed and needs addressing? Are there a couple of routes that need addressing or is there some simple way of looking at that?

[Jeffrey Bland]: I think so. the model that I have used, which I believe is factually correct, is that a person who is overloading their body’s detoxification system through a detox program, meaning that they are releasing more toxins from stored fat tissue or within the body than their detox system can manage, now what they are getting is an amplified toxicity. It is actually their body is now toxic because they are not able to manage the toxins that they are releasing. And so the way that you prevent that is to slow the release of toxins and to increase the body’s detoxification program or detoxification ability.

That is why I am not a big believer in fasting as a focus for detoxification. Because I think in fasting you get into nutritional depletion and that then lowers your body’s detoxification ability and makes you more vulnerable to the toxins that you are releasing to produce toxic symptoms. So the approach that we developed starting back in the early 1990s through the studies that we did was to make sure a person is getting augmented levels of the specific nutrients that are necessary for supporting the phase one and phase two detoxification processes and obviously getting proper fluids so they are flushing out these materials and not storing them in their body, these liberated toxins, and that they are taking in adequate calories, particularly in the way of specific protein that is necessary to support the proper detoxifications.

So it is not a fasting, it is what I would call a modified detoxification, clean, nutrient-rich dietary program. What that leads to over the course, in our experience, of 14 to 20 days is an extraordinarily successful with lower adverse signs and symptoms in the patient or the person getting clean. And when they get clean, they know it. They think clearly, the act clearly, the sleep better, they have more energy, the chronic pain is reduced. If you have never been through that it is hard to describe those feelings to a person until they have done it. It is an amazing experience.

[Damien Blenkinsopp]: Great, thank you very much. Rounding off the interview now and thank you very much for your time. It will be very great to get these details on the basis of your book. There is one thing about functional medicine that I have found as I have been kind of going through my journey is that there are lots of different providers of tests today. There are lots of different labs with Doctor’s Data, Metametrix, Genova Diagnostics, BioHealth – there are many different providers at the moment. And it seems a little less regulated than traditional medicine where – I mean, everything seems to go to [Lab Corp 00:57:19] or some other big lab that may be a bit more standardized. And the measures on the tests are also different.

So I think for many people that can be – for instance, if you go to several different functional providers, functional medicine providers, they are maybe going to favor different tests and so on. So could you talk a little bit about the journey of functional medicine in terms of using lab testing and where you think it is going and what kind of stage it is? Do you see it as anything that needs to happen going forward in terms of standardization or anything like that?

[Jeffrey Bland]: Yes, I think obviously many of these tests that we are talking about or we have alluded to are especially tests – it doesn’t mean that they are unregulated and they don’t have standards of identity, it just means that they are not in the standard and customary tests that all physicians use, like you would have if you went to your doc and had a physical exam and they did a blood test and you had 30 different things in your blood analyzed. Those would be kind of your standard things. So these are more specialized tests that are used within the functional medicine practitioner environment. And this is one of the reasons that I really think it is very useful for a person if they move down this road and as they get more into tuning up their health that they have a functional medicine provider as their ally because these are things that have been skilled in the art and have been trained to know what to use and how to interpret these tests and not to just assume that testing just for testing’s sake is beneficial. It is the right test for the right person or the right set of circumstances, and then the right interpretation of the results.

So my belief is that testing is part of the functional medicine model but it is not the functional medicine model in itself. Much of what you can learn about a person doesn’t need testing, it needs the right way of asking the questions. And that is what I have tried to bring out in my book. The questions you ask determine the answers you get. If you never ask the questions you are never going to get those answers. So it is all about the asking about the patient’s story, understanding the patient’s story, in which then specific tests become part of a defining of I guess taking the hypothesis to understanding so that you can design a specific program for that person. It is going to meet their need and lead to the health outcome that they are desiring.

[Damien Blenkinsopp]: Great, thank you very much for that. So looking forward is there anything that you are excited about, say the next five or ten years, about the use of biomarkers in functional medicine? Do you see any opportunities in the future where it will be more like looking at epigenetics or anything new on the horizon that might help functional medicine practitioners to get better diagnoses or help people better monitor their health and so on? Is there anything interesting you see ahead or that you would like to turn up in the future?

[Jeffrey Bland]: Absolutely so, and this is actually a wonderful place to kind of bring our discussion to a close because really I think it is real time. We are in a health revolution right now that is second to none. This is equivalent in its extraordinary discovery periods to that of the turn of the last century when the origin of infectious diseases was discovered as caused by microbes. And then from that therapy antibiotics were developed, which really transformed healthcare. We are having that same extraordinary revolution in thinking right now and it is around how we are going to manage chronic illness based upon these characteristics of dysfunction. And there are three intersecting changes that are occurring right now that I think are absolutely revolutionizing this field.

One we have talked about and that is the ‘omics’ revolution – genomics, proteiomics, metabolomics, that really allow us to analyze certain aspects of how are genes are expressed and how they are able to be induced to produce good health through activating our resilience genes. And every one of us has some areas of our genetic weak spots. Unfortunately most of us have – in fact, I would say everyone, has resilience genes that can kind of neutralize our response if we turn on our resilience genes. So I think that this particular period that we are undergoing right now in discovery is helping us to understand what are those characteristics and how do we measure them? Soon virtually everyone will be able to have a full gene analysis done, the full genomic analysis, for the cost of a normal lab test, probably somewhere in the range of less than a thousand dollars and eventually for a few hundred dollars. And that will ultimately become insurance reimbursable and we will all have the ticker tape of our genetic information.

That, coupled with the internet and social media where information is now being communicated, transferred, and analyzed in ways never before so that it gives power to the person to own their own genetic information, their own personal health information. And then lastly, big data now in the cloud with what is called informatics that is allowing these huge amounts of new data to be made available to people to be analyzed in such a way that it becomes sensible and a person knows what it means, not just a bunch of ones and zeros but actually operational and instructive about a person’s own personal health program.

Those three things, which we used to think were way out in the future are now happening in real time. The wearable devices that we have like FitBits and Jawbones and so forth and the new devices that are coming out to measure all sorts of biometrics and how that data that each one of us generates about ourselves each day goes to the cloud and gets analyzed and comes back to us and helps us to assess what we need to do to be healthy throughout the course of our life. It is a disruptive innovation that is changing healthcare. And we are all living through it right now. We have a generation of kids that are all social media savvy. They are very comfortable with sharing things that their parent’s generation never was willing to share about their health and their genes. And all of this is transformative.

Within the next ten to twenty years the rules of the road that we have lived with upon doctor’s owning information and everything is about disease diagnosis and all of that is going to go away. We are being replaced with a whole new system that will emerge underneath us with the kids that are growing up in the video game revolution and social media and the age of genomics. That will be transformative.

[Damien Blenkinsopp]: Well thank you Jeffrey, that sounds like a very exciting future and that fits very well with what we talk about often on this show. So it is certainly what I am excited about as well. Thank you so much for your time today, Jeffrey. I know you are a really busy man and I really appreciate your many, many decades of experience in coming on this show and sharing your opinions with us and your ideas.

[Jeffrey Bland]: I appreciate it very much and I hope we have given some good information to your listeners. Thanks a million.

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Today we’re looking at HRV- endurance training, adrenal fatigue, and future app developments.

If you didn’t listen to it, in Episode 1 we primarily looked at resistance training, or weight training.

Today we also look at some scenarios where the HRV metric can be confounded where an increase in it is not good, how it can be used to identify possible adrenal fatigue and how to improve its accuracy by combining it with Resting Heart Rate and qualitative measures.

Today’s guest is Simon Wegerif who founded ithlete, the first HRV app company, which appeared 5 years ago in 2009. In comparison to Andrew Flatt, whose focus was resistance training, Simon has a background in primarily endurance training and it was for this he originally became interested in HRV.

Since 2009, through working with its client base including a range of pro and amateur athletes and everyday gym goers, and now universities in connection with studies, ithlete has evolved its app to cater for specific scenarios like adrenal fatigue and understanding how individual factors are impacting training. Simon has been diligent in staying up to date with the research and adapting the ithlete app to take advantage of it as it evolves.

The show notes, biomarkers, and links to the apps, devices and labs and everything else mentioned are below. Enjoy the show and let me know what you think in the comments!

itunes quantified body

Show Notes

  • The status of research on Heart Rate Variability and some of the issues to overcome such as standardisation.
  • HRV as a predictor of endurance performance – now as effective as running times?
  • Using “Active Recovery” to recover quicker from endurance and resistance training.
  • True overtraining vs. non-functional overreaching – how to improve training results by understanding how HRV indicates these two .
  • How to diagnose potential adrenal fatigue with a combination of HRV and RHR (resting heart rate) metrics.
  • The one situation where you don’t want your parasympathetic to become dominant (or your HRV to be high).
  • The need for HRV benchmarks to be established in order to compare your “health future” to others and as a proxy for aging.
  • The Palo Alto Prize spurring on new investment in research to improving longevity based on using HRV as a feedback mechanism for experiments.
  • Using yoga breathing (Pranayama) to increase Heart Rate Variability by up to 5 points within a few days.
  • The biomarkers Simon tracks on a routine basis to monitor and improve his health, longevity and performance.
  • Simon’s one biggest recommendation on using body data to improve your health, longevity and performance.

Give some love to Simon on Twitter to thank him for this interview.
Click Here to let him know you enjoyed the show!

The Tracking

Biomarkers

  • Heart Rate Variability (HRV): Measures how your heart rate varies over time. Research studies link HRV to recovery status, stress and other aspects of human physiology.
  • Resting Heart Rate (RHR): Measure of your heart rate at rest (typically measured upon waking).
  • Calories: We discussed the merits of measuring calories in and out, the current hype cycle around ‘calorie counting’ apps and devices, and its relationship with weightloss.

Apps and Devices

  • ithlete HRV App: The app Simon developed which includes some of the RHR and adrenal fatigue functionality discussed during this episode.
  • Polar H7 Bluetooth Smart Heart Rate Sensor: A chest strap heart rate sensor that works with the ithlete and other HRV apps (Damien uses this one).

Simon Wegerif and ithlete

  • ithlete: Simon’s company and the HRV app with the same name.
  • You can also connect with Simon on twitter @SimonWegerif.

Other People, Books and Resources

Resources

People


Full Interview Transcript

Transcript - Click Here to Read
[Damien Blenkinsopp]: Hi, Simon. Thank you very much for making time today to come on the show.

[Simon Wegerif]: No problem, Damien. Really good to talk to you.

[Damien Blenkinsopp]: What I thought we would first do is quickly, where does ithlete fit in with the world of HRV apps and development, from your perspective?

[Simon Wegerif]: Okay, well, ithlete was the first HRV app available, and when I first started getting really interested in HRV, which was early 2009, I decided it was so interesting to me as an engineer by background, but also a keen recreational endurance athlete, trying to make the most of my own somewhat limited abilities, that the iPhone was just being launched early in 2009, and talking to a couple of people, I was looking for ways to realize my hopeful invention of a convenient, simple-to-use, but accurate HRV measuring device. And people said, you know, why don’t you do it as an app in the iPhone? So I started thinking about that, and I made that my target during 2009, and got the prototypes all done on an iPod Touch, and at that time, I think it was IOS version 2 was just coming out, so we were easily the first to bring even accurate heart rate measurement onto the iPhone, let alone HRV. So we’ve been doing this for a little while now, and the product, I think the current version of the app is relatively mature because of that.

It’s also — being the first gives you some advantages in the early — doctors in research started looking at it quite early on, and we’ve now got some good quality validation studies that have been done that show, in fact, the ithlete measurement to have an almost perfect correlation with the gold standard of ECG, which we’re very happy about. The ithlete finger sensor has also been validated.

[Damien Blenkinsopp]: Great, great. Well, you have three sensors. You’re using the finger sensor, the Bluetooth heart rate chest straps, and isn’t there another one?

[Simon Wegerif]: Yeah, the other one was actually the original one, Damien, so in the early days of the iPhone, there wasn’t any convenient and reliable way of getting a heart rate signal into the phone, so I designed a little adapter, a plug-in adapter which would go into the headset socket, which I still think was a good choice, because headset sockets are available, you know, on pretty much every phone, and the way they’re connected has remained standard, now, for three or four years. So it’s a little device which users can take from one phone to the next, be that iPhone, Android, or even Windows phones, if we do an app version for that. And that little receiver picks up the signal from the Polar type of chest strap, and, of course, that Polar transmission system has been around since the early 1980s, so there’s an awful lot of products in the market that support that.

In fact, although Bluetooth [Smarties 00:05:56] is, in many ways, the state of the art, and the finger sensor is the most convenient, we still sell a lot of the — what we call the little ECG receivers because of the massive installed base of Polar type straps and systems.

[Damien Blenkinsopp]: Okay, great. So I know you stay up-to-date with the research, and you’ve been following this since 2009 or before, so could you give us a bit of an overview, from your perspective, of the research? How much is there related to HRV? Where are the strongest areas, and, you know, how you look at it?

[Simon Wegerif]: Yeah, I think if you were to put heart rate variability into PubMed, which is the — you know, the recognized research database of peer-reviewed papers, I think you’d probably get about 14,000 hits. So there’s an awful lot of peer-reviewed research which has been done on HRV.

[Damien Blenkinsopp]: Do you mean 14,000 papers, separate papers?

[Simon Wegerif]: Yes, 14,000 separate papers, yeah.

[Damien Blenkinsopp]: Great, great.

[Simon Wegerif]: Which is quite a high volume. A lot of that is focused on disease state, so looking at autonomic dysfunction, for instance, in diabetes, cardiovascular diseases, cancer, and a lot of other disease states like that, but there is a fair body of research studies on sports performance and health as well. During my preparation for designing the ithlete app, I read about 500 papers during 2009, and I’ve now got about 1,000 in the collection, my collection that I’ve read.

Some of the papers have got some strikingly good methodologies and breakthroughs, and others are a bit weaker. I think one of areas where heart rate variability research has not done itself any favors is not standardizing in units or protocols. For instance, things like the duration of the measurement, the units that are going to be used, the position of the subjects, whether they’re lying down, walking around, standing, sitting, what are they doing. There hasn’t been much standardization there, I think partly because a standards document was never adopted in the industry.

[Damien Blenkinsopp]: So one thing I noticed about your ithlete app when I was playing around with it was that when you’re taking the reading, it’s got the breathing timer. It’s got this circle that moves up, in and out, with your breathing, which I thought was great to try and standardize that aspect a bit better in terms of how you’re breathing and just keep more rhythmic and controlled every time you’re doing it, instead of different. Is that why you put it in there, or?

[Simon Wegerif]: Yes. Breathing has a very important impact on heart rate variability, so when we talk about HRV, particularly in sports performance and everyday health use, we nearly always mean parasympathetic HRV, and parasympathetic HRV is primarily dependent on breathing. In fact, the HRV is caused as part of the breathing feedback loop with the brain. So as you breathe in, your heart rate gets faster; as you breathe out, your heart rate gets slower. And it always seemed to me, as an engineer, that unless you’re controlling your breathing in some way, that your HRV measurement process is going to be somewhat unpredictable, if you’re just relying on a breathing pattern which is uncontrolled. So controlling that breathing, but without creating stress, hopefully, in the user is the objective here, because everyone who knows much about HRV will know that stress lowers your HRV. So we don’t want to stress the person during the measurement, but we do want them to have a constant breathing pattern, and hopefully the ithlete breathing pattern is something that’s evolved over three generations of the app now, and we hope that people find it peaceful and relaxing to use.

[Damien Blenkinsopp]: Yeah, it’s kind of like this pulsing heart thing. I found it relaxing, and it’s just nice to have an indicator. Because I’ve used other apps, and, you know, they don’t have that. So every time you’re probably breathing a little bit differently, but you don’t notice it. So I thought it was a nice touch. Thanks for that overview.

So, you’ve done a lot of work in the endurance and aerobic areas. We haven’t looked at that yet on the show, so that’s what I’d like to explore a bit more with you. Any idiosyncrasies or differences compared to weight training, which we’ve looked at quite a lot with Andrew Flatt in the past. How would you say that it differs from weight training in the way HRV relates to endurance?

[Simon Wegerif]: Well, one thing, as a segue or a link from the body of research on HRV, Damien, is that a lot of the studies in the sports performance area have actually been done with endurance sports. So they’ve been done with running, cycling, rowing, cross country skiing, because, of course, Finland and the Nordic area has been one that has done a lot of adoption and research into HRV. So there is — the body of research in endurance sports is strong. It’s also something that I’ve been personally interested in, because one of the reasons I created the app originally was to improve my own performance, originally, in triathlon, but lately in long distance cycling.

And so HRV, interestingly, has been something which is really quite well proven and quite well applied to endurance sports. And one of the things about some of the research that’s come out in the past couple of years has been the very good correlations between changes in HRV and changes in performance. So there have been studies done at the national level on French swimmers where they measured their HRV before doing a weekly 400-meter pool time trial, and they found the correlation was so good between the individual’s change in HRV and their variation in performance on the Thursday time trial, that they said one or the other is good enough here. So if we measure their HRV, they don’t need to do the weekly time trial to assess performance improvement.

And a key researcher in this field also, Martin Buchheit, also found when club runners were training to improve their performance in 10K races, that only the runners that improved their HRV during — I think it was an 8-week training program. Only the ones that improved their HRV, improved their running times. The ones whose HRV didn’t improve, their running times didn’t improve, either.

So there’s been some very clear findings in the endurance area. And I think training guided by HRV is becoming more and more practical for endurance sports as a way of maximizing performance with the training time that’s available, but without risking overtraining.

[Damien Blenkinsopp]: Right, right. I know with respect to endurance, we’ve touched on this a bit with Andrew Flatt, he was talking about basically how he would be doing weight training, and his HRV would go down, but if he did a bit of aerobic as well, he would limit how far his HRV would drop the next day. How do you explain that? What’s going on there?

[Simon Wegerif]: Yeah, there’s been a pretty important study that came out, I think it was late last year from a couple of researchers in the University of Queensland in Australia, and again with Martin Buchheit involved, that built on work done by researcher Stephen Seiler, who’s been looking at the way, for instance, marathon, long distance runners have trained in Kenya for many years. And what he observed there is that they tend to follow a polarized approach to training. So the majority of their volume, say 80% of their training time, is conducted at what appears, to many athletes and coaches, to be really quite moderate paces, fully aerobic work. And in fact precisely defined, it’s a level of aerobic work below the first lactate threshold.

So essentially the lactate level in the blood is close to the athlete’s ordinary baseline. And recovery from that kind of aerobic work, although athletes can do habitually quite high volumes of that, you know, many hours a week, is very quick. And that’s reflected in HRV. But when you go above that threshold, then recovery takes much longer to achieve.

So in Andrew’s case, I think what he’s really enforcing is the fact that aerobic exercise really allows rapid recovery, and the fact that the metabolism is accelerated is helping to process the byproducts from the high intensity sessions and perform, essentially, what we call active recovery. Active recovery actually gets you back to baseline more quickly.

[Damien Blenkinsopp]: Does that reduce the stress, the stimulus to improve your body in any way? We’ve also spoken to, like, Doug McGuff of Body By Science. He talks about inroads, so, you know, one of the things about heavy weight training is you want to create a large enough stimulus to improve strength. So is this in any way — it sounds like it’s reducing, in a way, the stressor. Is that a correct way to look at it? I’m just wondering if that has an impact on how your body tries to compensate.

[Simon Wegerif]: Yeah, it does seem to be having that effect by stimulating the parasympathetic nervous system. And the parasympathetic nervous system is good for reducing inflammation, for rebuilding energy stores, glycogen in the liver, for ensuring that oxidative stress is reduced. And the really useful thing about long slow distance or aerobic training in endurance athletes is that it provides a good level of stimulus for mitochondria to adapt. So one of the things you want as an endurance athlete is an efficient metabolism with lots of mitochondria in the muscles, which are able to process fuels and turn those into energy. And what you also want is a metabolism that’s able to use fats as fuels. You know, your store of fats in any body, even thin people, is many, many thousands of calories, and fat is a very efficient way to store fuel. You know, it’s 9 calories per gram. Whereas, carbohydrate is 4.2 calories per gram, and carbohydrate is usually associated with quite a lot of water retained in the body as well. So if you can use fats as fuels, that’s a big advantage.

If you’re running a marathon, then you’ve only got enough glycogen for about — you’ve probably got about 800 grams. You know, you’ve probably got — your total body store is about 3,000 calories, of which your body will probably only allow you to use a couple of thousand, so your ability to supplement that glycogen fuel with fat stores is something that your body learns to do and learns to adapt to when you spend time training aerobically.

[Damien Blenkinsopp]: Yeah, we discussed this with Jimmy Moore. He’s done a lot of work with other people in keto diets and so on involved with training. So, yeah, it’s good for you to make that connection and bring that up in this context.

Okay, so kind of round off the impact — so you’re saying it helps recovery — it helps accelerate recovery by stimulating the parasympathetic system.

[Simon Wegerif]: That’s right, as well as building — building the cardiovascular system and energy stores and energy system to make you — make you efficient, really, and be able to go for a long time.

[Damien Blenkinsopp]: Are there any cases where we shouldn’t be doing this? If we’re just focused on HRV, it’s like, oh, well, it leads to a higher HRV, so — if we’re always just aiming to increase the HRV, which is part of the discussion I wanted to have today, so should we always be doing that? So if we’re weight training and we can do a little bit of aerobic to increase our HRV, so everyone be doing this?

[Simon Wegerif]: I think everybody should be doing a certain amount of it, but it’s not going to lead to good race pace performance unless it’s also complimented by some high intensity stuff. And the general adaptation syndrome of Selye, which was, you know, written a very long time ago, basically talks about stressing the system and then allowing time for it to recover, and when it recovers, it supercompensates, so the body is stronger than it was before. And high intensity work is a very good way of stressing the body sufficiently that it is stimulated to adapt and supercompensate compared to where it was before. And that’s a necessary component of high performance athletics.

[Damien Blenkinsopp]: Okay, okay. So it sounds like everyone — although it’s not going to lead to a higher baseline, by the sounds of it. If we think of we’re trying to increase our HRV over time in terms of kind of aggregate, rather than the ups and down adjustment cycle of just trying to time our training properly, doing a little bit of aerobic with our strength training probably isn’t going to increase the baseline. It just may help us to get back to another workout sooner than later in terms of recovering quicker. Is that a fair assumption?

[Simon Wegerif]: Yeah.

[Damien Blenkinsopp]: Or would that be, actually, kind of biasing the result, and it would be better to — I guess this area isn’t 100% clear as yet.

[Simon Wegerif]: It isn’t 100% clear. I’m trying to recall my own experience of doing a lot — because I’ve prepared for a pretty long cycling event across the Alps this summer, and I did a lot of hours of fully aerobic training, so I was very careful to keep my heart rate and intensity level below the first lactate threshold, and I accumulated a lot of hours, basically, about 15, 17 hours a week for about four or five weeks of this. I didn’t actually see my HRV baseline rise much. What I did notice was my resting heart rate went down during that period, though, and that was a very clear trend.

[Damien Blenkinsopp]: Okay, so let’s talk about that, because I know that’s something very important to ithlete. You track the HR, the resting heart rate, as well, and you use that in your assessment. And you see it as an important part. So what is the HR for you? What is it doing in terms of tracking and helping you to understand performance and recovery and so on?

[Simon Wegerif]: Well, resting heart rate, most people who do training and even people who know about health would recognize that a lower heart rate — a lower resting heart rate is very often a good thing. And most of the time, that it true, because it’s actually the ratio of your maximum heart rate to your resting heart rate that determines your VO2 max. So there is, for instance, a ready reckoner for VO2 max, which is your maximum heart rate divided by your resting heart rate times 15. So, you know, as your resting heart rate decreases, provided your maximum heart rate stays the same or only decreases a very little bit, then your VO2 max will increase.

Now, there are also situations, which can be due to either non-functional overreaching, so some states of overtraining, or even —

[Damien Blenkinsopp]: When we say non-functional overreaching, what does that mean?

[Simon Wegerif]: Well, non-functional overreaching is basically what you might think of as the third stage in progression of training load and recovery imbalance. So the first stage is shock, also known as the alarm stage, which is the body’s healthy response to a new stressor. And during that stage — so you do something intensive, your body is temporarily stressed. It reacts with an increased sympathetic tone, increased output of central stress hormones, increased adrenaline, norepinephrine, cortisol, and if you then allow time for the body to recover, then it supercompensates, and you actually end up you are a little bit fitter than you were before the stressor had been applied.

Now, overreaching is a deliberate imbalance of training and recovery, usually over a short period of time within a periodized block. So a lot of endurance training programs are periodized into a month or a 5-week block whereby you have a progressive overload, then, you know, ending up with a taper or a recovery week. And that is called functional overreaching, because you deliberately continue to stress the body, and then in the last week, you taper, and you supercompensate, and, you know, the benefits of training are imbedded in your system.

If the balance of training and recovery is such that, you know, your body really — it can’t cope with the amount of load that’s being applied, and that can include environmental conditions as well, so that can include bad diet, lack of sleep, all these other things which are, in fact, stressors to your body as well as training, then if, you know, after a short taper period you don’t recover and supercompensate, but you stay in the hole, as it were, then that’s non-functional overreach.

[Damien Blenkinsopp]: Uh-huh, okay.

[Simon Wegerif]: But people do even go beyond that. It is — yes, it is really — the way I would define non-functional overreaching is that when you take the training load away, you don’t see recovery or supercompensation within a few days or a week.

[Damien Blenkinsopp]: And does it take much longer, or would you have potentially basically lowered your baseline by overstressing the body?

[Simon Wegerif]: Yeah, and it can take weeks to recover from non-functional overreaching. And non-functional overreaching is still not as bad as true overtraining. True overtraining is really quite a serious condition, and it’s not that common, but it can takes months or even years to recover from. It can —

[Damien Blenkinsopp]: How would you differentiate the two?

[Simon Wegerif]: Yeah, true overtraining, again, is an extension of the states of overreaching, whereby you take away the training altogether, and the individual really remains in a chronically stressed state. I think it is quite rare, although certainly we’ve been contacted on a number of occasions by athletes and coaches who know that they are overtrained. And this is also known as the exhaustion phase in the General Adaptation Syndrome. And the body is basically continually failing to adapt to the chronic stress. And the chronic stress also starts to burn out the adrenal system, so the central nervous system starts to shut down production of central stress hormones. The adrenal glands themselves desensitize.

A sympathetic response is normally quite healthy.You know, when a person needs to have a fight or flight response, they want to be able to turn it on and turn it off again quickly. When somebody’s overtrained, that response is pretty much absent, to be honest.

[Damien Blenkinsopp]: Right. We talk a lot about the importance of parasympathetic. In one of our previous interviews, we talked about the fact that most people are sympathetic dominant, mostly because of lifestyle reasons today, and so on. So in the HRV Sense app, for instance, Ronda Collier, she noted that most people have a very high sympathetic in their LF, and their HF tends to be much lower. And over time, they can, you know, look at that for stress and so on. But now we’re talking about also that overdominance of parasympathetic can be a problem? Is that associated with adrenal fatigue?

[Simon Wegerif]: Yes, indeed. Once the body gets itself into this state whereby the sympathetic response is essentially impaired, then — it’s interesting. I mean, that’s a pretty bad state, right? I mean, that’s also a state where protein synthesis becomes impaired, so, you know, muscle damage becomes much more likely. Decreased testosterone and other anabolic markers, increased baseline cortisol, so basically, you know, the body is in quite a stressed state, although it’s sensitivity to the adrenal family of hormones has been reduced. And then, you know, parasympathetic becomes essentially dominant. You swing to a high HRV, which if you weren’t looking at heart rate, you might say that that’s a good state, right?

[Damien Blenkinsopp]: Right, right, right. So let’s be clear. What would the heart rate be doing that’s different to show that this is a negative HRV despite the fact that it’s high?

[Simon Wegerif]: Yeah, so what actually happens is that the resting heart rate decreases pretty significantly compared to your normal range. So all of the ithlete measures are based on solid statistics and smallest worthwhile change and things like that, so we’re always tracking rolling means and rolling standard deviations. We can look at the heart rate and see if that all of a sudden — you know, if that over a short period of time goes much lower than it should do normally, and coupled together with an unusually high HRV, then that is quite characteristic of parasympathetic dominant sympathetic burn out state.

[Damien Blenkinsopp]: Right, right. Have you come across many cases of this?

[Simon Wegerif]: Yeah, I’ve certainly see it in myself. We first came across it, because it’s not that well documented, so most of the textbook stuff on overtraining tends to talk about sympathetic dominance, and indeed that is the case through functional and non-functional overreaching. But then, you know, when people keep going, and there are some very motivated type A individuals that keep on going, and they get themselves further into this — into this truly overtrained state, the first time we —

[Damien Blenkinsopp]: Right. So would it be correct to say that your HRV would go down for a while, and if you ignore that, then you might get to this situation?

[Simon Wegerif]: Yes, absolutely. That is exactly what we see.

[Damien Blenkinsopp]: Right, right.

[Simon Wegerif]: The first time we noticed this, in fact, was in the beta testing of the original ithlete app in 2009, when we gave it to a national standard runner and triathlete, and he did a three-day running event in Southern England over the South Downs, and he said, ‘Hey, you know what, guys? My HRV was really high this morning, and I’m completely knackered. You know, what’s going on?’ And we started to look into it and talking to some researchers and developed this test, basically, out of that.

And we certainly have seen it a few — you know, a few times. I’ve seen it a couple of times myself. In fact, the day after I finished the Haute Route Alps, which was 1,000 kilometers in seven days across the Alps, I was six hours a day on the bike working quite hard, the day after that, the Sunday, my HRV all of a sudden swung from low, which had been progressively decreasing during the week, and it swung very high, associated with a much lower than normal resting heart rate, and ithlete went — gave me a straight red.

[Damien Blenkinsopp]: Right.

[Simon Wegerif]: So ithlete doesn’t mess about in that situation. It gives your a red card straight away.

[Damien Blenkinsopp]: It’s nice that it does that, ‘cause, you know, often I imagine most of the apps don’t pick that up, that scenario. So in terms of a swing of HRV, do you remember your — just to give people an idea, where did it kind of start from baseline, and it lowered steadily to what, and then it jumped up one day?

[Simon Wegerif]: Yeah, I can’t remember the numbers right now. I did do a blog post about it, in fact, so it’s on — yeah, myithlete.com/blog, I did a blog post about my HRV before, during and after this actual event. I think you can go look at that.

[Damien Blenkinsopp]: That’s good. So we’ll put a link in the show notes to help people. Okay, so this final thing on adrenal fatigue, is adrenal fatigue is a widely discussed topic today, because a lot of people, not just people who are training, but often it’s the weekend warriors, the people who are working during the week, and they got out and have pretty stressful jobs, and then they’re training at the weekends, or they’re doing triathletics and all these other things at the weekends. And there’s this question of when they start getting more and more tired is the adrenal fatigue. Doctors and clinicians argue about this and how to test for it. And many of the tests are considered not ideally accurate, there is saliva test, there is blood tests, and there’s a bit of discussion there. So I’m just wondering whether you think this would be a relevant biomarker, and if you’ve seen anyone try to compare it to some of those other adrenal fatigue tests?

[Simon Wegerif]: I haven’t. A practical test I could recommend for people, though, is if you suspect you might be starting to get adrenal fatigue, then the likelihood is that you won’t be able to manage high intensity exercise. You know, you simply — you hear comments like, ‘I was unable to get my heart rate or my power up into the right zone.’ You will notice that. And it is literally impossible. You just cannot manage the effort levels, no matter how hard you try. So your perceived exertion would go right up, but your metabolism and your body wouldn’t respond to the workload and energy levels that are required.

[Damien Blenkinsopp]: Yeah, yeah. So I noticed, also, that when you were talking about how to notice this, you know, you spoke about an athlete who came to you and said, ‘Look, my HRV’s really high, but I’m feeling terrible. I’m feeling really tired.’ So in ithlete, you have a bunch of indicators that you track whenever you track your HRV for training, in the morning you have sleep, fatigue, muscle, and stress, and mood, and diet. Do these filter into some kind of algorithm, or how are you using these to help people make decisions?

[Simon Wegerif]: They are going to. I mean, at the moment, these are quite widely used subjective metrics, and they are quite useful for tracking overall health and wellness, as well. So at the moment, it’s great for people to record those every morning, and on the ithlete, if they rotate the dashboard around to the landscape chart, they can visually for themselves see correlations between any one of those variables and their HRV, and in my case, I’m really not very good, if I’m lacking sleep, quality or quantity. So, you know, my HRV normally shows quite a good relationship with my sleep score. Other people —

[Damien Blenkinsopp]: Right. Is that the same for everyone, or do people have different weaknesses? You know, the high leverage weakness you’ve got to kind of avoid. So yours is sleep. Mine is probably sleep, too.

[Simon Wegerif]: No, I think people absolutely do have individual characteristics there. It could be stress for some people, or it could be diet in others, if they have particular dietary sensitivities. But what we are just starting to do, right now, in fact, is a cooperation with a UK university on some advanced statistical algorithms which will look for relationships between those individual subjective variables and the HRV over a period of time. So what we hope to be able to do within the next six to eight months or so is to be able to give users feedback and insight into their own data.

I — you know, for me, HRV has always been a journey of personal discovery. I’ve found out things about myself, what my body and my brain likes as assessed by HRV, and, you know, I’ve been able to keep my HRV sort of steadily trending upwards over the five years that I’ve been doing this; whereas, normally it would decline with age. But, yeah, what we want — what we aim to be able to do is to give users insights, exactly as you say, Damien, telling people, you know, over the past month, sleep was the most important factor for you, perhaps again, and diet was the second, and it seems like you’ve been having a lot of stress recently, and that’s been affecting you as well.

So I think there’s potential for this to go quite a long way, including things like, perhaps, looking at all the relationships between everything people are capturing, and then saying with some statistical confidence all of this stuff that you’re capturing isn’t explaining all the variation we’re seeing in your HRV, is there something else? Is there, for instance, travel?

You know, one of our — one of the members of our team just noticed that driving for periods above three hours was causing a big drop in his HRV the next day. So potentially we can also alert people to things that they’re not capturing or not trying to understand right now, but which nonetheless are affecting their health.

[Damien Blenkinsopp]: Yeah, yeah. So, yeah, just to be clear, because I didn’t bring this up before, but these ratings you enter into your app are basically from, you say sleep quality, and you just give a rating from weak — it’s kind of like 0 to 10, right?

[Simon Wegerif]: Yes.

[Damien Blenkinsopp]: Or you can put very strong, and that’s for each of them. So they’re qualitative measures, but as you say, you’re finding correlations with them, and you’re going to be looking into more of that.

[Simon Wegerif]: Yeah. We turn the position of the slider into a number, like you say, between 1 to 10, and I think that’s a technique — I think that’s called a visual analogue scale or something like that, and the statistics will be using those numbers to determine relations and give people feedback.

[Damien Blenkinsopp]: Right, great. Well, [00:35:23] we’ve explore a bunch of new topics and interesting scenarios that we hadn’t come up with before, because you’ve got this user base which is using ithlete. I think what would be interesting is, like, what do you see people mostly using this for, and what are the kind of biggest use cases, and most useful things people are using it for?

[Simon Wegerif]: We’ve got a wide variety of users. We’ve got well over 10,000 users now on the ithlete app, and they really vary. They do vary from weekend warriors to — all the way through to top professional athletes, both in team sports, endurance sports, things like boxing as well, through to health and wellness practitioners. So we certainly get quite a few bulk orders from chiropractors and holistic wellness practitioners and people like that. And I think it’s used for all kinds of things. It’s used by health conscious people who just think HRV is a good metric to track every day, and, of course, it is. It’s a sort of holistic measure of adaptation reserves or overall well being. So it’s a great thing for people to track.

I think in the more serious side of sports, people are looking in their training not to have dug themselves into too much of a hole, and they fairly quickly start to take the tool seriously when they get amber and red warnings, and they still go training on those days. They fairly quickly work out that that’s a bad idea, and they start to trust the tool more. We give them feedback on a day-to-day basis.

[Damien Blenkinsopp]: Is there any scenario where you wouldn’t trust it? I mean, we’ve highlighted one that you’ve identified and you’ve integrated now into ithlete, with that one HRV going up. Is there anything else you’ve kind of got on the horizon? Maybe there’s a couple of other scenarios that need to be looked into?

[Simon Wegerif]: Yes, definitely. One of those is taking readings at an unusual time. So the ithlete algorithms are based on you doing things at the same time every day. Ideally, it should be first thing in the morning, because then you haven’t got additional variables of drinking a coffee or not, or having something to eat, or looking at — opening emails, having an argument, anything like that. Those variabilities all eliminate it. And, of course, another advantage of doing it first thing in the morning is that you can plan the day ahead. So, you know, darn, I got an amber instead of a green, but it’s not too late, I can modify my training or something else that I was going to do today.

[Damien Blenkinsopp]: Yeah, that’s interesting, because in a future episode, I want to have someone talk about willpower, because I’ve read a fair amount about the correlation between HRV and willpower, and, you know, basically motivation and drive. So if I have a low HRV one day, I’m, like, okay, I’m going to take on less and less business tasks today. I’m going to focus maybe on one instead of trying to get five done. I kind of factor in like that. I mean, obviously you’re feeling like that as well, but I’m also kind of aware that maybe I need a recovery day in terms of just taking on work stressors and mental stressors and things like that, in order to be able to take on bigger stuff the next day and so on.

[Simon Wegerif]: Absolutely, or there might be some intervention which will help you a bit. So if I get an amber in the mornings, then I often, you know, I will change my training to an hour aerobic bike ride around a particular route in the local forest that I really enjoy, that, you know, is visually stimulating. And I know that will help me make the best of my current physiological state.

But back to the question you were asking about when would you not trust ithlete, or in fact any HRV product that compares to baseline, and that is if you get up significantly earlier or later than your normal time. So one of the things about the waking measurement is that you are taking it after you’ve had the cortisol awakening response, so basically when light starts to fall on the back of your eyes, even through your eyelids, it kicks off the cortisol awakening response, which basically gets your body ready to get up and start being active again. So it banishes the melatonin, and it starts the sympathetic nervous system to a certain extent, enough to get you out of bed and get moving in the morning.

Let’s say you normally do that at 7 a.m., and then one morning you have to get up at 4:30 in order to catch a plane or something like that. This is something that I noticed quite early on, that my HRV would, in that situation, be much higher than normal.

[Damien Blenkinsopp]: Ah, because parasympathetic is higher.

[Simon Wegerif]: Yeah, basically. Because my body was still in sleep mode, so the parasympathetic was dominant at that time.

[Damien Blenkinsopp]: So, basically, the circadian cycle is very important to control for.

[Simon Wegerif]: It is important to control for, and some people — I think everybody, once they realize that, that really your morning measurement should be +/- 45 minutes, something like that —

[Damien Blenkinsopp]: So I’m thinking jet lag is — because I just came from Europe to the U.S. a few weeks ago, and my HRV has been a little — I think I was surprised to see how high it was, given how tired I was feeling. So maybe that had some of the impact there.

[Simon Wegerif]: It could do. It could do.

[Damien Blenkinsopp]: Or do you think you adjust pretty quickly in terms of that cycle?

[Simon Wegerif]: I don’t think you do adjust that quickly. We’ve had so many stories reported back to us over the past few years. An Australian coach has said, ‘I never realized what an impact jet lag had on my body,’ and that was by doing HRV measurements, and he was flying backwards and forwards between Australia, Europe and America. And those are long haul flights. I think one rule of thumb is something like your body needs a day to adapt its circadian rhythm to each hour of time zone change. So if you’re doing all that trans-Atlantic or trans-Pacific travel, you’re going to have a really hard time getting adjusted, and your HRV is going to give you feedback on that.

[Damien Blenkinsopp]: Yeah. So the only other confounder is basically the issues is controlling for circadian rhythm and other things you’re introducing, like caffeine or those things. But in terms of actual scenarios, the only other one you’ve seen is where you continue to overtrain and eventually get to this adrenal fatigue situation, without introducing — and then the other scenarios are where you’ve introduced either a circadian or some other confounder in terms of stimulant or activity which is influencing your HRV?

[Simon Wegerif]: Yes, I would say so. Water has some interesting effects on HRV. Hydration level is something that — you know, some of the professional teams that are using ithlete, they want to control hydration level.

[Damien Blenkinsopp]: So are you saying dehydrated would lower your HRV, potentially?

[Simon Wegerif]: Yes, because it stresses the system, so, yes, that will tend to make you more sympathetic dominant. But, of course, that’s something that’s quickly fixable, right? You drink water, and within 15 minutes that HRV will have been restored, because your body absorbs water so quickly. So that will give you a false low.

[Damien Blenkinsopp]: Right.

[Simon Wegerif]: So if you woke up dehydrated and you were normally fully hydrated, you will get a falsely low — I mean, it is a low HRV at that point in time.

[Damien Blenkinsopp]: It’s relevant, yeah.

[Simon Wegerif]: But you have to take it — it’s relevant; it’s important, but you don’t have to take it easy the whole day —

[Damien Blenkinsopp]: Yes.

[Simon Wegerif]: — because recovery from that particular situation can be very rapid. You just drink large glasses of water and you’re right as rain.

[Damien Blenkinsopp]: That’s a good point. It’s a momentary HRV lapse, a decline. Are there any other scenarios where there are HRV’s you can quickly addressed? I’m thinking training scenarios. I mean, obviously, there’s, maybe a stress scenario, caffeine and things like that.

[Simon Wegerif]: Yeah, mental stress is important.

[Damien Blenkinsopp]: So people can account for those kind of things by — hopefully, if they’ve identified it, then they can retake their reading in an hour or so and see if it’s readapted to their usual baseline.

[Simon Wegerif]: Yes, they certainly could do that, yup.

[Damien Blenkinsopp]: Okay. Well, so you’ve talked about some of the things you’re going to be doing in the future with the algorithm and the correlation. Is there any other future developments and things that you — like, if you’re looking at the whole HRV app space, is there other things you’re looking forward to or that you see could be possible in the future, 5 or 10 years? Where do you see it all going?

[Simon Wegerif]: Well, what I personally hope for is that HRV, it is starting to get credibility now in sports training and sports performance. You know, it’s becoming, thanks to some of the really quality research that’s being done, it’s becoming more and more trusted. I’d like to see HRV trusted as a precursor to Western chronic disease, and in particular I mean conditions like high blood pressure. High blood pressure is an autonomic imbalance disease, and basically high blood pressure can certainly be caused by chronic stress over a period of time, and the blood pressure regulatory mechanism starts to go adrift. But you will see, in the case of not only high blood pressure, but type 2 diabetes as well, that HRV will go out of what ought to be considered acceptable normal ranges months or even years before those diseases take hold.

So what I’d like to see is HRV used as an ongoing wellness barometer, if you’d like. So I’d like to see normality of standards create for HRV measures, and for those actually to be something that people do, perhaps on their own initiative, but something that primary care physicians, general practitioners, etc., are happy to discuss.

[Damien Blenkinsopp]: Yeah, because — I mean, today we take our — if we go to the doctor for a standard checkup, we have our blood pressure and we have our heart rate, standard heart rate taken. What you’re suggesting is potentially HRV could be a better measure, and it should be included in those, if we could be more standardized and stuff, because you’d see it decline steadily over time if there were some chronic issues building.

[Simon Wegerif]: You would, and you would see it declining outside of a normal range. We exhibited — we launched the finger sensor in V3 of the Apple Consumer Electronics Show in Las Vegas in January. We probably did 200 demos during whatever it is, the three days that CES is on, and we had people who illustrated HRV values which, by looking at them, some of them were predictable, and in some cases, people really needed to pay attention. So we had a very large gentleman who came to see us, who said he got diabetes and he hadn’t been exercising recently, and he got 35 on the ithlete scale. And that shocked even him, because that is a very low number. I mean, that’s an extreme case, but —

[Damien Blenkinsopp]: Was that lying down or standing?

[Simon Wegerif]: No, that was sitting. So we did — all of these demos were done with people basically sitting at a table. But I would like to see some normative ranges exist for people. And also by tracking over weeks and months, that they’re able to do what I’ve seemed to been able to do, which is to basically find ways to keep my HRV increasing over the long term as opposed to declining with age. HRV is a very good forward looking indicator, and that’s why I sometimes call it a barometer. You know, it’s telling you about the weather to come, rather than the weather as it is right now. I would like to see it accepted and accredited.

And I think there’s been a useful start made in that area recently. There’s been this announcement about the Palo Alto prize, and that basically is, I think, either a half million or even $1 million award to researchers who can show initially in laboratory animals that they’ve developed techniques which would cause animals’ HRV not to decline over a period of time. The idea is that that will be applied to human studies later on, once the techniques are proven. So HRV is starting to become recognized now as a longevity indicator.

[Damien Blenkinsopp]: Right, right. You wouldn’t have seen it yet, but we also interviewed a guy named Todd Becker who’s very interested in hormesis and aging and longevity, and you might have read his stuff.

[Simon Wegerif]: Yup.

[Damien Blenkinsopp]: He plays around with that to increase HRV.

[Simon Wegerif]: I did read it. His article on HRV was excellent, really, really good.

[Damien Blenkinsopp]: Yeah, so he has some interesting points on that. Look out for the interview when it goes up, because it has some relation with this discussion.

So in terms of places where people could go to learn more about this, are there any people or particular journals where you think are good sources of information about HRV?

[Simon Wegerif]: One of my observations about HRV, there’s this massive body of research out there, but unfortunately it’s largely untapped, and I think that’s partly due to the impenetrable nature of medical research language. What we have tried to do is also to summarize a number of what we regard as some of the most important articles. So on the ithlete blog, we have done a number of research summaries where we’ve tried to take — captured the essence of what we regard to be some of the most important papers and put it up there for people to look at.

Also, we’re doing a new website where we’ll be putting more resources in there. I think Todd Becker’s article is an excellent introduction to HRV with a really good — a really good, if you like, approach to experimenting with different interventions on himself to see what made a difference. I think Andrew Flatt is doing some very good work at HRVtraining.com. There are a few sites around. And even Men’s Health carried an article or two on HRV over the past year.

[Damien Blenkinsopp]: Was that a good quality article, or was it just good that it’s getting the word out there?

[Simon Wegerif]: It’s good that it’s getting the word out there. I think reasonably brief at the moment. But HRV is getting more mentions in the mainstream press, which I think is important.

[Damien Blenkinsopp]: Great. Okay, so I’d like to round off with a couple of personal questions. I always like to get some information about how people like you, who’ve obviously spent a lot of time thinking about data on biology and working with it, actually make use of it. So what kind of data metrics do you track for your own body on a routine basis? HRV, I guess, obviously. But beyond HRV, or in the specific context of HRV?

[Simon Wegerif]: I’m always wrestling with how to quantify my training. So training load is something that’s interesting to me. And I don’t think that any of the existing measures are really adequate.

[Damien Blenkinsopp]: So is that — are you talking about cycling or — you’re talking about volume?

[Simon Wegerif]: Yeah, that is the point. So training load metrics, there are many of them. So how do you quantify any kind of workout? If it’s cycling, is it miles? Is that a good — is that a good indicator? Is it average heart rate? Is it something about zones, the amount of weighted addition of all the zones you are doing? In team sports, they use RPE a lot, which is rating of perceived exertion. They also do translations from GPS data using group statistics for acceleration levels and running speeds and things like that.

But all of this training load stuff, what are we trying to achieve exactly with respect to — you know, training is all about stimulus and adaptation. From what I can see in endurance sports, there’s two completely different kinds of stimulus that we provide to the body, both of which seem to be necessary, and both of which are very helpful. One is this aerobic stimulus, which some people call the long, slow distance, and the other one appears to be the high intensity stuff. So how should we quantify each of those, other than by observing Kenyan runners who win all the long distances races and seeing what they do? I’m really interested in the science and the biology and the physiology behind that.

There’s all the stuff about calories. How do we measure calories? Why do we measure calories? What exactly are we going to do with that information? That stuff is of interest to me. Calories was of interest, before I did this trans-Alpine cycling, because I wanted to lose weight, but I wanted to do it in a controlled way, and in a safe way as well. So I didn’t actually damage either my health or my sports performance, but I wanted to lose 7 kg, just a stone, a reasonable amount of weight, and I wanted to do it very safely.

[Damien Blenkinsopp]: So you focused on calories to do that?

[Simon Wegerif]: I ended up actually focusing on food types. So what I actually did as advised by my good friend, Dr. Mike T. Nelson, was actually just to deliberately introduce a lot more protein into my diet, and basically diet — there’s an easy way and a hard way to diet, and I think the hard way is to think about all the things that you can’t do. And I think the easy way is to introduce good stuff, and that will necessarily push out some of the other things.

And what I mean by that is — Mike’s advice, specifically, was to increase my protein intake dramatically. And one of the ways I chose to do that was by having a big omelet after training in the mornings every day. And that actually makes you much less hungry during the day for snack foods, biscuits, carbohydrates, things like that. I also asked my wife not to buy biscuits and not to put biscuits in the — or cookies in the cookie jar, so that those were just sort of taken out. I was also — with chocolate, I just said I’m only going to have two squares of 70% chocolate a day, and that’s okay. Because 70% cocoa chocolate is so strong that you don’t want lots of it anyway, but it does sort of just satisfy that need.

So by deliberately eating lots of protein, I basically pushed out quite a bit of carbohydrate, and that combined with the volume of training actually tailed my weight down quite nicely.

[Damien Blenkinsopp]: Right. You make an interesting point in calories, because there’s a lot of devices coming out to measure calories. One of the areas of investment. And obviously that’s been a huge focus for the last 30, 40 years in diet books and so on. However, there’s a fair amount of research now to say that calories are not necessarily the whole thing, input and output, and that it’s a bit more complex than that.

In our discussion with Jimmy Moore a couple of weeks back about focusing on fat. You focused on protein. He focuses on fat intake, and it has the same impact. It satiates you and you tend to lose weight, and you’re not counting calories.

Yeah, so this is arguing whether it is useful to count calories, and these are the kinds of discussions I love to bring up, because especially when the marketing and everything that is out there is saying, ‘Let’s count calories; it’s going to change our behaviors; it’s going to have an impact on our lives.’ But is it really as beneficial as it’s portrayed to be, or are there better methods, like we’re doing — we looked at using the ketonics, which measures your state of ketosis, and as long as you’re staying in a state of ketosis, you’re going to be losing weight. So there’s other approaches to it that may be more useful, depending on what you’re doing.

And the training load thing, I think, is also interesting, and difficult, as you said. There’s not really any measures. We talked to Doug McGuff from Body By Science. He has a very specific protocol which kind of allows to do that, but you have to use that exact training protocol; whereas, I think what we kind of really need to get to is like you were talking about, is we have the metabolic and the strength, or as you call it, the aerobic and the —

[Simon Wegerif]: The high intensity HIT.

[Damien Blenkinsopp]: The high intensity stimulus, and how do we quantify those? Is there any way to quantify those so that we can see what stressor we’re getting, and then we can see, oh, we got a decline in our HRV because it was that stressor. Right? And currently you’re trying to do this with qualitative measures, which is pretty much the best I’ve seen that exist today as well. I don’t know — so you haven’t seen anything? It seems you haven’t — on your journey looking for that, you haven’t yet found anything that might be better than a qualitative measure?

[Simon Wegerif]: No. I’m always looking for things which are practical, which people will actually do every day. So anything which is too complex to calculate, people might do it a few times out of interest, but then it’s not going to imbed itself as a habit.

One thing I will say about calories, though. This whole motto of ‘What gets measured gets done.’ So giving people some kind of feedback that they can relate to which motivates them is always important, and whether that’s steps or whether that’s calories, I personally don’t mind, so long as it motivates them to imbed good habits and to reach for smart targets and goals.

What I think the particular problem I have with calories is that, yes, perhaps you can measure calories out, calories expended. Calories coming in is pretty difficult, though, unless you’re really going to spend a lot of time not only looking at the back of food packets and weighing things out exactly, which can be done, but at the end of the day, it doesn’t seem to work out that well, either. I mean —

[Damien Blenkinsopp]: It’s very impractical. It’s very time consuming.

[Simon Wegerif]: It’s very impractical, and it doesn’t actually work out that well. So people who’ve tried to do this very exactly, like Nigel Mitchell, who is the consultant nutritionist for Team Sky and is a very well recognized and respected nutritionist, says that if you do this exercise exactly — so on professional cyclists, they use power meters. You can measure the exact number of joules that they have expended. They can also measure the efficiency of the cyclist in terms of oxygen consumption, they can work out very accurately how many calories in those guys should need, and even if you do do all the food weighing stuff and measuring and everything else like that, the weight balance doesn’t seem to come out exactly as you would have hoped. There’s some quite large inaccuracies in there, one of which I believe is potentially the fact that the calorie numbers on the back of the food packets are achieved by burning the product in pure oxygen and seeing how much heat it gives off, but to what extent does that really represent the way our digestive systems work? And do they always do the same thing with two forkfuls of pasta? Does it matter, you know, what else you’ve got in your stomach at the same time?

[Damien Blenkinsopp]: And your microbiome, which is another interview with recently did. Like, your microbiome can impact how you metabolize the food. So I think it is more than calories, and it seems like the research is steadily going towards that, but it actually seems pretty complex. You know, microbiome, the types of macro and micro nutrients that you’re consuming. But, as you say, if you’re counting calories, you’re potentially looking at helping yourself to behave better, so it potentially could help.

Just, I think there is a device and a crowd sourcing project which is tracking calorie input, so in a more convenient method, I think it’s still in crowd sourcing. I’ll put the link in the show notes, because I can’t remember the name of it, but it would be interesting to see if that one works out. Because, yeah, like noting down everything you eat is not something that I can see people doing for a very long time.

What has been the biggest insight about your own biology that you have drawn to date from any data or anything you’ve tracked?

[Simon Wegerif]: I will tell you, I haven’t mentioned before in this discussion, but it is actually HRV — so HRV biofeedback, which is another — another topic in its own right and may be one that you will cover in a future podcast, but one of the things in my journey to steadily increase my HRV was — I do tend to be quite a driven person. I do tend to get moderately stressed, and my wife is much calmer. She’s been doing yoga for a number of years, and she’s always told me, ‘Simon, you should try yoga breathing.’ And I must admit, I did poo-poo it a bit, until I actually had a chance to meet up with an old friend who was a yoga instructor, and he told me about breathing. And I started to relate that to HRV, and I built myself a little biofeedback app prototype, and that, over a period of just a few days, made a big change upwards in my baseline for about 5 or 6 ithlete points.

And that was a really — that was a really big insight for me, that I could increase my HRV and feel much better quickly by using basically guided, deep diaphragmatic breathing. And there are good reasons as to why that should work.

[Damien Blenkinsopp]: You were tracking — you were doing this for, like, what 10 minutes a day or something like this? And you were using an HRV device to see if you were raising it? Or were you just using the HRV for training every day, and just watching it? So it was like an experiment?

[Simon Wegerif]: It was like an experiment. I did my ithlete reading every morning, and then, I mean, you couldn’t help but notice how much it had swung upwards when I started doing this breathing practice. And what I found even more surprising was that when I experimented again by not doing it for a few days, my HRV remained elevated. So it seems to have a chronic effect on upwards HRV. And I think this is a technique that’s got a lot of potential for the future as well.

[Damien Blenkinsopp]: Yeah, very interesting. Great, great point. Okay, last question. What would be your number one recommendation to someone trying to use some form of data to make better decisions about their body’s health or performance?

[Simon Wegerif]: I think it would be do it consistently. Do it consistently. Preferably, you know, every day or several times a week, and do it for a period of time. And when you’re trying to — if it’s a measure that you’re trying to improve, like HRV, try to change just one thing at a time to see if that thing does make a difference. So just be a little bit scientific in what you do and how you do it. Because otherwise, you know, there’s so much data around now that actually deriving information from that data is in some ways getting harder, because there’s more and more data, more and more variation in it.

[Damien Blenkinsopp]: Great, great point. And yeah, the information overload is going to get worse as time goes on, because there’s so many devices and things coming out. I know I already have too many devices, and I’m trying to decide which ones I focus on. And HRV happens to be one I very consistently do, because it is very rewarding, and I notice the changes.

So Simon, thank you very much for your time today. It’s been a great discussion, and I can’t wait to put this out on the podcast.

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When we think about health risk, and reducing it, most of us are thinking about cancer, heart disease and strokes.

Autoimmune and other chronic health conditions aren’t top of mind, because they don’t tend to get the same attention in the media – and have much smaller research budgets currently.

But if you look at the numbers you are statistically much more likely to face autoimmune problems in your lifetime than heart disease or cancer or stroke.

In the US at any one time it’s estimated there are 9 million cases of Cancer, 22 million of heart disease and between 23.5 to 50 million cases of autoimmune disease. (Source: National Institutes of Health, American Autoimmune Related Diseases Association)

Autoimmune disease is becoming a growing collection of diseases as researchers identify more and more diseases which have autoimmune mechanisms behind them. Diseases assumed to be included are big names like Alzheimers, Parkinsons and Arthritis to name the best known.

I’m guessing that you did not miss the ALS ice bucket challenge to raise awareness and funding for Amyotrophic Lateral Sclerosis. 30,000 people have this condition in the US, and its one of the diseases which most likely falls into that 50 million bracket. Because of the small numbers it took a viral campaign to bring attention to ALS – which most people haven’t heard of.

But if we came to understand autoimmune diseases having a common mechanism – like mitochondrial health, that could quickly change how we look at treating all of them.

Today’s guest is currently running clinical trials to evaluate the impact on autoimmune disease of a “simple nutrient dense” protocol – a protocol that enabled the researcher herself to recover from one of the worst autoimmune diseases – Multiple Sclerosis. The basis for her protocol was supporting recovery and repair of the mitochondria.

Dr. Terry Wahls was diagnosed with secondary-progressive multiple sclerosis in 2003. This is the irreversible form of MS and by 2007 the disease had progressed to the point that she was restricted to a wheelchair and unable to walk.

But in 2007 she turned her condition around, taking her first steps within 3 months, and riding a bike again before the end of the year. Hers is the only known recovery from Secondary Progressive MS, and has been based on insights she took from published research on mice mitochondrial health amongst other things.

Dr. Wahls is also now the author of the Amazon Bestseller: “The Wahls Protocol: How I beat Progressive MS Using Paleo Principles and Functional Medecine” which describes her protocol.

In this interview we dig into the details of her current clinical trial, some of the biomarkers she tracks, and her views on linking mitochondrial health to autoimmune and chronic disease, and how nutrient based treatments can work to heal these conditions.

The show notes, biomarkers, lab test and links to Terry Wahls and everything else mentioned are below. Enjoy!

itunes quantified body

Show Notes

  • Terry Wahls explains her degree of recovery as it stands today including remaining symptoms from Secondary Progressive Multiple Sclerosis and gives the context to this recovery, as she is the only known case
  • An overview of the clinical trails that Dr. Wahls has been leading, their current status of progress, the results and the research to be done as next steps
  • The broader range of autoimmune, neurological and chronic diseases that Dr. Wahls is treating with her protocol
  • The top areas Dr. Wahls is receiving positive feedback as to efficacy of her protocol – including Multiple Sclerosis, Parkinsons, and other autoimmune diseases
  • Improvements in quality of life and performance that healthy controls, such as the researchers working on the trials, have experienced with the Wahls protocol
  • An overview of the Wahls protocol and how it works
  • The methylation, epigenetic and mitochondrial mechanisms behind disease and why the symptoms vary so much despite having similar mechanisms behind them
  • The concept of “nutritional reserve” and how it can be a balancing act as you recover to keep this building (especially where travel is an aspect of your lifestyle)
  • How the Wahls protocol provides for many many times the RDA nutritional recommendations and why
  • The list of biomarkers Dr. Wahls uses in her clinic, in her clinical trials for research and for her own personal tracking.
  • Dr. Wahls’ view of the effective use of the various testing labs currently available considering economics and insights or useful information they can provide.

Biomarkers in this Episode

  • Serum Vitamin and Nutrients: Dr. Wahls uses standard blood vitamin and nutrient labs to follow her own progress. She likes to see the values in the top quartile (top 25% of reference range), and mentioned specifically the B vitamins, this would be including Vitamin B12 and Vitamin B9 for example.
  • In Dr. Wahls Clinic she uses:

  • Lipids (e.g. LDL, HDL, Triglycerides, Total Cholesterol): Markers of cholesterol are commonly used with primary docs.
  • Homocysteine: An indicator of inflammation and of how well your methylation processes are running. Dr. Wahls likes to see this acutely improve.
  • hs-CRP (High Sensitivity C-Reactive Protein): A predictor for heart disease, more pain with fibromyalgaia and Terry uses to track progress via lowering inflammation. Dr. Wahls likes to see this improve significantly by declining, and that it takes some time to decline.
  • HbA1C (Glycated Hemoglobin): A proxy measure of your average blood glucose levels over the last 3 months.
  • Fasting Glucose: A measure of your blood glucose in a fasted state.
  • Micro Systems Questionnaire: Dr. Wahls uses a very detailed list of symptoms to use like an index to watch with parents, and watch their progress (e.g. as the number of symptoms decline).
  • In Dr. Wahls Clinical Study for learning purposes she uses:

  • NutrEval from Genova Diagnositics: Vitamin and anti-oxidant levels in the cell, How well enzymes are performing in the krebs cycle and electron transport chain and the fats.
  • Urine Toxicology: Using a challenge like DMSA, Dr. Wahls looks at the presence of heavy metals in the body.
  • Microbiome: Tests that look at the biome of the gut and the ratios of different bacteria that are occupying it.

Lab Tests from this Episode

  • NutrEval: Dr. Wahls uses this specific test in her current clinical trial – at this stage primarily to see what patterns emerge.

Other Resources Mentioned in this Episode


Interview Transcript

Transcript - Click Here to Read
[Damien Blenkinsopp]: So, Dr. Wahls, you had a diagnosis of secondary progressive multiple sclerosis, which is worst case, as I understand it. Could you explain briefly about what that diagnosis means?

[Dr. Terry Wahls]: Most people, I would say 80% of the folks with multiple sclerosis, are diagnosed with relapsing Multiple Sclerosis. And in that case there is an episodic worsening disease called the relapse, and improvement, called a remission. Most people’s relapse will be well within 15 years, and convert to secondary progressive.

So they have no more spontaneous improvement, they simply are experiencing the gradual sudden decline. In my case I was diagnosed in 2000 but within three years I had already transitioned to that steady decline and was in that secondary progressive phase.

[Damien Blenkinsopp]: All right, so in a typical situation is there any remission from the secondary progressive stage?

[Dr. Terry Wahls]: I don’t believe any have been reported other than mine in the scientific literature. There are some books talking about improvements, but if you are looking for a case report I am on the only one who has reported an improvement like that.

[Damien Blenkinsopp]: Great, so do you consider yourself in remission today? What remaining kind of symptoms do you have?

[Dr. Terry Wahls]: I am very clear that this is not a remission because this is not in a disease phase that has remission. The fact that I have improved to such a dramatic degree really means that the current understanding for multiple sclerosis has some gaps in it because this would be considered not possible. We have done clinical trials to show that in fact this level of improved function appears to be quite possible in others as well, not just me.

[Damien Blenkinsopp]: So today what symptoms do you still have? Or do you have any?

[Dr. Terry Wahls]: I am not as strong as a 58-year-old woman my age, so I can stand easily to give a lecture for an hour but if you ask me to stand for two hours that would be difficult. That is still fatiguing. I can go out and jog a mile and a half because I am continuing to improve. I have faith that will continue to improve.

My strength continues to improve remarkably but it is probably not quite as strong as you would expect for a normal, fully-healthy, athletic, 58-year-old woman. I want to stress the key point that I am continuing to steadily improve.

[Damien Blenkinsopp]: Great, that’s great to hear. I am very glad to hear that. What are the areas that you are targeting? You just mentioned your clinical trials. What are they targeting? I heard one explanation around your latest study was clinical trials are to prove the effectiveness of a nutrient-dense Paleo diet to reduce autoimmune disease symptoms. Is that kind of the best definition?

[Dr. Terry Wahls]: Actually, that’s really pretty close. I am very interested in diet and lifestyle and I studied that for traumatic brain injury and I am studying that for multiple sclerosis. We are writing grants to study it in other disease states as well, such as fibromyalgia and Parkinson’s disease. So we will see if we can get other people interested in funding it as well.

[Damien Blenkinsopp]: Great, great. So right now it is very multiple sclerosis-focused?

[Dr. Terry Wahls]: Right, so that is where I have the relationship and the funding sources, with a foundation that is particularly interested in multiple sclerosis-related research.

[Damien Blenkinsopp]: So the first study, the pilot study, was about 20 people. Could you give a very quick update on where your studies were?

[Dr. Terry Wahls]: Yeah we had initial funding to study 20 people using the diet, some targeted vitamins, meditative practice, exercise, and electrical stimulation of muscles. Because this was such a radically new concept the institutional review board, which is the safety committee that monitors research, told us that we can enroll ten, run the study with the ten, give them safety data, and then come back and enroll the second ten.

So we have published our results from the first ten that we got enrolled and that came out in the Journal of Alternative and Complementary Medicine. And the big challenge was finding other scientists who felt comfortable reviewing an intervention that was so broad-based, so that took a bit of time to find the appropriate reviews.

[Damien Blenkinsopp]: Okay, because normally they are trying to control the variables so it is changing one thing, but you have got many interventions stacked together there.

[Dr. Terry Wahls]: Right, and that is a very unusual study design. We were really testing with good people to implement the same, very complex regimen that I did and could it be done safely. It is called the safety feasibility study. So we want to know that people can do it and that you don’t hurt anyone. Because these are small studies all you are really hoping for is to have a trend in a favorable direction because it is [inaudible 00:09:23].

[Damien Blenkinsopp]: Okay, great. and you have another study underway now. Could you talk a little bit about that one?

[Dr. Terry Wahls]: Yes, so we have actually a couple of studies I am involved with. Because the first study used diet, vitamins, meditation exercise [inaudible – 00:09:43] and we wanted to begin to break apart the study to see how important those race components were.

So i have one study that is looking just at the exercise [inaudible 00:09:53] portion of the intervention and another study that we’re recruiting furiously for right now – which is a diet and lifestyle intervention where we are really just focusing on teaching them a Paleo diet that has been structured in a very specific way to maximize nutrient density.

[Damien Blenkinsopp]: So kind of summarize what the Wahls protocol is – how would you summarize it? Is it 80% nutrient?

[Dr. Terry Wahls]: This is really very intense nutrition. I stress vegetables, green leafy vegetables, sulfur-rich vegetables from the cabbage, onion, and mushroom family, and deeply colored. So if you’re a guy or you’re a very tall lady, that is 9 cups a day. If you are petite it is going to be much smaller, perhaps in the 4-6 cup range.

And the protein is sufficient protein, like 6 to 12 ounces of meat a day. And in the first level we can do it for vegetarians and vegans then as we advance I have some additional requirements to then move the diet to a more ketogenic diet for the more advanced person.

[Damien Blenkinsopp]: In terms of advanced do you mean people who are dealing with the worst severity of symptoms or as they get used to compliance and getting used to it?

[Dr. Terry Wahls]: Well we are testing in my clinical trial to see if the ketogenic version is more defective that the standard Wahls version, so I don’t have the answer yet. In my book I talk about why ketogenic diets may be beneficial and the research that is going on in the ketogenic diet around seizures, chronic headaches, schizophrenia, Parkinson’s, and my research in MS – there is also a lot of research with cancer and ketogenic diets.

This is a very exciting area and it may be another decade before we have the full answer, but I am thinking for those who are highly motivated, highly interested in a ketogenic diets, there are health benefits. I talk about the potential risks of a ketogenic diet as well. So it gets much, much harder to maintain really excellent nutrition while in ketosis over the long term.

[Damien Blenkinsopp]: Is that because you are limited in the vegetables you can eat?

[Dr. Terry Wahls]: Yes, absolutely.

[Damien Blenkinsopp]: Okay, great. So talking about your book a bit, the Wahls protocol is positioned a bit more broadly than just multiple sclerosis. Can you talk about who you are aiming at with the world’s protocol and the book?

[Dr. Terry Wahls]: So what i have discovered in my clinics time and time again is that by using the Wahls protocol to restore the health of the cell, the health of the person over the next three years steadily improves. They often need fewer and fewer drugs. The weight falls off without being hungry, blood sugars, blood pressures normalize often to the point where no medication is needed.

The most immediate people who are going to benefit are the folks with autoimmunity or folks with a lot of pain and the docs can’t make a diagnosis. But we’re also observing that people with medical problems requiring medication often find that their medication needs steadily decline. the mental health problems also often steadily improve – anxiety, depression, irritability, focus, autism, and other neurological disorders.

We have many, many folks with Parkinson’s who have reached out to say that their symptoms do not include [inaudible – 00:13:38] and of course the folks with MS who are telling us how much they have improved as well.

[Damien Blenkinsopp]: Right, so that was my next question – where are you getting the most feedback in society as you spread the Wahls protocol and the word about it? Which areas have you heard the most feedback from people that have these positive results?

[Dr. Terry Wahls]: Multiple sclerosis and then Parkinson’s probably next. Diabetes would be probably third and then fourth I would say I have so many folks with a wide variety of autoimmune problems that are telling us that symptoms have been markedly reduced. Many of these autoimmune diseases I have not encountered before so it just lets you know about the diversity of autoimmune problems with inflammatory bowel disease, psoriasis –

[Damien Blenkinsopp]: There are like over 160 classified –

[Dr. Terry Wahls]: Yeah, and we keep adding many, many more every years. I would not be surprised if in the next two decades we begin to rethink our autoimmunity to the point where it is a matter of nearly every chronic disease having some level of autoimmune component. That is my prediction but we will see if that turns out to be the case.

[Damien Blenkinsopp]: That is very interesting. So moving kind of away from health issues and also a bit more generally, on Dave Asprey’s Bulletproof Radio you mention that some of your research staff have been using the protocol and I think also they also followed the protocol so that they understand it and while they are all healthy they have noted some positive impacts as well.

[Dr. Terry Wahls]: Yeah, actually it’s really interesting. So students come volunteer in my lab and I ask them to fill out the forms and follow the diet for a couple of weeks just so they get a sense of what our subjects have to do. So these young kids are healthy, robust, and we think at the peak of their game and they nearly always discover that their attention improves, concentration, memory, sleep, and mood improves.

Several kids had their chronic headaches go away. And a couple others realized that some of their family’s health issues could be addressed by diet and lifestyle and this had a really nice favorable impact on their extended family.

[Damien Blenkinsopp]: That’s great to hear. We have been talking a lot about acute conditions before but in terms of long term disease prevention, risks, aging, and potentially talking about cognitive performance, improvements, less headaches, and so on, do you think there is a lot of application for these areas as well, beyond the acute illness and where it started from?

[Dr. Terry Wahls]: This will be very beneficial for chronic health problems. Certainly in my book I talk about autoimmunity a great deal and then I acknowledge that my other medical issues that we don’t think of traditionally as autoimmune also seem to be dramatically helped with weight issues, diabetes, high blood pressure, cholesterol problems, mental health, and the traumatic brain injuries that I followup and take care of.

[Damien Blenkinsopp]: That’s a very broad area. In term sof the areas you see it positively impacting, are there any similarities of the issues? What are the underlying mechanics? Like the way that you are looking at it today, how that is being addressed?

[Dr. Terry Wahls]: I am looking at the health of the cells and the effectiveness of the mitochondria. And so I am looking at the nutritional needs of the cell and how to provide them using food, because I think food is safer than supplements and probably much more effective. And so with just the mitochondria you need basically all the B vitamins and you are going to need minerals, magnesium, zinc, and sulphur.

You need a lot of fats, the omega-3 and omega-6 fats, the saturated fats, cholesterol fats, to make healthy membranes. Then you have to protect the mitochondria so things like zinc, mercury, and lead, and some of the [inaudible 00:17:51] that we take a lot of, like antibiotics, which are tough on our mitochondria. And by maximizing cellular nutrition then we start much more effectively having our epigenetics factor set.

We have basically more efficiency in all of the biochemical processes in ourselves, which over time will lead to healthier organs and of course a healthier person. Some things go away very quickly like the fatigue and the brain fog. Often that is dramatically better within 12 weeks. Things where you have to replace or rebuild proteins that may take one to seven years, depending on what organ in the body you are trying to rebuild.

[Damien Blenkinsopp]: Right, so do you have a theory as to why are mitochondria behind autoimmune disease? There is a whole variety of issues taking place in the body. Do you have some kind of underlying mechanism as to how this works and how the damage is caused to the mitochondria in the first place?

[Dr. Terry Wahls]: Well I think there are many, many reasons our mitochondria can get damaged. The toxic load that we are all exposed to continues to climb every year and many of these toxins will have negative impacts on some of the proteins involved in the mitochondria and how the mitochondria manages the electron transport chain. So that is one problem, straight up. Just direct toxic effects for mitochondria.

These toxins in addition to the direct toxic effects will interact with the DNA, putting adducts on the DNA, and causing certain parts of our DNA to be read and other parts to be silenced and not read, so that shifts how my DNA would have been read by the presence of these toxins. And that changes our biochemistry.

[Damien Blenkinsopp]: Are you referring to – is that working for methylation processes?

[Dr. Terry Wahls]: Methylation is one of the processes and I will also predict that we don’t really understand all the ways that epigenetics impact their DNA. Methylation is one way and changing the histone protein is another way. And we may find that there are even additional ways that we have not yet unraveled.

But clearly toxins are interacting with our DNA, turning genes on and off without changing the actual DNA sequence. So we have lots of toxins that are doing this. And some of those toxins, by the way, include the drugs that we take and the antibiotics and the things that have gotten into our groundwater. And of course all the food and indoor environments, etc.

[Damien Blenkinsopp]: Great, so in terms of I think for people at home to understand, it is like if the mitochondria are behind the problems you are encountering, why is there such a wide different variety of conditions, such as Parkinsons?

[Dr. Terry Wahls]: You know, that is really something I talked about in my book and that conventional medicine, over 100 generations of stuff. We have been classifying diseases based on the history, the symptoms, physical exam, and then more recently laboratory testing. And we did all of that before we understood the molecular basis, how these diseases evolve.

But what is startling to physicians and scientists, and medical students as well. Now that we begin to understand the molecular basis of these diseases, with what is going on at the molecular level, the cellular level, we are seeing that the diseases look more and more alike. There is often inappropriate inflammation of the body attacking itself or having too many inflammation molecules.

We have mitochondria that are not generating energy appropriately with too many free radicals being generated, causing early aging. We often have a sense of excessive toxic exposure and toxins are stored in the fats and in the tissues. We’re seeing the production of inflammatory molecules.

We often have problems with the gut with the wrong bacteria mix living in our bowels, created a leaky gut and allowing for contents within the bowels to slip into the bloodstream and bringing it along with them for some bacterial protocols with incompletely digested foods, all of which will create more inflammation in the body. What is so startling is we see those same core abnormalities whether or not the person has schizophrenia, depression, diabetes, MS, chronic fatigue, fibromyalgia.

We see a slightly different mix but those same, less-effective cellular processes are present to varying degrees in nearly every chronic medical problem, mental health problem, neurological problem, or autoimmune problem.

[Damien Blenkinsopp]: Yeah, do you think that the pattern that shows up in each person is probably down to genetics and epigenetics?

[Dr. Terry Wahls]: Well actually the pattern is maybe 5% or less epigenetics. The rest, the 95%, is due to the environment, and that includes diet, activity level, toxic exposure, and stress level, probably as the big four. Then infection, exposures, family relationships, social bonding, social networks, and all of that will interact probably through the person’s epigenetics to some degree directly to toxins in the cells and nutritional deficiencies to the cells themselves is another thing.

All of those are factors and because we’re all unique with our unique DNA, so even if i had a twin sister and we share the same DNA and we grew up in the same house we would still have differences in our environment and it would be enough to affect those genetics slightly differently and to create a different health status for both those individuals.

[Damien Blenkinsopp]: Right, another thing I think is interested is – I was diagnosed with chronic fatigue syndrome and one of the first things I was looking at was MS – multiple sclerosis – because I had difficulty walking and a symptoms list which kind of fits with that at first. As you were talking about it already, you are talking about the list of symptoms as a diagnosis but it can be very difficult to judge based on symptoms.

I think there are a lot of diseases which we have in categories which often have a list of very similar symptoms and the differential diagnosis isn’t being made in a lot of the cases and it is kind of a fuzzy line at the moment. So do you think instead of my presentation here which is potentially I have something which is chronic fatigue/MS, where I had that, and then somebody else has maybe 100% MS is the classification. And there are all these mixes out there but they are getting split into different categories based on who looks at it.

[Dr. Terry Wahls]: You know, one of the things I’m observing is that [inaudible 00:25:41] Clinic, where we treat people with chronic health problems and they can be mental health problems, physical problems and the big thing that they have to do is agree to the diet and the lifestyle, and [inaudible 00:25:53] for them.

And what I find is I am less and less interested in the names of their diseases and much more interested in diagnosing all their environmental factors addressing those. And I will use the same types of interventions across many disease states and I find that to me the most important thing I need to know is diagnosing their diet and lifestyle choices and exposures that they are doing and helping them address those. my young students are intrigued that my approach is so different to what they were taught. And it appears so remarkably effective, although making the diagnosis is far less important than understanding a person’s diet and lifestyle issues and diagnosing that.

[Damien Blenkinsopp]: Right, that is very interesting because then you can look at the weakest areas of someone’s lifestyle, if you have a blueprint for a more ideal lifestyle.

[Dr. Terry Wahls]: Oh yeah, and you have to work with them, work with their family, have them evolve this collaboratively. So if you are in my trial you have to evolve in one fell swoop in the trial, but if you’re in my clinic we negotiate with people to adopt these concepts at the pace they are willing to live with.

[Damien Blenkinsopp]: Yeah, because compliance can be an issue with a lot of these diets. So just going over the Wahls protocol in a bit more detail, there are some things that you want to remove? Can you talk quickly about the items you want to remove from a diet and why?

[Dr. Terry Wahls]: Well I look at what are the foods that at least in Westernized society are most likely to cause abnormal immune response and the top on is gluten-containing grains, the wheat, rye, and barley as most common. But many of the ancient grains have gluten so it is not – you want to reduce those gluten grains because the gluten and dairy overlap and you also take away all the dairy proteins, so we take out dairy as well.

And because the third most common is eggs we take out eggs and then in my book I give people directions on how to take out the next level of problems if that more simple approach doesn’t resolve things for them.

[Damien Blenkinsopp]: Yeah, so is that just [inaudible 00:28:20] or are there other items as well? Does it get more complex than that?

[Dr. Terry Wahls]: That’s the top three and then it’s a much more sophisticated conversation about what else to consider. And I am really very reluctant – some of the Paleo authors give people a very detailed elimination diet but from my perspective you are just increasing the risk of micronutrient deficiency when you have an excellent probability that just taking those three out would have a dramatic, favorable impact.

Now, if it doesn’t then you may need to go through a more comprehensive elimination diet in a step-wise fashion. That’s the approach that I am more comfortable with and I have had marvelous success.

[Damien Blenkinsopp]: Have you seen – because you emphasized it is pretty much a heavy intake of micronutrients in terms of the variety and the [inaudible 00:29:16]?

[Dr. Terry Wahls]: Oh yeah, and the rationale for that is I am a very simplistic thinker. So when I look at the literature I see the traditional society is still eating the traditional foods, traditional lifestyle, and eat radically different things in each locale but what is consistent is there is an extraordinary micronutrient density of vitamins, minerals, and fats per calorie.

Now, there is a huge variety in what the percent of fat, protein, and carb is across the various localities. So my interpretation of that data is that our mitochondria are actually quite flexible. They can burn sugar, fat, or protein and get energy for us to run the chemistry of life. But it appears that our ancestors identified what foods would give you the highest micronutrient density.

Sometimes it was going to be a fat-based diet, sometimes it was a protein-based diet, and sometimes it is a carbohydrate-based diet. So I then went around and used science to help me figure out what were these key micronutrients I could track as I designed my diet. So now we have 36 that we track and then I designed a diet using foods that I could get through agricultural means that would give me the various antibiotics, vitamins, minerals, and fats that science says my brain needs.

And once I redid my diet like that it was dramatic – within three months my fatigue was gone and I clearly was beginning to recover.

[Damien Blenkinsopp]: About your recovery, one of the things I heard you mention before is nutritional reserve and how at the beginning you would have something like a 36-hour crash window if you weren’t continuing to take in the amount of nutrients that you are currently doing.

[Dr. Terry Wahls]: Yeah, and now in retrospect I think in the first two years or even three years from my recovery is as I was improving I still hadn’t had enough recovery yet so that when I traveled, because I was now having enough energy to travel again, that my vegetable intake dropped and then my fatigue would come back, my brain fog would come back, and I would be craving greens. So I would come home to this huge salad bowl of greens which I would immediately scarf and begin feeling better.

[Damien Blenkinsopp]: Just out of interest, how long would it take you to feel better?

[Dr. Terry Wahls]: About 24 hours – actually probably 12, because I would eat that after I got home that night from my flight and then by morning my thinking was more clear and my energy was back up. And then I began to travel with a head of cabbage because that travels easily and you don’t need to refrigerate it.

I would just consume that and it seemed to work pretty well. Now I am well enough that I don’t need to travel with food, so if my vegetable function dips for a couple of days or a weekend that doesn’t bother me now. Again, because I think I have so flooded myself with nutrition that they just have a lot more reserve than they had before.

[Damien Blenkinsopp]: That is great – so the first 20 or 30 years of your life and you didn’t have multiple sclerosis, do you think eventually if you built up enough nutritional reserve you could walk around for a week – I imagine that in your 20s most people weren’t eating an ideal diet and you can eat that kind of thing, or do you think there is no way, like once you have had some kind of condition you already have to be very compliant with this for the rest of your life if you want to keep symptoms at bay?

[Dr. Terry Wahls]: Those are great questions. My observations from our clinical trial is if you deviate from the protocol you lose ground. If you go back to giving yourself substandard nutritional support and things will begin to decline and you will end up with more rapid aging and probably more diffuse symptoms.

[Damien Blenkinsopp]: All right – in terms of how much we’re talking about here, if we think about someone who has got a typical modern diet and someone else who has got a typical kind of Paleo diet, how much more vegetables are they eating every day?

[Dr. Terry Wahls]: Well when people come in – and I am trying to give this to you from memory here – and I believe that based on fruit and vegetable intake it was one-and-a-half servings a day. At 12 months the typical intake was seven-and-a-half. And most of our people are women and we just had a couple of guys so they were really doing an extraordinary amount of fruits and vegetables.

My nutrition colleagues told me that in the nutrition science world if you get someone to shift their vegetable intake just one serving up a day that is considered a phenomenal success. And for us to have shifted the vegetable intake from one-and-a-half up six more cups, she is thinking it was unheard of and no one had been able to do that previously.

[Damien Blenkinsopp]: Yeah, that’s pretty impressive and there are more benefits for the people on these trials than the average I guess. In terms of recommended daily amounts you are far exceeding the nutrition values of recommended daily amounts. What do you think about the recommended daily amounts of the vitamins and so on? Do you think they are sufficient for everyone and sufficient for some people?

[Dr. Terry Wahls]: Likely not because they are designed to prevent you from going into an acutely diseased state associated with that particular vitamin or mineral. So we will take, for example, vitamin C. They set a level to prevent you from acquiring scurvy, which is vitamin C deficiency.

But we don’t know what level is required for optimal health, which might be 50% more or 500% more, but I think what might be a more valid way of thinking about this would be if we looked at what were the RDAs that people hit who were eating traditional foods, traditional diets, and traditional societies, that likely those societies over time that figured out how to get these micronutrients for optimal health.

And when we use those values the intakes are two-to-ten-fold above the RDA depending on the nutrients. And actually that was one of my goals, to get my nutritional analysis pattern to look like hunter-gatherer societies to get two-to-ten-fold and we get two or maybe eight-and-a-half fold. We are very pleased.

[Damien Blenkinsopp]: And so from the safety standpoint of your pilot study, one of the ideas was to see if you are doing 1000% RDA?

[Dr. Terry Wahls]: We get as high as eight-and-a-half times the RDA from food. And again it looks very much like the hunter-gatherer societies. The biggest side effect was if you are overweight or obese you lost weight without being hungry and got back to a healthy diet again.

[Damien Blenkinsopp]: Okay, and there were no toxic issues at all?

[Dr. Terry Wahls]: No toxic issues. Some people had – some of the vitamins had some GI upset, some nausea. And we told them that if anything seemed to bother you just to skip it. So they did and we had a few people who couldn’t eat as many greens as we advocated so they just titrated down to what their tummies would agree to.

[Damien Blenkinsopp]: But I guess that would be down to like the ability to process – ?

[Dr. Terry Wahls]: Well that’s right. It’s microbial, it’s deficiencies of their own particular enzymes, so there is probably a combination of who have got living in the bowels and what was the efficiency of the set of enzymes that you have that you are born with. And it would seem that some people do not metabolize sulphur quite as well so they need either more sulphur or less sulphur in their diet and how their enzymes are working.

[Damien Blenkinsopp]: Right, I think some people have – I think I have a partial issue with this, detoxification of sulphur. So too much sulphur can cause issues because you have to detoxify it as well.

[Dr. Terry Wahls]: We are all unique. And I stress that in my book, that we are all unique. I have got a public health message out here that will be good for everyone, but I certainly can’t guarantee it will be good for an individual so they have to really pay attention to how well they feel on this and work with their personal stock because they definitely may need things adjusted because of their unique DNA and unique health issues.

[Damien Blenkinsopp]: So which types of biomarkers are you looking at when you are tracking this data and you are in the clinical trials?

[Dr. Terry Wahls]: It was divided into two questions in my clinical practice. We don’t do any fancy functional medicine testing. We do things that primary care docs will feel very comfortable using – lipids, glucose, hemoglobin A1c, B12, folate, C-reactive proteins, and homocysteine levels. Primary care docs should feel comfortable looking at that stuff. In my clinical trial we are doing things just to see how they change over time and I am not changing my protocol based on these results.

We are just trying to learn the mechanisms of what is going on. So we measure things like who and what is growing in the poop for microbial analysis, what heavy metals are showing up in the urine, so that is the toxicology. And that is done with a very mild kelator. Then I do a nutri-eval, which is by Genova Diagnostics, which gives me a detailed look at the vitamins and antioxidant levels within the cells, a really nice look at the generation of HET to the mitochondrial electron transport chain and how well that’s working.

It gives a nice look at the fats and how the fat metabolism is working and making the long chain fatty acids or arachidonic acids, [inaudible 00:40:01] acids. We get lots of detail that we will be able to use to write up our papers and project why we have these very lovely results that we’re seeing.

So that’s fun research stuff. It is not what I am doing in clinic and in clinic what I am finding is careful history, a thoughtful exam, and some very simple labs like primary care docs get a lot of the time.

[Damien Blenkinsopp]: Because you are working with patients who are working with other people so you are talking about the language here that you are enabling the patient by using language that they can talk to with other people easily?

[Dr. Terry Wahls]: Yes. So we want to address that lifestyle. We want to have some guidance. I do use these labs. You need to think about functional medicine things but you don’t have to spend tens of thousands of dollars for functional medicine assessments. You could just address all the lifestyle stuff very thoughtfully and very comprehensively, get someone to do a thoughtful history for you and I would say there is probably a 90% probability that your health will steadily improve as a consequence of those actions.

[Damien Blenkinsopp]: And you would be tracking that based on symptoms and how the patient feels?

[Dr. Terry Wahls]: Yeah, the most sensitive ritual that we have is what we call the medical symptoms questionnaire which I have got in my book. It’s a detailed list of questions asking about how your eyes and ears and nose – it goes through your entire organ system and you can get scores from zero to I think almost 300 points if everything is not working.

So that is a very nice way to look if the chemistry of all of your organs are working well or if there is some level of problem. And that is the best number for us to track with how well people are doing and how well we are doing for them.

[Damien Blenkinsopp]: Great. In terms of – like, you mentioned some things and everyone accepts today the chronic headache pains for example. Would you consider that as a condition, a symptom that shouldn’t be there?

[Dr. Terry Wahls]: Absolutely. And again, I have many people with chronic headache pains and we get them to address the diet and lifestyle issues. And those headaches finally resolved.

[Damien Blenkinsopp]: So amongst all the blood tests you have mentioned and you said they use them because it is easier to talk with our primary care doctors, do any of them ever stand out as interesting? You mentioned the symptoms list is actually the most interesting. But you mentioned inflammation markers, homocysteine -?

[Dr. Terry Wahls]: Well homocysteine and CRP are acutely – I would like to see those improve. That tells me there is too much inflammation or the brain can’t metabolize the vitamins very well. And then the hemoglobin A1c lets me know how many carbs they are eating, how much insulin they have to use, and trying to get that number lower and lower. That takes a little bit more time but again that is a very helpful intervention to follow.

[Damien Blenkinsopp]: Great so CRP, as far as I understand it that isn’t really related so much to autoimmunity. That would be more related to dietary inflammation?

[Dr. Terry Wahls]: And again I predict that in ten more years we are going to overlap that together. More and more disease states we are recognizing. If your C-reactive protein is elevated you have too much inflammation in the body and that is a predictor for worse heart disease, worse risk for stroke, more pain with your fibromyalgia, so it is an independent risk factor and if we get people on nine cups of vegetables a day, get rid of the gluten and dairy, that CRP will typically fall.

[Damien Blenkinsopp]: Okay, because I guess your protocol is so nutrition based, in terms of the tests you are doing I think it is mostly nutribalance and blood plasma tests for vitamins – what interesting things have you seen in terms of nutritional status? Have you seen any patterns in the people you get where it is showing up that their nutrient status is very low or with different patterns?

I spoke recently with William J. Walsh. He has worked with brain neurology for many years and he found some nutritional deficiencies were driving or often contributing to symptoms of schizophrenia or other diseases and correcting those would help them. So I am just wondering to what extent you might have seen some kind of patterns where specific nutrients are showing up a lot?

[Dr. Terry Wahls]: Those analyses are ongoing right now and I can’t comment yet.

[Damien Blenkinsopp]: Okay, no problem. If you were looking at – because we spoke a lot about mitochondria and what the status of those are and if you wanted to understand from a more testing standpoint the status of the mitochondria. Are there any particular tests you would look at with the nutrival test or any others that would be useful to understand what is going on with the mitochondria?

[Dr. Terry Wahls]: Nutrival is certainly one that I would use. Several of these functional labs have tests and use the nutrival, that can give you insights into how well the enzymes are performing at every step of the electron transport chain and the Kreb’s cycle. That can be very helpful to follow that over time and then provide nutritional support and free enzymatic steps that appear to be blocked.

And that would just – order the nutrival and follow those guides along. But again I remind your listeners that one can do that if they have had diet and lifestyle interventions very effectively for a year and haven’t gotten where they want to be. These tests are extraordinarily expensive and you follow them all the time and it is a $1000 to a $1500 excess, so it is not cheap. So from my experience at the VA I frankly don’t think it is clinically necessary for the vast majority of people.

[Damien Blenkinsopp]: Right, but for you it is more interesting to basically do a project and say I am going to use this protocol for six months and see what happens in terms of symptoms rather than doing tests to figure it out.

[Dr. Terry Wahls]: That would be my preference and I would certainly still work with the primary care doctor and have that basic primary care testing to help guide and refine things a bit. But I don’t think that it is – rarely do you need to spend $20,000 to $30,000 on testing to understand the mechanisms of why diet and lifestyle will make you better.

And that is what functional medicine testing does, it gives you the mechanism to explain why you should make these interventions and why they are going to help you. Or you could just make all the interventions to begin with and see if that would help. And then if it doesn’t then yes, you may need to spend a lot more money for a very thoughtful, functional medicine [inaudible 00:47:17]. But yeah, unless you have a lot of money to burn, try to do diet and lifestyle first.

[Damien Blenkinsopp]: Right, it sounds like a lot of these tests – you don’t see the value in them for most cases and it is better to spend some time and some money on the actual protocol as a test rather than spend the money on these tests which are currently a lot more expensive. You said the primary care tests are a lot more general?

[Dr. Terry Wahls]: Well you can easily spend $30,000 if you run down the functional medicine testing to understand everything that is potentially [inaudible 00:47:50] wrong with you. I think it is not money well spent for the vast majority of folks.

[Damien Blenkinsopp]: I see. One thing we didn’t look at but I heard you mention before is one of the issues you see with the mitochondria is membrane fluid – what is the issue around that?

[Dr. Terry Wahls]: Well it was probably in the 70s where we had a public health campaign against butter. You are also not supposed to use margarine with a lot of trans fats in it. And we have flipped out the beef with the deep fryers and fast food, and lard for vegetable oil, which increases the risk of trans fats. So our trans fat intake soared – and we all felt that was a good thing for us.

Now we realize trans fats are very rigid. They stop the fluidity of the membranes and it accelerates aging. It accelerates the risk for heart disease, cancer, dementia, and other neuroregenerative processes. Somehow after World War II we developed the fat theory for clogging of the arteries and then fat became demonized and so we switched to this low-fat diet but on a low-fat diet you don’t get enough of the fats that our membranes need to keep things nice and flexible and keep things fluid.

So you cannot have the bad fats, which are trans fats, vegetable oils that are heated, and you want to avoid those.

[Damien Blenkinsopp]: Have you looked at, I think it is called lipid exchange, where you purposely try to take in more fats and more fats of different types in order to promote – is that something that you have figured into your diet in terms of the fat intake?

[Dr. Terry Wahls]: We talked about fat at great lengths in the book and as I put people into ketosis we definitely increase the fats and have opinions about which fats they shoudl be eating, absolutely.

[Damien Blenkinsopp]: Another thing you mentioned earlier is supplements versus food. I know you are a proponent more of food, but you did take supplements to start with?

[Dr. Terry Wahls]: Yeah, I took supplements and they slowed my decline – they did not lead to recovery. When they added more supplements in the functional medicine folks that leveled things out and when I redid my diet is when I began to recover. So supplements targeted in a very, very thoughtful way may be useful but it is very difficult to have a big public health statement saying, ‘These are the supplements you ought to take.’ It really should be individualized based on that person’s story and their current health status.

[Damien Blenkinsopp]: Right. And you mentioned safety of supplements – what is your concern?

[Dr. Terry Wahls]: Well most of them are made in China now so I think people need to remember that and many of the supplements are made by genetically-modified bacteria. They do it, think about that as well.

[Damien Blenkinsopp]: Well I have lived in China and I have read the news a lot there so I can attest to the supplements used there.

[Dr. Terry Wahls]: Yeah, so they may be useful but you really have to think carefully about how useful they are.

[Damien Blenkinsopp]: And in terms of economics, I know some of the extremes for you guys and I think you actually grow some of the food in your back garden. Can you talk a little bit about the economics of you are a proponent of organics versus conventional? In terms of the economics of food, is it a lot more expensive?

[Dr. Terry Wahls]: I am going to vigorously disagree with this. I think the problem is people want someone else to cook the food and when you have someone else cook the food it is going to cost you more versus you buying the ingredients and cooking it yourself. And we have a number of lovely articles in the New York Times and I compared that – that are going to fast food restaurants and they cook the food versus you buy it and make it yourself. It is always cheaper to buy it yourself.

Now, if you want to go organic and grass-fed, which does have more health benefits, yes, that does become more expensive. But you can eat vegetables, clean protein, ditch the glutens, sugar, and processed foods for less if you cook it at home than if you are getting either fast food or something that corporate America has cooked for you.

So I like to see people go organic and get grass-fed if their monetary means allows that. You can still recover just eating more vegetables in the pattern that I have described. It will take you longer to clear all the toxins than if you were able to go grass-fed and organic. So you will begin to heal but it will take longer.

[Damien Blenkinsopp]: Right, now that is very – it is not yet proven by research. Is that something you are going to look at, the split of conventional processed – ?

[Dr. Terry Wahls]: That will be a wonderful project for us to do. We will see if we can get someone to pay for it.

[Damien Blenkinsopp]: Yeah, I bet you have got many projects in your head that you would like to do soon. What do you think will happen in this whole area in the next five or ten years in the area of testing and biomarkers and things like – well, what interesting things would you like to be able to test for?

[Dr. Terry Wahls]: I think the public is going to race out rapidly ahead in probably the medical field. I think it will be interesting to see ultimately that we could do rapid genetic testing and tell you which enzymes that you have are less effective and perhaps which vitamins you need to stress, which foods to stress, which foods to avoid. That would be very interesting.

And likely there will be a time that we can do that and then what we could probably do would just be the swish, gargle, and spit it out into a cup and get a readout of recommended dietary choices, recommended vitamin supplements.

[Damien Blenkinsopp]: Do you think that will be available within the next ten years?

[Dr. Terry Wahls]: I have no idea. I have to warm you I have clinic in two minutes so we should be wrapping this up.

[Damien Blenkinsopp]: Yeah, nearly there – great, and thanks for your time. What comes next in your research? What are your sort of next steps that you are looking at? I understand that you are crowdfunding projects?

[Dr. Terry Wahls]: So as a matter of fact tomorrow I will be talking with someone about a project that we are thinking about and throwing it up for crowdfunding. So I am going to be learning about that. I am submitting a grant to the MS Society and that is why I am feeling a lot of time pressure today because that is due here in the next couple of days.

And this Fall it is very exciting to know that the national MS Society here in the US is convening a programming meeting to talk about research priorities and programming for diet, lifestyle, and wellness. And they asked me to be one of their experts. So I was very excited about that. I thought that was –

[Damien Blenkinsopp]: Well that is a big milestone for you. That is kind of where you started all this.

[Dr. Terry Wahls]: Yeah, that will be huge. That will be very exciting.

[Damien Blenkinsopp]: That’s great to hear. So if you were going to track some biometrics of your own on a routine basis or do you track any biometrics for yourself?

[Dr. Terry Wahls]: Well I like to know where my vitamin D is. I like my B-vitamin levels at the top quarter of the reference range. And in general I am looking for nutrient biomarkers and I prefer they are in the top quarter.

[Damien Blenkinsopp]: Are you using nutrival or some other test for that?

[Dr. Terry Wahls]: No, that’s too expensive. I just use the straight primary care labs that folks get for these vitamin levels.

[Damien Blenkinsopp]: That is just plasma levels?

[Dr. Terry Wahls]: Yeah.

[Damien Blenkinsopp]: Great, okay. Well Terry, thank you very much for your time today. I know you have got another meeting.

[Dr. Terry Wahls]: Send me the link to the interview when it is available and I will shoot it to my social media team as well.

[Damien Blenkinsopp]: Great, I will do. It will go up in about three weeks’ time – that is when we are launching it.

[Dr. Terry Wahls]: Thank you very much.

[Damien Blenkinsopp]: Good luck with your meeting.

[Dr. Terry Wahls]: Okay, bye now.

[Damien Blenkinsopp]: Bye.

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