The Primary Causes Of Cancer And The Truth About How Keto Affects Cancer with Chad Macias

Content By: Ari Whitten
The Primary Causes Of Cancer And The Truth About How Keto Affects Cancer with Chad Macias

In this episode, I am speaking with Chad Macias – who is a cancer researcher, sports nutrition expert and trainer to professional athletes. He is currently pursuing postgraduate research in molecular oncology and has spent over 19 years conducting research and developing protocols in cellular and molecular physiology. We will talk about the primary causes of cancer and his take on the controversial claims about keto and cancer.

In this podcast, Chad will cover:

  • The primary causes of cancer (random genetic mutations, or something more?)

  • Keto controversy — can a ketogenic diet really help or cure cancer? 

  • The Gerson protocol – is it backed by the science?

  • The role of hormesis in cancer prevention

  • The exciting role of deuterium depletion in cancer treatment

  • His top cancer prevention tips

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The Primary Causes Of Cancer And The Truth About How Keto Affects Cancer with Chad Macias - Transcript

Ari Whitten:  Everyone, welcome to the Energy Blueprint Podcast. I am your host Ari Whitten and today I have with me Chad Macias, who is a cancer researcher and specifically… And actually in addition to being a cancer researcher, he has got a pretty diverse set of areas of expertise – cancer researcher/sports nutrition expert and trainer, and actually works with a lot of elite athletes, for example elite MMA athletes in the UFC. He is currently pursuing postgraduate research in molecular oncology. He spent over 19 years conducting research and developing protocols in cellular and molecular physiology. He is adjunct faculty at the University of San Diego and he is also a faculty member at the University of Western States Functional Medicine and Nutrition Program.

And he has developed some of the most advanced blood lactate testing and intermittent hypoxia protocols in the world. He founded the Institute for Human Kinetics in 2011 where he works with many of the world’s top athletes. In addition he was a two sport Olympic athlete. He also serves as the human performance specialist at Navy Special Warfare developing programs to prepare Navy SEALs for combat deployment through their Tactical Athlete Program and he heads OPIs, that is the… Wait, did we mention what OPI is, Chad?

Chad Macias:  I don’t think so.

Ari Whitten:  Okay. What is OPI?

Chad Macias:  It is a biomedical research group.

Ari Whitten:  Okay. He heads OPI’s research team and has the knowledge base to conduct medical and exercise physiology research in both humans and rodents. In this Podcast we are going to be talking mostly about, actually entirely about cancer and your research around that. So welcome to the show, Chad, such a pleasure to have you.

Chad Macias:  Thanks man. It is nice we could actually get together. It has been awhile, long time planning, so I appreciate you having me on.

The primary causes of cancer

Ari Whitten:  Yeah, yeah. Really a pleasure to have you. I want to start off with like big picture, totally zoomed out. You know, the broad 30,000 foot view of cancer and why we now have a cancer epidemic, why rates of cancer, of many different kinds of cancer are increasing. Having said that there’s lots of specific cancers that arise for different reasons and different combinations of genetic and environmental factors, what is your sort of paradigm of this broad landscape of the causes of cancer? If you can treat that as sort of a broad topic without, you know, getting too diverted by the specifics that some cancers may arise for other reasons.

Chad Macias:  Well it is a bit of the golden question. Etiology of cancer is pretty hotly debated amongst researchers. The somatic mutation hypothesis is what is currently favored. I personally believe that there is some version of that that will be accurate. And it is just in the sense that majority of all cancers arise from random DNA replication errors and they can arise from the various things that you stated. And I think that with the changes in obesity, that would be the direct pressure that you would see rates of cancer increasing in different types of cancers that may not have been as prevalent in say, the last 50 years. Outside of that, there really hasn’t been much change. And in fact, the survivability from cancer has significantly improved over the last 25 years. So I think we are on the right path in terms of heading towards cures, especially with immunotherapy. But I think isolating more specifically the causes behind the random replication errors has proved to be very difficult. I personally believe nutrition plays a larger role than has been given credit for and, as we know, there is some obvious low level inflammation that can come with different types of foods. And I think that, really simply in and of itself would contribute significantly to a lot of the undiscovered causes of those random mutations I believe will eventually be traced to something to that extent, but…

Ari Whitten:  Okay. Well I want to dig into a few aspects of what you said here. One is you used the phrase “random mutations” and I know that is kind of how it is spoken about in terms of the literature. Yet you also mentioned nutrition, but you also mentioned obesity, which is obviously tied into nutrition. If obesity is increasing the rates of these mutations, how can we call them random? I mean, can’t we reasonably say that it is being, these mutations are being increased as a result of, for example, obesity or poor nutrition?

Chad Macias:  I am sure it is probably possible. There is probably a way to run some type of regressional analysis. It is very difficult to do association type of research when the population has already been exposed to the variable that they may or may not be exposed to, to run that statistics properly. But I think more, you have to look at more that the random replication errors which already happen in general. And I think it is difficult to try to separate where those errors may increase or decrease when we can’t study them actively. And so it is probably a link that you will have a lot of indicators there, but not one you will find a smoking gun for. And I think that will reveal itself as science and as research gets better at looking at these things over the next three to five years. I believe the answer to your question will be yes. But right now we just don’t have enough data inputs to ask the right question.

Ari Whitten:  Okay. What about, I mean, just the very fact that cancer rates for so many different types of cancers have increased, rates of childhood cancers have increased. I am under the impression that they have really skyrocketed. How can we talk about these things as random DNA mutations when our genes aren’t changing over the last, let’s say 50 or 70 years. So if our genes aren’t changing, why is the rate of DNA mutations changing?

Chad Macias:  Well, I mean, it is a good question. I think the, you would have to look at each one of those inputs along with obesity, along with the exposure to various different chemicals that we live around, exposure to different types of wifi with 5G. All of these different factors certainly all contribute in a different way to those errors in replication that we see. So I think in that regard it would be like, it is very difficult to find a way to do regressional analysis with all of that included and even point to even two or three of them, because each one of them has such a strong input in various different cancers. So, you know, you might have, say wifi, heavily influenced wifi cancers will have a totally different input than say heavily influenced nutritional cancers like cancers of the digestive track and bowel cancers, for example, that are heavily, heavily influenced by nutrition. Probably the most influenced by nutrition is like, say bowel cancers where you have, you know, very little protection against all the things that we put through our body down there. So…

Ari Whitten:  Got you.There’s a whole bunch of different tangents I want to go on here, but basically what you are saying, I think, if I can translate it is from your perspective, probably on an individual level, you are probably under the belief that it is very likely that it will ultimately be found that there’s lots of environmental contributors to these DNA mutations. But speaking purely as an academic, as a researcher, you know, as of the current science as of 2019, you know, we don’t have like super conclusive evidence from randomized controlled trials where they followed people for 30 years and found that, you know, put two different groups of people on different diets for 30 years and found that, you know, group A has a 200% increased risk of cancer and therefore we can attribute that precisely to these particular dietary variables.

Chad Macias:  Right. It is hard. It really is hard with so many different types of cancers that are influenced through different factors. And I think it is only becoming more complex because our world is becoming more complex and technology is becoming more complex and all of the inputs and stressors and challenges to hormetic balance that our body goes through are all increasing in both volume and type. And, I think, you know, like anything else, we are seeing times we haven’t seen before where we are able to treat cancer better. But I don’t think we are any closer to understanding, you know, how or why it is starting to show up in different ways and more often in certain populations like you suggested. If I got honest with you, I completely avoid even thinking about the childhood cancer thing. I can’t even have a thought about it without tearing up, man.

It is just too hard for me. And I commend the people that study it. Eventually when I am done working in the area I am working with, I will go over there if some problem solvers are needed. But man, you are right. It has been increasing there, you know, pretty significantly and for pretty much every single cancer besides brain cancer. So, pretty alarming.

The link between mitochondria and cancer

Ari Whitten:  Yeah. Now, are you familiar with any research that has looked at the role of mitochondria and mitochondrial dysfunction in the context of cancer development? What do you perceive of that research as far as the role of mitochondria in the process of development, of oncogenesis, of tumor formation.

Chad Macias:  Well, I suppose that dysfunctional mitochondria could lead to a growth and, you know, there could be crazy mitosis there and you could see something that becomes, you know, malignant.

I don’t see mitochondrial dysfunction being a large catalyst to create a tumor because it just doesn’t have a lot of, like I can’t in my head as I am trying to think, I can’t draw a picture of how that would get from point A to point B. So the plausibility of it turning into a cancer and angiogenesis and all these things that need to take place, rapid proliferation to lead, for tumoral genesis, it is possible. Certainly, you know, the body is one of those things where you can never say this will never happen because the second you do, it happens. So, but it is not very plausible to think that that would be, because if that was the case I would think that cancer would be much higher in those with obesity and metabolic dysfunction that are, you know, diabetics. And granted, they do have higher rates, but I would think that it would be, I mean, it would probably be 30 or 40% higher than what we are seeing right now, if that was a thing because there is mitochondrial dysfunction across the board in those. Same with, like maybe endurance runners because I mean, they are basically, you know, lean diabetics, you know, professional endurance runners.

I mean that what they do with their bodies and the amount of carbohydrates they take in, that is about as unhealthy as you can get in terms of metabolic function and metabolic flexibility, so to speak. Despite it being great for performance, I think you would also see it in populations like that, if that was a thing. So…

Ari Whitten:  Got you. I think the main argument, as I understand it, and I recently interviewed Nasha Winters on the Podcast and the argument that, her paradigm is very mitochondria centric. And I think the crux of it is basically that mitochondria are critical in sensing what is going on in the cell and determining when the cell undergoes apoptosis and programed cell death. And if the mitochondria are not functioning well then they are not going to basically create that programed cell death and kill off the cell when there’s, enough mutations have occurred. And if they don’t, if that cell does not sort of commit suicide, then it can divide uncontrollably.

Chad Macias:  Well, in order for that to be true, the mitochondria would have to exist independent of the body because you have multiple genes, P53. You have specific cancer genes that are activated to fight cancer that are completely independent of the mitochondria. You have the immune system, which also is there to fight cancer, which is completely independent of mitochondria. So, that doesn’t make a lot of sense because the mitochondria is not responsible. Its job is not to fight cancer. There’s a multitude of genes and systems that are responsible for detecting and fighting it. And cancer is very cunning. What I would say is that the mitochondria would play a key role in helping cancerous cells that are already cancerous evade detection and continue their processes. It would play a central role there for sure. But in isolation, it really is not relevant in the hierarchy of what is happening and why leading to rapid proliferation angiogenesis and the cascade that leads for a cell to become cancerous. So that is not something

How epigenetics affect cancer growth

Ari Whitten:  Okay. So you mentioned nutrition. You mentioned obesity. You have even brought up like electromagnetic fields from wifi or 5G and things like that. I am curious at the mechanism level, how do you see these different kinds of forces converging at the cell level to initiate cancer development?

Chad Macias:  I think the most simplistic would be just changes on epigenetics and gene expression. And once you have a slight change in gene expression on mitosis, that is all that it takes. And from there, once a cell becomes cancerous, it already has the ability to communicate and facilitate all of the needs that it needs, that it can in order to facilitate angiogenesis and to generate cancer stem cells and a tumor micro environment and all those things that it needs to intravasate into like say to circulation or into the lymph nodes and things of that nature. So it just is going to set the ball rolling. And once the ball is rolling, you have got a cell that is out of control, it already has everything that it needs right at its fingertips to do what it needs to do.

Ari Whitten:  Got you. Okay. I want to dig into, I am actually, to be honest, kind of little surprised that you brought up the EMFs and wifi issue and 5G and things like that. I am curious, do you actually think that is a big factor and what, because, you know, I actually don’t have a strong position either way on this. I am kind of open to it and I feel like we don’t know enough yet. And there isn’t like a strong consensus in the science about it. I have seen research that definitely suggests harm and then there is other research that kind of suggests it is benign. What is your take on EMFs?

Chad Macias:  I agree with everything you just said on your kind of personal stance on it. I don’t think we know enough yet. But I think there is definitely a red flag and there is reason for alarm and reason to take a closer look at it. I think a lot of the areas that are controversial in cancer research, I have a much different perspective than most people. And it is because I am able to actually go in and look at, you know, some of the data that was used for aspartame. The rodent data that was used to suggest that it is safe for human consumption is not what a lot of people would think it is if you actually looked at the studies and you understand that you don’t terminate rodents before the end of an experiment and then draw conclusions from it.

So I think knowing what I know now about how science is conducted and how you can be disillusioned to think that there is going to be honesty in how experiments are conducted, industry experiments, I am highly skeptical of everything that has a cancer causing potential that is so broad. So I agree with you that the evidence is not there to draw those kind of conclusions yet, but I am very cautious about it. If I could avoid exposing my family to it, I certainly would, if that means anything.

Ari Whitten:  Yeah, I am with you. I have wired internet in my house. I don’t have wifi for that reason. Not because I am like, I think EMFs are the most terrible thing in the world and I am convinced from the science that they are awful and a huge contributor to disease. But basically just because I think they might be a contributor to disease and I think it is smart to operate based on the precautionary principle and just make some simple changes that you never even, you just make them once and then you never even think about them again.

Chad Macias:  Agreed. Yeah. I am on a wired internet now, too. Partly because wifi is horrible where I am at in unincorporated San Diego. But yeah, also for that same reason. Yeah, little small changes that are not much of an inconvenience, you know. Especially non nutritional changes. Nutritional changes are difficult, even for people who are disciplined, you know. Adherence is very hard if you don’t like what you are eating. So, but stuff like this, it

The link between hormesis and cancer prevention

Ari Whitten:  Yeah. You mentioned the word hormesis very much in passing a minute ago. I am curious if you see the lack of hormetic stressors, for example, things like exercise, things like fasting, exposures to heat and cold, you know, as opposed to being in indoor climate controlled environments. You have also, you know, in your bio you have done hypoxia protocols which is another form of hormesis interestingly enough. I know you used it more with training for athletes, but you have some, quite a bit of experience with that. I am just curious if you believe that the lack of exposure to hormetic stressors in terms of the modern lifestyle is a factor in cancer development.

Chad Macias:  I don’t know that it would be a factor in development. I think if you were going to develop it, you would develop it either way. I think for the cancers that are age and lifestyle related, I think it makes you way more resistant to those cancers. To the cancers that aren’t related to just age or lifestyle like, you know, obesity or smoking, things of that nature, I think the other cancers that originate from, you know, hereditary or other causes I don’t believe would be impacted by those things necessarily. But certainly, I mean, that would cover a majority of the cancers out there you would be more resistant to if you had those types of stressors.Especially, you know, as we are learning more about how light affects cells and heavy water and deuterium, and all of these things that science is starting to reveal to us. I think it has become way more clear that these stressors, when you include them, lead to much better cellular health, especially mitochondrial cellular health, I think is one of the things that you find. Yeah, definitely.

Ari Whitten:  Okay. So, one of the things you just mentioned there is this distinction between resistant to cancer versus the development of cancer. So can you explain that distinction a little more clearly? You are saying these hormetic stressors wouldn’t necessarily prevent the formation of it, but they would make you more resistant to it. What do you mean by that?

Chad Macias:  Yeah. Well, you know, for example, you know, when you are looking at something like say telomere length and things of this nature that age has a heavy effect on, I think that you are more resistant to certain types of cancers as those things start to play out in your life. And if you are good about exercising, exposing yourself to different types of light and grounding and, you know, different types of waters and all these different things and resisting, you know, blue light and do different stuff at different times of the day and all these different things that you can learn about, I think all of those things when you combine them together will make you much more resistant longterm to those cancers that are going to be predicated on, you know, seeing a change in how resistant we are to those types of cancers that are more, that you don’t really see in young people and that you don’t see in people who are not obese.

There are certain types of cancers that are going to be way more resisted and they may not be initiated. Because you would see those types of cancers in anybody once you reach a certain age, a lot of those cancers. But that is age-related when our cellular health is at such a minimal, our brain capacity, all these things change. So I think during the course of getting to that point, you are much more resistant to it if you adhere to the things that we know are beneficial

How sleep habits affect cancer

Ari Whitten:  Yeah. Got you. I am curious about the role of circadian rhythm and sleep. We know that sleep, for example, directly contributes to DNA damage. There is a bunch of circadian rhythm research looking at, you know, certainly artificial light exposure at night and suppression of melatonin and there’s links between melatonin and fighting cancer. And then there’s also this link with like autophagy and the feeding and fasting windows. For example, there is some research linking longer feeding windows to increased risk of breast cancer in women and things like that. So I am curious about how light and meal timing might relate to circadian rhythm and how that might affect pathways like melatonin and autophagy or other pathways that could impact on cancer development. Do you have any thoughts on that?

Chad Macias:  Well I would say that is all incredibly complex because you are converging multiple different areas of science and medicine.

Ari Whitten:  I like doing that. That is my thing.

Chad Macias:  Yeah. That actually is more difficult than studying cancer to be quite honest with you because there is such a broad affect in terms of health that there’s so many different things that it impacts in terms of disease. I think what is clear is that the end result of a lack of appropriate sleep and/or people who work through the night, I think the data is quite clear on mortality, comorbidities, early death, cancers. All of those things are way higher than the general population in night workers. You know, specifically like nurses are studied a lot in the literature. Things like that, I can think about off hand a few papers like that. So I think it is clear what it leads to. And again, I think those things you don’t see in people who are young unless you see something really off like that, somebody who works the night consistently over a three or five year period, you know. You have probably shortened your life by 20 years by doing that if you were to live at any other way like you were now but didn’t work through the night. So certainly I couldn’t give you specifics on, I mean, I could parse out the details and we can go in the weeds for sure. But it is very clear that the end result, when you don’t do those things appropriately, just simply not getting sleep right or sleeping during the window that was best intended for us, then there’s some pretty dire consequences that go along with it.

Ari Whitten:  Yeah. I just want to like point something out and I almost want to have you clarify it because the initial question I asked you at the start of this Podcast was sort of like, “What do you perceive to be the causes of cancer?” And it was, the way I interpreted your initial response was almost like the environmental causes don’t matter and have no impact. It is just random DNA mutations, which I know there is some segment of researchers who kind of hold that opinion. I personally think it is going to turn out to be wildly wrong. But then, you know, we have dug into all these other specific subtopics and I hear you basically saying, “Yeah, this could have a role in cancer development. Yeah, that probably does. Yeah, that probably does.” And so you are now painting a picture that is definitely not just random DNA mutations that are occurring just based on genetics without any influence from environment.

Chad Macias:  Well, no. So they are all random DNA replication errors. So the three causes of cancer, they are parsed out into an actual percentage. I will send you the, there is a good research paper on this I can send you afterwards. So whether it is environmental…

Ari Whitten:  Okay, we will link to it on the Podcast page, to this episode page. I will put it under your name actually, so

How nutrition affects cancer

Chad Macias:  Yes. And I will also be sending you about 40 papers once we dig deeper into like say specifically ketogenic diets and cancer and glioblastoma. I will send you about 40 papers for all the things I am talking about. But the three main causes of cancer would be hereditary, environmental and you know… So regardless of what three you are dealing with in terms of the different causes, they all lead to random replication errors, though. So regardless of what causes the random replication error, whether it is hereditary, whether it is environmental or whether it is something like say a heavily nutrition influence, because nutrition is not really, doesn’t really fall under environmental.

Ari Whitten:  It doesn’t? What does it fall under?

Chad Macias:  Well it does but it doesn’t because we can’t quantify it if we just look at it in that simplistic term.

So it would in a broad sense but, you know, environmental would be something like lung cancer, right? So lung cancer is going to be, you know, that is going to be about 97% environmental. So that is more like lifestyle related than you would consider it to be environmental depending on the paper, the journal. They all kind of use different terminology. But when we say environmental, for me, you are not talking about nutrition. So between those three inputs, they all lead to random replication errors from DNA, which also already happens independently of cancer. Right? We have random replication errors within all of ourselves, thousands of them at a time. It is when they become excessive in certain areas, that is when you can lead to an aberrant growth in mitosis and cancer cells.

Ari Whitten:  Yeah. So I think I am just getting hung up on the semantics of it, referring to it as “random errors.” It almost suggests that paradigm that I mentioned before that some people hold that it is like these things aren’t, they are not related to nutrition and lifestyle factors. They are just purely genetic and random and so I think it is just that phrase. But the picture that you are painting, the paradigm you actually hold is one of, “Yes, there’s very clear environmental and lifestyle factors that do influence the rate of these random errors occurring.” Is that accurate?

Chad Macias:  Yeah, sure. Because when you look at something, for example, like childhood cancers, right? How could environmental things affect children and cause cancers but we are not affected that way as adults? And, you know, there’s a lot of childhood cancers that you can’t explain through lifestyle related. They haven’t been obese. They have hardly been alive. They are three, four years old and getting cancer. So certainly there are a lot of people who do exactly what you are talking about that will say, “Oh, you know, cancer is a purely genetic thing.” That doesn’t even make any sense. Like what does smoking have to do with genetics? Clearly smoking causes cancer, right? So, no for sure. Yeah. No, not to get hung up on certain terms. But yes, they are all leading to random replication errors in cell division and things of that nature even though they have a direct input in that. But there’s already replication errors happening. So I think that is why they are referenced as random replication errors because they are already happening to begin with. Those things aren’t creating them. They are just influencing them in a different way.

Ari Whitten:  Got you. Thank you for clarifying. That makes a lot more sense to me now. I was like trying to make sense of what your actual paradigm is for a while there because I know you know a lot about nutrition and lifestyle factors and I am like, “Really? Does he really not think they are any significant factor in cancer development?” So…

Chad Macias:  I wish it was like that. But no, unfortunately they

How deuterium affects health

Ari Whitten:  Yeah. So, I want to go on one more little sort of digression before we get into like the metabolic theory of cancer and keto and all that sort of stuff. And this is something you brought up in passing. You mentioned how light affects cells and deuterium depleted water, which are cutting edge stuff. Obviously I have written a book on red light therapy light and my next book is going to be on light more broadly. So I am super geeky on the science around that topic. I am curious what you have found in relationship to light. How does that figure into all this?

Chad Macias:  Well, so the best that I can tell, and it is linked with deuterium and deuterium accumulation, is that it appears that exposure to different types of light, specifically sunlight at specific times of the day can potentially prevent deuterium accumulation in the cells, or it can inhibit the normal deuterium accumulation in cells. And deuterium accumulates in the cells as, one of the ways is as a result of carbohydrate ingestion, which really creates a challenge for me in knowing that because I love carbs. I am like a fat kid in an athlete’s body, you know, so I can just carb up all day long. I love carbs, you know. I can also eat keto and I enjoy it, you know, it is just one of those things where I can do that when it is related to a goal that is like sports oriented or something of that nature. I don’t have any problem being disciplined, but by all means I love carbs. So, but yeah, so with the way that deuterium is going to accumulate in the cells just based on the way most people eat, it appears that that has value in kind of reducing the deuterium accumulation. And the reason that is important is that it appears, we have enough literature to at least entertain the idea that deuterium accumulation in the cell can also affect growth signaling and…

Ari Whitten:  Sorry to interrupt. But real quick, let’s assume 95% of listeners don’t know what deuterium is. So can you just kind of quickly explain that and then go follow up on where you were headed there.

Chad Macias:  Yeah. So, do you think people are familiar with like heavy water and light water and those sort of…?

Ari Whitten:  Probably not. No. Man, that requires going into the weeds there a little bit… I mean, before the whole deuterium stuff came around in health, I had only heard of heavy water in the context of like, I think Nazi Germany. I remember seeing like history shows where they were working on like heavy water related stuff. And it was part of like the weapons manufacturing in Nazi Germany. That is the link in my mind. But outside of that I knew nothing about it until this whole health craze.

Chad Macias:  Right, so…What I am very not good at, I’d have to tell you, Ari, is creating layman’s versions of stuff. And I think I would feel poorly if I tried to give you a layman’s way to give that to the listeners. So, I think it is, you know, it is best described as is what it is. It is essentially kind of like a quantum biochemistry, if you will. If you had to classify it, it would be quantum biochemistry. And it is, you know, it is, how can we make it simple? It will definitely just be the weight of the water within our cells, I think would be the easiest way to put that without getting crazy into the weeds. And that can have an influence over how our cells signal to grow and create new cells, so mitosis. And deuterium can accumulate. And that water and the weight of that water can be influenced by nutrition, by sleep patterns and by exposure to light. And there’s probably other things that just haven’t been researched yet. So I think just looking at it from that perspective for the listeners, that is how light can influence the way that water is accumulated within our cells, within the mitochondria if you will. And so…

Ari Whitten:  And how does the deuterium figure into cancer development?

Chad Macias:  So I don’t know that it would influence the development of cancer. Certainly it could play a prominent role there in terms of rapid proliferation and getting that biomass started. I think the bigger concern would be about things that we could say now is that if you already have cancer, then certainly you don’t want to influence something that leads to cell division because that is the very definition of a rapid growing tumor and how it can affect the body and then metastasize.

Chad Macias:  So I think for somebody that already has cancer, you want to look at doing anything that can deplete deuterium from the cells. And so deuterium depleted water is one way to do that. Also the way that you can be influenced by sunlight, especially like in the morning for example, is one thing that you can use to kind of influence the deuterium content of the cell.

Ari Whitten:  So just to be clear, this, deuterium depleted water is water that you can drink that has been taken through a process to get rid of the deuterium?

Chad Macias:  Correct. Yes.

Ari Whitten:  Okay. There is research actually to show that that is beneficial on cancer outcomes?

Chad Macias:  Oh, brother, yes. It is impressive. There’s actually phase II clinical trials where they used deuterium depleted water to improve progression free survival in terminal cancer by years.

Ari Whitten:  Wow.

Chad Macias:  As a matter of fact, I have been contacted by NASA and talked to them a couple times because they are concerned about radiation exposure when astronauts go to Mars. They are concerned that the radiation exposure will lead to almost immediate cancer. And so we had discussions about things that they could do to try to combat that. And that is one of the things I suggested like, “Hey, have them drink deuterium depleted water for a couple of months before they go up there. And you know, let’s try to look at every little thing that could potentially create a problem for growth signaling if there was a cancer scenario.” So, yeah, deuterium depleted water is available commercially. People can also make it at home. I think…

Ari Whitten:  Make it at home. Oh, I haven’t heard that. Tell me about that.

Chad Macias:  So, here is the thing about that, though. So for it to be therapeutic in the cancer trials, it has to be a specific parts per million. I think it is right around, somewhere around 120. I can’t remember directly off the top of my head. I believe it is right around 120. But I don’t know off hand how you would secure that making it at home. But yes, to make it at home there’s all kinds of YouTube videos on it. It is really, really easy to Google search. But you basically just freeze water. As it starts to freeze and it builds up the layer on the top, you scrape it all off and then repeat the process. Eventually what you are left with is deuterium depleted water. So…

Ari Whitten:  So the deuterium, for whatever reason, the deuterium, the heavy water that is deuterium rich has a lower freezing point.

Chad Macias:  Yes. And so it will accumulate and enable you to kind of clear it out to where you will end up with some deuterium depleted water. So…

Ari Whitten:  I think it is, maybe I misspoke there. It is a higher temperature. Lower implies like lower temperature.

Chad Macias:  Higher…Right, exactly. So I don’t know how you would ensure, Ari, that you got that parts per million correct. Certainly if cost is an issue or somebody that just wanted to just kind of do it as a preventative maintenance, precautionary, I think it would be simple to just do that at home and make your own. But they do have it available commercially as well. But there is probably, I want to say about six to eight phase I/phase II clinical trials where it is being used to improve progression free survival. For me that is pretty powerful. It doesn’t get any better than that. It looks like it is a scalable thing based on the clinical trials results in the fact that they already made it to phase II. So pretty cool stuff.

Ari Whitten:  Interesting. Yeah. I am curious, if there is anything known about, for example, like tap water, you know, city water coming out of your tap versus like spring water versus glacial water as far as deuterium content in those different waters. Do you know anything about that?

Chad Macias:  I have read about it. The glacier water is a better source for less deuterium. I don’t know much about other water sources other than that. I mean, I have seen that factoid in reading about it that that is a better source of deuterium depleted water if you were just to list out what each type of water had in it existing. But I don’t know much about other water sources in terms of their deuterium content, to be quite honest with you.

Ari Whitten:  Got you. Well, it sounds like sunlight, which I am a huge fan of and is a big part of my recommendations in what I teach people, it sounds like that in and of itself will probably turn out to be a really powerful way to create deuterium depleted water inside your cells, which is probably ultimately where it really matters the most.

Chad Macias:  Yeah, it seems like it. And I think the more that we get people who are interested in studying this, because it is difficult to get something like that into a clinical trial, depending on its clinical utility, but it appears that it does have good clinical utility. And it is one of those things where I would love to see it thrown into as an adjunct into standard care into a cancer trial. Because I mean, why not? You throw exercise, you throw all these other things in there to try and make a difference, especially in terminal cancer, right? Where the battle ground is really at. And so yeah, I see it being something of great value moving forward in oncology treatment as the oncology world starts to embrace that there is other things out there, that we can use off label drugs. There is all these other things now that researchers go, “Wow, you know, this stuff is, there is other things that we can do outside of, you know, cut, burn and radiation.” So I definitely see that being something that we see here very shortly because it is already in play now.

The science on ketogenic diet and cancer treatment

Ari Whitten:  Yeah. Awesome. This is fascinating stuff. So I want to get into the metabolic theory of cancer and keto diets. So this has been written about by a few different people in recent years and kind of popularized this notion that, you know, for example, cancer feeds on sugar but not fat or ketones. And so if you go on a keto diet it kind of starves the cancer, you know, or reprograms the metabolism in a way that fights cancer. I know that you are pretty critical of some aspects of this. So what, why are you critical of this theory? What is wrong with it?

Chad Macias:  So there is a lot wrong with it, actually. It is pretty interesting to see how far this has come based off of what I could only describe as like, say bad science, is really what it comes down to. And I became really interested in this because it just became something I was very curious about. And cancer is always something I have wanted to study. My family has been affected by it. Most families have. My mom and aunt both had breast cancer. It has affected my wife as well. And so, you know, I kind of thought, you know, well maybe I can look at what is going on here. You know, I am a good thinker. Maybe I can help out here. I wouldn’t mind getting some education in this and seeing what I can do. I have done a lot in other fields I have worked in.

So that is what kind of pushed me down that path and was naturally guided to the keto for cancer discussion because it is so prevalent amongst the lay in social media. And then also in the research world, there is probably 400, you know, review papers on a ketogenic diet and cancer. And all 400 of them have specifically looked at rodent and cell culture data. So to get to where we are now, let me go back to the beginning so that people can understand really why I have been so critical. Because there has been a lot of very strong claims made about what the ketogenic diet can do for cancer and none of them are supported by any evidence in humans whatsoever. Not one of those claims. And so when you are making those kind of claims, and you and I both know that when they get filtered down to the layman, to the average person, what was said has been so diluted to begin with.

And if it is not based on accurate science, that is pretty dangerous. And so you can go into any chat room anywhere, in any type of social media, Instagram, Facebook, whatever it is, and you can find people giving each other advice on how to use a ketogenic diet to treat a family member or themselves with cancer. And that really is what kind of pushed me to say, “Well, hold on a second here. Let’s take a look at what is going on, because if that is the case, why isn’t that reflected in clinical trials?” And so when I look back to where this all started, around early 2000 you started seeing a series of cell culture papers being published that were looking at specifically glioblastoma. If I can remember correctly, I believe it is the U87 cell line, which was and still is pretty popular in studying glioblastoma.

And so what researchers were doing is they were allowing these glioblastoma brain cancer cells to adapt to the serum and the cell culture in that petri dish. And then they were investigating how they responded to glucose and fatty acids and proteins. And so they conducted these experiments and they were noticing, they were like, “Wow, you know, it really has an affinity for glucose and it doesn’t respond to fatty acids.” And so, you know, they continued doing more experiments. And this led to rodent studies. And that is pretty much where it stopped. And then the hysteria started. And then you had a lot of people who were fringe researchers in terms of, they are not oncologists and they are not medical doctors, right? So they don’t actually study cancer and they don’t actually treat patients, but they are studying ketogenic diets in rodents.

And that is where a majority of where this sensation that you see now on social media was started from, was a group of researchers who are what I would consider fringe in terms of cancer research. All well qualified, highly educated PhDs in biochemistry. And even some doctors that are not oncologists, but they are studying oncology and they are not working with human patients and they are drawing a lot of conclusions from their work. And it influenced everybody and it got really out of control. And so in looking at the clinical trials, I want to be at the forefront and the battleground of studying this. So I said, you know, I need to go get an education in cancer biology, which is where I am still currently doing that. I am still working towards my PhD in Molecular Oncology at [inaudible] University in Spain.

Started with my Master’s in Molecular Oncology at Center for Biomedical Studies also in Spain, which is the leading research facility for cancer research in the world. And I started asking questions. And when I looked at the clinical trials, which does exist in human patients and ketogenic diets, it is not improving progression free survival. And so why? Why is it not improving progression free survival there but it does in a majority of the rodent models, only a few of them does it not work, and in all of these cell culture studies? So I started looking at the cell culture studies to understand, well why is this showing up here but it doesn’t show up in human patients? Obviously there can be differences in between what happens in a petri dish and what happens in humans. But for the most part, what you see is fairly accurate of what you can loosely see biochemically within the biological individual.

And so when I looked at that, you start seeing all these papers that are recommending that you do not do cancer research when you allow the cells to adapt to the serum. So they lose their ability to differentiate, they lose their ability to be clonogenic to be tumorigenic. It changes their epigenetics. It prevents them from looking like the parent cell so they cannot recalculate anything that came from the actual original tumor. So it is a horrible place to examine what is going to happen with a substrate. And one thing that is very clear now when you look at cell culture studies that have specifically investigated this and the research studies that I will be sending you to put up on the page, I have got about 10 that specifically directly quote everything that I am telling you that say, “Do not conduct these types of experiments where you allow the cells to adapt to the serum.” They lose their fatty acid oxidation potential when you do that. So they cannot oxidize fatty acids when you allow them to adapt to a serum that has glucose or bovine or any of the other typical serums that you find. You can’t do it because you are going to get a picture that is incomplete where you think that they cannot use fatty acids but they actually can and sometimes at a higher rate.

Ari Whitten:  And so this is, just for anybody who got lost in the biochemistry that you are describing here, what you are basically saying is in the experimental model, you are going to draw the conclusion that these tumors are being starved on a low carb, you know, higher fat substrate. But in an actual living human being that would not occur and the tumors could maybe, it sounds like, easily adapt to burning fats or ketones for fuel. And maybe even, I don’t know, I don’t want to put words in your mouth, but maybe even preferentially use them for fuel or something to that effect.

Chad Macias:  Yes. Both of those can be true depending on the cancer. But to continue to draw the line from there, so that is exactly right. You have these cell culture, these petri dish experiments where they left glucose in there, the cells adapted to using glucose and not fat. When they introduced fatty acids, the cells couldn’t use them and they died. And so there is, it gives this illusion that that is what is going to happen in the individual. So they take those and they go to the rodent studies. Well, the same thing happens in a lot of the rodent studies. So that is going to bring about some pretty strong confirmation bias for researchers who are looking at this going, “Hey, wow, look, this is happening in the rodents, too.” So the rodent stuff, we will just keep very brief and very simple. Rodents have a basal metabolic rate that is seven to eight times higher than humans and a vastly, vastly, I’ll say it one more time, vastly different hepatic function compared to humans. It is a good model to rapidly induce obesity and look at changes in nutrition related to obesity influenced diseases, body mass and things like that. It is a great model to do that. It is a horrible model to investigate cancer when you are investigating how a high fat diet influences tumoral genesis. Horrible model to do that in. I see more value in jumping straight from cell culture to working with nonhuman primate like canine or monkeys and then humans then going to rodents because it will give off another illusion that you have this therapeutic intervention that you really don’t have because that environment will never exist in a human. So you get cell culture that went to rodent studies. The rodents happened to respond in a similar way that you saw in the cell culture.

There is a few different reasons also that there is problems with some of the rodent data that I will briefly mention. The group of researchers that was really spearheading this, Dominic D’Agostino, Tom Seyfried, those guys popularized this with a rodent model that they created themselves, the VMM3 model of metastasis. The problem with that is that it doesn’t have external validation. And for the listeners, what that means is that no other scientists or groups outside of these individuals use that model to study cancer and treat cancer with a ketogenic diet in that model. So the only ones to do it, they created it. And they started conducting these experiments in rodents and started drawing conclusions in humans saying, “Hey, you can use this in humans. It can be an adjunct, it might even replace chemo and radiation by itself,” which is crazy to say in a research study that you conducted on rodents. And so you have both rodents being an inappropriate place to investigate a high fat diet because of the changes in basal metabolic rate and the difference in hepatic function. And then you also have a group of researchers who are responsible for popularizing this diet and cancer intervention who used a rodent model that didn’t have external validation. So you have multiple different problems with the rodent side of the research as well.

Ari Whitten:  So I think I also heard, maybe I am interrupting your flow and you were going to get here, but,I think I also heard you say in another interview I listened to something to the effect of they actually miscited, you know, they made claims in their paper where they put citations next to it and the citations literally didn’t support the claims they were making.

Chad Macias:  Yeah. So, you know, I don’t want to throw too much mud because I try to get to a place where I can build bridges with people because I think we have a common goal to some extent. But certainly those research papers, there was references in there that were unrelated to the point. It wasn’t that the point was that it required a large amount of evidence. It was simply that when you started looking through some of the citations, they were like completely unrelated to what it needed to say. There was also a lot of things in the papers where they would make claims about biochemistry that, you know, “It is impossible to use fatty acids in brain cancer tumors because you don’t have the metabolic phenotype, you don’t have these biochemical milieu,” and all that stuff has been demonstrated to be false.

It was false when they said it. There was evidence to prove it was false when they said it. It has since been solidified as false with a lot of human data. So there was a lot of problems within their papers as well that you alluded to both with citations not being accurate and also an inaccurate description of what is actually happening within the tumor itself. Despite that they were describing what happens in rodents, they were still projecting that as that would be similar to what you would see in human patients. So if we fast forward to what happens in actual human patients, so let’s go to that data. We have talked about the problem with cell culture in rodents. So what happens in actual human patients? I actually have, there’s actually clinical trials that have been published.

A lot of people don’t realize that. I have got that data right here. So, the first study that was conducted by the Institute of Neurooncology Hospital at Frankfurt, it had 20 patients total, only 17 completed it. They had, they verified ketosis through urinary measures. The researchers were looking at what we call progression-free survival and overall survival. That is what matters in cancer. Progression-free survival is how long you can survive without the tumor itself, the cancer progressing any further with the treatment. Overall survival is achieved after five years of no progression from the cancer at all at the five year mark. That is considered overall survival. And so they, the researchers looked at overall survival and progression-free survival in a group of patients. They had different types of cancers. So you had glioblastoma, you had prostate, you had different types of cancers.

So the medium progression-free improvement was five weeks. None of the patients were, saw a change at six months where they weren’t progressing. So every single one of the patients had progressed by the six month mark. The average time before progression was about five weeks. So they did not achieve any significant progression-free survival in that group compared to what you would see with standard care. So the second study was with 12 patients at the Veterans Affair Hospital here in Pittsburgh. So they had patients that had prostate, melanoma, renal cell, pancreatic, colon, thyroid, head and neck and glioblastoma and lung cancer. Six patients discontinued treatment at four weeks due to the disease progressing. Two patients discontinued treatment at eight weeks, one due to a grade three weight loss, one due to disease progression. Three patients completed the 16 week trial.

Two of those patients died, one at 40 weeks one at 80 weeks with one patient reporting disease free at 131 weeks, which was the melanoma patient, which is, that type of melanoma was not terminal. So that was not unexpected. So you can see that when we look at the clinical trials that it has not led to any progression-free survival in the various forms of cancer that it has been investigated in.

Ari Whitten:  This, just to be clear, this was keto diets being investigated for these different types of…

Chad Macias:  What it was is it was a ketogenic diet used as what we call an adjunct to standard care. So the patients were still receiving chemo and radiation and they were introducing the ketogenic diet to try to improve the therapy itself. From a cancer biologist’s perspective, you use the ketogenic diet to sensitize the tumor to keto.

That is the hypothesis that has been put forward that it will sensitize it to the treatment because it is not going to have a fuel source. What we find when we actually started studying this a little bit closer is that we actually, Ari, found the complete opposite of that. And that is what makes this so frustrating is that the original cell cultures, not only were they conducted improperly, but it is actually the complete reverse when you do it properly. So when you actually investigate these things in cell culture, when you don’t allow the tumors to adapt to the serum and you introduce glucose or sugar and you introduce fat, fat is the preferred fuel source for glioblastoma, for brain cancer. And one of the things that… And the thing that I wanted to understand is why, again, why are these things happening? And if there is all this data in the cell culture and even with knowing why it is improper, you still want to find out what exactly is happening within a tumor.

How could the tumor use fat and how is it going to not be able to resist the treatment and how does it not resist the treatment? So I am asking all those questions at the same time. I study specifically glioblastoma. Myself, Tim Sharp and Brad Dieter are involved in a clinical trial at SUNY Upstate Medical Hospital University in New York where we are introducing a ketogenic diet as an adjunct for glioblastoma brain cancer patients. So we are actually trying to figure out ways for this to work and the reasons why it doesn’t work. And what that clinical trial has revealed to us is that when we start looking at the ways that a tumor can resist treatment, so why is a tumor terminal in this cancer but it is not in another cancer? And it is actually pretty simple. It comes down to antioxidant defense.

So you have chemo and you have radiation and they are trying to disrupt the DNA that the tumor is using to regenerate all the things it needs for fuel and biochemical needs. And it is also, we are using the keto which is trying to introduce cellular death and apoptosis, and it is inducing cytotoxicity in the cell which will lead to cell death. And the way that the tumor resists that is through antioxidant defense. So it wraps up glutathione production to resist the cytotoxicity that comes with chemo and radiation. So there’s a couple of noteworthy things that happen when we start looking at that really in depth, specifically in glioblastoma which is where a ketogenic diet has been prescribed the most is in brain cancer. So when you start looking at how does, how do brain cells produce glutathione to resist the chemo? And we start looking at it, it is actually produced through fatty acid oxidation. So fatty acids increase the ratio of NAD+ to NADH, and anytime you increase the ratio of NAD+ to NADH you are going to increase antioxidant production. And in fact, one of the chemotherapy drugs that is used specifically reduces NAD so that you can reduce that ratio and the antioxidant production. So fatty acids…

Ari Whitten:  Just to be clear, this process that you are talking about, I think it also involves things like sertuins and Nrf2 pathway. This process is profoundly beneficial to ramp this process up in normal healthy cells. But you are talking about when it is happening, when it is being ramped up, and the internal antioxidant defense system is being bolstered in tumor cells, that becomes their defense against things like chemo or radiation.

Chad Macias:  Yes. Correct. And so there is a couple of kind of large indicators of what is going on that a lot of these researchers seem to ignore. And so when you look at patients who are on chemo and radiation for any type of cancer, it doesn’t have to be brain cancer, one thing you notice is that regardless of the metabolic phenotype of the tumor… So some tumors do prefer to use sugar and/or glucose. That is true. There are tumors that will prefer to use sugar and glucose and as they change throughout tumor progression, that changes and they go to using more proteins. Or, like pancreatic cancer has an upregulation of autophagy. And there is all these just random different things for each cancers. But what you start to see is that these different types of tumors resist the therapies by switching over to oxidative phosphorylation.

So they all start using fatty acid as their main fuel source when you try to kill them. All of them, every one of these tumors that you find, the cells within them will start going to ox-phos to fight against the stress that is created by the treatment. And the reason that it can do that is, again, because fatty acids can support glutathione production in the mitochondria and the cytosol, and it was always thought that it was glucose through the pentose phosphate pathway that that is what was happening. But in fact, that is not the case. It is actually happening through fatty acid oxidation that it is increasing the NAD/NADH ratio.

Ari Whitten:  Yeah. So the bottom line…

Chad Macias:  So basically fatty acids and ketones can increase the NAD+ to NADH ratio, which will increase glutathione production and help the tumor resist the chemo and radiation. And when I start looking at, there are survivors which we call extreme survivors of glioblastomas and there’s a couple of survivors that have utilized a ketogenic diet. So it is like, okay, so if this is the case and I am so sure of myself, then how did this person survive despite using a ketogenic diet? So that is where IDH1 mutation comes in. So there’s different types of mutations that happen within glioblastomas.

Chad Macias:  There is several and that can actually define the type of brain tumor it is. And one of them is the IDH1/IDH2 mutation. And when we started to look at that a little bit closer, I had a feeling that we were going to find that fatty acid oxidation is down regulated in those with the IDH1 mutation and sure enough it is. So in the people that have an IDH1 mutation, they don’t have the ability to oxidize fatty acids to improve that NAD/NADH ratio and improve…

Ari Whitten:  This is specifically in the tumor cells or throughout all the cells.

Chad Macias:  Well, this would be specifically in the brain tumor cells.

Ari Whitten:  Interesting. And so a lot of this stuff is actually a little more specific to brain cancer in terms of like the glutathione production in glial brain cells is really where this plays out and it may play out in other areas.

Chad Macias:  I haven’t studied that in other cancers, but I have a feeling it will, not in all, but most will. It will be similar in that glutathione production is better supported through fatty acids. And that is clear by the fact that all tumors switch to oxidative phosphorylation when you introduce chemo and radiation. The second you introduce chemo and radiation, the tumor that had previously been living on glucose will immediately switch over to oxidative phosphorylation and start using fatty acids as its fuel source, also as its carbon source. So, tumors don’t just take glucose and fatty acids for fuel. They will break them down so they can get the carbon [inaudible] from it and they can take it and use it for building blocks in rapid proliferation. So that is another thing. People have a misconception that, you know, that glucose and fatty acids are only a fuel source and that you can starve the tumor.

They are not just used as a fuel source. And anytime you try to starve one of those fuel sources, the tumor will literally just adapt. It is such a reductionist approach that is totally ignorant of how intelligent cancer operates on. I just want to bang my head on the wall when people suggest stuff like that.

Ari Whitten:  Suggest like basically that cancer feeds on sugar and if you eat a low carb ketogenic diet you are starving the cancer. That level of reduction is what you are talking about that makes you want to bang your head against the wall.

Chad Macias:  Yeah, that is just ridiculous. You don’t think that we would be doing that as cancer researchers to help these patients live? Like, I mean it is just asinine to think that something so simplistic we wouldn’t just do it. You know, there is a lot of misconceptions about what happens in cancer research and you always hear Big Pharma and their influence.

Big Pharma is the reason why our rates of cancer death have dropped significantly. Even though chemo has its own set of problems that come along with it, it saves a ton of lives. And standard care is hands down the best way to go about it. If my children or my wife, as we are currently dealing with a cancer in the family, I will highly recommend standard care across the board if immunotherapy or a really attractive clinical trial is not available. It is hands down the best way to do things. And to think that you could still simplistically do something that we wouldn’t just do on our own accord. There’s no, Big Pharma doesn’t fund… The majority of cancer research is funded by the NIH or the university itself that conducts it. Big Pharma puts very little money into cancer research unless it is for the drug they are developing. So, and there hasn’t been very many drugs developed in the last 20 years for chemo or for radiotherapy, which is now majority done through laser, anyway.

Ari Whitten:  Got you. One more little digression, which is the Gerson diet and the, you know, kind of the vegan approach to cancer. There’s a little bit of a battle even among the people who think, you know, standard care, chemo radiation should be avoided. There is an internal battle where even within those people, there is a division where some people are more pro-keto and other people are more anti-keto, pro-vegan diet. Do you have any thoughts on that debate at all?

Chad Macias:  Yeah, sure, I do. I think that anybody arguing for the use of the ketogenic diet as an adjunct outside of a clinical trial setting doesn’t know what they are talking about. We don’t have any evidence in humans that this can improve progression-free survival. So I don’t understand why people continue to draw conclusions from studies that are not in humans to treat humans. The human data suggests it is not effective. So I would say that that is, they definitely should not be voicing their opinion if that is what their opinion is because it is not validated by evidence. So in looking at the side, the vegan or the juicing and the coffee enema side of things. So it sounds attractive and it seems intrinsic that you could be healthier by doing those things. The problem is the evidence is just not there.

I personally have investigated it. I have contacted the NIH about it. There has been research studies published on the Gerson methods and when researchers at the NIH and other cancer biologists looked at their data independently and asked for five year follow up from their cancer patients, it did not exist because they did not follow up with a single patient. So when these researchers track down all of these patients at five years, the group of 50 patients that they chose to track down, all but one was dead and the one that was alive still had cancer and died within a year. So the evidence would suggest they are not treating cancer at all. The evidence would suggest they are sloppily helping people with a method that I am not sure that has any value. There was probably a dozen reported cases of death from their methods from both the enemas gone wrong and also the use of raw liver led to a number of deaths here in San Diego that are all… I will happily also send those to you. All of this stuff is published in peer review, which is a wonderful. So there is no evidence for that.

Now with that being said, I know of a few different clinics where people that I have personally helped through the cancer journey have went where they used a combination of Gerson like method along with low dose chemo and a few other natural methods with success that I verified through MRI and pet scan at an oncology hospital that is well-respected here in the U S. So I do see value in using methods like that when they are combined with standard care. But when you have groups like the Gerson Hospital and other institutes that are using those as their standard care, I think it is a recipe to die and to die quickly. I don’t see any value in that stuff at all.

The best way to treat cancer

Ari Whitten:  Got you. Yeah. Do you think there is, and we spoke, you know, we kind of alluded to some possible ones earlier, but do you think there is any natural treatments that you would like, you know, wholeheartedly recommend or encourage people to look into? Let’s say in conjunction with standard of care, whether it is fasting or deuterium depleted water and things like that.

Chad Macias:  Absolutely. There is a ton of stuff that is heavily evidence based that you can look at. You just mentioned a few of them. Deuterium depleted water. You can look at circadian rhythm, how sunlight affects deuterium in the cells. You can look at things that… There is really strong cell culture and dosage is probably where you might run into some problems, but things like turmeric and different types of anti-inflammatories that, depending on where you are at with cancer because you don’t want to arm the body with anti-inflammatories during chemo resistance because that is how it resists the treatment. There is this kind of battle ground there where there is value with anti-inflammatories depending on what stage of cancer you are at and things of that nature, which is why it is good to have somebody guiding you through these journeys that has the experience. But…

Ari Whitten:  Yes, certainly in the context of cancer prevention. In somebody who doesn’t yet have it.

Chad Macias:  Yeah. When you shift over to the prevention, yes. All those things go well with prevention. You can also take a look at things like a Mediterranean diet and things that kind of more, or lower carb that would also reduce your exposure to things like deuterium. But certainly there is a whole realm of healers out there, whether it is naturopaths or functional medicine specialists or even if you are in allopathic medicine, there is integrated medical specialists and fields now that I think has a ton of value in prevention and treatment of cancer. I think allopathic medicine by itself is pretty limited. It is, you know, cut and burn, you know, for cancer. And that is really all there is. I mean, they usually don’t even advise cancer patients on nutrition when they are in front of the oncologist.

Ari Whitten:  I have heard stories from people with cancer that literally, you know, ask their oncologist about nutrition and the oncologist will say… I have heard this multiple times, where the oncologist will say something like, you know, “It doesn’t matter if you eat McDonald’s and candy bars or whatever, you know, organic food you want to eat. It doesn’t make any difference.”

Chad Macias:  Yeah. There is a lot of oncologists who say that because they are lazy and don’t give a crap and it hurts me to hear that. But it is definitely true. There’s also some that will say that because they want the patient to be as happy as they can be, and depending on the scenario that actually may be the right thing is to, you know, because…

Ari Whitten:  If it is like a terminal cancer and people would you suffer unnecessarily from also changing their diet.

Chad Macias:  Well, because muscle wasting becomes such an issue for cancer patients, right? I mean, you die from metastasis or you die from wasting away. You die from, you know… So I think that a lot of times just the fact that they can eat is a plus for an oncologist. So, but that is not who you are referencing. You are not referencing the person that is concerned about their patient that just wants them to eat because they are worried about them wasting away because that is what will kill them, not even necessarily the tumor itself. And so I think the people that just, you know, don’t care enough to give a recommendation or to refer them out to an RD or somebody at the hospital, that is just unacceptable and completely ridiculous and far too common.

And it is really unfortunate because certainly nutrition has value in at least, you know, being slightly resistant to just the therapy that you are going through. And like you mentioned, fasting. Like we know that if you fast before chemotherapy it can almost completely reduce the side effects to nothing. And that is extremely powerful. You know, if you are an oncologist, you owe it to your patients to go to conferences and listen to people like me talk about what is in the literature and what we see and how you can translate that over to your patients for clinical utility. And that is a great example of a tool that you can use.

Ari Whitten:  And just real quick, you know, before we started recording this Podcast, you mentioned something to me as we were talking and I said, “You have got to bring that up in the Podcast.” So, you mentioned basically exactly what you were saying is there is a ton of oncologists who are just, you know, they have their training from medical school, from their residency, and they kind of know what they know, but they are not necessarily keeping up with all the latest advancements in, you know, from cancer researchers such as yourself. And they don’t know, you know, what has been published in many cases, the latest science that has emerged in the last couple of years.

Chad Macias:  Yeah, exactly. I think it is actually a huge problem in the field of oncology is there is a large disconnect between what we are looking at in scientific research and clinical trials and what they have knowledge of that we are doing. And I think that they should attend these conferences where we are, you know… They have a general knowledge of these chemotherapy or what we prescribe for this and we are going to use radiation or whatever protocols they have at the university or the hospital that they are at. And that is kind of a lot of times how they go at it. And, you know, I am not trying to take a knock on anybody but you certainly need to be aware of the ever changing landscape. Immunotherapy will all but make me completely redundant within 10 years. And that is great news. I don’t want to have a job studying cancer because if I don’t then everybody is living and that is great.

But that is where it is headed. And I think it is so foolish for them to not be aware of clinical trials, to go on to and do a simple search. If you are an oncologist and you treat brain cancer patients, stay up on what clinical trials are there. Maybe you can recommend your patient there if you haven’t given them any rounds of chemo or radiation. And there is a promising immunotherapy trial at like, for example, here at UCSD in California where they are pioneering that. You would want to be aware of that. That is going to give your patients the best chance to survive. And they just don’t get that. And so that is one of the things that I do is, Tim Sharp and myself, we will go around to different nutrition conferences. And in fact University of Western States has sent us to conferences to talk about, you know, we have created poster presentations and we have written, you know, letter to the editors about some of these researchers. And we present that data as to the problems and also what you can do about them, solutions. We don’t just talk about what is wrong. We also talk about what the solutions are as well.

Ari Whitten:  Awesome. Chad, this has been phenomenal. I have really enjoyed this. This is absolutely fascinating stuff. Thank you so much for coming on the show. Last thing that I want to ask from you, just real quick, if you could give, and you don’t have to go in detail, but just your top two or three things that you think are the most important things. You know, having said that this is somewhat speculative when we talk about causes of cancer, but for people who are interested in how to prevent cancer, what are your top two or three things that you would say to somebody who says, “I want to make sure that I, you know, do as much as possible to live to a hundred without ever getting cancer.”

Chad Macias:  So I would say from a nutrition perspective consider a Mediterranean diet. It appears that that is likely the best case scenario for longterm avoidance of cancer from a nutrition perspective without creating any problems anywhere else. I think that would be what my nutrition recommendation would be. Create a type of protocol or an awareness about the small little tools that you can have in your tool bag like dealing with blue light, like grounding and getting sunlight early in the morning, being conscious of deuterium or maybe even deuterium depleted water. That would be number two. Number three…

Ari Whitten:  I will just translate that for everybody listening is sign up for the Energy Blueprint.

Chad Macias:  Yeah, no, all those things…

Ari Whitten:  I will give a little pitch for my own program where I talk in depth about those things.

Chad Macias:  It is totally appropriate. And if I were to recommend anybody I would recommend you. So that is fine, that is great.

Ari Whitten:  Thank you, that means a lot to me, thank you.

Chad Macias:  No, your work is exactly what people should read if that is what they are curious about from the perspective of light and how light affects various different aspects of health. I am sure you have covered all of them. In reading some of it, I have seen you covered the majority of the things that I could think of off the top of my head. So, yeah, certainly reading a book that can educate you on how to use light so you are not relying upon, you know, something on social media. Go to the subject matter experts like Ari that have written these books. Look at the peer reviewed literature also to guide you when you are doing these things. And lastly, the third thing would be just to use common sense and avoid the obvious, you know. Don’t live under power lines and then wonder why your child has some obscure, rare cancer. I mean, use common sense, which doesn’t seem to be so common nowadays. But nevertheless just avoid the obvious that you know is not healthy for you because we oftentimes know things aren’t in our best interest and we do them anyway. So please just, that would be like not smoking, not living near power lines, you know, trying to avoid your exposure to 5G and things of that nature.

Ari Whitten:  Yeah, beautiful. Chad, this was seriously awesome. One of my favorite Podcasts, so educational. I learned a bunch of new stuff, too. And really, thank you so much for coming on the show.Thank you also for spending a huge amount of time with me. I really appreciate it. For anybody listening who wants to either follow you, I don’t know if you, do work with people directly like one-on-one? But maybe you can feel free to just let people know where they can follow your work or reach you if they want to work with you.

Chad Macias:  Well, I mean I mainly exist within the research realm and then we do a lot of work with elite athletes. So I am easily accessible, though, on social media. You know, Chad Macias on Facebook. I am on Instagram as well. I am happy to answer any questions that you have about cancer. You could send me a message, send me a friend request. I am easily approachable. Outside of that, be looking for lots of research papers to be published, which I will put out through my social media. And then I will leave any, I will leave my email address with all the research studies I send to Ari to put up and feel free to contact me that way.

Ari Whitten:  Beautiful. Chad, thank you again. I know you have got to run. I got my kids waiting for me to go for a little outdoor adventure while we still have got some sunlight here in San Diego. And I am sure you are very busy as well. Thank you again, and I look forward to more future conversations with you.

Chad Macias:  Sounds good. Thank you very much, brother. I appreciate it.

Ari Whitten:  Yeah, thank you.

The Primary Causes Of Cancer And The Truth About How Keto Affects Cancer with Chad Macias – Show Notes

The primary causes of cancer (4:47)
The link between mitochondria and cancer (12:58)
How epigenetics affects cancer growth (17:12)
The link between hormesis and cancer (21:17)
How sleep habits affect cancer (25:20)
How nutrition affects cancer (29:01)
Deuterium depleted water (32:43)
The science on ketogenic diet and cancer treatment (42:46)
The best way to treat cancer (1:12:41)


Listen in to Dr. Nasha Winters about some different approaches to cancer treatment.

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