Written by Christopher Kelly
Feb. 18, 2016
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Christopher: Hello and welcome to the Nourish Balance Thrive podcast. My name is Christopher Kelly. Today I'm joined by Travis Christofferson. Hi, Travis.
Travis: Hello.
Christopher: Thank you so much for joining me. I'm extremely grateful. I've just finished reading for the second time your book, Tripping Over the Truth: The Return of the Metabolic Theory of Cancer. It's a fantastic read. I highly recommend it to anyone.
I've got Travis on to talk about the ketogenic diet and how it might be a therapeutic agent for cancer. Yeah. I'm very excited. Why don't we start by me asking how it was that you became interested in biology in the first place? There are two reasons I'm asking that question. The first is I want everyone listening to know. The second is I may end up copying you.
Travis: I guess it go way back as a kid. I've always been interested in just how your body works. The people that are in this field, that's usually how it starts. I think they just have a fundamental curiosity about why they work, how their body works, why they get sick, and they pay attention. The best doctors are the ones that are taking notes of their own body and doing experiments on themselves. So I always had that kind of fundamental curiosity.
Then in grad school I was doing a course on sort of cancer theory. That's what I ran into, this book called Cancer as a Metabolic Disease by Tom Seyfried. That kind of just set me off into curiosity and obsession with this theory. I went on and saw Tom, interviewed him, and that only made it grow and grow. This was about 2012.
About the same time The Emperor of All Maladies came out. It was such a fascinating book. It's a Pulitzer Prize-winning book. If you haven't read it you should read it. It's so extraordinarily well written. It's called The Biography of Cancer. It's this tomb of cancer, of how we've come to know the disease starting way back in history, and how therapy has sort of played catch-up with what we knew about it or sometimes led in some cases.
I thought that Tom's book deserved a sort of The Emperor of All Maladies type book to kind of piggyback it because obviously he had written science book but this book, there was such a rich story to it going all the way back to Otto Warburg and this metabolism of the cancer that -- the basic research that went on through the century starting with him who is this fascinating figure and then it got lost as we discovered DNA, and now it's had this resurgence.
I've always kind of dabbled with writing. So I had that intense curiosity we begin with and then I just really wanted to tell that story because it was such a deserving story.
Christopher: He says dabbled with writing. That was kind of one of the things I was blown away by in the book. Dominic D'agostino said the same thing. I don't know if you heard the Tim Ferriss podcast. He referred to you as one of the most talented writes he'd ever read. He's clearly a well-read guy.
Travis: Yeah. He's being overly generous.
Christopher: Yeah. No. It's a really great book. So can you just repeat the name of the book, the Pulitzer Prize book, that I should read next?
Travis: Yeah. It's called The Emperor of All Maladies.
Christopher: Right. Okay. Well, I'll definitely link to that.
Travis: Yeah. It'll walk you through the history of cancer. It leaves you with a depressing conclusion because it's gene-centric. It's based on the somatic mutation theory of cancer. So you walk away with kind of this "Oh, boy. We're kind of in this therapeutic checkmate and we don't know where to go from here."
Christopher: Right. The next place we should go is just to describe sort of succinctly the difference between this genetic theory and the metabolic theory that's described in your book.
Travis: Absolutely. Yeah. So the dominant theory of cancer right now is called the somatic mutation theory of cancer. That has been the dominant theory for the better part of the 20th Century. What it states simply is that cancer rises from sort of the sequential lesions to DNAs, mutations to DNA that can happen from radiation, just general cell repair, general cell division, carcinogens of course.
So you get this sequential series of rewiring to the cell circuitry that results in uncontrolled proliferation and all the hallmark features of cancer, metastasis, growing new vessels and so forth. That's still the dominant theory. It's still in textbooks as the leading theory of cancer. The cancer biologists who get the most money in the world still are flying that flag.
So the metabolic theory contrasts from that pretty profoundly. What it contends is that cancer is precipitated by damage to mitochondria. So cancer is a metabolic disease. What it is is it's a loss of the ability to respirate or to generate enough energy aerobically. So the cancer cell has to then switch to this sort of ancient method of energy generation which is anaerobic energy generation with the generation of lactic acid.
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When the cell does this it then sends out a signal, the mitochondria sends a signal to the nucleus saying, "Okay. We need to upregulate this type of energy creation." And then you see this epigenetic response which is upregulates all the important oncogenes.
Now, the most important part of this theory is that it transitions cancer away from this disease of accidents, this disease of entropy, this disease of disorder, and makes it look like a disease of order, a systemic disease that is being driven from somewhere. It's an epigenetic disease.
So this metabolic theory takes us to that point. It says okay, the trigger is damage to mitochondria. Incidentally everything that causes cancer damages mitochondria, viruses, radiation, carcinogens. It can also cause mutations to DNA but it also causes profound damage to mitochondria. When you look at the mitochondria cancer cells they're very defunct. They have all kinds of protein abnormalities. There are less of them. So it takes us to this point where okay, cancer is a preprogrammed response to this.
Now there's a new model of cancer called the activist theory. I'd love to tell you about that if that's the next question.
Christopher: Yes. Of course. Okay. We'll save that one. We'll finish this one. That's the next one then.
Travis: Okay. We're to that point. Cancer looks like an orderly disease. Now, the atavistic model is championed by guy named Paul Davies who is also an Englishman. You should be very proud. It seems like a lot of great minds come from your country. Isaac Newton.
So Paul Davies is this world-famous cosmologist. He grew up in London, post-World War II. He worked with Stephen Hawking. He's done really profound work in theoretical physics himself. Then he kind of became a Carl Sagan type figure where he sort of became his bridge between theoretical physics and the rest of us. He's very good at explaining it. He's written 30 books. He's spoken at Google. He's talking to the Dalai Lama at the EU. So he's a very prominent figure. He's very good at solving very complex and hard problems, big questions.
In 2006 Anna Barker became the deputy director of the NCI. She really wanted to disrupt the way things were there. One of the programs she initiated was called Physical Sciences-Oncology Centers. The idea was cancer is this complex monster. Cancer appears as a novel. It just doesn't fall within the normal rules of disease.
She was thinking who's better at solving these sort of complex issues than physicists. She was a big fan of Paul Davies. So she called him up and said, "Hey, I'd like you to help us with cancer." His quote was "What? I know nothing of cancer." She's like "Perfect. I want you to look at this from the ground up with fresh eyes." So he did that. It kind of tapered back in what he was doing and started diving into cancer. This was about 2008.
He's come up with this theory of cancer called the atavistic model. The profound difference is it's not a disease of disorder. He thinks genetic mutations are a trigger. They are not the cause of cancer. What he thinks it is is this unfolding of a preprogrammed epigenetic program that's been embedded in our DNA since the dawn of time. He took the 300-foot view of cancer. He sort of cherry picked the data which are so much. There are 3 million articles in PubMed when you type in the word cancer. So he just kind connected the dots with this basic research.
When you look at DNA, it's a snapshot of our evolutionary sweep through time starting with life when it began 4 billion years ago. And then about 1.5 billion years ago life began this track to multicellularity. Before that the biological imperative was just to divide. Single cell organisms, their only imperative is to divide and replicate and replicate. So that entrenched program is retained in our DNA.
Now, when cells began multicellular living there was a new set of rules. They had to differentiate and stop dividing and live within the collective. So when you look at cancer what it's doing is so unique. It reexpresses all these fetal genes. When you look at an embryo go through the process, it recapitulates this sweep of evolutionary time. The fetal genes are the first genes to evolve. Cancer is reexpressing these very, very early genes when the biological imperative was just to replicate
It gives us very clear picture of what cancer is. It's the first explanation of it as a biological phenomenon. It gives hope because now when you look at it as an epigenetic disease that's unfolding, this preprogrammed set of genes, it gives a whole new way to approach it therapeutically.
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Christopher: That makes sense. The epigenetic is interesting because it can be influenced. So what can we do?
Travis: Well, there's a lot. So from the metabolic theory what you're trying to do is sort of restore mitochondrial function or to have mitochondrial biogenesis which is just mitochondrial division. You can do that in a number of ways. The ketogenic diet is a great way to do that. It enhances mitochondrial biogenesis. It increases the efficiency of mitochondria. Another way is periodic fasting. There are all these drugs that influence metabolic pathways. The beautiful thing is they all seem to synergize and overlap. Dichloroacetate or DCA is another one. Metformin is an amazing drug. It's a type II diabetes drug that kind of been repurposed as a potential oncology drug. In a lot of these labs we're seeing tremendous overlap of these different therapies that kind of go from this metabolic angle.
Now, from Dr. Davies' angle, when you look at it, the idea is to exploit the expression of these early genes and your healthy cells' expression of newer genes. One way to do that, for example, is -- the expression that cancer cell is doing is way back, a billion years ago. So back then it was the Proterozoic ocean. The atmosphere had far less oxygen. So the cancer cell has adapted to less oxygen, that's why the Warburg effect, that's why all the lactic acid and. So you can exploit that difference through the ketogenic diet and hyperbaric oxygen.
Another way is when it goes back to these suite of genes, it's bypassing the adaptive immune system which evolved about 400 million years ago. So the cancer cells essentially decoupled from your adaptive immune response. When you go back in the literature you see cancer patients that had bad infections. They had high fevers and then all of a sudden they get to spontaneous remission. There is no good explanation for that. That vanished from the literature when past year came around and we really started having sterile surgical technique and so forth. The idea is that cancer can't withstand the sort of infection that healthy cells can because they've decoupled from the immune system.
Now, you could potentially exploit that. You could vaccinate a cancer patient from, say, Listeria or another type of disease, and then deliberately infect them hoping to exploit that difference. The idea sounds crazy but when you look at it through the theory it's not crazy. I suspect that some of these new viral therapies, partially that's probably how they're working.
Christopher: That's incredible. So the ketogenic diet exactly the mechanism by which it works against cancer.
Travis: The ketogenic diet is fascinating. Biochemically as you transition to ketone bodies obviously you're lowering blood glucose, systemic blood glucose, and that is the preferred field of a cancer cell. When you look at a PET scan that's what you're seeing, this voracious appetite that cancer has for glucose. So you're transitioning away from that fuel and you're upregulating ketone bodies as a circulating form of fuel.
Now, there is some debate whether cancer cells can fully utilize ketones or not. I think the overwhelming degree of basic research is on the side that they have very dysfunctional use of ketone bodies. All the enzymes for ketolysis are downregulated. There's less mitochondria, like we said earlier. So they have a hard time using -- and you can prove this just right in the lab in cell cultures even if you give them the same amount of glucose within the Petri dish, just add ketones and they start to slow their growth.
So it's not just an energy replacement. The ketone bodies are also doing other things, some kind of signaling mechanism. This transition puts tremendous pressure on cancer cells and at the same time is sort of gives healthy cells this robust ability to withstand chemotherapy. That's been proven. You can take cancer patients and fast them 48 to 72 hours, kind of jumpstart them into ketosis before chemotherapy and have much less side effects, measurable side effects like hair loss, mouth soreness, vomiting, things like that, they feel better. All the evidence suggests that it enhances the efficacy of chemotherapy including radiation. So it kind of got this dual purpose. It should be the base of every therapy because it kind of preps the landscape to accept most kinds of therapy.
Christopher: Yeah. I know. That's incredible. So I guess the burning question is can all cancers be treated with this type of therapy? I should give credit here to Dr. Tommy Wood. He pointed me at some studies of women with breast cancer where they've seen some upregulation of ketone metabolism. I'm wondering. Is this just for certain types of cancer?
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Travis: Good question. We won't have the answers to that for quite some time. It's safe to say that we know everybody has a distinct metabolic entity. So the efficacy of it from individual to individual will likely vary quite significantly.
There are clinical trials right now for glioblastoma. It kind of lends itself extremely well to glioblastoma because the brain has a unique metabolism because it's exclusively glucose but then when you shift to a ketogenic diet it shifts primarily to ketone bodies, like 80% ketone bodies.
Christopher: Is it really as much as that? That's more than I've ever heard before.
Travis: Yeah. It's very, very high. It could be 60%. I could be wrong on that. There are very small neurons that don't even have mitochondria. So physically they're not [0:16:09] [Indiscernible]. So they have to rely on glucose. So you'll always have some glucose metabolism to some degree. Yeah. It's kind of this one or other metabolism. Most trials begin with glioblastoma, and that's the trial that's going on right now in Arizona with Dr. Adrienne Scheck. We should have results with that trial by April, she told me.
So it lends itself well to glioblastoma. Anecdotally there are so many people trying this, I've heard tremendous stories. There's a kid in Norway right now that is doing it for -- I think it's plasmablastic lymphoma which is a very rare cancer. Its prognosis is about eight months. I think his first diagnosis was about three years ago. So he went through two rounds of chemo, two different types, and had very little effect on his tumor. So he switched to the metabolic therapy. He switched to a restricted ketogenic diet, some very long term fasting in there with DCA, with metformin, and the tumor has shrunk and remains stable now for three years. His oncologist is like "Keep doing what you're doing."
These metabolic therapies are very, very good at managing cancer. They probably won't be a cure. They probably won't, in most cases, get rid of it especially the tough cases but they've slow to or they just keep it static. They buy time to where you can do other things. We're going to need a very good cancer sidle drug, something that goes in and sort of mops up the cells at that point.
Christopher: Right. So one of the criticisms I've seen of the studies that have been done was that they're all from the same line of glioblastoma cells. So maybe the treatment was specific to those particular types of cell.
Travis: Yeah. That's where it got started. The beautiful thing about this is it operates the framework of the theory. So the theory is you're exploiting this metabolic intransigence of the cancer cell. That extends to 95% of cancers. The majority of work has been in glioblastoma but the framework of the theory suggests it should have an effect on every type. With these anecdotal cases you hear about, that seems to be what's going on but we can't have definitive answers until we get very good trials.
Christopher: So do you think that would be the first cancer that we might see a cure for, the glionlastoma?
Travis: That is such a tough one. Glioblastoma, it's got a set course. Usually it's about a year, give or take a month, from time of diagnosis to the time of death. It's a very, very brutal cancer, one of the hardest to even get. Standard of care is just palliative care which is buying a month or two at the most. So it would be difficult to say that's the first one that will be cured by this but it's potentially one of the ones will have the best benefit if that makes sense.
Christopher: It does. Yes. I think it's really interesting. Can you talk about how some of these cancers show up in a PET scan?
Travis: Yeah. PET scan is radiolabeled glucose. What you do is you inject the patient with this fluorinated glucose that then systemically gets distributed throughout the body. You lay there for about an hour. You can't move or you'll get kind of a noise if the muscles take too much of the glucose. So you just sit there and let the tumor do its thing. The tumor is upregulated to just compete with healthy cells for that circulating glucose. So it sucks it in and hoards it within the cell. So that's how you get the image. The image is sort of this subatomic cascade of imaging that you're able to pitch up.
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Christopher: Okay. This is so simple, even I can understand it. You put this patient in a scanner and these tumors light up because of the way that it's uptaking these glucose. So then at that point is it not obvious that maybe a therapy that restricts glucose in some way would be helpful as a therapy? It just seems too good to be true. I'm just wondering why it's taking so long for anybody to think of this as a therapy.
Travis: Yeah. That's where the mind inevitably goes when you start talking about this. I think there's probably a tipping point. The trial that Adrienne is doing in Arizona is just using a standard ketogenic diet. For some people, that doesn't drive down blood glucose very far. You get upregulation of ketone bodies but not to a huge degree. So the question is if the cancer cells are fixed with this metabolism what would it take to get them to where you're killing them, they're choked off.
We know you can drive this further. You can drive blood glucose way, way down. When you look at the '50s and '60s when fasting was kind of the in vogue treatment for obesity, there were people that did -- I think the world record for longest fast is a year and 17 days with no food. It was a 450-pound man. So his blood glucose kind of planed off I think in the '60s but you can go even further than that. Now we have exogenous ketone supplementation and drugs that inhibit gluconeogenesis. So with those tools theoretically we can drive down blood glucose very, very far at the same time upregulate ketones to pseudonatural levels.
There probably is some tipping point where we get a patient to where the cancer begins to die because you've changed the physiological landscape so much. It's going to be tough to get that passed in IRB, that sort of trial. I've seen protocols. People have written protocols to do it. Protocols I've seen where you give them drugs so the body can't make glucose through gluconeogenesis. And then you drive it down so far that you could then actually inject glucose into like a jugular vein to supply the -- or the carotid artery, supply the brain with glucose if you go too far.
So yeah, you're along the right track, and there are people thinking along those lines but I think this moves so slow and it's just going to take a long time for IRBs to get comfortable with this idea and doctors to be willing to even do that sort of trial.
Christopher: That's so interesting. Gluconeogenesis seems to be the most hated pathway by all people trying to get into ketosis. So what were these drugs originally developed for?
Travis: Well, one of the good ones is metformin. Metformin is an incredible drug. It's a type II diabetes drug that now we're finding has all these interesting properties including [0:23:05] [Indiscernible] it's either 25% or 30% reduction in a diagnosis of cancer if you're on metformin. It reduces the probability you're going to get cancer. Dominic D'agostino's experimenting with it. There's a lot of experimentation with it as a cancer drug. No one really knows how it works but it's operating through probably a variety of mechanisms. So that's one.
There are others. I think phenylbutyrate is a good gluconeogenesis inhibitor. There are others but they don't come to mind right now but there's a host of drugs that will do that.
Christopher: Right. I didn't understand that metformin was a gluconeogenesis inhibitor. I didn't understand that that's how it worked.
Travis: Yeah. That's one of the mechanisms. It's also inhibiting complex 1 electron transport chain.
Christopher: That doesn't sound good.
Travis: Exactly. This where biology gets so complex because ROS we've been always told as bad. Reactive oxygen species or free radicals are bad but it's a signaling phenomenon. In other cases it's good. Metformin, it also trims down the gut biome. There's a sect of biologists who believe it's acting in that way. All these things intersect. Eventually it will sort out how it's working, but it's going to take a long time.
Christopher: Yeah. I know. Tommy and I have talked about this previously on podcast, the reactive oxygen species. I lived in fear of oxidative stress for a number of years before Tommy started sending me all these papers that show that exercise is in fact an antioxidant, and that when you do more exercise, sure, you generate more energy and maybe some more reactive oxygen species but there's also signaling mechanisms that upregulate our production of antioxidants. So the whole thing cancels out or maybe more than that cancels it out. It's so complicated.
Travis: Yeah. It is. I was listening to you and Tommy on Robb Wolf's podcast as you guys were sorting through the murky waters of insulin resistance and iron overload and overall with the gut biome.
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All these things overlap and intersect. Yeah. You get these exponential layers of complexity that you're trying to work through.
Christopher: It just makes it even sillier when you go in to your specialist. So I go and see the doctor and I complain I'm tired and maybe I've got some G.I. complaints. Where am I going to go? It doesn't make any sense that kind of way, dividing complexity anymore.
Travis: Yeah. Tommy said something very interesting to me. There's this basic science we have in biology where you focus on one thing. It could be like one protein, one pathway. I think of Dr. Ko who I wrote about in my book. She's a brilliant biophysicist. She looked at ATPase, this enzyme that generates ATP from the electron transport chain, for I think over a decade. That was just to sort out the functionality of this one amazing protein. We need these people to do that basic work but then we need these people to step back like Paul Davies, and connect all these dots.
Biology is lacking because we don't have that sort of differentiation. Physics has that. Physics has experimental physicists and theoretical physicists. The theoretical physicists will just look back and cherry pick the experimental data and drive new theory. Einstein came up with this theory just by thinking about it. His theory guided the next experiments that would sort of prove it. So they overlap and contrast. Cancer biology, especially, has a very, very lacking of this sort of give-take relationship with theory and experimentation.
Christopher: You're reminding me actually. I had a conversation recently with a former colleague. I used to work at quantitative hedge funds. He was one of the mathematicians, one of the quants that worked at that fund. He kind of noted that in physics there are tons and tons of data so you can just come up with an idea and test it with a supercomputer and find out whether your answer is correct in a relatively short period of time. In biology, especially in nutrition, you really can't do that. There's not much data at all with respect to physics.
Travis: Yeah. The data contradicts each other. I heard a stat from the NCI that said up to 80% of the basic research in cancer biology is not reproducible which means the science is probably wrong. When you sort through these studies you have to get good at ferreting out the good from the bad. It's an art form. It's like Warren Buffett picking stocks. He does this in a room in Omaha where he sits and just reads through accounting statements and somehow magically picks the companies that are going to thrive. It's kind of the same thing with science. You have to get really good at discerning the good studies from the bad and sort out that mess. Even the good studies, there's contradiction because biological systems are just so inherently complex and don't lend themselves well to really clean experiments.
Christopher: Right. I know I'm getting a little bit off track now but I can't resist to ask you this question. So maybe I'll just take a bunch of runs and control trials. The only criteria I use to pick them are the number of subjects and some other kind of fairly arbitrary things that I can select as maybe search criteria or in a database, and then I put those all together, I sum them all together and then try and come up with a conclusion based on the sum of all of them. Based on what you just said, doesn't that sound like a terrible idea?
Travis: Yeah.
Christopher: Isn't it the golden standard of science? People would refer to that as the golden standard.
Travis: Yeah. Right. Those are notoriously just fraught with landmines. I don't know if you've read Good Calories, Bad Calories.
Christopher: That's one of the few books I should have read by now.
Travis: Yeah. Gary Taubes. He walks you through exactly that, how we've gotten that wrong with dietary pyramid throughout the century. These large scale studies are just inherently flawed from the very beginning. Yeah. It's a good way, I think, to get clues. You can kind of look at broad trends but there's so much more complexity. You have to control so many variables. Yeah. You're right. That is notoriously bad way to draw conclusions.
Christopher: So tell me what you know about the ketone supplements that just seem to be suddenly coming onto the market. I was taking them a couple of years ago. They were just catastrophically awful but I was willing to go through that. It's funny. That's how I came to the ketogenic diet was for reasons of performance. I'm a mountain biker. It gets me great results on the bike, both on and off the bike. I can still think clearly once I finished my race which is kind of nice.
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It seems like an obvious supplement for me to take you especially right before a bike race, the ketone supplements. Now it looks like the applications for those supplements could be much broader. Tell me what you know about how they're being used for the therapy of cancer.
Travis: Well, they're not being used that I know of right now. I'm sure there are individuals using them know on their own but not as a standard of care type thing. I think they will have their place. As we move forward with these metabolic therapies that's going to be part of the puzzle, one of the pieces of the puzzle for sure. There are a lot of questions with them. Dominic D'agostino who I collaborate with on a lot of stuff, that's his line of research, is exogenous supplementation.
There are clearly many, many questions but one of the biggest things that have come out of ketone research is the signaling properties of ketones. We've always thought of them as just an energy substrate. You can even think of them as another macromolecular food group. There's fats, carbohydrates, ketone bodies and so forth, protein. So we kind of always look to them as this one-dimensional way as just an energy substrate but it goes much, much deeper than that. They have very, very, very deep signaling properties and turn on variety pathways, a lot of anti-inflammatory pathways. All of those are going to be sorted out.
In my mind what I think we were designed to go through periodic times of starvation. I think that's a time of renewal. When you're in ketosis, when you can't get enough food or it's wintertime and you can only kill one mammoth, it's this time when all this mitochondrial renewal, all these pathways gets turned on. We've stepped so far outside of that now with our Western culture that we're constantly inundated with food, with carbohydrates. Like Dr. Veitch at the NIH said, it's not normal to have a McDonald's and a delicatessen on every corner. It's normal to starve periodically.
So this inundation with abundance has left us in a bad state. If you extrapolate the curve for type II diabetes, it's 1 in 10. I think it goes to 1 in 4 if you just keep going on the path we're going, and Alzheimer's and all these things that appear to be caused by dysfunctional metabolism. Alzheimer's looks like it's a form of what's called type III diabetes, a form of sugar, metabolic dysfunction.
In my mind, my construct of human metabolism, I think that we're designed to have ketones flow through our bodies at certain times. What are the questions about doing it while you're eating Western diet and supplementing with ketones? I don't know. I don't know if you're going to get a bang for your buck that way. There are a lot of details to be sorted out but they're going to have their place for sure.
Christopher: Do you think it's a bad idea to constantly be in ketosis? We know that it's sending a signal maybe to your genes, perhaps a period of not very much food and starvation. Do you think it's a good idea to be constantly in ketosis if you're a healthy person?
Travis: That's the next $10 million question. You hit on it right there. I haven't found a good answer to that myself, and I've tried. Peter Attia who is this nutritional guru who's mostly in ketogenic diet, I've looked for him to say but he won't commit to that answer. Dominic, same thing. It's certainly not natural, I think, to be in nutritional ketosis for a very, very long time. That doesn't mean it's not the optimal physiological state. It very well may be but we just don't know. That's the question right now that remains to be answered. You're going to have to do long term trials, and those are just difficult.
There are two studies, one at the National Institute of Aging and one at the University of Wisconsin on caloric restriction in monkeys, and they kind of run parallel. They started in the '80s. We've started to get data from those. Kind of the consensus from those is caloric restriction helps but not as much as we thought. What happened was one study used a very high sugar diet. The other study used a very low sugar diet. So the study with a high sugar diet, even the restricted monkeys were much, much worse off. So kind of the conclusion that comes out of that is caloric restriction helps but dietary composition might even be more important particularly with sugar. So we do know that at least within primates.
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Christopher: Blimey! I just wondered where to take this interview next. How is this going to become the standard of care? How is anyone even going to take this stuff seriously?
Travis: That's a great question. The more I watch the way cancer studies sort of unfold it is such a slow moving kind of haphazard process. It's easy to get depressed. One of the biggest pieces to come is going to be this trial in Arizona. It's a ketogenic diet with standard of care radiation for glioblastoma. If the results come good out of that trial, the point of this being an efficacious treatment, I think that's when you're going to get this first kind of awakening of dietary use for cancer.
It's a notoriously hard thing to convince people of because diets have always been associated with fats. If you bring up the idea of a diet in cancer, doctors typically kind of gloss over and say, "Oh, God. Here we go again." That's going to be the first step.
Then these antidotal stories of people that just keep popping up using all these therapies, they're going to be the next piece. 3-bromopyruvate, which is this drug that operates through metabolism, I think, is going to be the final piece because it appears to be a fantastic cancer sidle drug. It's fantastic at killing cancer cells. So that should be the final piece. That's the final piece in the puzzle for this metabolic type of therapy.
An interesting story about how slow this all moves, there was a doctor, I think his name was Halsted, at the beginning of the of the 20th Century who came up with this -- he was a surgeon. It's kind of an interesting and funny story. He got trained in Europe where all the doctors get trained in America. They went to Europe, particularly in Germany. He developed this cocaine habit over there. So he came back to America. The treatment for cocaine addiction was heroin. So this guy throughout his entire career he'd scrub out in the middle surgery and get his heroine fix just so he could keep his hand steady. That's neither here nor there, beside the point.
He was kind of the pioneering surgeon in America. He came up with this surgery called the radical mastectomy. The idea was you had to get every single cancer cell out if you could. So if a woman came in with breast cancer, if it was a small lump they'd take everything they could from the farthest proximity. You take lymph nodes, parts of collarbone, parts of ribs, kind of this horribly disfiguring surgery. It was never questioned. If you got diagnosed with cancer and you walked in it's like "Do you want the radical mastectomy?" The woman would say, "Yeah. It gives me my best chance." The doctor would say, "Yes, it does."
This went on for I think about 80 years until in the mid '80s when cancer patient advocacy groups started questioning if it was even necessary. They finally did these huge large scale studies and they found out that a local lumpectomy was just as efficacious as this radical mastectomy. Women went through almost close to a century of this horrible surgery where it was unnecessary. So that kind of illustrates how haphazard and kind of clunky this therapy goes because you don't get good answers until you do large scale trials, and those are so hard and so expensive that it's this very slow moving process. I'm sure we're going to see that with regard to all these metabolic therapies.
Christopher: I mean theory it should go faster, shouldn't it? Whenever I think about this problem it's well, you got to eat something. Why not this? It's a very, I think, low risk intervention. What you're talking about there is surgery, like a change in the way they do surgery. That seems like a much bigger thing and maybe that would take more time to change. I interviewed Dominic at least a year ago, maybe even two years ago. It doesn't seem like too much has changed since then.
Travis: Yeah. I think it is catching on to some degree. I spoke at Paleo f(x) and talked to quite a few people that their doctors had prescribed or suggested the ketogenic diet. One was at the Mayo Clinic. Where I live here in Rapid City, South Dakota, we have a very standard of care conservative oncology center. I just heard that one of the oncologists suggested the ketogenic diet. So I think the next generation is obviously going to be more attuned to this than the old guard. It's definitely catching on.
[0:40:13]
Another place that this has a great potential is this idea of recurrence because once you've been treated -- say, you have surgery and chemotherapy or whatever targeted drugs you can get, and you're sent home. You have this kind of purgatory where you're waiting to see if it grows back. You know your five-year survival rate. Maybe you have a coin flip of it reoccurring within those five years. So what do you do in that meantime? Most people don't know what to do. They're right there trying to eat right but they don't know what that means. They go through all this introspection.
This is when I think this kind of dietary protocol can shine because it really does rejuvenate -- from the metabolic theory you have this chance, this window of opportunity to kind of change the landscape of your body, to reduce inflammation, to restore mitochondria, to do all these things to prevent a recurrence.
I wrote an article about this in my website. Recurrence is not what we always thought it was. We always thought it was like this one smoldering cell that got left behind. Usually that's not the case. I shouldn't say that. In the percentage of the cases that's not the case. It's something like 20% if I remember right. It's in the article. Twenty percent or so of the cases of recurrence are in new cancer. So what that means is you haven't changed whatever conditions your body had that allowed that first cancer to develop. You have this opportunity to change those conditions, this epigenetic landscape once you've been sent home. That's another kind of less, I guess, publicized use that I think should be more explored.
Christopher: Yeah. I know. That makes sense. So it's not really about what was there. It's more about the environment. So you see that with bacteria as well. It's not like it contaminated with this bacteria. It's that you're creating the environment in your gut where it really likes to grow.
Travis: Exactly. Right.
Christopher: So my personal experience with this has been within my family. Nobody wants to take the ketogenic or high fat diet seriously for weight loss until it's cancer, and then no, no, it's not an option because these ketogenic diets, they cause weight loss and cachexia, so they could be really dangerous for someone with cancer.
Travis: Right. I'm sure there are doctors who do say that. The biggest fear nutritionally for an oncologist is cachexia because it's this kind of wasting away that you can do nothing about nutritionally. That's probably coming from signaling from the tumor itself. It doesn't have a lot to do with nutrition. I think it's a separate entity. That is a problem.
I've just gone through this with my mom who was diagnosed with endometrial cancer about six months ago.
Christopher: Oh, no. I'm sorry.
Travis: The first thing we did of course was put her on this diet. She's got a very standard of care oncologist who didn't want to hear anything of it. I think she even steered her away just because of the weight loss issue. Same thing with the trial I spoke about where they'd fast the patients before chemotherapy. The doctor who did that, his name is Valter Longo. He's at the University of Southern California. He had a brutal time convincing oncologist to do this protocol. They're like "No. I'm not going to do that. It's crazy to do it to my patients." Finally they convinced enough of them to do it. It helped them. It helped them get through the chemotherapy. It helped them I think with efficacy of the chemotherapy. Yeah. There's a contradiction in thinking with what the diet does and what the traditional oncologist view of what cancer is.
Christopher: That's been certainly my own experience is that being in ketosis, the state of ketosis, it doesn't really say anything about weight loss or energy balance at all. It was like a completely separate problem.
Travis: Right. Yeah. Exactly.
Christopher: Well, this has been fantastic. Thank you so much. Where can people go to find out, obviously, the book, Tripping Over the Truth, which I will link to in the show notes? So tell us about your articles on the Robb Wolf website because those are fantastic.
Travis: Dominic D'agostino and I wrote a series about the history of the ketogenic diet. It was actually supposed to be the sample chapter for a book that we're collaborating on for publisher but our agents kind of steered us in a different direction, towards a more prescriptive book. This one was kind of a historical narrative.
[0:45:05]
I didn't want it to go to waste. We didn't want it to go to waste. So Robb Wolf was kind enough to put it on his website. It kind of walks people through the history of the ketogenic diet, how it got started which I think is fascinating. It goes way back to the '20s. It was a standard of care for epilepsy and then it got just lost once anti-seizure drugs came out in the mid '30s and just relegated to this kind of side note in textbooks.
And then it had this course resurgence in the mid '90s because of Jim Abrahams. He's the founder of the Charlie Foundation. Of course he did this media campaign to kind of bring it out from out from the shadows. So it kind of highlights that story of the ketogenic diet and where it's going in the future and what we've learned so far.
That's on Robb Wolf's website. It's called The Origin and Future of the Ketogenic Diet. Dominic and I are trying to set up a blog so we can kind of just shuttle out some of this content that we kind of gathered up together. I think it's going to be called metabolic optimization. It's actually a web address. We should have that up and running hopefully within a couple of weeks.
Christopher: Excellent. Does Dominic really write? I just can't believe it. It really annoys me when people are so good at so many different things. So here's this guy, Dominic D'agostino, this amazing scientist who interviews and presents beautifully. He can deadlift 175,000 pounds in six hours or whatever it is. And he writes like that too.
Travis: Yeah. He actually sets the Guinness Book of World Record squat record. It was something like I think 175,000 pounds within six hours.
Christopher: Yeah. That's what you wrote in the book. I just remember reading it this morning.
Travis: Yeah. He's definitely multidimensional, a very, very skilled, great scientist, wonderful guy, just so nice. We've been collaborating on this book together. It's a joy to work with him.
Christopher: Is that your full time job is now, as an author?
Travis: Yes. That's what I'm doing 100% of the time right now.
Christopher: That's fantastic. I will of course link all these resources. Yeah. Let me know if there's anything I can do for you. I'm not a scientist but I am a computer scientist. If you need like programming stuff done, if you got an interesting stuff in the lab or you hear of anything that needs doing in Python or WordPress blog or something you should let me know. I'd love to get involved with that kind of thing.
Travis: Yeah. That stuff always overlaps so I'll let you know.
Christopher: I know. Yeah. I say to people I really want to replicate your education but then I remember that I actually enjoy doing computer science at university. I wouldn't have that now if I've taken some other routes. That's difficult.
Travis: Yeah. The most interesting you find kind of have this diverse background. Yeah.
Christopher: Excellent. Thank you so much for your time. I really appreciate this, Travis.
Travis: Yeah. Thank you so much, Chris. Take care.
Christopher: Cheers then. Bye-bye.
Travis: All right. Bye-bye.
[0:48:04] End of Audio
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