Mitochondria, the power plants of our body, get damaged through aging and other stressors. Lipid Replacement Therapy (LRT) is a tool being used to repair part of this damage to mitochondrial membranes, and can help people recover and optimize their energy levels.

The mitochondria is often described as the “powerhouse” of the cell and it supplies the energy the body needs to function properly and efficiently.

Previously, we have discussed mitochondria as related to cancer, in episode 16 with Dr. Thomas Seyfried and in episode 3 where Dr. Terry Wahls described mitochondrial health and the link to autoimmune disorders.

This episode will focus on mitochondrial function and the symptoms we experience when our mitochondria have sustained damage from either environmental factors, natural aging, or other exposures. Often this leads to general fatigue, cognitive decline, or physical decline and the effects can be seen in patients who suffer from chronic fatigue illnesses, neurodegenerative disorders, cancer and various other diseases.

Lipid Replacement Therapy (LRT) has been shown to repair the mitochondrial membrane damage and improve symptoms for many patients suffering from these chronic diseases and other natural aging symptoms.

One of the things we’ve done with the aging process is we’ve taken people that were fatigued, 90 years old plus, we’ve improved their mitochondrial function to a 30 year old. And they’ve gained all kinds of function in the process. Mental function, physical function, you name it.
– Garth Nicolson PhD

Today’s guest is Dr. Garth Nicolson who is an extremely accomplished research scientist best known for his work with Gulf War Syndrome, and Lipid Replacement Therapy (LRT). He is the president, founder, chief scientific officer, and researcher at The Institute for Molecular Medicine in Huntington Beach, CA where he conducts most of his current research.

He was the leading authority serving the United States House of Representatives on the study of the cause, treatment and prevention of Gulf War Syndrome on suspicion of biological warfare. For his service he was conferred honorary Colonel of the US Army Special Forces and honorary US Navy SEAL.

He has published over 600 peer reviewed research papers and served on the editorial boards of 30 scientific journals. In 2003 he introduced LRT and its benefits for the first time, shedding light on the importance of mitochondrial function and repair of damaged membranes and its benefits for aging, cancer and chronic disease states.

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

  • Mitochondrial function decline is the underlying problem in many chronic diseases (6:43).
  • Mitochondria are the powerhouse of the cell providing energy – like a battery – which fuels the cell’s function (7:43).
  • Oxidative damage to the lipid membrane of the mitochondria is the most universal cause of damage (8:38).
  • Damage to the lipid membrane harms the phospholipid molecules causing “leakiness” across the membrane (11:30).
  • If you don’t produce enough energy in a cell, you lose the function of that cell (13:15).
  • Damage to the energy process in a system can occur during aging, chronic illness, viral/bacterial infection, toxic exposure, etc. (13:55).
  • Some patients have restored their endocrine systems by repairing their mitochondria in some way (15:53).
  • Chronic fatigue illnesses (chronic fatigue syndrome, fibromyalgia, etc.) are directly related to loss of mitochondrial function, which is mostly true for many other diseases as well, such as cancer and neurodegenerative disorders (16:45).
  • Much of the mitochondrial function decline occurs because of the natural aging process (18:46).
  • For instance, improving the function of a 90 year old, fatigued patient greatly improves mental and physical functions for the patient (19:01).
  • Repairing the mitochondrial function for patients who have any of these diseases is not a cure-all, however it is a step in the right direction and definitely supports the overall recovery for the patient (21:21).
  • Dr. Nicolson discusses the importance of lipid replacement therapy (LRT) as a way to replace damaged membrane phospholipids to improve mitochondrial function (22:48).
  • LRT also functions to detox and repair chemically damaged cells as the lipids delivered to the system can soak any chemicals out from the membranes and remove them from the body (27:11).
  • Dr. Nicolson works with populations who have had particular exposures however everyone has been exposed to various chemicals throughout their lifetime (31:05).
  • Using both LRT and infrared saunas can speed up the long, slow process of detoxification and recovery (32:47).
  • LRT can reduce the symptoms of detoxification and recovery; for example LRT used in conjunction with chemotherapy for cancer patients helps the patient manage the side effects of the cancer treatments (34:50).
  • Patients generally see improvement of symptoms between 10 days and 3 months after the start of LRT but when therapy is removed the mitochondrial function declines again and symptoms return (36:39).
  • Mitochondrial function can be measured directly by testing the mitochondrial membranes in the white blood cells (38:38).
  • LRT is becoming more popular especially with naturopathic doctors and individual people as you do not need a prescription to obtain these natural supplements (40:37).
  • An increased dose of lipids is crucial for patients with severe chemical damage or mitochondrial damage so luckily no one has reported negative side effects yet as lipids are natural substances of the body anyways (44:37)!
  • Cholesterol markers and homocysteine levels have been shown to improve when using LRT (45:48).
  • LRT is proving to be effective as an anti-aging treatment, a therapy for various diseases processes, and as a co-treatment option for cancer patients to reduce negative side effects and fatigue related to traditional therapies (46:29).
  • LRT works well at improving energy systems however dosages, etc. do have to be optimized to work with each person’s unique system (50:26).
  • LRT is a lifelong solution and a long term treatment because we are constantly exposed to new toxins, infections, and traumas throughout our lives (52:17).
  • The minimum supplement needed for LRT is NT factor lipids. (55:32).

Garth Nicolson PhD

Tools & Tactics


  • Lipid Replacement Therapy (LRT): Used to restore and repair mitochondria function by replacing damaged lipids in the membrane and restoring the mitochondria’s ability to produce energy for the cell. (See relevant lipid supplements below).
  • Infrared Sauna: Used to remove fat soluble toxins in particular from the body. Garth Nicolson recommends using this along side LRT to help with the removal of chemicals from the cells, which tends to improve results.


  • NT Factor EnergyLipids: NT Factor is the lipid based supplement that is the main component used in LRT. There are a variety of products including this one, which contain NT Factor. Read more about these on, as recommended for use by Dr. Nicolson.
  • NT Factor Energy Wafers: The specific NT Factor product that is “child friendly”, as the wafers easily dissolve in the mouth and do not need to be swallowed.
  • ATP Fuel: In addition to NT Factor, this supplement also contains NADH and coenzyme Q10 which also aid in the energy production cycle in a cell.



  • Cholesterol: A cholesterol panel covers a number of markers related to lipoproteins (such as HDL and LDL) in the blood. LDL and HDL are standard markers used to track cardiovascular risk. Dr. Nicolson has seen LDL drop and HDL increase with use of LRT – which typically indicates improvement and lower cardiovascular risk.
  • Homocysteine: A marker often used to assess cardiovascular risk. Higher values relate to increase cardio risk. This marker is often related to methylation SNPs like MTHFR as discussed in episode 5 with Ben Lynch. Dr. Nicolson has seen homocysteine levels drop with LRT also.
  • Mitochondrial Membrane Potential: An approach to assessing the health and functioning of a cell’s mitochondria by looking at it’s potential or voltage. In the same way as with a battery, if it is functioning, the outer membrane of mitochondria has an electric output and thus a voltage.

Lab Tests, Devices and Apps

  • Inner Mitochondrial Membrane Potential via Rhodamine 123: The status and functioning of the mitochondria are assessed via analysis of mitochondria inside white blood cells with the dye rhodamine 123 and a fluorescence microscope (see study here). The test provides a quantitative fluorescence value indicating the health of the mitochondria and integrity of the membrane. This test is not easily accessible and is used for research purposes.

Other People, Books & Resources


Full Interview Transcript

Click Here to Read Transcript
[Damien Blenkinsopp]: Garth, thank you so much for joining us on the show.

[Garth Nicolson]: Well it’s a pleasure to be on your program.

[Damien Blenkinsopp]: To start off with, I was really interested to find out how you first started working with mitochondrial function. Where it first came up for you, and you started taking an interest in it.

[Garth Nicolson]: Well this really goes back to our work on Gulf War veterans. And from that we did work on civilians with Chronic Fatigue Syndrome, Fibromyalgia Syndrome and related fatiguing illnesses. And one of the underlying problems in all of these – and it turns out any chronic disease – is mitochondrial function. There’s just not enough energy around to provide all the necessary high energy molecules in a cell to perform all the functions necessary.

Then you get into energy deficits, and if the energy deficits are systemic, well you can have a chronic condition with lack of energy, lack of mental alertness, all kinds of other additional problems. Because basically every cell requires energy to perform. And some cells, such as the nervous system, require a lot of it – six times what most cells require – and so they’re particularly sensitive to losses in energy function.

[Damien Blenkinsopp]: It sounds like there’s a wide variety of symptoms that could be reflecting some kind of mitochondrial function damage, or interruption. Is that the case? Is it quite a wide variety of symptoms?

[Garth Nicolson]: There are a wide variety of symptoms associated with loss of mitochondrial function. And as I mentioned before, the mitochondria provide energy to your cells. In fact, almost all the energy is provided by mitochondrial function in our cells.

If you’re breathing oxygen, you’re using that oxygen to provide it to mitochondria, so they can convert it to energy, along with other molecules that they use in the process called Electron Transport System. And it’s a complicated conversion system which converts, essentially, stores that you have in your cells to high energy molecules that you need for doing a number of different functions.

Now in different clinical conditions, we find that these people have given signs and symptoms, but often they’re also related to mitochondrial function, because a lot of these problems arise when there isn’t enough energy left for cells to perform their functions necessary, and consequently this can have profound effects.

[Damien Blenkinsopp]: Right, and what kinds of damage can interfere with mitochondrial function?

[Garth Nicolson]: Well there are a variety of different types of damage. We’ve concentrated on damage to the lipid membrane of the mitochondria, because this turns out to be the most sensitive form of damage, or the most universal form of damage that we find in mitochondria. They’re particularly sensitive to oxidative damage.

And oxidative damage can occur, for example, during infection, during high performance issues, if you get run down – for example, physically, mentally, you name it – or because of infections or other damages, disease associated damages, mitochondrial function suffers. And in order to recover from all of these, you do have to have mitochondrial function available, because you can’t repair and recover without it.

[Damien Blenkinsopp]: So are we all constantly repairing the lipid membranes, as you are talking about? Is this a constant? Because when you mentioned, for instance, high performance, could that be someone like an athlete, or someone who’s heavily into fitness? Are they constantly causing this type of damage with oxidative stress, which then has to be repaired?

[Garth Nicolson]: Well, that’s true, but it’s also true during aging, for example, where our membranes normally get damaged during aging processes. And mitochondrial membranes are particularly sensitive to aging, and as we age, they get more damaged. And so if you look at a 90 year old, many of these 90 plus year old people have lost almost half their mitochondrial function.

And a lot of that is due to accumulated damage in the mitochondria, and a lot of the damage is due to the damage to the mitochondrial membrane. And the inner mitochondrial membrane is integral to our production of energy, and if that’s damaged, they become leaky, and lose function, and they can’t maintain the trans-membrane potential, the electrical potential across the inner mitochondrial membrane, which is absolutely necessary to produce high energy molecules.

[Damien Blenkinsopp]: Right, right. Well to take a step back, when you’re talking about trans-membrane, what’s the function of the membrane in terms of generating electricity? Because basically the mitochondria are a bit like our power cells, you know our batteries, which feed our cells and the rest of our body with energy. But how do they do that, and what’s the role of the membrane in that process?

[Garth Nicolson]: Well I always liken mitochondria to the little batteries inside our cells. And like any battery, it has to be insulated to selectively permit a trans-membrane potential across different membranes in our mitochondria. It’s a biological membrane instead of a synthetic membrane that we have in batteries, but it provides the same kind of insulation necessary to separate electrical charges.

And so when this separation of electrical charges occurs, you can make a battery out of it. Essentially that battery drives the production of high energy molecules in the mitochondria just as it does in a normal battery.

[Damien Blenkinsopp]: Great. And what types of damage are we talking about when we’re talking about this membrane getting damaged?

[Garth Nicolson]: Well there’s certain molecules in the membrane. It can be the phospholipids that make up the matrix of the membrane. But when they’re damaged, there can be enhanced leakiness across the membrane. So it’s like you get a leakiness if you take the insulation off a battery it will leak, and you’ll lose the charge of the battery.

The same thing in the mitochondria. If they become leaky, and the inner membrane becomes leaky, you can lose the trans-membrane potential, and then you can’t form the high energy molecules. There are also some critical lipid molecules, like cardiolipin, that are exquisitely sensitive, in fact, to oxidative damage. And when they’re damaged, this results in loss of function. So these different types of things are very important, the direct function and the trans-membrane potential.

[Damien Blenkinsopp]: So these are different types of fat molecules that we need in the membrane for it to function optimally. And it’s kind of like holes have been punched in the surface of the membrane, and molecules have been knocked out of it? Is that a way to look at it?

[Garth Nicolson]: It’s a little more subtle than that. When oxidative damage occurs, think of the lipid chains that are going into the membrane, into the hydrophobic matrix of the membrane, you can think of kinks getting in those chains after they’ve been oxidatively damaged. And those kinks mean that the lipids can’t fit together as well, and there’s a certain rate of leakiness across the membrane.

[Damien Blenkinsopp]: Great. Is this something anyone should be concerned about, in terms of the type of damage? You just referred to a 90 year old, the damage that’s gone on to them.

What kind if symptoms could someone think of if, maybe they don’t have a chronic disease like some of the ones you referred to, but are there other indicators that potentially they have some aspect of mitochondrial damage, in terms of some symptoms they could look out for which might identify that?

You were referring to, like brain fog, or other symptoms. Are there obvious ones, or is it always very different, and it’s kind of difficult to differentiate this to other things that might be going on?

[Garth Nicolson]: Well, obviously a number of different factors can cause problems with your central nervous system, for example, your peripheral nerves and other systems of your cells, but one of the things that can happen is that if the energy systems inside the cells get run down, they don’t function as well. It’s as simple as that.

So if you don’t produce enough energy in your cells, your cells can’t function as well. So all the different functions that cells do, of course the nervous system, the function is to transmit nerve impulses, if they’re not functioning properly then the nerve impulses can’t be transmitted properly. And so that leads to a loss of function.

Now this can occur when people get run down. And they can get run down for a variety of reasons. They can lose their energy stores, for example, or they can have them damaged through the mitochondrial damage that I was talking about. Some of this occurs naturally, and it’s reversed by rebuilding things like the membrane as it’s damaged.

And if there’s some process that prevents that rebuilding of the membrane, then this will persist. For example, during infection we know that a variety of different types of infections – viral, bacterial and so on – cause an increase in the what are called reactive oxygen species, or ROS. And these damage the membranes of the cell, and in particular they can damage the inner mitochondrial membrane and cause loss of function.

So these are things that can happen. So it can happen during infection, it can happen during aging, it can happen during a chronic illness. It can happen when you get run down, for example, or you have exposures of various types that are toxic. So under a variety of different conditions you can have damage done to your mitochondria, which means loss of function, and your body cannot repair itself as well without that energy that’s necessary to do it.

[Damien Blenkinsopp]: Great. And I guess an important differentiation I just wanted to point out here is a lot of people talk about adrenal fatigue, and if one of the symptoms is fatigue, basically having low energy – which I guess would be one of the outputs of mitochondrial damage – how do you differentiate it, or is it possible to differentiate it, to something which someone would diagnose as adrenal fatigue? Or how do you look at that?

[Garth Nicolson]: Well they go hand in hand, because for the adrenal gland to function, it requires energy. So if there’s an energy deficit in the adrenal gland, then that’s not producing the correct hormones and everything that your body needs. Cytokines and so on. So this sends up the deficit, and this can cause a problem. So they’re inter-related.

[Damien Blenkinsopp]: Right, right. And it sounds like you’d think mitochondrial damage might be a pre-cursor to adrenal fatigue, often.

[Garth Nicolson]: It could be a pre-cursor to adrenal fatigue. And so we’ve seen people that have managed to repair their endocrine systems by repairing their mitochondria. So at least we know, and at least in some patients, that’s reversible.

Now in other patients they may have either genetic defects, or toxic exposures, or something like that, that’s damaging specifically those particular adrenal glands. So that’s a different issue. But we do know that these things are inter-related. If you don’t have the energy, you can’t repair.

[Damien Blenkinsopp]: So you’ve worked, in your clinical studies and your patient population, you’ve worked with Gulf War illness and Chronic Fatigue Syndrome and some others. Could you give us a brief explanation, for the audience, what are the issues that these people have? How critical are they, what kind of situation are they in? Before we talk about the lipid replacement therapy and what it was able to do.

[Garth Nicolson]: Well there’s quite a bit of variation on the signs and symptoms of people with chronic illnesses, and a variety of different sorts. We started working with what are called Fatiguing illnesses, because Chronic Fatigue is the hallmark of those illnesses, and that’s directly related to mitochondrial function. So that was a good place to start.

A lot of other diseases, mitochondrial function may be thought of as a side issue; although it’s important it may not be the primary clinical manifestation of the disease process. Nonetheless, it’s still important [for] practically any chronic illness.

If you take something like a neurodegenerative disease, for example, mitochondrial function is intimately tied up with neurodegeneration. You cannot repair your nervous system if you don’t have the energy available to do it. So if mitochondrial function goes down, you’re particularly susceptible to neural damage. And to have that process going on, it can exacerbate it.

So this is one of the things that we are trying to work with, how to improve mitochondrial function, how to help people with a variety of chronic illnesses.

So we started with the fatiguing illnesses, and Gulf War Illnesses are really one of the fatiguing illnesses, but Chronic Fatigue Syndrome is another one, Fibromyalgia syndrome is another. Fibromyalgia syndrome is a little different because it’s also characterized by widespread pain, in part, we think, that’s due to mitochondrial function problems as well. The nervous system not operating properly. But there are some other factors as well.

So all these issues have as an underlying commonality loss of mitochondrial function. In a variety of different diseases, that’s true. And it’s true in infections, it’s true in toxic exposures, it’s true in a wide variety of different diseases. Cancer, you name it, practically every disease you can think of has a problem with mitochondrial function. They can’t keep up the repair process.

[Damien Blenkinsopp]: Are there other, beyond the ones we’ve already discussed, are there other types of patient populations, or other use cases you’ve looked at for lipid replacement therapy? You mentioned anti-aging as well. Have you worked with people for that area also?

[Garth Nicolson]: Exactly. Well, anti-aging is probably the normal manifestation of mitochondrial functions. I mentioned as you age you lose mitochondrial function naturally. And there’s an increase in the oxidative damage that occurs in all of our cells, so we need to reverse that process.

And so, one of the things we’ve done with the aging process is we’ve taken people that were fatigued, 90 years old plus, we’ve improved their mitochondrial function to a 30 year old. And they’ve gained all kinds of function in the process. Mental function, physical function, you name it. Every system that seems to be important improves.

[Damien Blenkinsopp]: In terms of the studies you’ve done, are these all based on studies, or is some of this based on patient population, other studies? Because I’ve seen some of your presentations, looking at your studies and work on the fatigue cases and the Gulf War Syndrome. So are all of the studies basically based on those patient populations versus the anti-aging, or have you also done studies on anti-aging also?

[Garth Nicolson]: Well we’ve done some studies where we’ve included older people in our studies, and that’s where we see the anti-aging effect. So with those older cohorts of patients – well they really are, they’re subjects, not patients, because their main problem is they’re elderly and they have fatigue issues. So we can’t categorize them as a disease process, because it’s a natural process of aging.

So they are fatigue subjects. So they have chronic fatigue, but they don’t have a disease called Chronic Fatigue syndrome, or Myalgic Encephalopathy, or something like that. They have fatigue problems. So we work with people like that as well.

We’ve also worked with cancer patients, we’ve worked with people with chemical exposures, we’ve worked with people with infections. For example, there are a wide variety of chronic infections that we work with, like Lyme disease, mycoplasma infection, so on and so forth. Were, again, in the chronic disease process, it’s always an issue. Mitochondrial function is always an issue.

[Damien Blenkinsopp]: Right. Would you say it’s going to be helpful in most situations to have some kind of lipid replacement therapy as a support for your mitochondria? In terms of the disease process, to give an idea, what kind of results do you get from people? Can you get people back to resolution? Or is this basically managing symptoms, managing the damage of mitochondria, kind of therapy?

[Garth Nicolson]: Well it depends on the situation. If we take normal, healthy people that can get run down for one reason or another, yes we can bring them completely back by repairing their mitochondrial function.

If you take people that are in a disease process, usually these processes are much more complex than just mitochondrial function. Mitochondria being one part of the problem that they have. And we can repair that part, but there are other elements that have to be taken care of as well. For example, if you take somebody with a neurodegenerative disease, does just repairing their mitochondria reverse the process? No. There’s some other elements that are involved.

Does it help? Yes, it seems to help people with cognitive loss and so on and so forth. But it doesn’t reverse it or completely cure the problem. That would be a pretty simplistic approach to these complex, multi-factorial issues. But, we do know that this is an important element in all of these processes.

[Damien Blenkinsopp]: Do you feel like it provides a support to get people to recovery? That it’s an important ingredient in your practice? You feel like it helps people to recover by giving them that mitochondria energy, thus supporting things like the immune system, and other systems of the body?

[Garth Nicolson]: Absolutely. If you’re talking about the immune system, for example, it requires energy to function. So if your energy goes down, your system might be less capable. So, it’s absolutely important there.

And it’s absolutely important for any type of recovery, because what is recovery? Generally it’s repairing our cellular processes and our system processes, our organ processes, and that requires energy. That just doesn’t happen naturally without energy.

[Damien Blenkinsopp]: Okay, so let’s get kind of concrete here, for the audience listening at home. What is lipid replacement therapy? What does that actually involve, what do people do when they’re taking lipid replacement therapy?

[Garth Nicolson]: Well this is a particular type of lipid, this is not just the normal gross lipids that people might think of. These are very particular membrane lipids, so these are lipids that make up the membranes of all our cells. And of course as I mentioned before the membrane is an integral part of the mitochondria, but they’re also an integral part of other organelles within the cell.

Membranes, in fact, are absolutely essential for the function of all of our cells. And they get damaged, they get run down, we have to replace the molecules and the membrane occasionally. And some of the most sensitive molecules are the lipid molecules, because they’re very sensitive to oxidative damage, which can occur in any disease process, infection, or whatever.

So this is something that has to be replaced. And we came up with this idea, well we need to replace the membrane lipids, which are primarily a class of lipids called glycerophospholipids, that don’t need a lot of other things. That’s what we need to help repair the, more or less the matrix of the membrane.

So if we supply that in purified form, undamaged form – which is very important – then we should be able to help repair this process, because we have natural systems in our body to replace these lipids as they’re damaged. Because we evolved with the mechanism to help repair and replenish our membranes.
The problem is we can’t keep with the damage, and that’s when the disease process can occur. So to help it along, if we provide the lipids, well we can help that process.

Now people say well, you can buy all kinds of different stuff at the store. Well, the reason it doesn’t do it is a lot of those lipids are already damaged, they’re already oxidized, they’re not the right kind of lipids, and so on. So they’re not very helpful. And even a lot of supplements that people buy in the store are not very helpful, because even if they have lipids they’re not the right kind of lipids, or they’re already damaged, or they’re damaged during the shelf-life.

These are very sensitive issues, which we’ve tried to overcome with the products that are designed to survive and provide our bodies with exactly the right lipids that we need to repair our membranes and restore function.

[Damien Blenkinsopp]: So, would it be correct to, because you provide these in pill form. So is it these are things we can get from food, but we get them in very low quantities, so it’s like having a very high dose of the reduced form? The active form versus the oxidized form of these lipids?

[Garth Nicolson]: Well that’s part of it, but a lot of the lipids are damaged already by the time we take then in in the foods, and unfortunately, our transport systems, they can’t readily acknowledge a damaged lipid from a properly pristine, undamaged lipid. And so a lot of these things might get transported in as well. Or at least they’re transported in, too much of it is transported in if it’s damaged.

So we kind of flood the system with undamaged lipids, and that helps the whole process move very smoothly. It also helps remove the damaged lipids, which is one thing we’re working on now, is how to take people who are chemically damaged – and I can talk about that later – help them remove those damaged chemicals from their bodies.

And it turns out that the replacement therapy can help do that, because it’s an energy driven process, so it helps provide energy, but it also is very dependent upon moving what we call hydrophobic molecules out of the cells. And the lipids that we provide have a very important part of their structure, a hydrophobic part of their structure, which helps remove these molecules.

So if they’re present in quite a bit of excess it can help remove these damaging chemicals from our system. And that’s one thing we’re working on right now.

[Damien Blenkinsopp]: That sounds very interesting. We’ve spoken about detoxification before. So, just to take a step back, when you say chemically damaged people, what kind of things has happened to these people?

[Garth Nicolson]: Well often people with chemical damage due to illness could be anything from herbicides, for example, to very industrial chemicals, and so on and so forth. Often damaging chemicals are chemicals that we would classify as hydrophobic chemicals. That is, they don’t like water. They like fat, essentially.

So they concentrate in our membranes, they concentrate in the fatty parts of our cells and lipid droplets, and so on. And they can remain there indefinitely. And they can bleed out very slowly and cause problems with the cellular mechanisms. So to get rid of these, we need a system to remove them.

But the system that we have for detoxification is an energy dependent system, at least one of the most important ones. So by providing mitochondrial energy, that helps in that process. But it also helps remove them because, it turns out, the lipids that we provide kind of soak up these molecules, because it will bind to the lipids and it helps them be excreted from our cells and from our system, so they naturally come out in the GI system.

[Damien Blenkinsopp]: So that sounds like the new molecules that you’re providing are basically replacing the ones which have absorbed the toxins, the chemicals, the fat soluble chemicals, and are thereby displacing them and allowing the body to remove them.

[Garth Nicolson]: Well that’s basically it, but it’s providing a different store, or different storehouse for these chemicals to move into, but a storehouse that we can eliminate. And that’s the important thing is to do that.

One of the mechanisms for moving chemicals that’s most important for these very damaging chemicals that concentrate in our cells is that there are enzymatic mechanisms, to conjugate the offending chemicals with other hydrophobic molecules within the cells, to make them more easily removable.

Well when that happens, if we have somebody’s undergoing lipid replacement therapy, there are a lot of these lipid droplets around and lipid carriers around, which could help soak these conjugated chemicals up and remove them from our systems.

So it’s a process, it’s a very slow and steady process of removal. It doesn’t, of course, happen over night, but it’s a natural system for removal of damaging offending chemicals from our bodies. And this just takes it to a maximum advantage by providing some of the things necessary for it to operate in the first place.

[Damien Blenkinsopp]: So out of interest, because we’ve spoken quite a bit about detoxification, and also the kinds of tests involved in measuring things like mercury, lead, and other toxins. Are you able to test these chemicals in fats and see the change, and how long does it take? Does it take a month, two months?

[Garth Nicolson]: Again, we’re not talking about heavy metals, because that’s a different process of removal. We’re talking about chemicals that partition themselves into the fatty portions of your cells. Well these chemicals, and they could be, for example, herbicides or any number of different chemicals.

[Garth Nicolson]: Yeah, a lot of the chemicals that damage our cells are very hydrophobic, and they partition into the fats of the cell, the fat systems and the membranes of the cell. They have to be removed or eventually they’ll interfere with the function. That removal process is slow. It does not happen over night.

So it’s a very slow process of bleeding them out and removing them from the stores, and so on and so forth. So one of the first things that you can see, for example, if you give somebody lipid replacement therapy, is you might actually see an increase in the number of these chemicals that are being excreted, that are being at least mobilized as well.

So there may be an increase in the blood levels of these, because they’re being brought out of the cells and being transported to the brush border cells in the intestines, and then secreted there. But again, there are a number of different mechanisms, this being just one of them.

[Damien Blenkinsopp]: I’m guessing this is a new area, it sounds like you’re more focused on this recently?

[Garth Nicolson]: This is a very new area of ours that we planned to get very focused on because it’s so important, so necessary to help these people, many of whom have been damaged for decades without much help at all.

[Damien Blenkinsopp]: So just out of interest, are there any specific exposures? And is it people working in factories, or is it people who have detoxification systems which aren’t functioning, or perhaps they have some methylation or other issues, which they’ve lived a pretty normal life, compared to most people. It’s not like they’ve been in any specific situation which could have exposed them to more chemicals.

What kind of populations are you dealing with here?

[Garth Nicolson]: We work with the populations that are sick in general, although a variety of different individuals may be exposed to chemicals, because they are all over the place in our modern environment. And people will have tremendous variation in their sensitivities to these chemicals.

So you may have somebody that’s been normally and naturally exposed who’s becoming sick because of it, and other people not at all. Because there’s such a range of sensitivities to these.

So we’ve worked with people who’ve had specific exposure. For example Vietnam war veterans who’ve had exposure to Agent Orange, which is a particularly nasty chemical that takes a long time to remove from the body. Or Gulf War veterans that are exposed to petrochemicals in the forms of fumes, and exhausts, and oil fires, and so on and so forth, during the first Gulf War, and some during the second Gulf War.

So these are people that have had chemical exposures above and beyond the normal types of exposures that we might see. But in the industrial environment that we’re in, there are a lot of people that get exposed to various chemicals.

If you work in the petrol-chemical industry, for example, you could be exposed fairly easily, and it may not cause any problems with you but there are other individuals who have severe problems because of it.

So again, there’s a wide range of different sensitivities to these different chemicals that are seemingly in our population.

[Damien Blenkinsopp]: Great. I just want to bring it up, because I know a lot of people talk about infrared saunas, and saunas in general when it comes to fat detoxing from the fat soluble toxins like the ones we’re talking about. So, do you have a viewpoint on that, on the effectiveness of infrared sauna? Is it something you’ve ever gotten involved with, and could you compare it to your process?

[Garth Nicolson]: We’ve looked a bit into that, and yes the use of infrared saunas to actually bring the chemicals out in your sweat, which is what it really does. But if you do these at least a minimum two times a week, you’ll slowly start to deplete some of the chemicals from your body.

What we found is if you add our lipid replacement therapy on top of that, you can accelerate the process of removing the chemicals from your body that way. So again, this can be an adjunct to a variety of very well established methods for detoxification.

[Damien Blenkinsopp]: Great. Have you seen complete recoveries, or to what degree have people recovered from their health? Because we’re talking about people that are quite sick.

[Garth Nicolson]: Well, we’re in the beginning process of this right now. So this long term goal of ours, but again, this is just the beginning, and we’re seeing some responses. We’re seeing people that are feeling better, getting better. But again, it’s a long, slow process for recovery.

And again, there may be other types of damage along the way that we discover that these individuals have. Most of these chronic illnesses are multi-factorial. There’s not just one problem, generally these people have a number of problems, this being one of them. But this is something that we can approach.

[Damien Blenkinsopp]: Absolutely. So it sounds like an on-going process of a year. We’re talking really long term, just to give people an idea.

[Garth Nicolson]: We’re talking long term. Particularly when it comes to removing offending chemicals from your body, it’s a long term process. Same thing with removal of heavy metals from your body, it’s not a short term process.

It can take years to remove heavy metals from your body, and the same thing is true with chemicals that build up in your body. It can take a long time to really get rid of them. And in fact, if you mobilize them too quickly, you can really make people feel sick in the process. So it’s better to do it naturally and slowly.

[Damien Blenkinsopp]: So, I’m glad you brought this up, because we’ve spoken about these kind of topics quite often on the podcast before. It’s nice to get that. Is there anything you have to do in terms of supporting them?

Because you mentioned that some people can get sick if it comes up too fast. Is there anything else that you do for them while you’re using the lipid replacement therapy to support detox, or as long as you go at a reasonable rate, which I imagine is a reasonable dose?

[Garth Nicolson]: What we have found is that lipid replacement therapy actually reduces the symptoms of detoxification, reduces the symptoms, for example, of cancer chemotherapy. So it is very significant in our studies with the cancer patients. They’ve showed really quite a dramatic decrease in the side effects due to chemotherapy, because it causes a lot of damage to our normal systems, and the lipid replacement therapy helps repair those normal systems.

So you get a reduction in the associate problems, very adverse events that occur during cancer therapies. So, you could figure that is, again, when you’re repairing the normal mechanisms of the cells, the tissues, and this helps the overall process.

[Damien Blenkinsopp]: Right, right. So you’re saying a lot of the symptoms people have when they’re going to a detoxification process, or, as you’re saying, chemotherapy or exposure to other toxins or when they’re ill, is due to mitochondrial damage, right?

So when you’re supporting the mitochondria with lipid replacement therapy, it helps to manage the symptoms as well in that process and reduce them, because there’s not as much damage going on.

[Garth Nicolson]: Well it does, and not only that, it helps accessory systems as well, because a lot of the signs and symptoms that we see that are associated with damage are release of chemical messengers like cytokines, that cause all kinds of problems in the body, and so on.

And damaged tissues can initiate this whole process. So if you reduce the damage, you can reduce these accessory damage response systems from exacerbating the signs and symptoms in these patients.

[Damien Blenkinsopp]: Great. One thing I wanted to kind of make clear to people, what kind of results, because when I was watching some of your clinical studies you were looking at. Over the few months you were giving lipid replacement therapy, could you talk about what kind of impacts it generally has on the people?

If we’re talking about say the chronic fatigue, or in the Gulf Syndrome cases, the ones I saw, what kind of time-lines did you walk through in your clinical studies? And also, it was interesting what happens when you stopped the therapy.

[Garth Nicolson]: This is a process that takes time. You don’t repair your mitochondria overnight. It takes days to weeks. The process can begin fairly soon after you take the lipid replacement, but it takes time to fully repair the mitochondria.

And we’ve seen, again, that it can take, depending upon the different formulations of lipids, anywhere from 10 days to three months, depending on the formulation, depending on the patient type, to reach an equilibrium of repair. And these people see a maximum benefit in that time. But they do see benefit fairly, fairly soon.

[Damien Blenkinsopp]: And then what happens when you stop the therapy? Depending on the condition. So when it’s in a chronic condition, like Chronic Fatigue Syndrome, or Gulf Syndrome, where they have some kind of infection or some underlying cause, then what happens when you stop the therapy?

[Garth Nicolson]: Well then it slowly returns back. As the mitochondria get damaged again, it will slowly go back to the way it was before you started the therapy. And one of the trials that we did was called a cross-over trial, where we take patients, and they’re on part placebo and part the lipid replacement therapy, but they don’t know when they get it.

And what we found was when they get the lipid replacement therapy, they improved. They had reductions in fatigue with 35 to 45%, enhancement of mitochondrial function was a little bit less than that in terms of percentage, but very significant. But when we switched them to placebo, it slowly started to go back again.

[Damien Blenkinsopp]: Yeah.

[Garth Nicolson]: And they wondered what was going on, because it wasn’t having the same effect. So we could prove that it was in fact the lipid replacement therapy that was giving them the benefit, not a placebo effect.

[Damien Blenkinsopp]: Great, thank you very much for that. And so, what were you using to assess mitochondrial function in terms of tests?

[Garth Nicolson]: Well what we do is we take a blood sample from patients, we isolate the white blood cells which have mitochondria – the red blood cells do not have mitochondria – and we can measure the mitochondrial function directly.

And what we’ve done actually, more recently, is we’ve measured the membrane potential of the inner mitochondrial membrane using a special redox dye, called rhodamine 123, and see that fluorescent dye in the mitochondria. If the mitochondria are fully functioning, they will reduce that dye and it will fluoresce.

And if they’re not functioning, they can’t reduce it, and the mitochondria won’t fluoresce. So you can see it visually in a microscope and you can quantitate the fluorescence so we can get a quantitative value.

[Damien Blenkinsopp]: Great, great. So this is your own lab tests that you developed for this purpose?

[Garth Nicolson]: Well other people really developed the tests, we just adapted it to what we were doing.

[Damien Blenkinsopp]: Great. Well I guess what I wanted to say is it’s a pretty unique [test], like we wouldn’t expect to find it outside of research, apart from potentially your practice, and some other specific areas.

[Garth Nicolson]: This is a very specific research type of test, and you won’t find it in your normal doctors office, that’s for sure. Because it requires some complicated machinery, like a cell sorter and fluorescent tools, fluorescent light sources, and so on and so forth. So, it’s a bit complicated, but it works in a research environment.

[Damien Blenkinsopp]: So it’s not something you use on your patient population, I guess it’s cost prohibitive. It sounds like quite complex.

[Garth Nicolson]: Well it is, and speed is very important. So you have to have a very fresh sample. Often if you’re not doing the test immediately or soon, you could get variable results. So to get the best results, speed is very important. So, generally you have to have this complicated equipment on hand to do it. And the technical expertise to do it.

[Damien Blenkinsopp]: So, how well accepted is lipid replacement therapy? We’ve spoken with functional medicine doctors here, and we’ve looked at functional medicine quite a bit, contemporary medicine is there of course also, and in the research studies.

Is there a lot of support for it right now, or is it still something quite niche that basically there’s not very many people using?

[Garth Nicolson]: Well more and more are using it, because more and more people are finding out about it. And we published some 28 papers on this process. So, it’s well-known in the literature. We published a number of reviews on it now.

Less known in the general population of physicians, more in the naturopathic medicine areas, mainly because I get around and talk to these people, and then they get informed that way, through conferences and so on. So it’s becoming more and more well-known, and even people outside the medical area will find out about it through broadcasts like yours, for example.

They can buy this stuff over the counter, it’s not something they need their physician’s prescription for. These are natural supplements. It’s the lipids that are in our membranes all along. So, it’s not a drug, it’s not anything but what’s there. We just have to provide it in a way that’s not damaged.

[Damien Blenkinsopp]: Well so I’ve got to ask you the question, are you using lipid replacement therapy yourself?

[Garth Nicolson]: Absolutely.

[Damien Blenkinsopp]: Okay. How long have you been using it?

[Garth Nicolson]: Well, I’ve been using it for years now. It was very effective for me in terms of reduction of fatigue. And for example, recently I got an influenza virus, unfortunately. It kind of knocked me down, and this helped the repair process. I recovered much more quickly than normal, and so I think it’s very useful for that.

[Damien Blenkinsopp]: What kind of dose are you taking? Let’s talk about practicals here. Because I’m taking ATP Fuel, for example, because I’ve had my own issues and it was recommended to me. And your research was recommended to me, so that’s kind of where I came into it.

So I’ve been taking that for a while, the ATP Fuel. And you have the NT Factor, which is a part of that. Is that actually your company who supplies that, or is that another company?

[Garth Nicolson]: I’m in a non-profit organization. We’re not really a company, but we do consult with companies like Researched Nutritionals that makes the ATP Fuel, [and] Nutritional Therapeutics in New York which makes the NT Factor, the lipids.

In fact, the Researched Nutritionals uses the NT factor product in their own product. They add some other things as well. So, ATP Fuel is an excellent product for these chemical exposure patients. In fact, I’ve just been going back and forth with the President of Research Nutritionals because we need to increase the amount of NT Factor, which is the lipids, to that product to really help these individuals.

So what we found is that more of the NT Factor is actually better. You might want to supplement your ATP Fuel with some NT Factor Lipid Wafers. By the way this is an excellent product.

We use these with children, for example, that have autism spectrum disorders, and these children have mitochondrial function problems. They readily take these wafers, and they don’t take pills. You can’t get them to take a pill.

[Damien Blenkinsopp]: Right, right.

[Garth Nicolson]: But these wafers are very tasty, and they’re creamy, they melt in your mouth because they’re lipids. So they like these creamy things, and so we have no problem with the compliance, even with difficult cases like these autistic children.

These are things that we work with on a daily basis, and we’re trying to improve our products as we go. Recently we found that although ATP Fuel is a really good product, I’m saying for the chemically exposed individuals that we need to increase the amount of NT Factor with the lipids in that product.

[Damien Blenkinsopp]: So just for the audience, the ATP Fuel has co-enzyme 10 and NADH added to it. Obviously, say that the dose of the lipids, which you say is the most important, this is kind of the innovation here, the lipid replacement therapy.

[Garth Nicolson]: That seems to be the most important thing because if you leave that out, it’s not very effective. If you put it in, it’s very effective. So it is a combination, but it’s a critical part of that combination.

[Damien Blenkinsopp]: Let’s just talk downsides here. Are there any downsides you know to this, and are there any safety issues? I just want to make that clear in terms of, maybe if you overdose it. You’re talking about increasing a dose for chemically exposed people. Is there any downside or risk to taking a lot of this?

[Garth Nicolson]: We’ve never seen any safety issues with the NT Factor lipids. As a matter of fact, we’ve given approximately 40,000,000 doses of this to patients without any recorded evidence of a real side effect.

And the reason for that is these are natural molecules that are in our cells and our systems all along. So we’re not giving our systems anything that’s different. We’re not giving them a drug, we’re not giving them something that they don’t see all the time anyway. I don’t know that it has any toxicity.

There are some studies that had been done in animals, where they’ve been given tremendous doses, without any effect at all. And we’ve had patients that have been on, oh, up to several grams per day of the NT Factor lipids without any [negative], as a matter of fact more positive effects. Their blood lipids had more normalized, they’ve had a lot of really positive things happen to them.

[Damien Blenkinsopp]: So that’s interesting. What kind of quantitative changes have you seen in terms of, are you talking about cholesterol markers?

[Garth Nicolson]: Yes.

[Damien Blenkinsopp]: Have those changed as well?

[Garth Nicolson]: Cholesterol markers and bad and good lipids. For example, lipoproteins, we’ve seen a move in the right direction. We’ve seen reductions in a product that’s associated with Heart Disease, homocysteine.

We’ve seen in elderly patients a reduction over time in homocysteine levels, which are directly related to coronary, artery disease and heart attack. So these are some of the beneficial things that we’ve seen in patients taking this long term.

[Damien Blenkinsopp]: Great, great, thank you for that. So, are there things that you’re looking for in the next five or ten years, where you think there’s going to be some more changes or innovation? Or is there anything you’re kind of excited about the opportunity of this, to help more people or to improve it?

[Garth Nicolson]: Well we’re doing an anti-aging study right now, which I’m very excited about. It’s actually going on in Uruguay. A colleague of mine who is there is a specialist on sperm function, and he takes care of men with fertility problems. But as we age, our sperm function declines, and that’s what I’m interested in as a test model for anti-aging.

So far what we’ve seen is that even in vitro, if you take sperm they have a certain lifetime. So if you take older men they have less of a lifetime, that is they can be for a while, but then they start losing motility more rapidly than younger men. But if we put in the NT Factor in it, we can help restore the function of the sperm even from older men.

So the next step is that we’re going to go from these in vitro experiments, which are very interesting, sperm motility, to in vivo experiments where we look at actual men with fertility problems that have functional problems with their sperm motility, and see if we can help repair that process.

But in terms of it’s anti-aging, which is what I’m really looking for, long range, this is an interesting model to look at. So whenever we have systems that undergo slow degeneration, like sperm function over time, if we can reverse that process, that means that we’re having an anti-aging effect, and it’s very clear, it’s very specific, and very quantitative effect. And so that’s one of the systems that we’re looking at, and I’m very excited about.

And we also have a number of different diseases processes that we’re very interested in, and we’re trying to intervene and see if we can help. Neurodegenerative diseases is one thing I’m very interested in. That’s obviously a very long term and slow process to eventually recruit patients in that area.

Another thing is reducing the adverse effects of cancer in cancer therapy. So there are two aspects of this. If some person has cancer, often they have what’s known as cancer associated fatigue, in the absence of any therapy. And of course the NT Factor will help patients with that.

We’ve seen a 30% reduction in that fatigue with patients with long-term cancer, that have had cancer associated fatigue. But it’s really reducing the side effects of cancer therapy that is most interesting, because we’ve seen reductions in side effects to chemotherapy that are really dramatic. So there’s reductions, for example, not only in fatigue but in vomiting, and malaise, and a number of other side effects – headaches, for example, and so on – associated with chemotherapy.

I think the reason for that is we’re helping repair the normal systems very rapidly in these patients after their burst of chemotherapy. So you might ask, well does this interfere with the therapy? And the answer is no, because it turns out there’s a window of therapy which is very short for the cancer, but it’s very long for the normal systems.

So these chemotherapeutic drugs attack the cancer very quickly, but then they have lingering effects on our normal systems for months, literally, after the therapy is over. So, what this does is the NT Factor helps reverse that process of damage after the therapy.

[Damien Blenkinsopp]: It sounds like you’re saying that there’s no risk of them providing a protective effect to the cancer cells themselves, provided that you introduce a timing?

[Garth Nicolson]: Well what we do is we put it in after the therapy. Because we know the damage to the cancer cells occurs very quickly. Generally, within hours after the therapy is administered. Whereas the damage to the normal systems occurs for weeks, or even months later. So we allow the therapy to occur and then next day, the following day, we start the lipid replacement to help repair the normal systems.

[Damien Blenkinsopp]: This is really interesting work. You must be really excited about all of these projects you’ve been working on.

[Garth Nicolson]: There’s something new every day!

[Damien Blenkinsopp]: And luckily you have lipid replacement therapy to keep your energy up, so you can keep focused on them all.

[Garth Nicolson]: Well I’m taking it, and so far it’s been a real help. I know that personally. But every individual will have to see what’s optimal for them. Some people will find they have to take a bit more of the lipid replacement than other people, and that may have to do with their transport systems that bring these lipids into their bodies and cells, and everybody’s different in that regard as well.

So, the same thing with detoxification. We have systems in place to help detoxify us, but it’s working so poorly for most people, or their systems are swamped out with these dangerous chemicals and they can’t keep up with the damage, and so this helps accelerate the removal of chemicals.

And also, we know that’s an energy dependent process. So it helps rebuild the energy systems that are necessary for detoxification. Because detoxification just doesn’t occur naturally, it requires energy.

So if you don’t have the cellular energy necessary, you can give them all kinds of different things, and you’re not going to see much improvement, or at least you could see much better improvement if you repair their energy systems at the same time. So I think for any detoxification, mitochondrial repair is really important, because it really helps accelerate the detoxification process.

[Damien Blenkinsopp]: Great, great, thank you. There is a cost side of this kind of therapy.

So, in terms of monitoring, how do you assess whether someone should remain on the treatment? Is it purely based on symptoms resolution, or whatever they’re trying to achieve, or do you have any markers? You brought up the homocysteine, for example. So if they had raised homocysteine and it leveled out, you could say, okay now I can take you off the therapy, because you’ve got to that critical [point].

[Garth Nicolson]: Well, actually, here’s the problem that we have in the modern environment. We don’t stop people from being exposed. We don’t stop people from getting sick, we don’t stop people from getting into automobile accidents, or whatever. We can’t do that, but what we can help them do is repair once it occurs.

We can help repair and accelerate the healing process due to trauma. We can help the healing process due to infection. We can help the process due to long term treatment of a chronic condition. All of that means that this is a long term solution, not a quick fix. And that’s why I’m taking this for the rest of my life.

And I put my father on it when he was 92, and he had much better cognition, he had less fatigue issues, and was more ambulatory, and clearer thinking, and so on and so forth. And he lived another eight or nine years. He was a coronary patient and he was on his last legs when he started.

So I think it’s never too soon. Just like it’s never too soon to stop smoking, it’s never too soon to start taking lipid replacement therapy. And yes, you may have to take it for the rest of your life if you want the benefit.

[Damien Blenkinsopp]: Well, I think I’m certainly going to stay on it. And I’m very glad to have you on the show to spread the information about this. It’s been very useful to me.

In terms of other people who, besides yourself, you would recommend to talk to about mitochondria, or lipid replacement therapy. Is there anyone else who’s done work which you would reference which is interesting, that have done a lot of work in this area?

[Garth Nicolson]: People can go to our publications, because they can see what we’ve cited in terms of the references, and the groups, and so on. Yes, there are other people working on different aspects of it. For example, there are some groups in Europe that are using intravenous lipids – similar type but not the same – and they’re getting very good results with that.

We prefer the oral supplements because obviously you can’t go in every day for an intravenous lipid replacement therapy. So, we prefer people take it orally, because we know we have the mechanism in our brush border cells lining our guts to bring these lipids in naturally, because they’re essential lipids. So, this is a very natural process that we’re supplementing, essentially.

And I think people need to find out about this. The ATP Fuel that you mentioned is primarily available through physicians and naturopaths, and professional health people, but there are also a lot of people out there maybe listening that want to know where can I get this stuff on my own.

And there’s a website called, where they can buy all these products over the counter, because they’re just natural supplements. And so, that’s where they can go, to find these lipids replacement therapy products, and find out more about it. And they can go to our website, the Institute for Molecular Medicine, which is It’s like a media .org, and they can see the scientific results and the clinical trials.

[Damien Blenkinsopp]: Great, thank you so much. We’re going to put all of this in the show notes so people have all the references to everything we’ve spoken about today. Would you recommend they take the straight version of NT Factor? Because there’s these different combinations of things.

[Garth Nicolson]: Well it depends on what people want to do, and it also depends in a lot of cases on what people could afford if they’re buying supplements and stuff. The minimum thing they need is the NT Factor lipids.

Now, the more complex formulations like the one you’re taking cost more because they have a lot of other ingredients that are very costly. But if they want the initial punch, they need to take at a minimum the NT Factor lipids.

[Damien Blenkinsopp]: I see, that sounds like the big lever.

So Garth, thank you so much for your time today. Just on a personal note, are there any data metrics that you track for yourself? Either on a routine basis or a once yearly basis for your health, longevity, or performance?

[Garth Nicolson]: Well of course we look routinely at membrane lipids, for example, in our blood. We look at things like homocysteine and so on – and my levels are very low. I find that I feel better on NT Factor and, by the way, I have gone on a trip recently and I forgot to take it along, and I suffered because of it.

[Damien Blenkinsopp]: Oh no.

[Garth Nicolson ]: I feel very strongly about taking it on a daily basis. So I’ve seen it in myself. I mean I know that I can recover much faster from travel associated problems, for example, from illnesses and so on and so forth if I take the NT Factor.

And that’s what other people reported back to us as well, it’s not just my own personal results. We get a lot of feedback from a lot of people who are taking this, and now tens of millions of doses have been given to patients and subjects and so on, in various forms, and so far we haven’t had any complaints. And that’s a good news.

[Damien Blenkinsopp]: Its great news, it’s amazing news. Thank you very much for your time today, Garth. Its been great to have you on the show.

[Garth Nicolson]: Sure. Thanks for having me.

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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


  • 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


  • 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.


  • 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


  • 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.



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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A walk-through of a practical framework designed to achieve what most of us believe is impossible – completely eliminate aging. Learn about the 7 ways we age, and how scientists are trying to design tools to repair each one of them.

Today is our first episode on aging. Longevity is a subject close to my heart, and I’ve been following the career of this episode’s guest for many years.

Dr. Aubrey de Grey is a visionary and general strategist in the field of longevity and anti-aging. He applies the concepts of planning, investment, and risk management to the science of aging so that we get there as soon as possible, within our lifetimes. The basis of his plan is the seven “Strategies for Engineered Negligible Senescence” that offer a practical route to longer life.

“[The] seven major categories… was really the big breakthrough that allowed me to see that the repair of damage was not only the most promising approach to combating aging with medicine, it was actually a feasible approach that could realistically be implemented within a matter of decades.”
– Dr. Aubrey de Grey, PhD

Dr. de Grey may be the greatest activist for longevity of our time. He’s the Chief Science Officer for the SENS Research Foundation, a not-for-profit organization funding research into longevity around the world. He’s authored two books; Ending Aging: The Rejuvenation Breakthroughs that Could Reverse Human Aging in our Lifetime in 2008 and The Mitochondrial Free-Radical Theory of Aging, for which he received his PhD in 1999.

In today’s interview we examine popular longevity strategies such as caloric restriction and telomerase therapies, as well as those covered by his own research. His viewpoints on these topics contrast greatly to those you may see in the press, and offer important insights into whether we should make use of these existing strategies.

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!

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Show Notes

  • Aging as a medical problem versus “Aging as a disease” (3:55).
  • The relationship of aging to illness (4:35).
  • The difference between “diseases of old age” and general illness (6:51).
  • The relationship between aging and cellular damage (7:51).
  • How the “seven categories of aging damage” make the longevity problem solvable (9:28).
  • The roadmap to the end of aging (“Bridging”) (12 :12).
  • The roadmap to the end of aging (“Longevity escape velocity”) (14:16).
  • Are we waiting for expansions in biotechnology to achieve better longevity? (15:00).
  • Dr. de Grey’s and SENS’ research resources (16:13).
  • Mitochondrial damage as it relates to aging (17:48).
  • Changes in mitochondrial theory since Dr. de Grey’s first book (19:22).
  • The uncertainty as to whether mitochondrial disease affects aging (20:35).
  • The indirect route by which mitochondria may affect health (21:24).
  • Mitochondrial damage and the “metabolic theory of cancer” (24:09).
  • How current trends, such as calorie restriction, fit into the SENS theory (26:51).
  • Intermittent fasting versus long term calorie restriction (30:21).
  • How telomeres and telomerase affect aging (31:20).
  • The balance between telomerase and cancer (32:58).
  • Do telomeres really effect cell function and aging? (36:04).
  • The difficulty in finding biomarkers valuable for tracking physiological age (36:54).
  • The difference between useful biomarkers and transitory blood metabolites (40:02).
  • What can be done, today, to increase longevity? (41:13).
  • Managing longevity by managing an individual’s health risk factors (43:23).
  • More about the SENS Research Foundation and the Methuselah Foundation (45:45).
  • What biomarkers does Dr. de Grey, personally, track? (50:28).
  • The Palo Alto Longevity Competition (53:13).

Thank Dr. Aubrey de Grey on Twitter for this interview.
Click Here to let him know you enjoyed the show or what you’ve learned from it.

Dr. Aubrey de Grey, PhD & S.E.N.S.

Aubrey de Grey

S.E.N.S. Research Foundation

  • SENS Research Foundation: Foundation for the research of “Strategies for Engineered Negligible Senescence” (SENS) founded by Dr. de Grey as an offshoot of The Methuselah Foundation.
  • SENS’ tax deductible donation page: SENS is a U.S. 501-C3 tax-exempt nonprofit organization, which can also accept tax deductible donations from citizens of the UK and most of mainland Europe. By donating, you’ll be in good company. Peter Thiel, the billionaire entrepreneur, VC and co-founder of paypal, donated $3.5 million to its activities.

The Tracking

Biomarkers & Frameworks

  • 7 Types of Aging Damage Framework: The framework Aubrey discussed in this episode which he has developed as the foundation of the plan to end aging.
  • Insulin: Probably the best indicator for overall metabolic function and health. Blood insulin levels begin to rise when muscle cells (primarily) become insulin resistant, meaning they are not taking up glucose properly. Insulin resistance is a precursor to diabetes.
  • Triglycerides: An indicator of general metabolic health. The seven types of aging damage are based on the inevitable damage arising from the metabolisms of life, and maintaining general health is a factor in keeping this damage in check.
  • Homocysteine: Dr. de Grey tracks his homocysteine levels only because it’s been slightly elevated in his personal history, and not because he feels it’s a general biomarker for aging. This is a great example of personalizing your biomarker monitoring plan.
  • Telomere length and Telomerase: While Dr. de Grey did not feel telomere length or telomerase levels were valuable as an indicator of aging, he did discuss their potential value for the function of high-turnover cells as well as the possible cancer risk associated with telomere extension.

Lab Tests, Devices and Apps

  • 23andMe genetic testing: Dr. de Grey discussed the value of understanding one’s personal health risks and predispositions via genetic testing.

Other People, Resources and Books



  • Methuselah Foundation: The Methuselah Foundation was co-founded by Dave Gobel and Aubrey de Grey in 2003 to shed light on the processes of aging and finds ways to extend healthy life.
  • The Palo Alto Longevity Prize: The Palo Alto Longevity Prize is a $1 million life science competition dedicated to ending aging. Aubrey de Grey is on the board of advisors.
  • Moscow Institute of Physics and Technology: Doctor Aubrey de Grey is an Adjunct Professor at the Moscow Institute of Physics and Technology (MIPT). According to his onsite bio, “[MIPT], better known as ‘Phystech’, is one of the best educational and research institutions in Europe, attracting the most talented students from all over Russia in the field of physics and mathematics.”

Full Interview Transcript

Transcript - Click Here to Read

[Damien Blenkinsopp]: Aubrey, thank you very much for coming on the show.

[Aubrey de Grey]: My pleasure, thank you for having me.

[Damien Blenkinsopp]: So, aging is a disease. Obviously this isn’t what everyone thinks today, so why would you describe aging as a disease?

[Aubrey de Grey]: Well, it is actually because that is a controversial use of terminology I don’t tend to do that. I tend to try to sidestep the ambiguity of the terminology, first of all, and cut to the chase. So let’s say whether or not we choose to call aging a disease, what we can certainly say is that it is a medical problem. It is bad for you. It makes your body and your head work less well, and eventually it kills you. And that is what I call a medical problem.

[Damien Blenkinsopp]: Okay, fine. When you are looking at it from this perspective, are there things in previous interviews where I have seen. When we are young we can die and we can get injured from certain things. And when we age, when we are older in our 40s and 50s, we tend to get other health conditions which you could say are linked to aging. Are there certain conditions where you could say that if we didn’t age, we wouldn’t have to put up with these health or functionality restrictions?

[Aubrey de Grey]: Actually, yeah. And actually let me elaborate on that by referencing your first question about the age. I think the big problem with telemetry, with the use of the word ‘disease’ is not so much that we don’t call aging a disease. The problem is that we do call things like Alzheimer’s disease and cancer and atherosclerosis – we call them diseases. That is the mistake and the reason it is the mistake is because actually the difference between those things and the things that we rightly call diseases like infections is a much bigger difference, both in terms of the symptoms and the progression of the symptoms and the ways that we might be able to treat them. That is a much bigger difference than the difference between both of these, on the one hand. And the aspect with aging that we don’t call a disease – like declining function of the immune system or a loss of muscle or gaining of fat or whatever.

I think that if we are looking truly accurate and instructive, useful classification, if you like, of the various ways in which we can get sick then a much better one is to say that aging conflicts with everything that goes wrong with the body or the mind, predominantly for those people who were born a long time ago. And diseases are things that can affect young people just as much as older people.

[Damien Blenkinsopp]: Right, so the distinction – just to give some examples to the audience, would it be things like Alzheimer’s, Parkinson’s, even multiple sclerosis? I don’t think people tend to get that before the age of 30, for instance. Cardiovascular disease – would all of these kind of things be linked into that area?

[Aubrey de Grey]: Kind of, yeah. Certainly multiple sclerosis a bit of a gray area, whether you would really call it an aspect of aging – not just because it happens rather earlier than the other diseases you listed, but also because it certainly doesn’t happen to everybody. Whereas the diseases of old age, the commonest ones – whether it is cardiovascular disease, cancers, Alzheimer’s, these things tend to affect everybody at more or less the same age. Of course, some people die of one thing and some people die of another thing, but the only real reason for that is because of small differences in the rates at which different people accumulate the damage that results in these diseases. But most people who die of cancer die with Alzheimer’s in some level or other. Most people who die of atherosclerosis die with cancer. It is just that it hasn’t got so far along.

[Damien Blenkinsopp]: Right, so in your book The End of Aging, you describe the seven causes of aging. Would all of these be classified – would it be correct to call them some type of damage to the body?

[Aubrey de Grey]: I would call them damage, yes. In fact this is another kind of terminology question. I would say really that the best way to define the use of the word damage, in relation to aging, is that we would say that damage consists of exactly those changes to the structure and composition of the body at the molecular and cellular level that on the one hand arise as side effects of being alive in the first place, side effects of the stuff that the body does to keep us alive from one day to the next. On the other hand, they accumulate throughout life. They get progressively more and more abundant and eventually they get more abundant than the amount that the body is set up to tolerate, so that means they start to impair and eventually completely eliminate their physiological function.

[Damien Blenkinsopp]: Right, so there are clearly changes which take place because of aging, because of the processes that are going on as we are living.

[Aubrey de Grey]: I would say that they are aging, it is not so much by aging or they think they are aging, but the nature of aging is the changes in molecular and cellular structure.

[Damien Blenkinsopp]: Right. That is a nice way to put it because most of us think of aging as what we are looking at outside the body – the wrinkles and when you are looking at people you can see that aging. but in a respect we could say that the actual things you have defined and are changing within the body would be aging. so could you please outline what those are and which ones are the most important for you or if they are all the same? What is this kind of framework that you have and which ones are you most focused on currently?

[Aubrey de Grey]: The classification – there are seven major categories. It was really the big breakthrough that allowed me to see that the repair of damage was not only the most promising approach to combating aging with medicine, it was actually a feasible approach that could realistically be implemented within a matter of decades. If you have got 1,000 different things to deal with, then 1,000 different therapies are going to take a long time to develop. Well, if you can classify them into a much more manageable number of categories, such that within each category you are basically doing the same treatment for every example within the category and then the whole thing becomes much more feasible-looking, and that is exactly what I was able to do. So the categories are very simple things like having progressively-fewer cells in a particular organ or tissue because cells are dying and not being automatically replaced by the division of other cell. Or we accumulate molecular waste products in the cell because the cell is creating this waste product as a byproduct of something it needs to do. And the cell does not have any machinery either to break it down or to excrete it, so it accumulates.

Now, in each of these things we can look at and we can point to particular diseases and disabilities of old age that are predominantly caused by one or another of these things, so that is what we work on. And yes, we feel that all seven of these categories of damage are equally important. Certainly – well, there is one exception I guess, which is mitochondrial mutations where we can’t 100% certainly say it matters as much as the others. Actually, it might matter more than many of the others, we don’t know. But all the others we can say they matter pretty much equally as much because we can go into a particular nature, age, relation, or [pathology 00:11:42] and kill people at more or less the same age driven by that damage.

[Damien Blenkinsopp]: I see, so you are saying that pathology can be linked to each of these aging processes?

[Aubrey de Grey]: Yes, for example, molecular garbage inside the cell I just mentioned, that is definitely the reason we get heart disease, atherosclerosis – molecular garbage outside the cell is a major cause of heart disease in certain areas. Cell loss is the major cause of Parkinson’s disease, and so on.

[Damien Blenkinsopp]: Great. Thanks for that clarification. So you have outlined a roadmap to basically end aging and you have brought to light two concepts that I understand there are like bridges and there is something called longevity escape philosophy. Did you explain how these are eventually going to end aging or stop us from having to go through this process of aging?

[Aubrey de Grey]: Sure. So first of all, let me talk about bridges. That is actually not my terminology – that comes mainly from [Ray Kurzweil 00:12:40] who has often pointed out that there is a certain amount that we can do today to postpone the ill health of old age, and that is good. That is all very well. But there is actually more. Maybe we will be able, some of us anyway, to postpone the ill health of old age today with methods already available well enough to still be around in time for therapies that are not yet developed, because they haven’t yet been developed. If that can be done then of course we get an additional amount of life and we may be around for the next generation therapy, and so on.

And that concept – well, he normally talked about three major failures – what we can do today, what we might be able to do in the next couple of decades with our technology, and then what we might be able to do in decades after that using more of the non-biological solutions such as nanotechnology. And that is a fine way of putting it. Certainly the biotechnological approaches that he favored are pretty much identical to the ones I favor. And nanotechnology is certainly not an area in which I can claim much expertise, but I think he is more or less on the mark there, as well.

There are some where we part, actually, Ray and myself, as to how beneficial for most people what things are today, things that you can do already. And I think that [Bridge 1 00:12:40] as he calls it may not be much of a bridge, but by large the concept – we stand together on this concept. So the longevity escape philosophy, which you mentioned, is indeed from a phrase that I invented. And here I am not splitting the process of getting from here to indefinite longevity into that particular number of phases, like three – I am just saying that once we get a certain way along this process we are safe because we will be improving the quality and comprehensiveness of these therapies fast enough to stay one step ahead of the problem, essentially be repairing the damage that we couldn’t yet repair well enough that the overall abundance of damage will at no point reach a level that exceeds what the bod is set up to tolerate.

[Damien Blenkinsopp]: Right, and this relies on the concept that medical technology and biotechnology will be advancing exponentially?

[Aubrey de Grey]: Oh not at all and this is something which – and again I talk a lot with respect to I owe to information technology that we can see there is an accelerating track where progress is made at a faster rate as time goes on. In the case of longevity escape philosophy that may well happen, but the key point is it does not need to happen. In fact, if we are able to say 20 years from now or 30 years from now to reach this point where people are eventually not getting older, they are getting repaired as fast as they are aging, then it turns out that thereafter we can actually proceed at only that same pace and perhaps even slow down a little bit and will still be doing well enough simply because the rate at which the damage we cannot yet repair is accumulating will diminish as the types of damage that we can’t yet repair become fewer and fewer.

[Damien Blenkinsopp]: Great. Thank you for those clarifications. So what, for you, is the first and most important step? Right now are you really focusing – because you do funding of research and you kind of prioritize things – are you kind of prioritizing any of these steps in particular? Are you are trying to spread your investments so that you kind of manage the risk?

[Aubrey de Grey]: Very much the last, we are spreading. We have our fingers in all of these fires because we feel it is pretty stupid if we focused on some of them and then the other ones didn’t get done by us or by anybody else and people carry on dying on schedule even though most of the problems have been fixed. So we need to make sure, especially for the areas which are least fashionable, are being most severely neglected by other people, that it is vital for us to move forward. In fact, that is the only criteria that we use that really does determine what we choose to work on and not to work on. So the real manifestation of it is that we do very little work in stem cells. Stem cell work is very limited simply because so many other people are already working in that area. It is very burgeoning, very fashionable. So our work effort would be a bit of a drop in the ocean where we are the leading group working in many of the other areas.

[Damien Blenkinsopp]: Great, so basically you are choosing the least fashionable topics so that other things get pushed on it? And we actually do need to fix all of these problems. I mean, that is your assumption – in order to extend life and create longevity?

[Aubrey de Grey]: That’s right. I don’t think it is even an assumption, I think we know it.

[Damien Blenkinsopp]: Okay, great, great. So one of your other books looks specifically at mitochondrial mutations and the free radical theory of disease. Why did you specifically write a book about that topic?

[Aubrey de Grey]: Great question. So that was a long time ago. That book was published in 1999 and it is actually the only other book I have written. I have only written two books total. It was simply the first area that I got interested in when I decided I wanted to work on aging, whether it being to do something about it. Of course, I started out knowing nothing about that subject. In fact, I didn’t know all that much biology. I had been a computer scientist for my research career until that point. So I had a lot to learn. And obviously you learn some things before other things just by random chance. I ended up gravitating into the area of mitochondrial mutations as my main focus before I got interested in the other things.

So for the first few years of my career in gerontology in the late 90s, that was what I was working on and that was where I published my first half dozen papers or so. And my very first paper came to the attention of a publisher who did low print run academic books and said – anyway, what I wrote, so he said that he liked what I did and asked if I could go on writing a book, so I said all right, and that was the result. So the material in there covers pretty much my first three or four years or gerontology research. And it actually was also the [inaudible 00:19:08] idea was cemented to the University of Cambridge and I got the PHD for it.

[Damien Blenkinsopp]: Great. So would everything you wrote in there still be valid today or are there things you have discovered which you would change, some of that?

[Aubrey de Grey]: So the fantastic thing is that more or less everything is actually still true. There have been, of course, some minor discoveries that have changed things, but the broad sway of what I was writing there is certainly still true with one big exception. That big exception is exactly the exception that you like to have – namely, as time has gone on, new techniques, new ideas, and new discoveries have been made that essentially provide shortcuts – they have made the job of fixing this problem easier. And that is true also for the book that I wrote for ending aging, which is not nearly half as long ago as I wrote the mitochondrial and free radical theory book. So, they are pretty good, the lead idea of standing the test of time so well – the seven point plan that we work on is pretty much identical to what I was describing more than ten years ago or 12 years ago. So that is really circumstantial, but nevertheless quite strong evidence that we are on the right line, that there is more to this robustly standing the test of time.

[Damien Blenkinsopp]: Well congratulations because that is not an easy feat given how everything is changing so fast in biology and so on. So you have talked a bit about – one thing you mentioned earlier was except for when you are talking about the seven different areas and causes of aging, you said that mitochondrial damage may or may not be one of the most important ones. Why is there that area of uncertainty around mitochondria specifically?

[Aubrey de Grey]: Simply because there is no one major pathology we can point to where we can say clearly that there is a chain of events from this particular type of damage to that particular pathology. In the case of every other – the other six types of damage, we can point to a particular pathology and say that it is established. It is not even a hypothesis, it is actually known and absolutely agreed that the main driver of that pathology is a lifelong accumulation of that particular type of damage.

[Damien Blenkinsopp]: Great. So is that because we need to do more research to understand properly this mechanism in mitochondrial damage so we can say that we understand it less than the others?

[Aubrey de Grey]: I don’t think so, actually. I think the reason is the actual fact of the biology, rather than our understanding of the biology. I think it is possible that mitochondrial mutations simply don’t matter very much in aging, but it is more likely that they do matter but only by a very indirect route. And if it is indirect then it may be very placebic and it is something that affects pretty much all aspects of aging but in a subtle manner. So if you look at my book in 1999, you will see that there is some discussion of a rather elaborate mechanism – in fact, it is so elaborate that a lot of people just didn’t like it because it was too elaborate, which basically says that if mitochondrial mutations are accumulating even to relatively low levels, they may be able to be disproportionately toxic by essentially damaging molecules in the blood stream. And if they do that then those molecules can get into other cells and spread the damage around and kind of amplify it. This model is still very much a hypothesis and it has by no means been shown to be true, but it hasn’t been shown to be false either. And in fact bits of it, occasionally here and there, end up acquiring little bits of supporting data. There was a paper actually put out in [inaudible 00:22:54] just a few weeks ago, which was the first one to support one little technical detail of that hypothesis which previously had been completely controversial.

[Damien Blenkinsopp]: Great, great. It seems to me that mitochondria have become quite fashionable lately, just from my perspective. I don’t know if you would agree with that, when you are talking about the least fashionable versus the quite fashionable. There are a lot of supplements that tend to target more mitochondria and the word just tends to come up a lot more.

[Aubrey de Grey]: So yes, in a general sense mitochondria are very fashionable. Lots of people work on them. They have the major pre-eminent conferences on mitochondria that are bigger than ever, and so on. But the particular question of how we might be able to restore health to cells that have been taken over by mitochondrial mutation, that is obviously a very, very narrow area within mitochondriology and that is not fashionable at all. We don’t know, but we think it’s because people think it can’t be done. It’s a nature of science that people work on, things that they think they can succeed on and get published and promote and those things. And that means the hardest things often don’t get worked on at all.

[Damien Blenkinsopp]: Right, absolutely. So like Dr. Thomas Seyfried is well-known for his ideas around mitochondrial and metabolism and cancer. Do your ideas connect with his or are they different?

[Aubrey de Grey]: I don’t actually know that name. Tell me about this guy and his ideas.

[Damien Blenkinsopp]: With the metabolic theory of cancer?

[Aubrey de Grey]: Okay, there are various metabolic theories of cancer, but go on – tell me the ideas a little bit and I will tell you what I think of them.

[Damien Blenkinsopp]: Well, the idea is basically about free radical damage of the MT DNA and once that is damaged the mitochondria are not functioning so they are not giving sufficient energy to the cells. The idea is that from there the cells start behaving in a different manner, which includes cancer.

[Aubrey de Grey]: All right, so certainly stated that simplistically that theory is not correct. Variations of it –

[Damien Blenkinsopp]: I am sure I am not doing it justice at all.

[Aubrey de Grey]: Variations on that idea may have some validity. Certainly we see in aging that normal cells that are not cancerous at all accumulate mitochondrial mutations. Only a small minority of cells do that, but the ones that do get completely taken over by that mutation. In cancer we don’t see those same mutations. We do see some mutations sometimes and certainly one thing that we see much more ubiquitously is a depression of mitochondrial function even in the absence of any actual mutations. So the [inaudible 00:25:36] and we certainly have a number of theories out there that describe how cancer cells may obtain some kind of advantage then and protect themselves from the immune system, for example, by doing things like that or reducing their oxidative metabolism. So if that is the general theory that is being put forward, then yes, there is a certain amount of validity to it. But the thing that counts is that there are an awful lot of ways this can occur. There are an awful lot of ways that cancer health can discover to escape the normal controls that stop cells from dividing when they shouldn’t. So they have to do a bunch of things like breaking down the intracellular matrix, they have to ignore the signals that tell them not to divide, they have to ignore signals that tell them to die. They have to, as I say, resist the attack from the immune system. All of these things are really hard and any cancer that has reached a size where it has come to the notice of the clinician it has already jumped through a million hoops. So there are a lot of different ways to be that way.

[Damien Blenkinsopp]: Great, thank you. So today we have a lot of things in the press – there are a lot of products and there is a fair amount of research around topics which supposedly could help to give us longevity. Some of these are caloric restriction and linked to that fasting, autophagy, mitophagy and then we have the telomeres, telomerase and some others. For any of these things that are available today, and we can stop and look at them separately, I understand that you feel that none of them are actually targeting any of the seven areas, or any of the seven causes of disease sufficiently to actually extend our life. So could you talk a little bit about why you feel that is? Perhaps you want to tackle the biggest one, which is caloric restriction, for example?

[Aubrey de Grey]: Yes, by and large the simple approaches that we have today are not even hypothesized to actually repair damage the way that science is trying to do. So the best that could be said about these things, the proponents will say, is that they may slow down the subsequent accumulation of more damage. So that is still good. That means you are postponing the age at which the damage reaches an abundance that is insupportable, but of course the later you start the older you are when you start doing it. And then even if it works, the less benefit you are going to get because you have already accumulated all the damage at the original rates. So that is bad enough, but yeah. So you can say I am also very pessimistic about the ability of the approaches even to slow down the accumulation of damage by a meaningful amount. In very short-lived species calorie restriction is very effective. We can certainly increase the lifespan of a mouse from let’s say two-and-a-half years to three-and-a-half years using calorie restrictions, and that is pretty impressive. But if we go further down the evolutionary chain and we ask about small invertebrates like worms, for example, that normally live only a few weeks, it turns out that calorie restriction can do a great deal more. You can multiply the longevity of a worm by a factor of maybe three or four by calorie restriction.

The unfortunate thing is that this correlation, this inverse correlation between the natural span of the species and the extent to which that lifespan can be multiplied by calorie restriction works the other way as well. So 20 years ago people did a calorie restriction experiment on dogs and they only got a 10% increase in lifespan instead of the 40% that you might get in mice. And more recently we had a couple of experiments that on for more than 20 year looking at monkeys under calorie restriction. They finally reported and they got less than 10% – in fact, one of them was basically faster. So it is not looking too good. The worst of it is that this is what we should have expected because it actually was predicted by evolutionary theory – especially simply because long famines are not so frequent as short famines. We are unlikely to have the ability – to have evolved the ability – to respond to long famines in a manner that would increase our evolutionary fitness whereas short famines we experience frequently enough irrespective of how long the actual lifespan is that it makes sense to have that ability.

[Damien Blenkinsopp]: That’s great. And of course, currently the more fashionable topic around caloric restriction and fasting is intermittent fasting, which is typically anything between 18 and 24 hours for most people. Do you have a different view of that and the idea of this, which is activation of autophagy which can help to clear up some of the cellular garbage?

[Aubrey de Grey]: No, it is absolutely the same. The kinds of metabolic changes and expression changes that are induced are basically identical, and a good approximation – whether you have continuous calorie restriction or intermittent fasting or whether you use drugs that essentially trick the body into thinking it is on calorie restriction when it isn’t like [rapamycin 00:30:59] or whether you use genetic modifications in model organisms that trick the body in that way, by turning on the same pathway. It is no surprise. All of these things are turning on the same response, they are just turning it on in different ways. So of course you are going to get the same response.

[Damien Blenkinsopp]: Great, thank you very much. So the other big area – I guess you could tell me if you see this as the other big area because you do a lot of these interviews and you probably get the same kind of rejections. I think the other big area is telomeres and telomerase, which has become very fashionable now. And I understand that of course you think that isn’t an area that is going to help us?

[Aubrey de Grey]: Sure, so the telomere is a critical part of the cell and the organism and we definitely need to understand how it changes with aging and the extent to which those changes are good or bad. But we definitely cannot say at this point that the changes we see during aging are uniformly bad and therefore the thing to do would be to stop those changes from happening. The reason we can’t say that is because it seems that large animals, or large mammals and certainly humans, have made use of the telomere as a kind of way to get a tradeoff – get the best of both worlds between two important aspects of aging. One of them being the inability of the cell to – well, let me back up and say it a little differently.

One of them being the increasing inability of cells to divide and the other being the increasing tendency of cells to get into a state where they divide when we wish they didn’t. Most of our cells, let’s remember, do not divide – or if they do, they only divide fairly rarely, on demand. Like, for example, skin cells – the bottom layer of the skin that divide like crazy when you have a cut, to close the wound. It is only a small proportion of our cells, a few cell types, the stem cells of rapidly renewing tissues like blood which divide regularly. Those are the only cells that have a potential problem of telomere shortening.

Telomere shortening is something that happens when cells divide because of the nature of DNA replication and eventually when cells have divided enough they end up getting telomeres that are so short that bad things happen in the cell. I won’t take the time to go into what bad things, but the cell basically gets unhappy.

So cells that divide rapidly need to compensate for this and they have an enzyme called telomerase which does so. They certainly don’t need that capacity because they don’t divide often enough. They just don’t make the same amount of telomerase. Now, most people believe that the reason why they don’t make it is so that if they mutate, or become cancerous, then the cancer will not be able to grow large enough to kill us because that will require enough cell division that the telomeres will get short and bad things will happen to the cancer cells and the cancer will just wither away. So the question is if we want to do better than what evolution has done, how do we address this tradeoff?

One way might be to make most of our cells create more telomerase, more of this enzyme. That would allow cells in the blood, for example, to divide more than they currently do. And that would be interesting because it might make the blood continue to work better and the gut continue to work better, and so on, but it would run the risk of exacerbating cancer. The alternative is to go the exact opposite direction to bear down on to telomerase and make it less of it. That might be a really good way to suppress cancer but it might exacerbate the more degenerative aspects in that it makes our blood age faster, for example. We simply don’t know which of these factors is going to better because really it is not just which of those things you do, it is also how you cope with the side effects that you are creating. You are going to make one or other sides of the equation worse, you have got to find some secondary therapy to alleviate that and we of course don’t know yet.

So a number of people are working on the telomerase stimulation side of the equation, going to rescue the aging of dividing cells by giving more telomerase and then trying to find some other way to deal with any cancer problems that might arise. And we are going the other way and saying we are still with cancer by suppressing telomerase and left the other cells to deal with the cell division problems that might arise.

[Damien Blenkinsopp]: Right. And that seems to be because cancer is one of the most sure things which is actually going to kill us versus the other side of the equation, which you are saying is more of a functional impact rather than a kind of end of life kind of impact?

[Aubrey de Grey]: Well, I wouldn’t quite put it like that. I mean, there is still the big question of the extent to which telomere shortening really contributes to the pathologies of old age, so definitely telomeres get shorter in the blood in older people, but nobody has really been able to show they get so short they cause loss of function. So we actually may not need to worry about that in a currently normal lifetime But for sure, if we were to suppress telomerate in the manner that I have been talking as an anti cancer therapy, then we would create a problem even if the problem doesn’t already exist.

[Damien Blenkinsopp]: Right – when we are dealing with really complex problems it has been shown that can often be the case for therapies. So a key thing we talk about in this podcast is any aspects of quantification and with respect to longevity I am wondering if there is anything that you feel that is worth monitoring to track how we are aging? Now, currently it is fashionable with telomeres to measure the telomeres and they have indexes which say your telomeres versus someone else your age are above average or below average in terms of how many you have left, basically. Are there any biomarkers that you feel can validly track the progress of aging and perhaps how it varies between different people based on their lifestyles, their genetics, or any other factors that might be affecting the rate at which they age?

[Aubrey de Grey]: That is a really tough question. They don’t actually age, the Natural Institute of Health paid a huge amount of money several years ago, many years ago now, into a long-term study trying to identify biomarkers of aging that were really reliable and it was basically completely unsuccessful. They basically found nothing. Now, people haven’t given up on this but the reason they haven’t given up is the complexity. Essentially there are a couple other things you can die of, so how do you put aside whether one means by a biomarker of aging. Well, you have to define that some how, its another way of saying the predictor of how long you are going to live, what your remaining longevity is, or that you will remain in healthy longevity, but then you have to define health and it gets a little bit fuzzy as well. So it is actually quite hard to even define what you mean by biomarker of aging, but even once you have gotten past that difficulty, because there are so many different things that go wrong you don’t expect to have one simple or even fairly simple number that says something like this.

You expect, one would think, that as you get older you are as old as your weakest link. So you are going to expect that you would want to measure a lot of things and each of them points to a probability of getting a severe case of this or that type of age-related pathology in this or that amount of time. And certainly some things are more influential than others. These things affect each other and we may be able to point to things that are a bit more indicative overall of the probability of death or disease of all types in old age. But it is a very – it is not an exact science, put it like that. I have been lucky enough to have my biological age tested, which I have been able to do maybe four times now over the past decade or more. The test I have been able to get done on me involved measuring probably 150 different things in my blood as well as all manner of physiological and cognitive tests. There is no one number that comes out of that, really. There is no one useful number. The only thing that really usually comes out of it is what to pay most attention to, what seems to be changing more rapidly or seems to be problematic levels or that of other people of your own chronological age, those sorts of things.

[Damien Blenkinsopp]: Right, so there are 130 markers. Would many of those fit within your seven areas of damage and kind of be related to that?

[Aubrey de Grey]: Oh certainly. Certainly not now because the things that one measures in the blood aren’t metabolized. These are small molecules that are constantly being ingested into the body or synthesized by the body or destroyed by the body or excreted from the body. The blood stream is just this pipeline, right? It is just this network of roads that take things from one place to another and particularly it shortens molecules whereas the seven types of damage that I talk about, types of molecules or cells, the molecular or cellular changes that accumulate over time. So in other words, yes, the concentration of a particular small molecule in the blood may change but that is because of subtle changes in the set point, in the equilibrium between synthesis and destruction or ingestion and excretion of those molecules, which are kind of readouts of the level of damage elsewhere – maybe of the activity of enzymes or the activities or numbers of certain cells, for example. But they are not the damage itself, they are readouts of the damage.

[Damien Blenkinsopp]: Okay, great. So if we wanted to live longer today – I mean, I know one answer which we are going to definitely come up with at the end which we need to talk about, like helping you fund the different areas because you see that as the most important to targeting these areas that we are not really looking at – but for the people at home who are concerned about their longevity, what would be the best strategy for them in terms of thinking about their own health?

[Aubrey de Grey]: I wish I had a better answer to this, I really do. Certainly I know that there are some people – if you are an unlucky person, so Ray Kurzweil – come back to Ray Kurzweil again because of course he is well-known as someone who thinks that one can make a big difference to one’s longevity using supplements and so on. He probably is making a substantial difference to his own longevity that way, but that is because his own longevity by default was probably going to be rather shorter than average. He has a lot of cardiovascular disease in his family, he came down with type 2 diabetes in his 30s, which is pretty unusual even though it is not unheard of. And he has been able to really completely fix that using his regime that he developed himself and I totally applaud that. What I can’t do is say that this would apply to people who are already doing okay, especially those doing better than average, like me. Only if you are somehow unlucky, we have simple ways that may be able to somewhat normalize your rate of aging. Now, of course, on top of that, there is the fact that there are plenty of ways to substantially shorten your longevity by smoking or getting seriously overweight or eating a very poor diet, for example, but you didn’t need me to tell you that. I bet your mother told you.

So unfortunately over and above that, as things stand, we cannot point to anything that can appreciably help most people. And that of course is why I always say the only thing you can really do is buy more time – not by extending the time that you stay healthy but by reducing the time before therapy had come along that would actually do much more than anything that exists today.

[Damien Blenkinsopp]: Right. So I will kind of run by you the way I think about this and see if you have ideas on this, to see if this is a decent idea or not. The way I talk to my friends and stuff when they ask me these kinds of questions is I say that basically you want to manage your biggest risks, right? So if you were talking about Ray Kurzweil has cardiovascular risk in his family. For instance, you had a 23&Me or other set of genetic tests which point out that with some probability you have – for instance, I have a higher risk of lung cancer than most people and a couple of other things in my profile and people have different risks. So I suggest they look at that and then potentially they look for the biomarkers related to that on an ongoing basis rather than the genetic longer-term risk. And they monitor that and they also look into the things that can reduce that specific health risk and to reduce the risk and to limit the risk of them actually getting that biggest risk. So it is kind of plugging the biggest gaps they have of shortening their lifespan. I am just wondering if you think that is a reasonable approach?

[Aubrey de Grey]: For sure. I think in general for most people if you have got a risk factor that puts you at risk of being considerably shorter length than average, then you are going to know about it as a consequence of the kinds of metabolic tests I was talking about. But there can certainly be exceptions to that, things that truly don’t really affect your health as measured in normal ways, so that is all they do. Like suddenly some of them bite you in the backside. So that is the kind of thing that 23&me analysis might lower. But one also has got to be extremely careful in evaluating that kind of data because ultimately it arises from basic science. It arises from people studying particular genetic variations in the population and identifying correlations between those variants and the instance of this or that to these. And those studies are notoriously difficult to do and they have a notoriously low level of reproducibility because different populations are different and because sample sizes are limited, and so on and so forth.

[Damien Blenkinsopp]: Thank you. I always appreciate your answers because they provide a different context and perspective to everyone else so it is always very interesting to get that feedback. Let’s talk a little bit about SENS organization and what you’re up to there because this is your vision basically for making it happen. So you have different activities – and I also want to know a little bit about the [Methuselah Foundation 00:45:56] which you were formerly part of. And I understand that has some similar activities although it is going about it in a different way.

[Aubrey de Grey]: Sure, and let me actually start with the Methuselah Foundation because that makes more sense chronologically. The Methuselah Foundation is a charity, a 501-C3, that was created by myself and a businessman from Virginia named David Gobel in 2002, late 2002. Our goal was, of course, was to hasten the defeat of ageing but we didn’t have any money. So we started out creating a prize pot creating competitions in which we encouraged people to give up money that would go into a prize box and that the competition would be to beat the prevailing world record for mouse longevity. So with all you had to do the mouse that lived longer than any mouse had ever lived before. And of course we weren’t saying how things would be done and we set things up so that even a small improvement would be enough to win some proportion of the prize box. And it worked.

Basically our goal was to raise the profile of longevity research to get the word out and to get people more interested in the possibility of developing medicine to postpone ill health of old age. Well, we were bringing all this money in and right about 2005 or so we had enough money that we felt we could spend some of the prize pot in advance on actually pursuing specific research projects. So that is what we started to do and then things started going pretty well in that regard. But then we had a problem which we started to recognize in about 2008, which was that if you are a research organization you have got to obviously impress people with your competence and you have got your feet on the ground and everything like that and you are doing the right stuff. Well, if you are a PR organization, to get people motivated and so on, then you want to be the opposite – you want to be very popular, sensational, and glitzy. So we felt that it would actually serve the mission better if these two themes of our activities were between two different organizations, which would thereby be able to have very different styles, discourse, and styles of communication. So that is why we created the SENS Research Foundation, which was started in 2009.

SENS Research, of course, is also a charity – a 501-C3 so anyone can get tax back. And because this is going out internationally I should probably mention that we have a subsidiary in the UK which is able to take tax-deductible donations not only for UK citizens but also from most of mainland Europe. And if anyone wants to know about that they can contact us on the website and we will tell them more.

[Damien Blenkinsopp]: Thanks. We will put all the links in the show notes.

[Aubrey de Grey]: Excellent, thank you so much. So we created the SENS Research Foundation and it has been a truly, and the Methuselah Foundation and all the assets that have been given us research into the new foundation, so both foundations have been made in parallel since that time and I think we have both done pretty well and it is pretty good. So SENS Research Foundation, to go into a bit more detail – we are headquartered in Mountain View, California, just a little south of San Francisco. We have about 5,000 square feet of space in a facility, most of which is lab space. We have a variety of projects going on here. We actually have more than two-thirds of our research budget is not in our facility but rather in five university labs, again most in the USA, but some elsewhere. We have on outside Cambridge, Biotechnology Institute, and these projects are focused on all of the various areas of research there that SENS describes.

[Damien Blenkinsopp]: Yes, and I don’t think we have actually said what SENS stands for – Strategies for Engineered Negligible Senescence.

[Aubrey de Grey]: That’s right. We don’t often try to spell that out because it is a bit of a tongue twister. The name originally arose because of – well, basically historical reasons within gerontology. The phrase ‘negligible senescence’ already had a particular technical meaning and it seemed like a good place to start. But it is a bit of a tongue twister so we don’t bother to get people to remember that anymore.

[Damien Blenkinsopp]: Great, thanks. I will put links to all of those, of course, in the show notes. One last thing I just want to ask you, Aubrey, is from a personal stance you have said every few years you are going to test 130 markers or so of your own. Are there any specific things that you feel are important for you to personally track about your body for longevity, health, or performance?

[Aubrey de Grey]: Well, yeah. I mean, I think that first of all, coming back to something that we were talking about earlier, if any one marker is out of whack, you know, it seems like it is really telling a much more pessimistic story than the rest, then you have certainly got to try to ask yourself why, ask yourself whether it really is an outlier, whether it actually has that much impact given everything else as people say, things like that – but it is definitely not something that would be a good idea to ignore. So my one outlier the past couple of times I have done this kind of thing has been homocysteine, and I have no – I am not really sure why my homocysteine level is unusually high because everything else that it is supposed to interact with has not – but it is still something that I pay attention to.

From that, I can certainly say that there are certain things that are really at the nexus of metabolism, things that really if they are extremely good then you will be pretty safe, pretty much with whatever else is happening. Insulin is the best one. And of course, insulin is the hormone that mediates the absorption of sugar after you eat a sugar-rich meal so that the overall concentration of sugar in the bloodstream is maintained at as constant a level as possible. And the precursor of diabetes, type 2 diabetes, is something called insulin resistance, where the cells that take up sugar in response to insulin, which are mainly muscle cells, start to be a little sluggish about it and to only respond when they are given a large amount of insulin. So if your insulin is high, then even if your glucose tolerance, as it’s called, your ability to normalize your glucose in the blood is still good, then the indication is that it won’t be good for very long. Whereas glucose tolerance is good and also your insulin is really low then that says that you are in the best possible state. I would say if you have one thing, that would be it.

Perhaps another one would be triglycerides, whether it is a type of fat which seems to be good to have very little of in your blood stream and again, I am pleased to say that I do.

[Damien Blenkinsopp]: Thank you very much because those are basically the biggest diseases that we have today, like metabolic syndrome, so those are good markers for that. I guess one of the confusions with biomarkers we are always facing is that we are not sure if it is the end point. So one last question I did have for you was on a Palo Alto longevity prize. I am not sure if you know about that?

[Aubrey de Grey]: I certainly do and I am invited to it.

[Damien Blenkinsopp]: Oh, great. Because I understand they are running a competition or they have been running a competition for heart rate variability in connection with longevity.

[Aubrey de Grey]: That’s right, yes. So, businessman in the Bay Area in Joon Yun has put up a million dollars as a prize fund for progress against aging. It is divided, actually, into two separate prizes. One of them is looking specifically at heart rate variability, as you say, but the other one is a bit more general. It is looking at what they call homeostatic control or something like that. I forget the exact terminology. But the point here is that the competition is for the attempt to actually extend longevity [inaudible 00:54:06] in this manner. And I think this is great. I mean, the heart rate variability aspect is a bit unusual for people who have not really bought into the idea that this could be a real fulcrum of aging but it might be. And we think it is great to encourage research in any area that hasn’t been terribly well looked at. The main thing is simply putting a million dollars on the table as a great way to get people pretty excited, and a lot of people are paying attention now, especially since in the Bay Area there is a lot of identity of people interested in longevity in general. It’s a great way for a research foundation to be located. So yes, I absolutely applaud them for doing this.

[Damien Blenkinsopp]: Great to hear you are part of that also because we had heard of that from one of our previous guests. Aubrey, thank you so much for your time today. I love to hear all your different ideas of course because you are working at a very high level compared to most people, so you have this perspective that stands back a bit, which can be very helpful to people. Thank you so much for your time and have a great day.

[Aubrey de Grey]: Thank you, and to you. Bye.

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Are your autoimmune and chronic health issues driven by mitochondrial damage? Could nutritional and other simple approaches targeting improved mitochondrial function provide the answer to many of our modern day ailments?

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.

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.

“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.”
– Terry Wahls

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.

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

What You’ll Learn

  • 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.

Thank Terry Wahls on Twitter for this interview.
Click Here to let her know you enjoyed the show!

Dr. Terry Wahls and the Wahls Protocol

Specific Research & Studies

Tools & Tactics

Diet & Nutrition

  • The Wahls Protocol: Incorporates the nutritional, exercise and lifestyle guidelines that Terry Wahls has tested, devised and which she is working on validating through clinical trials.
  • Increase Nutrient Density: A key pillar of the Wahl’s protocol is to increse the nutrient density of the diet. The idea is to provide sufficient nutrients for the body to be able to repair the functioning of the mitochondria, which as a knock on effect reduces autoimmunity.
  • Learning How to Cook: In her years of experience working with MS patients Terry has found that one of the most important steps is that a person (or family) learn how to cook the types of nutrient dense meals that fit with the Wahls protocol. In her experience this is the biggest hurdle that people wanting to implement the Wahl’s protocol face. This includes the basics, such as how to stock your kitchen with the right foods, to having clear recipes that fit with the protocol. Having recipes for smoothies, juices, salads, soups, and other meals that can be quickly prepared and are of reasonable budget make or break the protocol for most people.



  • 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

  • NutrEval: Dr. Wahls uses this specific test in her current clinical trial – at this stage primarily to see what patterns emerge.

Other People, Books & Resources

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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