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Deuterium Depletion: Powerful Health Hack for Energy, Cancer Prevention, and more, with Dr. László Boros

In this episode, I am speaking with UCLA professor Dr. László Boros—an expert on metabolic water biochemistry–on why a strange substance you’ve never heard of called “deuterium” could be the hidden key to unlocking vibrant health, preventing disease, and having high energy levels.

In this podcast, Dr. Boros will cover:

  • What deuterium is (and how it harms the body)
  • The best lifestyle habits for lowering deuterium levels in the body
  • How to test and measure deuterium levels in the body
  • How light can support deuterium depletion
  • How mitochondria are affected by deuterium 
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Deuterium Depletion: Powerful Health Hack for Energy, Cancer Prevention, and more, with Dr. László Boros – Transcript

Ari Whitten:  Hey there! Welcome to The Energy Blueprint Podcast. I’m your host, Ari Whitten, and today I have with me Dr. László Boros, who is a professor of pediatrics at UCLA and the co-director of the Stable Isotope Research Laboratory at the Los Angeles Biomedical Research Institute, with a primary focus on studying cancer cell metabolism. He was born and educated in Hungary, and his medical background includes three years of gastroenterology and pancreatology, focusing on chronic pancreatitis and pancreatic cancer. He’s an internationally-proclaimed expert of metabolic water biochemistry, as well as deuterium-mediated kinetic isotopic effects and health and disease. So I’m sure that many people listening to that are probably like, what the heck did he just say? And I promise you, we’re going to do a good job of simplifying what this is all about.

I want to just say at the beginning of this, the primary focus here is something called deuterium. And we’re going to talk a lot about this compound in the body called deuterium, and how it accumulates in water in our cells, and how we can deplete it. And what it does when it accumulates—the harms that it can do when it accumulates in our cells—and one of those is cancer, which is why Dr. Boros has such an interest in cancer—or I should say, maybe why he has such an interest in deuterium, from the background in cancer research. And there’s also some research linking this compound, deuterium—this accumulation of it—to a range of other health problems, and there’s research currently being conducted in relationship to chronic fatigue specifically. So we’re going to be talking all about deuterium, and it is a complex topic, but I’m going to do my best to ask simple questions and simplify. And I’m sure Dr. Boros is going to keep that in mind as well, and do his best to make everything as simple and easy to understand as possible. So, welcome to the show, Dr. Boros, it’s such a pleasure to have you.

Dr. László Boros:  Right. Thank you very much. It’s an honor to be part of the show.

Ari Whitten:  Yeah, thank you. So, first of all, I would love for you to tell a little bit about your background of how you became interested in deuterium. I was watching one of your presentations earlier today and you were telling the story of kind of this dinner party in Hungary where this guy approached you and started talking to you about this deuterium-depleted water and how amazing it was. So can you kind of talk about how you became interested in the first place? And then I also want to just talk about what deuterium is.

Dr. László Boros:  Yeah, so I’m a medical doctor, but I do research and I teach biochemistry medicine, or biochemistry—and indeed, in Los Angeles, we had a dinner with a Hungarian friends were one of the participants approached me—who was actually involved in freight or shipping—with this water, which was a deuterium-depleted water, and he was telling me how wonderful it is. Like, anybody else, I was skeptic at first, so I just told him, “Listen, if that’s just the scenario, just drink as much as you can.” Yet I was not really after this, until—actually, I got a contract with the guy who makes this water in Hungary. His name is Dr. Gabor Somlyai, and he was studying this water for quite a long time.

He’s a biologist by training, and I did not know much about this water until he was pursuing studies to UCLA. I actually run a metabolic profiling laboratory services at UCLA, so my job is practically to look at compounds and look at their biochemical or metabolic effects, and if there is an effect, then we have a certain type of trace of technology which is very sensitive in studying metabolism. And if there is in effect, then we interpret it from the medicine or from the basic science point of view. Now, interestingly and surprisingly, this water—after they paid the full price for running a complete UCLA-based basic science studies—this water had a dose-dependent effect on certain biochemical platforms in the cells including mitochondrial energy production, mitochondrial substrate oxidation, based on the deuterium content of the water.

Now deuterium is a heavy isotope of hydrogen. Hydrogen comes in three forms—or three flavors: two of them are stabilized [peroxide], meaning that they do not really radiate any bad stuff. Those are hydrogen and deuterium. Deuterium has one extra neutron next to the proton. We know hydrogen has a proton, and deuterium has a proton and a neutron, so it makes it twice as heavy. It’s like a very heavy twin brother, twice the weight and obviously—

The process of deuterium depletion

Ari Whitten:  Just to clarify, a twin brother of normal water or normal hydrogen?

Dr. László Boros:  Well, hydrogen, and when it gets attached to oxygen, then it makes heavy water. So heavy hydrogen exists in nature, attached to various other atoms— carbon or nitrogen or oxygen most often—and actually hydrogen and deuterium—those are called elements—those are atoms because they only have protons and electrons and neutrons. Hydrogen is the first and the smallest and the fastest and the most active element in nature; it’s actually the first atom in the periodic table. It only has one bond proton. There’s no simpler scenario or atomic particle than hydrogen. And when you attach a nitrogen to it, it actually makes it twice as heavy. So in nature, the largest isotope effect is between hydrogen and deuterium. There’s no other atom that has this doubling of mass effect. Every other isotope has a fraction of the implicated fraction of increasing mass. And this doubling of weight or doubling or mass is really a big burden on any biological process that transfers or moves this hydrogen.

Deuterium makes this transfer process very difficult to carry out by cells. And just to go back to your original question, when it comes to heavy water, which my friend was talking about—this heavy water depleted from drinking water, meaning that the water is more light—they can deplete the water means that the hydrogen pool of water has less deuterium. In nature, there is about 155 deuterium for every million hydrogens. That’s 155 PPM—that’s the water in the Pacific Ocean as the largest water pool and the highest, most abundant deuterium source—and everything that is fractionated, evaporated, removed by any physical method from the oceanic water for example, by vapor, by formation of clouds who have less deuterium—and that’s why we call the deuterium depletion: when the extra fraction or the new fractional water has less deuterium, and this is what we call in nature: deuterium depletion.

Interestingly, when you have clouds that fly over or kind of spread out over lands and you had rain, those have less deuterium because of this evaporation process. It gets rid of deuterium somewhat because deuterium is heavier—or it has different physical chemical characteristics. It makes water more viscous, it makes water more heavy, and it changes its freezing and cooling and melting temperatures. And that’s why practically physics and physical processes constantly deplete deuterium or constantly changes the hydrogen-deuterium ratio in water, and also in molecules that are actually synthesized for water and all molecules—all organic molecules are synthesized from water because photosynthesis breaks water with the energy of light, and it’s also [deuterium]-discrimination process.

So after I talked to my friend—after we finished this study—we have learned through our experimental design that actually deuterium-depleted water has a large effect on energy production, especially in mitochondria, which is dose-dependent. And the fact is linear, meaning that the change of dose causes the same amount of change in energy production. So we figured there’s a very basic biochemical constrain—that type of interrelationship between deuterium content of water and energy production of sales.

What “deuterium-rich water” isw

Ari Whitten:  Okay, so let me jump in here for a moment, I want to make sure that we don’t lose people who don’t have any familiarity with some of this stuff and maybe never took college or high school chemistry. So, first of all, just water is H2O—two hydrogens and an oxygen. We have lots of water in our bodies and our cells and our mitochondria, obviously. Deuterium—is it D2O? Is it one normal hydrogen and one deuterium in place of that normal hydrogen that’s attached to the oxygen? So what is “heavy water” or “deuterium-rich water”?

Dr. László Boros:  So there’s light water, there are semi-heavy water, and there’s heavy water. And you’re right, light water is H20, semi-heavy water is DHO, and heavy water is D2O. So in other words, if you don’t have any hydrogen replaced by deuterium, that’s light water. If you have one hydrogen replaced by deuterium, that’s semi-heavy water. If you have two deuterium replacing hydrogens, that’s heavy water.

Ari Whitten:  Okay, so just to correct a common misunderstanding that so many people have, we all think water is H2O—we are bodies—we drink H2O; our bodies, our cells, are filled with H2O—that’s actually not true. Our cells are filled mostly with H2O, but with some DHO and some D2O in there as well.

Dr. László Boros:  Yes.

Ari Whitten:  And basically the gist of this whole concept is that more of this DHO or D2O—more of this deuterium accumulated in our cells—is linked with various kinds of harm. Correct?

Dr. László Boros:  Diseases including… It deprives energy, metabolism, energy production, and as a consequence of that, you’re right, it harms the cells.

The role deuterium plays in biology

Ari Whitten:  Okay. But I want to get into some of the mechanisms of how it causes harm. But first, I’m curious: does deuterium play any positive role in the body? Is there any beneficial reason—any beneficial purpose it’s serving? Or is it the case that just, the less deuterium we have in our bodies, if we could deplete it all the way down to zero parts per million, that would just provide progressively more benefits. Is there any kind of middle ground where we want to have sort of an optimal range, or it’s just, less is better?

Dr. László Boros:  Well, different biomolecules have different amounts of deuterium. We believe that the biological range—or the biological relevant range—is somewhere between 95 to 120 PPM. Most of the tumor accumulates in DNA, or nucleic acid simply because they have hydrogen bonds. And because hydrogen is so active and structurally so active, that actually bonds the helices of the two sugar skeletons of the two helices of DNA. There’s actually deuterium in DNA, and actually that makes DNA to grow bacteria. Bacterial DNA depends on deuterium to grow constantly, and this is actually yeast and bacteria [-growth] requirement to actually collect retained deuterium. So based on phenotype, based on cell type, deuterium has a biological role to control cell proliferation or cell growth. So cells—or prokaryotic cells, who actually specialize on continuous growth and fermentation of substrates—they collect retained deuterium, and that’s their purpose, practically.

So deuterium has a role in biology. Certain phenotypes or certain types of cells like to accumulate deuterium for their constant role as more like a competitive biological behavior. But it’s not very compatible with eukaryote or mammalian cells, which do not divide on a constant basis, unless they become cancerous. And those cells actually limit their own deuterium by these organelles—mitochondria—which are able to deplete deuterium for the cell, and this deuterium-depleted water can actually produce certain DNA with limited number of deuterium, and those DNA size—the size of DNA in cells that can limit or control deuterium—can be contained in a nucleus. So practically the difference between a bacteria and a liver cell, for example, is that the liver cell is able to deplete deuterium. So it wraps up its DNA, and pack it into a nucleus, and it can sit there for a certain period of time, and it only transcribes genes for normal cell function.

Prokaryotes, or bacteria, cannot do this simply because they don’t have the tools to deplete deuterium—they don’t have mitochondria. In fact, they retain deuterium for constant growth. It’s a very competitive and a very efficient way of surviving in nature. Yet, metabolically, it’s a very harmful way of living in an organized—or in a host organism were actually continued cell proliferation is really not a desired pattern.

Deuterium and the mitochondria

Ari Whitten:  Gotcha. So let’s jump to mitochondria first, and then this primary mechanism of how this deuterium is causing harm. I know there’s a few—probably several—nuances here as far as you mentioned there, that mitochondria are built with the capacity to deplete deuterium, but there’s also this element of how deuterium can damage mitochondria. So what’s the mechanism there of how this accumulation of deuterium at higher levels causes harm to our cells and to our mitochondria?

Dr. László Boros:  What we need to know about mitochondria, it actually uses these very delicate proteins—we call them nanomotors—and literally they are actually nanomotors that spin in the inner membrane. Mitochondria has two membranes: there’s an outer membrane and there’s an inner membrane, and between these two membranes, there’s a space—we call it intermembrane space. And what mitochondria do is it takes in nutrients mostly in the form of oxaloacetate or acetyl coenzyme A, but actually it’s an organic molecule. And actually, mitochondria would harvest the hydrogen from these organic molecules, and CO2—carbon dioxide—is the product of this proton or hydrogen harvest station process. This hydrogen is actually pushed in between of those two membranes, and when they return into the mitochondria, they rotate these nanomotors. And by rotating these nanomotors by an electromagnetic force, the actually get transferred to the membrane using these nanomotors.

In the meantime, ATP—or adenosine triphosphate—is produced, which is our energy currency in our cell. But these nanomotors are very sensitive to the effect of deuterium, meaning that it’s a very fast, rapidly-rotating protein. You can imagine, at maximum velocity, they rotate at 9000 rotations per minute—so these are actually a form of a racecar engine or rotating parts. So if you throw a particle that is twice as heavy as the—it’s more like sand in an engine, there’s an unbalancing effect of deuterium. So they got to physically break these nanomotors besides other harms that they can deliver: they alter the structure of proteins, proteins don’t fit anymore, proteins are not able to smoothly change their confirmations…

As you mentioned in the beginning, it’s a very complicated picture. But what we need to focus on is practically how deuterium damages the physiological structure of mitochondria, including the rotating parts and also the structural parts, which actually keep these elements in place more like the building blocks of the structures. And as a result of that, mitochondria need to work with as little deuterium as possible, meaning that our food, our contaminated water from the environment, has to be depleted of deuterium before they get into the mitochondria, just to make sure they don’t cause any harm.

Ari Whitten:  So what actually is the element that’s causing harm here? Is it that the deuterium atom itself is larger than a normal hydrogen atom? And so when it’s pushed through this nanomotor, that’s what’s pumping the ATPase pumps onto the mitochondria when it’s being pushed through that pipe—is it literally just too big? Such that it’s kind of plugging or scraping up the pipe?

Dr. László Boros:  Yeah, you can imagine a football game, which you just actually throw in a medicine ball instead of a football. So it’s twice as heavy, it’s twice as big, and it’s really not compatible with this dynamics of the game itself. So you can imagine, if you just change the ball of a football game twice as heavy, twice as large, the whole game will stop because actually it’s not designed—those players would not know what to do with it. So that’s how surprising—that’s how shocking it is for mitochondria whenever deuterium gets in there. It just actually changes the whole game—it just actually, because of its weight, it just breaks things. It’s like a bull in a China store, practically—it’s too heavy, too large to fit in proteins and actually to participate in any rotating movements. That’s why it’s actually very harmful for mitochondria, because of its physical properties.

Ari Whitten:  Now, so I want to dig into this a little bit more because, let’s say someone has very low deuterium levels versus very high deuterium. So let’s say, if someone’s got a hundred parts per million in their cell water—and we can talk later about the ways to measure this; I know there’s some methods of actually assessing how much deuterium is in your body—but let’s say someone’s got 100 parts per million deuterium versus 150 parts per million or 160. Either way, there’s still quite a bit of deuterium in there, or there’s still some deuterium in there that the mitochondria are having to deal with. Now, obviously they have to deal with more, and the scenario where there’s 150 or 160 compared to 100—but either way, there’s still some deuterium that’s passing through those ATPase pumps. What is actually the difference in terms of the damage being done to mitochondria if you’re at 100 parts per million versus 150?

Dr. László Boros:  Yeah, so here’s the catch: usually mitochondria should not have any deuterium because whatever is in the environment, your biochemistry is pretty much like a chemical protective fence around the mitochondria. Nobody disputes that biophysics is important in understanding the damage delivered by deuterium in the mitochondria. It’s actually biochemistry that protects the mitochondria, so neither of 155 nor 100 PPM can get close to the mitochondria at that level, as far as deuterium counts. Deuterium should not reach mitochondria from the environment. This is why our body has so many filtering layers and so many biochemical mechanisms to actually get rid of deuterium before it could get into the mitochondria.

Ari Whitten:  Okay, so let me just interject here real quick. So basically, what you’re saying is, some body tissues may have, let’s say, 150 or 120 or 100 parts per million of deuterium, but at the mitochondria level, we should have water that’s inside of the mitochondria that is completely purified of deuterium and has no deuterium. However, in some scenarios—which I would love to talk about next as far as why that happens—but in some scenarios, for whatever reasons of dysfunction, the mitochondria starts to get deuterium inside of there. Is that accurate?

Dr. László Boros:  That’s right. So mitochondria produces its own water, which I didn’t mention. When protons get into the matrix or into the inner mitochondrial space, oxygen is waiting, and water is produced. Because oxygen is reduced by hydrogen or oxygen is bound to hydrogen. Two hydrogens—actually metabolic water—is what is in mitochondria and then water is produced from food. It’s not from outside—mitochondria produce its own water. We call it matrix water or metabolic water. And the hydrogens come from food, from organic molecules that we oxidize—we burn in the mitochondria. It’s, for example, like your car engine: you have to use fuel to be burned and actually water is producing your engine, but the oxygen comes from air. So it’s practically the same scenario: you’re burning an organic material and you have to look at your food, what’s the [deuterium/different] content in your food to determine what’s that unique content in your mitochondria.

So if your food has 100 PPM through glycolysis, through fatty acids synthesis, through various interchanged reactions, your cells—your body’s trying to get rid of deuterium from food or from food components. So by the time they get to the mitochondria, they don’t have deuterium. Practically, this is how you protect your mitochondria. You actually use a lot of biochemical reactions and exchange—change hydrogens, or deuterium to hydrogen, from cellular water, which is also coming from mitochondria. So practically, your inner water production system is protecting your deuterium-depleted water production system, or inner water protects your substrates, your food items or food components. By the time they get that down to the mitochondria, they don’t contain any deuterium either. So practically, environment, and the load of your food—of deuterium—will determine how much of this deuterium will get down eventually to mitochondria. And if there is a damage, it is occurring through food, it’s not occurring through [water,

Ari Whitten:  So what is the—I want to say, rate-limiting step, but that’s not quite the right word in this context—but where are these major checkpoints that are kind of preventing this deuterium from getting into the mitochondria, and which one is the sort of the “key one”, if there is such a thing? The “key one” where most of the dysfunction occurs that allows this deterioration to start leaking into mitochondria.

Dr. László Boros:  It’s a process called glycolysis. Glycolysis is how you break down glucose. The third step of glycolysis is an isomerase—it’s actually called hexaphosphate isomerase. I don’t want to scare people away, that’s why I was not mentioning biochemical reactions by name, but we have to, after all, if we want to understand this.

Ari Whitten:  But this is part of the Krebs cycle or the citric acid cycle?

Dr. László Boros:  It’s not the Krebs cycle, yet—it’s actually glycolysis. Glycolysis has three particular steps that actually deplete deuterium very rapidly from glucose. One is this hexaphosphate isomerase, which specifically turns glucose 6-phosphate into fructose 6-phosphate. The second reaction is called triosephosphate isomerase, which actually turns glyceride high 3-phosphate into phosphate glyceride. And the third one is called enolase. Enolase takes out a whole water molecule from glucose simply because oxygen and two hydrogens are leaving simply because they want to get—glycolysis has 10 steps set practically to check on every hydrogen on glucose to make sure it’s not deuterium. So before glucose gets into the mitochondria, it has to go through glycolysis, it has to break down from a 6-carbon metabolite into two 3-carbon products. We call them pyruvate acid or pyruvate.

This pyruvate is the source of mitochondrial substrate oxidation. But by the time glucose turns into pyruvate acid, it should not have any deuterium unless there’s too much deuterium in the environment. So this depletion process is not complete, not very efficient. And that happens, which we know unfortunately now, because of the environment and because we eat a lot of sugar or actually ketogenic diets that don’t have deuterium. In nature, nature makes sure that the fat—or the ketogenic substrates—don’t have deuterium, and that’s simply because in nature, fat can only be produced from mitochondrial metabolites, specifically from citric acid. So every fat source in nature is from mitochondrial source, so it’s deuterium-depleted. So comparing sugar-ketogenic diet with glucogenic diet with glucose or carbohydrate diets, the main difference is their deuterium content.

If the glucose is too extensively entering mitochondria, or glycolysis is not efficient because there’s environmental deuterium exposure that is higher than expected for glycolysis to work, then there’s a chance—there’s a possibility that, eventually, deuterium can get into the mitochondria. It’s not desired. But they believe that nutritional and dietary recommendations that include too much carbohydrates can eventually damage mitochondria simply because of the substrate that enters mitochondria have higher deuterium content that mitochondria can handle.

So glycolysis, membrane transport of glucose, glycolysis several times. If you eat a glucose molecule, it goes through glycolysis in red blood cells, then it goes to glycolysis in liver cells, and it goes to glycolysis in target cells. So actually, it’s not only one time, but it’s actually at least three or four times of glycolysis before any substrate gets into the mitochondria. So our body at different tissues—at different tissue levels—has glycolysis just ready to deplete deuterium as much as possible. These steps are repeated in every cell. And after all, they are so intense and so rapid, so by the time your substrate get to the target cell—mitochondria—they should not have deuterium. And practically, this is what biochemistry is about: how do you get deuterium from organic molecules?

How deuterium leaves the body

Ari Whitten:  Gotcha. Okay, so there’s a few nuances I want to dig into here. First layer is—and I think these are pretty quick answers—but the first layer is: when these glucose molecules are going through glycolysis outside of the mitochondria in these multiple steps—you said red blood cells, liver, and then the target cell—they’re being stripped of deuterium, and then where is that deuterium going? How is it leaving the body?

Dr. László Boros:  Deuterium gets in through the water. So the reaction works that, actually, dropping a deuterium from glucose and getting the hydrogen from water. So that’s how it gets exchanged: in the deuterium that was dropped, gets it past through the water, water gets out of the cell, and becomes urine, after all.

Ari Whitten:  Urine, or also exhaled as well?

Dr. László Boros:  Urine, or exhaled, or actually, it becomes poop, or become part of feces. Because we just learned very recently that our cells are able to ship lactate out to the gut, where actually these bacteria—the prokaryotes—are waiting to collect deuterium from lactic acid. And actually, what they return is a short-chain fatty acid called propionic acid. So what we are describing here is a bunch of biochemicals—set of biochemical reactions—and collaboration between different type of cells—and even bacteria of the gut—simply just to get rid of deuterium as much as possible.

Ari Whitten:  So that may be another mechanism by which a dysfunctional gut microbiome contributes to poor health by preventing adequate depletion of deuterium.

Dr. László Boros:  Right, you’re correct.

Ari Whitten:  Okay. The next layer of the story, I’ve heard some people say—and I think maybe even you say this—that mitochondria are depleting deuterium. But it sounds like, in what you just described, that it’s not necessarily the mitochondria—it’s more of the steps before the glucose molecules or some of these other molecules are arriving at the mitochondria, it’s the steps before they get there that are depleting the deuterium. Which one is it?

Dr. László Boros:  Yeah, but mitochondria also retained this mechanism or the ability to deplete deuterium in case there’s too much deuterium in the environment. So the previous or the proceeding mechanisms or the reactions are not able to get rid of them all. If there’s too much environmental deuterium load, glucose is above the natural enrichment—which unfortunately is the case in GMO foods—then your mitochondria has to have its own mechanisms to actually get deuterium. And the way mitochondria do this, is that when—it’s called the urea cycle, you probably heard about the urea cycle, which takes place in the mitochondria—it actually takes heavy water out of the mitochondria, and urea is produced.

So mitochondria has these FO elements next to the nanomotors, so the nanomotor does not get deuterium, but actually deuterium is getting collected into these protein sacks—the sack that is actually on the side of these nanomotors. And there are gating mechanisms, there are actually filters of protons that enter the nanomotors. If the proton is too big—in that case, it’s deuterium—it’s actually sent to the other way to this FO subunit, which collects deuterium. And when this gets too heavy, then this sack, will be disassembled from the nanomotor and it will be replaced. And you’re right, mitochondria has its own ability to deplete deuterium or filter out deuterium. That’s practically kind of the last resort of the cell to protect their mitochondria. The mitochondria has its own defense system, yet they have to maintain this simply because sometimes, the environment or the tumor load is so high that the precursor mechanisms—the predecessor mechanism that protect the mitochondria are not sufficient. Mitochondria has to take care of its own—or, of their own, and a urea cycle and these deuterium-collecting proteins in mitochondria can actually accomplish this.

Ari Whitten:  Okay. And then if somehow all of these mechanisms are being overloaded constantly, then you still accumulate too much deuterium in the mitochondria where they start to damage these nanomotors. Is that correct?

Dr. László Boros:  Yeah, nanomotors break, and the mitochondria die, and you set up a whole set of diseases.

Ari Whitten:  Including cancer.

Dr. László Boros:  Including cancer, diabetes, obesity—these are cellular metabolic diseases because of the broken nanomotors. Once the nanomotors break, then the biological oxidation process slow down—this macromolecular crowding cells are not able to get rid of glucose or fatty acids. Fatty acids started accumulating, especially they are loaded with deuterium, and as a result of that, there’s this metabolic crowding and because of this crowding, there’s a whole host of no degenerative or cellular degenerated diseases, which actually will end up in the form of cancer, diabetes, obesity, [ocular] diseases, you name it. Practically, I believe that, besides breaking bones, all chronic diseases relate to some kind of a tissue-specific deuterium overload, and they can be actually improved by depleting deuterium one way or another, [inaudible] aspect of it. But practically, deuterium [does] balance when we talk about diseases, and the primary mechanism is practically too much deuterium breaking too many nanomotors in too many mitochondria.

Deuterium as a major contributing factor in many diseases

Ari Whitten:  Okay. Well I don’t want to gloss over what you just said because I think that’s a very big claim, and I want to emphasize it. So you believe that this deuterium story is central—is a big contributing causal factor to a huge array of diseases. Is that accurate?

Dr. László Boros:  On a tissue-specific manners, certainly. And I’m seeing this as a medicinal biochemist; it’s just not a medical opinion. It’s a medicinal biochemistry scenario. So we are actually exploring mechanisms. We are not suggesting as a disease or even a treatment, it’s practically an underlying tissue-specific mechanism behind disease. How to treat this, how to get rid of it, how to solve this problem—that’s a whole different matter. We’re talking about mechanisms, and obviously there’s many different set of those—dietary lifestyles, there’s pharmaceutical, there’s this many approaches, which is not part of this discussion. You’re actually looking at very basic biochemical medicine or biochemical mechanism to explain disease itself.

Ari Whitten:  Okay. But so you do believe it is a big factor in many diseases.

Dr. László Boros:  It’s a big factor in many, many diseases. That’s right.

Aging and deuterium depletion

Ari Whitten:  Okay. I want to come back to one layer of the story that you were just explaining: so we have all these sort of checks and balances and steps of depleting deuterium before these molecules ever arrive in the mitochondria. You’ve mentioned that a big factor is obviously the load of deuterium in the diet and the environment, but is it also the case that these internal checks and balances and systems to deplete deuterium that glycolysis, as well as the mitochondria, that those parts also become dysfunctional in a certain way? Let me ask this a different way: would it be the case that somebody who is young and healthy and physically fit and eats a very good diet—irrespective of the deuterium content, but just somebody who’s very fit and young—would they have a greater capacity to deplete deuterium at all those steps, than somebody who’s older and obese and sedentary and unhealthy?

Dr. László Boros:  Yeah, that’s right. That’s all we believe. Aging, which is what you’re talking about, is practically a deuterium-related process. Actually, the cleaning or filtering out deuterium, it actually gets less efficient by aging. It’s practically just because these mechanisms—these proteins—they’re replaceable mechanisms, they actually are wearing out.

I’ll give you an example: your car filters out gasoline at three different places. The gasoline filter at the tank, the gasoline filter at the carburetor, and the gas filter at the entrance of the gasoline mixture with air. Air filter and the gasoline filter, they just filter constantly . Now if any of those filters get clogged up, over time, it will load deuterium to the next filter layers. So practically, your systems fail over time to get rid of deuterium completely, and this is pretty much the same in the human body. When glycolysis is less able to handle flocks—meaning that your [glucose] is not as intense—in that case scenario, we actually have more deuterium to get into the mitochondria to match—your mitochondria has its own filtering system, but if it’s overloaded over time, then mitochondria start dying.

So practically, this filter system—as they are lined up to each other—they fail in the same sequence, practically. And aging, we believe, is dependent on oxygen delivery, depending on greeting functions, depending on heart rate, and eventually metabolic water production. And this metabolic water production is very important, very crucial, and is necessary to get rid of deuterium very efficiently. So it’s not necessarily just different filtering, but all the mechanisms and all the linked biochemical reactions that actually get rid of deuterium. Filtering is one thing, but getting rid of it is another. If your oil filter is clogged up, if your air filter is clogged up, if your gasoline filter is clogged up, then you have no ways of filtering out or getting rid of deuterium. So practically, all these mechanisms have to be in place, and over time, we actually exhaust one another. Practically, you have to deal with this scenario over a longer period of time when you age.

And you are right: the systems, when they actually fail one another, then aging and diseases may occur. Yet disease is not as important as natural aging. I believe in our low-deuterium environment, but over time, as every moving part is getting worn out, nanomotors get worn out, their replacement is not as rapid, the removal of deuterium is not—even the filtering is effective—the removal is not as efficient. You have less urine, you have less hormonal regulation. So all these mechanisms playing the same direction is filtering out and getting rid of deuterium. Any part of this process is somewhat diminished or compromised, then you might have a problem of deuterium accumulation, and it’s just a different ways of what’s the underlying mechanism that contributes to deuterium accumulation the most. But usually it’s the complement systems together that eventually fail, and that’s why it’s close to a terminal situation. When somebody has too much deuterium, then there’s no way to get rid of it through breathing or through saliva or through urine or feces. In that case, you actually end up with extra excess deuterium, which has never stayed in the [inaudible] of cellular functions.

How to build up a higher mitochondrial capacity

Ari Whitten:  Gotcha. This is fascinating stuff. My mind’s like overflowing with questions here, but one layer, just to segue from what you’re just talking about there—where my mind is going is: mitochondrial capacity. I know you said there’s a whole bunch of steps before the deuterium ever arrives at the mitochondria, but let’s just say the capacity of mitochondria to deplete deuterium is very important. Is it just aging, or is it also a person’s lifestyle habits that contribute to their mitochondrial capacity? I’ll give you an example: we know from studies looking at muscle biopsies and assessing mitochondrial capacity, that from the ages of 40 to 70, most people lose about half of their mitochondrial capacity. But when you look at studies of specifically 7-year-olds who have been exercisers for their entire life, they don’t lose half of their mitochondrial capacity, and they have mitochondrial capacity similar to 40 year olds. So I’m just wondering, that seems like it would be a big factor, to me, in retaining the capacity to deplete deuterium. And I’m also thinking that probably exercise also stimulates these glycolytic pathways. So I’m wondering if that system can be sort of exercised and built up to a higher capacity through physical exercise as well.

Dr. László Boros:  That’s right. Exercise actually makes the gut—the microbiome—more involved in deuterium deficiency because you produce more lactate, and lactate gets shipped to the microbiome, and then you get a ketone body back for oxidation.  These individuals may not live much longer, even though they have retained some mitochondrial mass, simply because they might not be able to get rid of deuterium, even though they can filter out, after all—they might not be able to get rid of it as efficiently. So it’s only a guarantee of longer, more quality life, if all these mechanisms stay in place. And you are right, number of mitochondria can be used or can be actually maintained at high levels, and these individuals have better quality of life. It’s not necessarily a longer lifespan—it may be somewhat longer than the average population. But practically, when it comes to getting rid of deuterium, that’s the key, after all, to understanding aging, or the time of death.

They die of different causes because once you compromise circulation, once you compromise heart muscle function, once you compromise joint functions—meaning that you have more inflammation in your joints—let’s say you load your physical exercise by physical exercise, you actually will wear out your muscle mitochondria more than, let’s say, your skin or your gut cell mitochondria. If you load certain cell systems or certain organs, for example, circulatory organs or lungs and heart, even though you are accustomed to higher exercise levels and you have higher mitochondria numbers in your cells, their function is not necessarily filtering deuterium; their function is producing more ATP in a low-deuterium environment.

Once your glycolysis or once your additional mechanisms are not as efficient, unfortunately, even though you have more mitochondria, they might not work as efficiently as you believe, or they might not be able to deliver as much ATP as you believe, as you hope for. After all, exercise is very important to make sure that you have a quality of life and you actually carry on with better health. And no question, exercise is very important, especially with good nutrition.

Good nutrition is—in my view, in my terms—is actually a natural ketogenic type of eating, so less carbohydrates and less proteins. Usually these people who exercise more, they actually eat more protein-rich diets, which may not be as favorable as far as mitochondria [had go]. You can induce mitochondrial number in muscle cells, definitely, but based on how you feed these mitochondria, it’s because of the mitochondrial high turnover, because there are so many mitochondria actually perishing and these mitochondria rebuild at higher rates—these may be augmenting on tissues, depending on what kind of source—what food source you eat, what’s the deuterium level—so all these complex scenarios come down to one very important question is that, practically, how you can maintain strength and how you can maintain ATP synthesis at a higher rate based on your exercise pattern; how you can involve your gut bacteria; how you understand this very complex system, after all, to beat it; and how to get rid of deuterium at a constant level. And if you actually do it in a smart way, meaning that you know how to protect those mitochondria—not only produce them, but how to protect them—that’s practically a ketogenic/low-deuterium diet—then you have a very good chance of living a very good, happy life. With a good exercise pattern, you can enjoy it for a better health, definitely.

How much exercise you should actually get

Ari Whitten:  Okay. So just to be clear, you don’t think exercise necessarily bolsters the systems to deplete deuterium that well?

Dr. László Boros:  It is necessary but it’s a moderate exercise. You don’t do the exhaustive type. The exercise is not a strain on your system. The overdone type of exercise pattern is not necessarily healthy, but the regular exercise—the moderate exercise, the constant exercise—is actually very good simply because it does not exhaust an energy-producing system, but actually it ups it to a higher demand. So exercise, again, has different levels and different scales, and in that way, you have to find the one that is actually serving your heart the best. And for some reason, the exercise pattern or type of exercise that you deliver—you can be a bike, or you can be a runner, you can be a weightlifter, you can be a body builder, you can be a swimmer—there’s many different ways of exercising. I think the best ways to exercise is practically find a moderate-demanding level that is not very exhaustive of your cellular systems, but maintain these high energy-producing mitochondria in good shape. And if that’s scenario, if that’s the case, then you have a good chance to live a very happy, innovative, productive, joyful life.

Ari Whitten:  Okay. And I know you alluded to this a minute ago, but—so you’re saying, avoid exhaustive exercise for what reason? You’re worried about it damaging what?

Dr. László Boros:  Yeah, it’s practically high-velocity, it’s a high demand on your energy-producing system. Your mitochondria, after all—mitochondria can be rebuilt and you see high number of mitochondria, but it may be also a high turnover. Turnover, we mean that it’s a new synthesis based on the death rate of mitochondria—that’s the turnover.

So exercise, for example, when you look at competitive sports, you can only do it for a certain period of time of your life, simply because it would actually damage physically—and also metabolically—your organs, meaning that if you are a body-builder or a long distance runner, you have to do it in just in a moderate fashion in-between competitions. Meaning that, you have to keep yourself in a good shape, yet you don’t have to run a marathon every day. Practically, you have to prepare for those challenges, but you don’t have to overload your system. You don’t have to exhaust your system on a regular basis because that may not serve the purpose of staying in good health. Yet challenge is very important. Exercise is very important. But you have to adjust to the kind of optimal level that your body can handle.

Just be a kind of careful how much you load and how constantly you load your body, simply because your nanomotors are very valuable. Your mitochondria are very valuable simply because they deplete deuterium for you. And for those reasons, you have to consider all these scenarios before you actually engage in any type of [inaudible] sports. They’re all good, very important, very, very. I start every day with 30 push-ups, I walk my dogs every day. So I do exercise routinely, but it’s comfortable—this is how much I feel comfortable with. I know it has a good strain on my body. It actually serves a better health, but I don’t do extremes just because I have to challenge myself. I try to find a middle way of finding a routine that is actually serving my mental and my physical health.

Other ways to deplete deuterium

Ari Whitten:  Gotcha. I have a random question before we dig into the deuterium depletion a bit more, and something forgot to ask earlier, which is: we talked about some of these pathways of elimination, so exhaling the water with deuterium, excreting via the urine or via the fecal route—what about sweating? I’m curious, have you measured the content of deuterium in sweat, and is that higher than sort of normal? Meaning, is that a pathway of elimination for deuterium? So if someone goes in a sauna frequently, would that be helpful in depleting deuterium?

Dr. László Boros:  Yes, indeed. There’s many ways of getting rid of deuterium. Sweating is one of them—saliva, lacrimation, body vacs…

Ari Whitten:  I don’t think we want to cry our way to deuterium depletion. That doesn’t sound like—

Dr. László Boros:  No but actually, through your nostrils because it’s connected directly to every gland of your body. It’s not necessarily tears, it’s actually more like vapor in your nostrils, that comes also from your lacrimal glands. Every gland of your body, including your skin and your saliva—and any way you look in your body, there’s  sebaceous and also sort of the [backs] producing glands—they all get rid of deuterium one way or another. Usually the lowest deuterium’s in your breath, but your saliva, your urine, your fecal matter, and your sweat, they have higher deuterium, and they are all mechanisms of getting rid of deuterium from your body. 

Ari Whitten:  Got it. What about sunlight? I’ve heard that light and sunlight—you alluded to this with photosynthesis earlier—but I’m also wondering about the capacity of light, whether it’s UV light. I’ve heard some kind of mixed stories. Some people claiming it’s the UV—the ultraviolet light—other people saying it’s the red and near-infrared wavelengths—the capacity of that light to interact with our cells and our mitochondria in a way that it helps deuterium depletion. I’ve tried to look into this and I haven’t been able to find a whole lot of research, but what’s your take on this?

Dr. László Boros:  I sent you a good paper, it was written by a colleague of mine, Dr. Andrei Sommer, he is a physician scientist in Germany. He exposed cells to red light, low-energy laser red beams, and actually he measured ATP synthase and ATP production in the presence of red light. And in fact, red light improves ATP synthesis by making water less viscous. So changing waters physical viscosity improves energy production—ATP synthesis, simply because more viscous water is able to move and participate in sovereign and also in structural obligations, per se, in mitochondria. So you’re right when it comes to interfacial water or the water that is in the mitochondria—which is interfacial water and more like surface water or structural water—light has a great effect, especially with red light, because that’s the most penetrating. Red light has a great effect on lowering viscosity and improving ATP synthesis and energy homelessness.

Ari Whitten:  But how does that specifically connect to deuterium?

Dr. László Boros:  Once deuterium makes water more heavy or makes it more viscous, if you expose your mitochondria to red light, it actually makes even semi-heavy water more viscous. That water is able to move faster, can leave this [as participating in] the urea cycle. So after all, exposing your mitochondria to red light, it actually makes every kind of water that you can find in mitochondria more viscous. And if that’s the case, then your mitochondrial nanomotors are able to function and rotate more efficiently. This is what we found. If you actually increase a red light exposure, then your water viscosity in your mitochondria—including the deuterium water—is decreased. So mitochondrial functions are increased in energy production, production is increased.

Ari Whitten:  Got it. I think I know which paper you’re referring to, I think I cited that in my—

Dr. László Boros:  It just says, “Red Light, Water Viscosity”—“Red Light decreases Water Viscosity and improves ATP Synthesis”.

Ari Whitten:  Right, I’m familiar with that paper. But I guess my question is: where is that deuterium going? Or, what is the red light doing that’s—if the water’s getting thinner and more able to move easily—these ATP motors are able to rotate more efficiently in the thinner water—the lighter water, where did the deuterium go to make that happen?

Dr. László Boros:  Yeah. So again, you have to kind of imagine mitochondria as water layers. It’s not really [back] water that flows around, it’s actually water layer on top of the other layer. And then these layers move easier to each other. It’s easier to move deuterium towards nitrogen—which is the urea cycle—meaning that you can actually mix this pool more efficiently even though it’s surface water. You can actually get rid of deuterium by more attraction towards nitrogen, which is the urea cycle’s purpose. So actually you can faster exchange those layers so they actually move faster, so your water dynamics in your mitochondria is much improved after red light exposure. So this constant deuterium-filtering, constant deuterium-binding urea cycle, they actually have more efficiency of removing a heavy, hydrogen-loaded, deuterium-loaded water—meaning that your deuterium—your heavy or semi-heavy water is cleared from the mitochondria simply because the water will be more viscous.

Ari Whitten:  Okay. So it’s the water near the membranes is becoming thinner and cleared of the deuterium.

Dr. László Boros:  That’s right.

Ari Whitten:  And so the deuterium is still sort of there in the cell, but it’s being moved out of the area next to the membrane where the motors are. Is that correct?

Dr. László Boros:  Yeah. Well, yes, indeed. You can actually bind heavy water to nitrogen, to urea itself, because urea takes them out. But for that, you have to move those layers. Urea does not pick up light water as efficiently as heavy water. So once those layers are moving because they are thinner—they are more viscous—then you actually get rid of more deuterium over a shorter period of time, meaning that it’s just a more dynamic process.

Ari Whitten:  Gotcha. Okay. So, just a couple more questions here—and thank you for your time, by the way.

Dr. László Boros:  Of course.

Testing and measuring deuterium levels in your body

Ari Whitten:  So one layer is: with mitochondrial health, there is some… We know from lots and lots of lines of research that mitochondria are obviously extremely important in health and disease prevention. Obviously energy—which is a big concern of people listening to this process—the way I conceptualize the story of chronic fatigue is very mitochondria-centric. And I believe that’s what the evidence points to. So mitochondria are really important. However, there aren’t a lot of really good tests that we have to directly assess mitochondrial function. Now, I was doing an interview with someone recently and he had just done a deuterium test on his body, and was really excited about it because he was basically thinking that measuring deuterium levels in your body is a really good proxy for assessing your mitochondrial health. So, in other words, if you have low deuterium levels, that is a sign that you have highly functioning, healthy mitochondria. So my question is, first of all: do you think that’s accurate to say that?

Dr. László Boros:  Yeah, that’s a very fair statement. That’s a very good assessment. Yes, that’s right.

Ari Whitten:  Okay. And then the second question is—I know there’s a couple different methods of measuring deuterium: there’s the breath, and I believe there’s also the urine, and then I think there’s also an MRI scan of your body.

Dr. László Boros:  That’s right.

Ari Whitten:  Do you have any thoughts on—if all of those are valid, or if one wants to measure deuterium, is there one that’s better than another?

Dr. László Boros:  Yes, so… MRI—or magnetic resonance—is, by definition, a proton spectrum. So you actually resonate protons and deuterium compromise the resonance. So actually MRI is a straightforward deuterium-measuring device indirectly. Now, the Yale University Department of Radiology—they just started deuterium metabolic imaging, and that means they actually measure deuterium. They now take deuterium scans, and those are interchangeable. So practically, proton or deuterium spectra in MRI image by density, you can tell what’s the cells’ deuterium content in comparison with other tissues. So it’s a good indirect deuterium-measuring device—MRI—so you can actually measure deuterium content or at least have a look at deuterium content of tissues, using MRI. It has a different view or different analysis tool to measure deuterium in tissues using MRI, but it’s a very much possible.

Ari Whitten:  Probably also very cost-prohibitive for most people, I would imagine.

Dr. László Boros:  Yeah, I think, after all, using a low magnetic field T-1 sequence, that’s probably your best bet. Using gate 1.5 Tesla magnet, and using a T-1 sequence, it’s practically just how fast do your protons return to their lattice, how fast the protons are able to reach into their normal position once the radio frequency stir enough—and that depends on deuterium.

Ari Whitten:  Right… So MRIs are probably the most accurate, it sounds like, but also probably the most costly, and probably so expensive that they would be inaccessible for most people.

Dr. László Boros:  Well, it depends on how you approach this. It cost about $400-$500, and you’re right, it may be expensive, but since you can look at multiple organs in the same time, it may be also—if you are, in general, interested in your body’s deuterium distribution, that probably is cost-effective. But if you are actually interested in just one particular tissue type, then it’s probably expense. You’re right, it’s maybe too expensive.

Now they’re all spectral phenomena—say it again? Did you have a question?

Ari Whitten:  If I may ask: so there’s these other methods of breath-testing and urine-testing—do you feel that those are worthwhile, or it’s one of these things where they’re just not giving enough data to be [worth your money]?

Dr. László Boros:  In health, in general, you have to measure it before you make any kind of assessment. Of course, they are very crucial because from those numbers, you know how your body’s able to deplete deuterium. I give you a scenario: your breath is actually coming from your metabolic water. At least some of it because it’s the vein of circulation—the veins take the blood back to your lungs, and your lungs’ vapor is practically what you measure in your breath test. Usually the breath-deuterium content tells you how efficiently your body is able to deplete deuterium compared to the environment or deuterium exposure. And if you compare this to saliva and urine and you see this window between your urine, saliva, and your breath—if those numbers are similar to each other, then you know you’re metabolically not very efficient of depleting deuterium. But if your saliva and your breath test shows a larger difference, then you know, at least, your body’s able to produce more deuterium-depleted water, and your deuterium depletion process to your metabolism is more efficient. So practically, these three numbers, just like in any laboratory medicine, you measure simply just to know which way these parameters are moving, where you are at any given time, what is the environment exposure—you always have to do these measurements based on your original, and then when you apply a depletion method, how efficiently they work, you have to look at your—it’s more like a One Sample t-Test or like a self—I don’t want to say self-experiment because we don’t do human studies, we don’t do this study for human study purposes—we do is for informational purposes, but that’s practically what it is.

At UCLA, now we are carrying out pre-clinical experiments in—for example—in the department of pediatrics where we actually look at deuterium content of cells, look at deuterium exposure of cells, and we look at their cell death rate, practically, and that, practically, just depending on deuterium content of the environment. So deuterium content of your body is a very important marker of where you are and which way you should start depleting. The healthy deuterium content in breath would be probably below 130 PPM—we don’t see this, unfortunately. We are overloaded of the team as a population, because of food and many other reasons. Obviously, the environment and the global temperature changes—they all play a very significant role in this process. But once you actually start depleting—how efficiently you deplete, and how fast you reach this biologically-required range of 130 PPM, for that reason, you have to measure.

Ari Whitten:  And just to be clear, the range is 132… what?

Dr. László Boros:  We believe that anything below 130 in your breath is close to the desired range. Anything below 135 in your saliva and urine—because I told you, those are higher than your breath samples—those should be below 135. You want to be on the safe side, is probably below 125 when it comes to breath samples—that’s what I like. And urine is probably below 130 or around 130 in urine and saliva. But practically, those are the required numbers. We don’t see those in the general population.

Ari Whitten:  How do you know those numbers are indicative of the amount of deuterium in the actual body? Meaning, is it possible that someone could have low levels in their body? Like, if you did an MRI scan, you’d show low levels in the cells in the tissues, but they’re just very efficient at getting rid of deuterium so that higher levels are showing up in their saliva or urine—is that a possible scenario, or not so much?

Dr. László Boros:  Yeah, so these are surrogate markers. Whatever is in your breath, it’s not the same as what’s in your tissues. It’s just practically a surrogate marker of what is your breath and usually what is your tissue. If your breath shows up at a certain level, what’s the value of your tissues? Obviously to start depleting, or to see depletion, it’s going to show up in your breath first.

So it’s practically a surrogate marker of what your body’s deuterium content is. Obviously you have to measure a multiple of samples, and more desirable would be an MRI study, which shows you your tissue deuterium content. Since people don’t have the money most of the time to do these types of tests, then we are actually—and it’s more invasive and it has to be medically indicated. So that’s a more complicated situation. But actually the measuring breath, saliva, and urine is the fastest, dirtiest, cheapest, I believe, and most informative surrogate—

Ari Whitten:  And it is accurate and validated?

Dr. László Boros:  It’s accurate enough. Let’s put it this way: it’s clinically not validated. Again, it’s for informal—it’s, for me, informational purposes. I want to know what my deuterium level is. I can just breathe my breathing into a [cold] tube, it’s noninvasive. You can just do it winter time on a cold window, you can collect your breath in many different ways—it’s practically just, you have to have a cold water, or you just need to condense your breath. So for informational purposes, it’s an excellent method. Obviously when it comes to clinical trials—which, at UCLA, we are pursuing very soon and currently carrying out studies—but practically, there are more accurate measurements. You’re right, there’s more creative approaches, and clinically we will position it. This is actually—deuterium story is when the biohacking is moving into mainstream evidence-based medicine.

So we are not doing it the other way around, and this is my mission as a UCLA professor of pediatrics and a full faculty member of UCLA. After publishing over a hundred papers in the medical literature and having an impact factor or whatever it is, it doesn’t matter—but I’m a very accomplished academic scientist who has been doing this for a long time in the academic setting, and I’m a medicinal biochemist. I don’t do these just like on my free time. So I have been studying these constrained models for a very long time and we have published very influential papers. We just got cited by Switzerland from the Department of Pediatrics, and we wrote very important papers to explain how fatty acid, how deuterium-depleted water in various [sack] compartment should measure up, after all, for health and for [curity] purposes, but practically the surrogate marker—it’s actually just an indicated marker of how much deuterium might be in your body. It’s not an accurate measure, no way, but it’s a good kind of look at it, and there’s going to be much more clinically-positioned cast laboratory test for that, which will enter mainstream medicine. Currently it’s an integrative alternative medical approach and it’s in the biohacking arena, but it’s going be evidence-based [inaudible] and mixed medicine. How long it will take, I don’t know yet, probably a few years—but we are carrying out those studies, definitely.

Benefits of drinking deuterium-depleted water

Ari Whitten:  So one layer is: with mitochondrial health, there is some… We know from lots and lots of lines of research that mitochondria are obviously extremely important in health and disease prevention. Obviously energy—which is a big concern of people listening to this process—the way I conceptualize the story of chronic fatigue is very mitochondria-centric. And I believe that’s what the evidence points to. So mitochondria are really important. However, there aren’t a lot of really good tests that we have to directly assess mitochondrial function. Now, I was doing an interview with someone recently and he had just done a deuterium test on his body, and was really excited about it because he was basically thinking that measuring deuterium levels in your body is a really good proxy for assessing your mitochondrial health. So, in other words, if you have low deuterium levels, that is a sign that you have highly functioning, healthy mitochondria. So my question is, first of all: do you think that’s accurate to say that?

Dr. László Boros:  Yeah, that’s a very fair statement. That’s a very good assessment. Yes, that’s right.

Ari Whitten:  Okay. And then the second question is—I know there’s a couple different methods of measuring deuterium: there’s the breath, and I believe there’s also the urine, and then I think there’s also an MRI scan of your body.

Dr. László Boros:  That’s right.

Ari Whitten:  Do you have any thoughts on—if all of those are valid, or if one wants to measure deuterium, is there one that’s better than another?

Dr. László Boros:  Yes, so… MRI—or magnetic resonance—is, by definition, a proton spectrum. So you actually resonate protons and deuterium compromise the resonance. So actually MRI is a straightforward deuterium-measuring device indirectly. Now, the Yale University Department of Radiology—they just started deuterium metabolic imaging, and that means they actually measure deuterium. They now take deuterium scans, and those are interchangeable. So practically, proton or deuterium spectra in MRI image by density, you can tell what’s the cells’ deuterium content in comparison with other tissues. So it’s a good indirect deuterium-measuring device—MRI—so you can actually measure deuterium content or at least have a look at deuterium content of tissues, using MRI. It has a different view or different analysis tool to measure deuterium in tissues using MRI, but it’s a very much possible.

Ari Whitten:  Probably also very cost-prohibitive for most people, I would imagine.

Dr. László Boros:  Yeah, I think, after all, using a low magnetic field T-1 sequence, that’s probably your best bet. Using gate 1.5 Tesla magnet, and using a T-1 sequence, it’s practically just how fast do your protons return to their lattice, how fast the protons are able to reach into their normal position once the radio frequency stir enough—and that depends on deuterium.

Ari Whitten:  Right… So MRIs are probably the most accurate, it sounds like, but also probably the most costly, and probably so expensive that they would be inaccessible for most people.

Dr. László Boros:  Well, it depends on how you approach this. It cost about $400-$500, and you’re right, it may be expensive, but since you can look at multiple organs in the same time, it may be also—if you are, in general, interested in your body’s deuterium distribution, that probably is cost-effective. But if you are actually interested in just one particular tissue type, then it’s probably expense. You’re right, it’s maybe too expensive.

Now they’re all spectral phenomena—say it again? Did you have a question?

Ari Whitten:  If I may ask: so there’s these other methods of breath-testing and urine-testing—do you feel that those are worthwhile, or it’s one of these things where they’re just not giving enough data to be [worth your money]?

Dr. László Boros:  In health, in general, you have to measure it before you make any kind of assessment. Of course, they are very crucial because from those numbers, you know how your body’s able to deplete deuterium. I give you a scenario: your breath is actually coming from your metabolic water. At least some of it because it’s the vein of circulation—the veins take the blood back to your lungs, and your lungs’ vapor is practically what you measure in your breath test. Usually the breath-deuterium content tells you how efficiently your body is able to deplete deuterium compared to the environment or deuterium exposure. And if you compare this to saliva and urine and you see this window between your urine, saliva, and your breath—if those numbers are similar to each other, then you know you’re metabolically not very efficient of depleting deuterium. But if your saliva and your breath test shows a larger difference, then you know, at least, your body’s able to produce more deuterium-depleted water, and your deuterium depletion process to your metabolism is more efficient. So practically, these three numbers, just like in any laboratory medicine, you measure simply just to know which way these parameters are moving, where you are at any given time, what is the environment exposure—you always have to do these measurements based on your original, and then when you apply a depletion method, how efficiently they work, you have to look at your—it’s more like a One Sample t-Test or like a self—I don’t want to say self-experiment because we don’t do human studies, we don’t do this study for human study purposes—we do is for informational purposes, but that’s practically what it is.

At UCLA, now we are carrying out pre-clinical experiments in—for example—in the department of pediatrics where we actually look at deuterium content of cells, look at deuterium exposure of cells, and we look at their cell death rate, practically, and that, practically, just depending on deuterium content of the environment. So deuterium content of your body is a very important marker of where you are and which way you should start depleting. The healthy deuterium content in breath would be probably below 130 PPM—we don’t see this, unfortunately. We are overloaded of the team as a population, because of food and many other reasons. Obviously, the environment and the global temperature changes—they all play a very significant role in this process. But once you actually start depleting—how efficiently you deplete, and how fast you reach this biologically-required range of 130 PPM, for that reason, you have to measure.

Ari Whitten:  And just to be clear, the range is 132… what?

Dr. László Boros:  We believe that anything below 130 in your breath is close to the desired range. Anything below 135 in your saliva and urine—because I told you, those are higher than your breath samples—those should be below 135. You want to be on the safe side, is probably below 125 when it comes to breath samples—that’s what I like. And urine is probably below 130 or around 130 in urine and saliva. But practically, those are the required numbers. We don’t see those in the general population.

Ari Whitten:  How do you know those numbers are indicative of the amount of deuterium in the actual body? Meaning, is it possible that someone could have low levels in their body? Like, if you did an MRI scan, you’d show low levels in the cells in the tissues, but they’re just very efficient at getting rid of deuterium so that higher levels are showing up in their saliva or urine—is that a possible scenario, or not so much?

Dr. László Boros:  Yeah, so these are surrogate markers. Whatever is in your breath, it’s not the same as what’s in your tissues. It’s just practically a surrogate marker of what is your breath and usually what is your tissue. If your breath shows up at a certain level, what’s the value of your tissues? Obviously to start depleting, or to see depletion, it’s going to show up in your breath first.

So it’s practically a surrogate marker of what your body’s deuterium content is. Obviously you have to measure a multiple of samples, and more desirable would be an MRI study, which shows you your tissue deuterium content. Since people don’t have the money most of the time to do these types of tests, then we are actually—and it’s more invasive and it has to be medically indicated. So that’s a more complicated situation. But actually the measuring breath, saliva, and urine is the fastest, dirtiest, cheapest, I believe, and most informative surrogate—

Ari Whitten:  And it is accurate and validated?

Dr. László Boros:  It’s accurate enough. Let’s put it this way: it’s clinically not validated. Again, it’s for informal—it’s, for me, informational purposes. I want to know what my deuterium level is. I can just breathe my breathing into a [cold] tube, it’s noninvasive. You can just do it winter time on a cold window, you can collect your breath in many different ways—it’s practically just, you have to have a cold water, or you just need to condense your breath. So for informational purposes, it’s an excellent method. Obviously when it comes to clinical trials—which, at UCLA, we are pursuing very soon and currently carrying out studies—but practically, there are more accurate measurements. You’re right, there’s more creative approaches, and clinically we will position it. This is actually—deuterium story is when the biohacking is moving into mainstream evidence-based medicine.

So we are not doing it the other way around, and this is my mission as a UCLA professor of pediatrics and a full faculty member of UCLA. After publishing over a hundred papers in the medical literature and having an impact factor or whatever it is, it doesn’t matter—but I’m a very accomplished academic scientist who has been doing this for a long time in the academic setting, and I’m a medicinal biochemist. I don’t do these just like on my free time. So I have been studying these constrained models for a very long time and we have published very influential papers. We just got cited by Switzerland from the Department of Pediatrics, and we wrote very important papers to explain how fatty acid, how deuterium-depleted water in various [sack] compartment should measure up, after all, for health and for [curity] purposes, but practically the surrogate marker—it’s actually just an indicated marker of how much deuterium might be in your body. It’s not an accurate measure, no way, but it’s a good kind of look at it, and there’s going to be much more clinically-positioned cast laboratory test for that, which will enter mainstream medicine. Currently it’s an integrative alternative medical approach and it’s in the biohacking arena, but it’s going be evidence-based [inaudible] and mixed medicine. How long it will take, I don’t know yet, probably a few years—but we are carrying out those studies, definitely.

Eating a natural ketogenic diet

Ari Whitten:  Gotcha. Last question—again, thank you so much for going over time here. This is much longer than I anticipated, but it’s just a fascinating discussion. I have so many questions, I want to keep you here for three hours. But, last question: you’ve obviously mentioned ketogenic diets, fats being lower in deuterium content—

Dr. László Boros:  Natural ketogenic, so grass-fed animals.

Ari Whitten:  Okay. I’m wondering—there are obviously a lot of carbohydrate-containing foods, for example, berries, for example, lentils—that are decidedly associated with health benefits and disease-prevention benefits, and are associated with longer life and so on. I’m just wondering how you square that with the recommendation. I mean, obviously we can certainly agree to avoid things like, wheat flours and added sugars and refined carbohydrate products, and no one would debate that. But is there really an argument to exclude things like berries, just because they’re higher in deuterium content?

Dr. László Boros:  Well, actually they’re natural. What the species—the plants that you mentioned, they actually produce sugar, which is very interesting. Lentils, for example, or beans, for example—they produce actual sugar, which is actually deuterium-depleted. There’s a great paper about it that actually there are some plant-sugar sources that are actually not only depleted, but they are depleted on specific carbons that are getting oxidized in our system. So it seems that nature figured it out. Not every sugar source is bad. It’s actually the fruits—they’re like—high-photon pressure, summer, early-fall type of fruits that are highest in, in sugar and deuterium. But actually, if you look at lentils or beans or some other…

Ari Whitten:  I would love to, to get that link with you and see what the breakdown of—

Dr. László Boros:  I can send you the paper, definitely. If you actually to look at our medical hypothesis paper, the water exchange reactions—actually we released those papers—which are actually deuterium-depleted sugars. So some foods, some plants are very healthy, especially because of their low-deuterium sugar and their high-fiber chemical fat content, so those are just fine to me.

Ari Whitten:  Okay. And things—obviously fat-rich plants—so I’m guessing things like avocados and nuts and flax seeds and things like that would be very low in deuterium.

Dr. László Boros:  Yeah, you’re right on.

Ari Whitten:  Okay. Excellent. Dr. Boros, this has been absolutely fascinating. Maybe you win the prize for the most fascinating subject matter I’ve ever covered on this podcast. I’m really excited to see this whole field of deuterium and disease and health evolve. I think it’s fascinating. I need to get a couple of papers from you. We’re going to share them on this podcast page. It’ll be at theenergyblueprint.com/deuterium, for people listening, and you might have to Google how to spell that, but it’s D-E-U-T-E-R-I-U-M. Again, Dr. Boros, thank you so much. Is there any place that people can follow your work, or do you have anything you want to direct people to?

Dr. László Boros:  My website is a lászlógboros—just my full name without spaces or dots—www.laszlogboros.com, and you can find all information as far as deuterium depletion. Now we use depletion—if it’s deuterium depletion—it’s D-E-U-P-L and the rest of the depletion word, but practically… I’ll send you those papers—you can go to my website—I’ll send you that information to complete this podcast. It was very honoring. If you have questions, just email me—

Ari Whitten:  Thank you so much.

Dr. László Boros:  —and I will send information to have for your audience.

Ari Whitten:  Yeah, this was an absolute pleasure. Do you have—in your lab, do you do any sort of deuterium testing? Do you want to let people know about that, if that’s something you do?

Dr. László Boros:  We don’t do currently, at UCLA, deuterium testing. There are various ways of testing deuterium, there are reference laboratories in the United States where you can actually have your deuterium tested of water or any type of sample you might have. You just make arrangements with them.

Ari Whitten:  Okay. And if somebody does want to test it, you would recommend saliva, breath, and urine—to get all three measurements?

Dr. László Boros:  I would recommend you do breath, definitely, saliva or—so it doesn’t have to be three samples—breath, saliva, or urine. I think that’s the most useful scenario.

Ari Whitten:  Okay, beautiful. Dr. Boros, thank you again. It was really an honor to have you on, and fascinating stuff. Thank you so much.

Dr. László Boros:  Thank you. Have a good evening.

Deuterium Depletion: Powerful Health Hack for Energy, Cancer Prevention, and more, with Dr. László Boros –Show Notes

The process of deuterium depletion (5:38)
What “Deuterium-Rich Water” is (10:31)
The role deuterium plays in biology (12:04)
Deuterium and the mitochondria (15:42)
How deuterium leaves the body (30:28)
Deuterium as a major contributing factor in many diseases (36:41)
Aging and deuterium depletion (38:03)
How to build up a higher mitochondrial capacity (43:09)
How much exercise you should actually get (48:59)
Other ways to deplete deuterium (53:18)
Testing and measuring deuterium levels in your body (1:00:33)
Benefits of drinking deuterium-depleted water (1:12:57)
Eating a natural ketogenic diet (1:21:41)

Links

Creativity, Transformation, Flow, Growth, Purpose, and Finding Your "Madness" with Dr. Reef Karim
Listen to the podcast with Dr. Reef Karim on how to Master Your Madness
Listen to the second podcast with Dr. Boros about how deuterium affects health.

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