Welcome to Pushing the Limits, the show that helps you reach your full potential with your host Lisa Tamati, brought to you by lisatamati.com.
Lisa Tamati: Everyone, welcome back this week to Pushing the Limits. Another fabulous episode in store for you today. Today I have the science writer Travis Chrristofferson to guest. Now, he is the author of Tripping over the Truth—the history of cancer, basically, and looking at the metabolic approach to cancer. We've done a few episodes along this theme, and hope it's helping people.
I'm getting a lot of feedback from people who are dealing with cancer or loved ones with cancer, and they're loving this content, so I hope you enjoy this episode. He is also the author of a book called Curable, which is looking at the state of the health system and where it's broken, and what we need to do to fix it, and some of the issues that are involved.
He's also authored a number of other books with one book with Dr Dom D'Agostino, who was also previously on this podcast about the past and future of keto, ketones, and what they are. He's also the author of a book called The Fourth Fuel, which is a deep dive into ketones as well. Fascinating gentleman—incredible work that he does. I hope you enjoy the show. Before we head over to the show with Travis, just please check out services that we offer.
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Hi everyone. I am super excited this morning. Absolutely stoked for this interview. I have Travis Christofferson with me, who is an amazing man with an incredible history of writing absolutely astounding books. Books like Curable, like Tripping over the Truth. He authored one with a—co -authored with Dr. Dom D'Agostino, who I’m also a fan of. Travis, welcome to the show.
Firstly, you're an incredible writer. The research and stuff that you've done is just absolutely mind-blowing, so we're going to dig into that today. So welcome to the show, Travis.
Travis Christofferson: Thanks for having me, Lisa. Appreciate it. Thank you for the kind words.
Lisa: Oh, I really, really mean them. It's your work and the works, say, of Dr Dom who's also been on here. I had Dr Charles Meakin and Maggie and Bradley Jones from the CanceRevolution. All of these amazing people have really contributed, I feel, to my personal life story with my mom. As my listeners know, we've been dealing with lymphoma, and touch wood, right now, we're looking very good. There's no cancer to be found anywhere.
I'm just desperate to get this information out there. Because what I'm realising so much now that I've been in this sort of space for the last eight, nine months, is that most people still have no idea of the somatic mutation theory—is not what they think it is. They don't know anything about the metabolic approach to cancer. They don't know about any off-label drug combinations. Just so many things they don't know, so that's what we want to dig into today.
Travis, can you give us a little bit of a background on yourself before we dig into your amazing research?
Travis: Yeah, yeah. My background is very nonlinear. I started off my undergraduate degree was in biochemistry. Then life sort of interceded, and I actually jumped into the family business; got married; had two children. But I always wanted to go back. So I went back to finish my master's degree, which I had started, but I only had three credits to finish. They were kind enough to let me do an independent studies class.
So I did it on cancer metabolism, they let me choose the topic. I just happened to be leafing through my Kindle and I ran into this book called Cancer as a Metabolic Disease by Tom Seyfried. Yeah, you're nodding your head. I'm sure you're aware of it. Yeah, it's a foundation for a lot of what you're talking about, and it just blew me away. I learned cancer from a standard textbook that it was extremely dogmatic theory—that the cancer was caused by somatic mutations.
That's somatic mutation theory—that there's a series of sequential mutations that sort of rewire the cellular circuitry towards uncontrolled growth. That was what cancer was. This book was this textbook sort of book that walked through over 100 years of evidence showing that—proposing a new theory, I guess is a way to say, that cancer was precipitated by metabolism rather than genetic mutations.
The amount of evidence to me was just astonishing—good evidence from credible labs, and so I did my thesis on that. That inspired me to look at it because it was such a beautiful story. I, like, I've always enjoyed writing. I just read The Emperor of All Maladies, which is literally a biography of cancer, which marches through all the history, but never looks at cancer from any other lens other than this dogmatic viewpoint of the somatic mutation theory.
The metabolic theory of cancer lended itself really well to a book because it's a story of a scientist named Otto Warburg, who in the 20s proposed this theory, and he was an absolutely brilliant biochemist. He'd won the Nobel Prize. He was nominated for three Nobels in three separate achievements. He was regarded as probably the premier biochemist of the 20th century.
But then he proposed this cancer theory, and by the time he died in 1970, it was really sort of ridiculed as a simplistic model of cancer. Then, the years go on and the somatic mutation theories locked down. We enter this era of targeted therapy, which was extraordinarily underwhelming.
The Cancer Genome Atlas project kicked off, which was to be the Manhattan Project to cancer, and really find those series of mutations that were causative for each type of cancer. It didn't come anywhere near that. It really just created this wake of confusion.
There was this rekindling of Warburg’s original theory, and it's still going on. It's still this disease that is so incredibly complex, that nobody can say with confidence that we absolutely know what it is. But what we do know is these new theories have a ton of data, a ton of credibility, and are sort of emerging now, and getting the attention they deserve, I guess.
Lisa: Yeah, and this is the thing, like, Warburg’s, this was 1924 or something that he did the original discovery, and it was the sort of direction we were going until the whole genetic side of things came into play, I think, in the 50s and 60s. Correct me if I'm wrong, and then from then on, it was like, ‘No, that's old hat. We're not going down that route anymore. This is far more sexy to be studying genetics and stuff.’
The basis of all this is that people thought that it was a genetic mutation that causes cancer or a number of genetic mutations, and that they'd be able to hone in on this and find the answer. Literally billions of dollars and decades have gone into this. Now, it's very hard to walk that back to justify that you've gone down this road.
Then, you come along with people like Richard Veech and Thomas Seyfried, who go, ‘Hang on a minute. What Otto Warburg was talking about is still very interesting,’ and start to go into that whole metabolic side of cancer, and the opposition is just huge. I mean, getting this information out because we were up against, I mean, you've written a book called Curable as well, about the state of the whole health system.
In New Zealand, it's no different than in America, really. It's a disaster, isn't it? Why do we not always follow the actual science? If it was just about the actual science, we’d be so much further ahead than what we are.
Travis: Right, right. Yeah. You get into this institutional inertia from these massive systems, right? Yeah, Curable was really smart by looking at this chart that showed the life expectancy of people, and I think it was 50 in developed countries versus their per capita healthcare expenditure. In the United States, we spend far more than anybody else per person on health care, but have the lowest life expectancy.
How could that be? Clearly we're doing something very wrong. The healthcare system is entirely inefficient if that's the case. It's just that was the 30,000 foot view in what are we doing wrong. When you really look deep, the two problems really are variation in treatment, overtreatment. The drug development process, I think, is one of the main problems, too.
When you look at drugs are developed for a very small indication for a disease once it's manifested, right? You don't want to get to that point. You should—when you consider your lifetime, you can think of it as a tree, so you sort of age at the trunk. Then, as you get older, chronic diseases start to branch off.
You want to get down to this trunk. What are the fundamental processes that are going on that lead to these diseases? We don't focus on that. We're terrible at focusing on prevention. We focus on the disease. Trying to treat it once it's already manifest, which is an absolutely horrible strategy. I think that's the third bucket, is we just don't try to prevent disease as well as we should.
Lisa: Yeah. I mean, that's what I'm all about, is try to get into that space before we get to that point. Even like convincing your local GPs to do a blood test every few months, so that you can see how you're doing.
It's like driving a car without a dashboard, in my opinion, when we can have these tests. These tests are cheap and available and would save us millions of dollars if we could just get them done early, so that we can prevent things from happening, or we get the early signs of things happening.
This is why I love doing this podcast because I want to help people to be in that preventative space. Because it's bloody awful, having experienced that in my own family for the last six, seven years. Because prior to cancer, we had an aneurysm journey with mum that she wasn't meant to survive either. Realising there was nothing there, and if I'd done a little bit of prevention, maybe it wouldn't have happened.
You can't prevent everything because we don't know everything. But there's a lot I could have done and to be in that space now to help other people stop. But going down that path is—or at least delaying. We have the technology now to really be living a long time. The ageing code has been cracked by people like David Sinclair and many, many others. We're starting to work this stuff out.
But at the same time, we're dying earlier now. We're living—disease—the last 20, 30 years of a person's life is often full of disability, disease, pain, and suffering. Yes, we're keeping them medically alive with all the great drugs and things that we have, but the quality of life is very poor, often, and nobody wants that.
So, Incurable, like, what do you think we can do to change the system? This is the $60 million question here. Yeah, how do you change and solutions?
Travis: You have to change, I think, you have to change incentive structures. In the US, we have a fee for—largely a fee for service system. So doctors get paid for every drug they prescribe every procedure. That's why there's this big incentive to overtreat and very little incentive to prevent. But there's ideas, like, one they're doing down south is where they give primary care clinics a big bolus of money per patient.
They say, ‘Okay, you can keep that money if your patients don't need procedures and things like that.” So now the doctors are completely incentivized to keep their patients healthy. That's the first thing, is you have to incentivize the doctors to be preventative in nature. Then, when you look at the science, like, one example is insulin resistance, which leads to diabetes. We know worldwide diabetes is an epidemic.
The way doctors and primary care clinics diagnose it is by a rise in blood sugar. But if you just tested like you were talking about earlier that we have these lab tests. If you just tested for fasting insulin regularly, you can see when people are becoming to become insulin resistant, decades before blood sugar starts to rise. This is where you have with this perfect window and intervene, but we don't do that.
It's very reversible. It's through lifestyle. People become motivated when they see laboratory numbers, and you talk to them what this means. That is a very one of those, again, back to that trunk of the tree, one of those fundamental core processes that accelerates ageing.
It just completely alters your energy metabolism, and your body becomes starved of energy, which it needs to repair DNA, to clean up different proteins, to do all these housekeeping processes, and slowly lead to all chronic disease, neurodegeneration, cardiovascular cancer. That's just one simple thing. One blood test where we could be extraordinarily proactive, but most doctors when you write, ‘I want an insulin test,’ and they'll ask, ‘Why do you want that?’
Yeah, so it's just we have to change the framework. They have to get different training and on what these are early on. Institutions have incredible inertia. To change them takes what we knew—smoking killed people, but it took decades before the smoking—they slowly went down, but they—eventually, they get there.
Lisa: Exactly. That's a really good analogy because we were told back in the 50s that it was healthy to smoke. I mean, my mom smoked throughout her pregnancy with me. I developed cancer where there was no—cancer, sorry, asthma—where there was none in the family history. She was told that it was healthy to do so by the medical profession.
This is the thing, it does take these long periods of time, and you think, ‘Well, that was way back then in the dark ages, they wouldn't do that now.’ But we're still bumbling along that sort of an approach. Coming back to the insulin resistance, if there was one thing that I can get people to do, is easy sort of things, like, well they’re not easy, but they’re simple: lifestyle interventions.
It's not sexy when I'm working with a client and I ask them if they can change the diet, if they can, start cutting back on the carbs, and maybe doing a keto diet, or going in that direction, cutting out the crappy fats in the diet. These simple things that people can do that bring massive, massive, but nobody wants to do the hard work, and it isn't, like, ‘I love food.’ It's a daily battle.
We all have that daily battle, but if you understand the—just how important this part of the puzzle is—not just the food thing, but just bits of a big piece of it. Like how our standard diet, you guys call it the standard American diet, it's pretty much the standard diet here in New Zealand, too, is just riddled with carbs and poor fats, processed foods, pesticides, herbicide. All the horrible things that go into our food chain, which is a completely another discussion.
But there is an opportunity to do something and then you add on, of course, the exercise, and these are two, but they're very—they're so too simple. They're people when they hear, ‘You've got to start exercising a little bit more and cutting back and changing what you're eating and doing some, perhaps, intermittent fasting or something.’ Then, ‘Where's the magic pill? I want the magic pill approach.’ Because that's where we've been conditioned to.
With the blood sugar and the insulin that is—you can look at a person mostly in their 40s who's got a muffin top going on, and you know that stuff’s happening in the—that they're down that pathway of metabolic dysregulation, that they're in the initial stages, and it isn't—it's not just because you age. This is what's ageing you. We've got it backwards, like it's not inevitable.
If you've got a—if you can still see your stomach, if you can still see your core—your muscles and your core, I always think that's a really good indication. You don't have to have the super six-pack. But if you can actually see that you've got musculature there, then you probably haven't gotten a metabolic dysregulation. That's a completely unscientific way of looking at it, but it's the way I look at it. It's simple.
Travis: It's valid. Yeah, and it's funny to me. You'd look at the animal kingdom, and lions will steer. They all look fit, right? They're living in this biological niche that they've lived in, that they evolved in over thousands of years. Humans, we lived in that—our niche for millions of years, but then all of a sudden, the last 10 to 12,000 years because of agricultural technology, we've all of a sudden been completely thrown out of it.
You would never walk around and eat wheat grain. The savanna, just the energy expenditure to do that before combines was, it would make no sense. So we've completely altered our diet in the last 10,000 years. Of course, we don't know better than evolution. We'd like to think that we know better, but that's a drastic dietary shift towards a massive amount of processed food and carbohydrates and oils that we never ate all these foods that we just never encountered.
It seems pretty obvious there would be consequences. When you look at the human race, we do look curiously sickly compared to other animals. We just do, and I don't think we're supposed to live this way and feel this way. The majority of people, and you're right, it's just a combination of probably a terrible diet and just not moving enough because we were designed to go out and have to work every day to catch food.
That's what we evolved, and when you uncouple your physiology from that environmental niche, you see all kinds of problems. It's very clear. You can study hunter gatherer societies, more traditional societies, you'll never see somebody overweight. You'll never see insulin resistance. In particular, you'll never see systemic chronic inflammation.
The majority of people in the Western world as they age, they'll get more and more chronic inflammation. It just—it should go back to baseline after an infection, but it just steps up and stays there. That's a very new phenomenon for our species. That's another—if there's two root causes of disease, it's insulin resistance and chronic inflammation.
Lisa: It’s just so, so true, and this is for everything from arthritis to heart disease to Alzheimer's. This is where when you understand cellular health a little bit, and you understand how you can improve cellular health, and get rid of inflammatory markers or work towards that, then you're getting towards that way higher up the line, like all of these diseases.
If I'm working with a client knows all how can you take a similar approach with someone with cancer with someone with Alzheimer's? Because at the top of the apex is a problem of cellular dysregulation, and if we can get those cells operating, how they should be in each of the organs, and we're gonna have a good basis.
You don't even need to know the specifics of that particular disease, like to the detail that a specialist would know. Because you understand how to get these inflammatory processes under control or what direction to go to in order to do that. These things become sort of panaceas. In the background. I've got a hyperbaric oxygen chamber. I don’t know if you notice that. That thing's sitting heavily.
Travis: Yep, I got one, too.
Lisa: You got one, too. Brilliant. It's a mild, mild one. There’s obviously better ones. I've had lots of podcasts on hyperbaric oxygen therapy, but that is one of those things that could attack all layers of inflammation—that inflammation in the body, inflammatory cytokines and chemokines, and all of that sort of stuff. On a—so becomes a sort of a panacea. Hyperbaric, like, there are so many things that people go, ‘It can't possibly help all of that.’
Well, it can, because it's providing oxygen to otherwise hypoxic tissue. It's creating more stem cell production. It's doing—attacking the inflammation. These are all baseline ageing processes that we're undergoing. But that's too simple, and the hyperbaric is one of those other things that is like, why isn't this in every person's household, at least or not in every doctor's office? Why?
Travis: Why isn't it studied more, right? It's so simple and cheap. Why aren’t there more clinical trials? But it's interesting to me, not just the food composition, but the amounts that we eat, and the fact we eat every day. That certainly didn't go on throughout our evolutionary history. There was times we had periodic food scarcity a lot where you just couldn't get calories. The wintertime, whenever. It's an evolution. It appears that evolution has built in a powerful signal to that.
When you're in a caloric deficiency, you switch your metabolism—I'm sure you've talked about this in your podcast—to something called ketosis where you completely shift what you're burning to these little small molecules that come from fat, and they're just absolutely fascinating.
It sounds like snake oil. When you look at the data, the clinical trials that have been done, everything from Alzheimer's to Parkinson's to cancer to diabetes, the data is remarkable. That's another way we've completely stepped out of that. Something that evolution baked into us that we just don't utilise. There's probably a lot of people in the Western world that never enter the state of ketosis in their life.
We still don't know, should you be continuously or periodically, those are questions that need to be worked out. But it's—what happens is absolutely markable. When you just go for about 16 hours without eating, your immune system completely shifts all those proinflammatory monocytes retreat back into your bone marrow. They infiltrate tissues and leave the tissues, go into the bone marrow, so you enter this state of low inflammation.
The, when you eat, when you think about eating, what it is, is it's really a wholesale invasion from the outside world. Your body has no idea what could be in there. There could be pathogenic bacteria. There's certainly bacteria. There's virus remnants. There's all kinds of things—different proteins that are not typically encountered.
Your immune system mobilises every time you eat. If you're eating constantly, you're in this constant state of mobilising the immune system, and it never really gets to rest. So that has implications for autoimmunity, for really every chronic inflammatory disease we just talked about.
Lisa: That's just the absolute goal. Of course, you've written the book, The Fourth Fuel, ketones. What is your take on, like, the keto diet? There's so many different types of keto diets for starters. There's the modified Atkins versus the hardcore stuff and the four to one ratio and all of these sort of things. For the average person getting into something like this, where would you start if you're wanting to do a keto diet?
I mean, obviously, if you've got someone like mum with cancer, she’s on a super strict keto diet. I'm pretty well and healthy. I do have carbs in the mix. If I'm doing a lot of aerobic activity in sport and things—a little bit more, and cycling in and out of things. But where can we start with this whole ketosis, and can you explain a little bit?
I'm still learning. There's so much going on on ketosis and ketones. Where am I going with this question? Yep. Like, what—when we go into this fasted state, and we start producing our own bodies’ ketones, what actually happens in the body? You've explained that the monocytes retreat back into the bone marrow, what else is going on? Because for the brain, for the heart, this is the perfect food as well. So for someone with Alzheimer's listening to this or dementia or anything like that.
Travis: It's interesting. When you stop eating carbohydrates or you fast one or the other, ketosis really is something that happens during the fasted state. When you look at a ketogenic diet, it's really the nutritional maintenance of the fasting state. It's like a sort of a trick to maintain that fasted state. What happens is, you have about 24 to 36 hours of carbohydrates stored up in the form of glycogen in your liver and muscle.
When you stop eating, you burn through that quickly. Now, your body has sort of a crisis to face, how does it get fuel? It will begin to mobilise the fat that you have. That fat spills out in your bloodstream; it goes into the liver. It begins this process of beta-oxidation where your enzymes cleave off to carbon units and you can burn that fat. But when you have a caloric deficit, it does this process so fast that it spills out these two carbon units. Some of those get converted by enzymes in the cell's cytoplasm into these ketone bodies—acetyl acetate and then beta hydroxybutyrate.
Those then enter the systemic circulation to take the place of glucose. Their glucose will never go down below a certain level, but it will drop to where you need some sort of replacement. Especially for the brain, which is a huge metabolic sink, and it can only burn glucose or ketones. It can't burn fats like most other cells. The brain costs us about 20% of our energy metabolism. The ketones will enter the brain and the heart and the muscle and replace glucose.
Now, what makes them unique is number one as a fuel, there is more thermodynamic energy per carbon unit than glucose, so they burn hotter. You get more ATP per carbon unit. It's—that's why Dr Veech called it a super fuel. But beyond that, they're doing just an incredible amount of other things. They enter the metabolism differently. They don't go down the glycolytic pathway. They enter the mitochondria and get burned oxidatively right away.
When they do that, they shift the ratio of these coenzyme couples, and coenzyme couples are like the money in the economy. That's what our body creates, and then diffuses out to use for energy, right? It's just like money in economy. So it charges the ratio of those coenzymes couples towards there's more energy. Now those do everything, and one of the main things they do is they recharge the antioxidant glutathione.
One thing you can notice when you shift somebody to ketosis is they have a huge antioxidant capacity. When you do it to mice, you can give them a lethal radiation dose where 70% of the mice die when they're in a carbohydrate metabolism. When they're in the ketosis, none of the mice die.
Travis: That is pretty profound.
Travis: Radiation is—it's just free radicals. It's what David Sinclair would say is slowly ageing us over time. So you get this robust way that you can deal with this constant sort of damaging presence in our lives. I'm really interested if we can do long-term trials to see if it really does slow down the ageing process.
But there's all kinds of diseases that are oxidative in nature. When someone's going through chemotherapy, which is an oxidative drug and radiation is pure oxidation. When you have somebody fast and this clinical trial has been done before chemo or radiation, the side effects are so far diminished and not the subjective side effects like fatigue, they are too, but the ones you can count.
Like, the number of times a person throws up goes from six a day to zero; the number of mouth sores; the amount of hair loss. So you get this protective effect in healthy cells while at the same time cancer cells don't like ketones. Everyone knows they love sugar. I think most people have heard that statement before, and it's true. They absolutely have a voracious appetite for sugar.
So they—when there's less blood sugar and more ketones, they are oxidatively stressed, so that oxidative chemotherapy and radiation effectively kills them easier. It's this kind of dream therapeutic scenario for cancer therapy. That's where I feel it should be studied, is alongside standard of care to see if you can improve survival and improve people's quality of life during that process.
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This is just so, like, I know Valter Longo did the research, like, getting people to fast 48 to 72 hours. I think it was before the chemo, and had a hell of a time convincing the oncologist to let him do that because it was—
Travis: You read the paper. Yeah, that's right, it was in the paper.
Lisa: Yeah, there is this fear like that cancer patients obviously lose weight, cachexia is a real problem. But that's a really different mechanism. Like, what we're trying to do here is a short, sharp, hermetic stress basic on the body that sends a body into this whole state that you've mentioned where it's actually protective, and it's an acquired state.
When you put the chemo in, which goes after the rapidly proliferating cells, which are the cancer cells, which is great, but it also goes after the stomach lining. That's why you vomit. It also goes after your hair follicles because—so all of those things are much, much less when you have a little bit of a fast before you chemo.
Yet, when you—like my mum has been on temozolomide. It was one of the chemos, and I got a very mild dose.I didn't go like the full, like, they want to go maximum tolerable dose, and I was like, ‘No, we want to do smaller dose.’ Did my research, fought hard to get what I wanted along with immunotherapy, rituximab.
Still did genetic testing to see that she would respond to those drugs, by the way, that was quite interesting with the IGCC. But then fasting prior and being in ketosis prior, and she's come through that really, really well as someone that is an eighty year old.
I mean, we actually got on top of the cancer, was no longer visible in the MRI before we started the chemo. But I put that in the mix as well because I didn't want—I know how nasty cancer can be and it can change its metabolism, and I just wanted to make sure that we keep this stuff gone.
Temozolomide is a milder form. It's not like some of the heavier, heavier duty ones. But that whole process, when I sit in the chemo room with all the other patients, no given orange juice and sandwiches to eat for their lunch. On the way out of the oncologist office, he says, ‘Oh Isobel, you've lost a kilo. You better start eating your pudding,’ and I'm like, therein lies the problem.
This is what my haematologist and oncologist are telling us to do. They just completely—I mean, they know that PET scans, how they diagnose cancer, use a form of sugar to see where the cancer is sucking it up. I mean, they know that, so why the hell would you put in sugar into the diet?
Travis: There's more data than that. There is data where colon cancer and brain cancer that shows the degree of insulin resistance correlates to a worse outcome.
Travis: All this is known in the literature. The problem is it's just not taught unless an oncologist digs up themselves. If you read Curable, we're beyond the point where a doctor, a single doctor can practise medicine. It is far too complex. There’s too many studies, too much data. We have to be pickers. We have to be teams to where they're specialists on each of these branches.
I can envision a future where there's medical oncology, radiation oncology, and metabolic oncology, and these teams come up with treatment plans. But yeah, it's horribly unfortunate that it's not there. It's always a patient—the patient has to find these things on their own and bring them to the doctor. If the doctor’s resistant, then they typically do it on their own.
Sadly, a lot of this is financial because all these things—how do you get paid for a 48-hour fast?
Travis: They don't, and so there's no incentive to do that. There's no incentive for the clinical trials because no one really knows how to make money off of it. It's—they're stranded in what we call this financial purgatory. It's really unfortunate.
Lisa: Yep. This is why it's so important for people to listen to episodes like this, so they can educate themselves in it. It isn't the ideal way for us to be getting help. I mean, especially when you're facing a life threatening illness, you want someone to just, ‘Tell me what to do,’ right? Unfortunately, you can't do that. You can't let—
Travis: You know, Lisa, it is changing. Like, we just talked about the slow social inertia. This metabolic therapeutic conference that I go to every year that Dominic D'Agostino puts on. I've been going to it since the beginning. The first year, I think, there was about 80 to 90 people there. It's tiny, and this is all based on, like, ketogenic diets, just metabolic therapies for various diseases.
This last year, there was 16—or last, like, two or three weeks ago, I was just there in California, there was 1600 people.
Travis: Clinicians from all over. There's a guy from— Jethro Hu, who from Cedars-Sinai, impeccable reputation, doing the, gave the data on a, phase one data on a clinic—on a ketogenic diet for glioblastoma. It was compelling enough that they're doing a phase two trial there. My foundation is helping out with that trial. It'll be a huge multicenter, the largest study ever done on ketogenic diet therapy for brain cancer, so it's changing. It is changing. Yeah, so it wouldn't surprise me if you do run into a clinician that is up in the literature; that endorses these things. But not all of them will.
Lisa: No, what I'm finding is that the functional medicine community are very much up on this. But they're general practitioners generally, right? They're not necessarily your oncologist. Then, you get a couple of integrative oncologists who are starting to bring this into play, but they usually have to step outside the system in order to practise, which means that you have to pay privately for them, right?
Because they are not allowed to practise with it and bring these things into the practice. Like, an oncologist can't tell you about diet because they're not a nutritionist. They can't step outside the standard of care. Because their arse will be on the line basically, and people just need to understand. I understand that they have limitations, and that they have rules and stuff. But as the patient or as a loved one of the patient, you need to understand that that is the situation.
That's how there’s different rules at play. You can't just go in and hand over all your power and expect that you're going to get the best in the world information because you're not. You're going to get the information that that person has been taught for a status. You're gonna get the information that's allowed by that institution. You're gonna have hundreds of years of medical system inertia, basically, like you said so beautifully in behind stopping you getting it.
I mean, I'm dealing with a patient at the moment whose mum—a client whose his mum has COVID, and we're trying to get the doctor to consider—she's in a rest home—ivermectin. There's 64 trials that are extremely good evidence. She's 88 and has comorbidities and stuff, but they won't look at it. It's not a licensed medicine in New Zealand. Well, that's wrong for starters because it is.
But that's the take of the rest home, and that's what they're sticking to. I mean, I lost my dad 18 months ago. He developed sepsis after an aortic aneurysm blew out in his main aorta and he had a massive operation, survived that. But I was aware of all the research around intravenous vitamin C and sepsis and Dr. Marik’s work and many of the others, Berry Fowler and so on. I was desperate to get him intravenous vitamin C.
Now, they had run out of options. He was dying and they would not let me do it. I fought for 15 days against the Ethics Committee. against every—I had to get every staff member's approval in the entire ICU unit—all the doctors, all of the nurses. If one spoke against me, I was out.
It took me 15 days to fight through all of this while I'm trying to fight for my dad's life, right? To be able to do something as simple as giving him intravenous vitamin C when they have no other options. And I lost my dad, you know? It was just devastating.
Travis: Yeah, that’s tragic. The end of the line when it's—all of medicine is risk/reward, right? You can understand a risky intervention on somebody that's mildly ill.
But when somebody's at death's door, and you're talking about something like IV vitamin C, some of our states in the US, we have the right to try law where doctors are absolved of liability, and the patients are more or less given the right to try end-of-life interventions that may or may not save them, but it's the right to try, and I wholeheartedly believe in that, especially with something that is benign or something like IV vitamin C. They should have the right to try.
Lisa: This was—I came with the clinical research. They said, ‘We're not interested in clinical research. It's a legal issue.’ I found a legal loophole eventually, and then had my GP who dad had been under, was allowed to come into the hospital and administer it under her licence and come in and do it. She would, but they only let me do it once. Then, they stopped me doing it the second. Of course, he needed every six hours, and by then, he was at death’s doorstep.
It did actually turn around all the markers initially, but I couldn't get the second one in in time. They stopped me and it took me 18 hours. I mean, I fought with everything—everything I had, and I lost that battle. So vitamin C, for me is a big part of what I’m trying to get that research out there. Now, this cancer journey, it's, like, keep getting slapped around the face. But—
Travis: I'm slightly—I can't stand loss of control. I have a hard time flying. To be locked in the medical system, that profound loss of control is absolutely horrific.
Lisa: Me too.
Travis: What drove me crazy with COVID was you had these monoclonal antibodies that were extremely—worked well, right? Very few side effects. They would not prescribe them for—they'd only give them to people that were high risk. Now, you have this phenomenon of long COVID, and people that were marathon runners who got COVID and are still suffering years later. Why wouldn't they change that indication to prevent long COVID?
It was never an option unless you had money. You notice that all the people that are connected or rich, they got the monoclonal antibodies instantaneously. Whereas if any one of us would have walked into, like, ‘You're not high risk. Go home.’ That drives me crazy that we don't.
In Canada—I was in Canada for a few weeks during COVID, and they were doing that up there. They're starting to do the monoclonal’s for just kind of anybody. Just to prevent long COVID because they understood the implications. But yeah, we just never—just when you look at the system, it will drive you crazy. You don't—logic is—just rarely operates logically.
Lisa: Especially in this COVID world, it’s like even all logic has gone out the door. But I don't think we'll open up that monster because it's huge. But the monoclonal antibodies and intravenous vitamin C for COVID, and hyperbaric, and things like that are not being explored to the extent that they need to be explored. This is just—that's another tragedy that's happening and people are dying, left, right and, centre, when we could have saved them in early intervention.
Early intervention, like, just doing something earlier instead of waiting until their oxygen levels are so low, and they're already in dire straits. Instead of just giving them a Panadol and telling them to sit at home and wait and see whether they start dying or not, right? It's for me, it's just—but let's get back to the cancer topic.
Because I wanted to talk a little bit, like, I listened to your interview with Dr Jason Fung who I really want to get on the podcast to, if you can give me an intro, and credible man. He’d written The Cancer Code. You were talking earlier about the abscopal effect, which I—when I was looking with mum and lymphoma, and we were looking at radiation, we didn't actually have to go down that path yet. Touch wood.
I was trying to explain the abscopal effect and the protocol that I was after. I just like they—just looked at me as if I come off another planet. They didn't know what the abscopal effect was. One of them did and said, ‘That's rubbish.’ It's just like why? So the abscopal effect, just for people who are listening who may have to go through radiation or whatever for their cancers, what is that and how does that work? Because that's really interesting.
Travis: Yeah, it is interesting. Immunotherapy has got a long history and it goes way back. It goes—it really goes way back. When you look in the literature, there was all these documented cases of people before sterile surgical technique, where they would get this horrible sort of post surgery infection, and then their cancer would go into remission afterwards.
They had no explanation for that other than the immune system was highly activated, and it somehow finally noticed the cancer and attacked the cancer. That was the most logical explanation. They sort of, kind of dismissed that. Immunotherapies then went by the wayside. Now, with this resurgence of checkpoint inhibitors and immunotherapies, the abscopal effect has come back.
What the abscopal effect is occasionally when you target even a single tumour site, even if somebody has metastatic cancer, multiple tumours, you can target a single tumour site, and the immune system, it roughs up the cell and exposes antigens to where the immune system can finally notice it, and lock on and then get activated and attack the cancer.
There's these documented things during—abscopal effects during radiation throughout the years. But then, when immunotherapies came along, those numbers of those abscopal effects documented sort of skyrocketed. There's a few clinical trials have been done. One is on breast cancer, where they give a much lower dose of radiation, while concurrently somebody is on a checkpoint inhibitor.
They'll only target one tumour site. They'll hit it with this low dose of radiation while on the check—the immunotherapy, and it'll activate the immune system to attack the cancer systemically. They showed a much longer survival in early stage breast cancer doing this in a small, small clinical trial.
But you're right, it's not one of these things that—I think there are some clinical trials that are proposed to continue to study this. But it's one of those things, it's kind of—there's very little risk and why wouldn't you try that? If it's—if you weren't getting full radiation, why would you just try the single tumour site.
Lisa: This is sort of aimed at like—when the cell is destroyed by the radiation for the one bit of description, it sort of uncovers the cancer cell, so that the immune system then recognizes it and goes, ‘Oh, I've seen that over there in the liver. Oh, we're gonna go over there and attack that as well.’ Because before they didn't have an explanation as to why this was happening. But they were just noticing that this was a bit the immune system was suddenly able to.
This is also why, as we get older, we get more cancers because the immune system is deteriorating and not doing its job well. On that front, I'd like to ask your opinion. I put you on the spot, perhaps, but you might not know. But peptides therapy.
What's your take on things like thymosin alpha 1, IgD 25, and things like that? Especially pharmacy thymosin alpha 1 seems to be very interesting to reboot our immune system. I've got my mum on it. That was a mission getting that into New Zealand, I can tell you. big fights with MedSafe trying to get that in, but what's your take on that?
Travis: I think, Lisa, we're just at the forefront of immunotherapy, and the immune system is absolutely incredibly complex, right? The way Siddhartha Mukherjee described it, as there's an icefall you're climbing and we just got the first pick axe, and now we can kind of pull up and look and see how far we can go. So it's incredibly exciting—immunotherapies.
It's really difficult because the immune system has got two jobs. They're two extraordinarily different difficult jobs to survey for cancer and try to get rid of it early. Also, it's designed all these checkpoints to not attack ourselves, which if it does, that leads to autoimmunity. It's got this incredible sort of engineering tension between it, where it doesn't want to attack cells.
That's why cancer is so good at evading. It's got this immuno-evasion quality because it is a self cell, and that the immune system you know is trained not to attack so, right? That essentially when you target with radiation, you could potentially expose some of the proteins that are not—look a little different than self, and that's why the immune system can finally lock on.
But peptides, tweaking the immune system, turning the dials a little this way and that, I think we’ll only get better at it, but it's going to be a—it's just going to be a trial and error long, long journey.
Lisa: Yeah, it is and it's exciting stuff that's coming down the line. I heard in that interview with Dr Fung as well that you would—he was talking about, like, the early detection of cancer, and I know that you're a part of AVRT and Zero Life Sciences, which I want to get into. He was talking about—we've got metastases as an early stage event, not a late stage event.
Like, we've sort of pictured it as like, you have a tumour growing, and then a piece of it will break off. That will go around the system, and it will lodge somewhere else, and it will start growing. Whereas Dr Fung was saying, Actually, those pieces breaking off all the time, and very—from a very early—but most of them get killed off in the bloodstream, because it's a very foreign environment for that cell.
It doesn't make it, but when it does go right around and comes back down to the tumour where it started from, it's now had a selection pressure, where it's actually gotten stronger. So you've made a stronger cancer cell. How that sort of related into then the heterogeneity of tumours, like, they have different genetic mutations in different parts of the tumour.
It's like, how can that be, if it's a somatic mutation theory, there should be three or four genes we should be able to target that the whole tumour should disappear, right? But actually, different parts of the tumour have different genetic mutations. His explanation for that was that it was coming around, and it was resettling back down on the tumour, but had different selection pressures going on, so it was evolving over time and getting stronger.
Did I butcher that?
Travis: Not at all. No, that's correct. If you know that sort of the competing theories on that, the somatic mutation theory contends that cancer is caused by a series of sequential mutations, right? That leads to the clonal cell cell theory, where this one cell gains this ability to be a cancer cell. Then you get subclonal populations that could have additional mutations.
When you sample a tumour site, you will find cells with different mutations, and presumably, they all have that founding set of one, two, or three driver mutations, that kick—precipitated the disease. You can sample metastatic sites, and find even different mutational profile—additional mutations.
It's—the heterogeneity is incredibly large, much more than people thought before the Cancer Genome Atlas project. It creates this game of whack-a-mole for this idea of targeted therapy, right? You could target one mutation, but cells got a mutation in that same system pathway, somewhere further down the line that would render that drug ineffectual. That's the problem with that paradigm of targeted mutations.
But the other theory is that these mutations are more of a side effect from the prime cause of the disease, which is, in my mind, would best be described as a metabolic epigenetic disease. When you look at what a cancer cell is, they—all types of cancer have the same hallmark features. They're all burning sugar. They do this metabolic shift. They're all immortal. They don't die. They evade the immune system.
There's all these very defined definitions of what cancer is doing. How can that be from a series of random mutations? We know these mutations are random when you sample, for example, 100 women with breast cancer. Ten of them will have this mutation; some of them will have one mutation completely somewhere else. It's, there's very—there's some consistency.
But there's even cases of cancer with no driving mutations, but it is a histologically identical, definitely neoplastic cancer cell. If you told a physicist that, I think they just laugh, and they do laugh.
Paul Davies was recruited into the—in the cancer program by Anna Barker, and he looked at the somatic mutation theory and just thought it was ridiculous. That it stuck around this long was crazy.
If we look at cancer then as the prime drivers being metabolic and epigenetic, that means that all of those things potentially could be modifiable, right? We don't have to target mutations. We can look for ways to change the way cells are expressing genes and so forth, and metabolising substrates, and things like that. There's all kinds of ways to do that.
Like, for example, ketones are what's called a JAK inhibitors, so they do change genetic expression. I think that is the future of cancer therapy, and there's beginning to be epigenetic targeted drugs now, but it's just getting started, and we all know how long this takes to get meaningful therapies in the clinic.
Lisa: Thirty, fifty years.
Travis: Yeah, and this is science. We tend to think we're in this modern era, but with regard to cancer, we are really—we’ll look back 200 years now, realise that we were just in the Dark Ages.
Lisa: Yeah, yeah,
Travis: We're still using radiation, which was invented about 110 years ago; chemotherapy was invented around World War II, and that's still the mainstays of cancer treatments. When you look at the other advances in computers and technology, it's just the most slow moving. It's just lagging so far behind.
Lisa: Yeah. Even when the research is done and there's compelling evidence, it still takes another few years to get into the actual clinic on the ground. This is where someone like in my situation and many of the people that I'm working with, situation is that, okay, we haven't got all the political studies, and we're facing end-of-life situations, we're going to have to make calls ourselves, and we have to do the best with what we have.
This is why gathering this information and sharing this information, so that people can make the very best decision that they can make, and it's not always going to be right. I was talking to my mum about this yesterday, and how much it weighs on me being responsible for the decisions that I make for her health.
In my case, the way I looked at it was I went and got, like, 14 of the world's best doctors on this. I sold a house, spent the lot of that money on having these doctors’ opinions and protocols and things developed for her. Then, I act like the CEO, and I make the decisions, what we actually put in the mix. Not everybody has that ability to do that. Financially, it's been very draining on our entire family.
But whatever, like, for me, it's like, whatever. I don't care if I lose everything. The pursuit of saving a loved one is for me a good exchange if that's what it takes. But also having the mental ability to research and to do all of this, and people who are actually sick, how the hell are they going to do that?
If they haven't got a driving person behind them who's able to do that, they're sort of left struggling to find this information, and it still weighs on me heavily, because if I make the wrong decision, she will pay the price.
Travis: You shouldn't put the tremendous amount of pressure on yourself, because medicine is practice under a cloud of uncertainty every day. You can go from one example to the next for that.
Say you come in, someone comes in with primary diagnosis of primary prostate cancer. There's five treatment options: there's surgery; there's watch and wait; do nothing. Then there's three different forms of radiation.
Those five treatment modalities have never been compared head-to-head. We do not know which one's better than the other. So watch and wait may be the best option, which is doing nothing, but that's terribly—when you say the word cancer, that's terrifying. Then the proton beam, the most advanced, most expensive sort of therapy in the five, is what's getting prescribed the most, but nobody knows that's the best still.
Every day doctors are—and when you do those head-to-head clinical trials, you find out that decades of what was thought was the best treatment paradigm is not. If you look at the, for example, a radical mastectomy that went on for 80 years before they finally did the trial, saying a simple lumpectomy is just as good. Women were disfigured, literally for 80 years. It's so bad.
It's uncertain. All we can know is what data we have. Then, you measure that through a risk/ reward lens. For example, fasting before chemo, that's very safe. We know that it's free. So some like that with low risk, but could have a potential reward. That's, to me, seems like an easy decision.
Some repurposed drugs that show very good—improves survival outcomes when people are on them with them that are low risk. We know the side effect profile, and that's very mild, that seems like an easy decision. You just—all we have is the data we have, and then you look at the risk/reward and make those decisions. But I think, yeah, bravo for what you're doing. It's the right way to approach it. I wish the whole medical system would approach it that way.
Lisa: Well, this is the thing, you have to do it because you don't have—you can't rely. This is the thing, this is not against the individual doctors or anything like that, but the system is broken. They're really good doctors, and they're really overwhelmed doctors who are trying to, I mean, if you've got 500 patients, and you've got your two minutes, basically, 15 minutes with each one—
Travis: I know.
Lisa: How the hell are you going to get to anywhere?
Travis: Right. I make the point all the time: it's not—this is not against the doctors. This is just a system, right? This is this systemic problem.
Lisa: Yeah, and we got it, and this is why we're doing what we're doing. I wanted to just go into the soil analysis, can you talk a bit about that? Because that was good a lot. I don't want to butcher it. We're looking at basically an analogy of a plant being in the right soil. Can you share that story with us?
Travis: Yeah. I think Jason Fung kind of, that’s his line.
Lisa: Yeah, yeah.
Travis: The soil hypothesis is where—
Lisa: That’s the one.
Travis: —the way cancer develops is the soil, right? The systemic sort of microenvironment around our cells is just as important as whatever molecular events precipitate cancer. That microenvironment is—could be causing those molecular events. That's kind of the seed/soil hypothesis.
What it takes—what we know when you look at the evidence, is it takes sort of a subclinical, chronic irritant over time, to where a cancer cell or cell starts to take on this phenotype of a cancer cell, and it happens over decades. A virus can do that, a sort of subclinical infection that lingers. Damage, obviously, from smoking, that's a physical and chemical damage that just happens daily.
You get this—this changes the entire sort of microenvironment around cells to where it's highly inflammatory. That begins to change the way the genes that are being expressed in the cell. It begins to revert back to the genes, the very early genes, that we express during embryology. This goes back to this evolutionary idea of what cancer is.
When you think about our tenure on the planet, life began about 3 billion years ago, and it began as single cellular organisms. Their biological imperative is just to divide—divide, divide, replicative immortality, right? Then, somewhere along the line, the cells started living together in a group. That's when mitochondria allowed for that, and then multicellular life took off. That was a very special event. We don't know how the probability of that ever happening again.
We know what happened once on planet Earth, so it's pretty special that we're even here. But when cells begin to live together, they have to sign a contract with each other not to stop the binding and behave for the benefit of the collective. What happens: the cancer cell will start to re-express these very, very early genes, our earliest genes in our DNA, that go back to this time of unicellularity.
Again, they adopt this biological imperative of replicative immortality. It's funny the way life builds on itself. We don't ever reinvent things. We always build off what evolution gave us before. So those are the genes that are expressed early on in embryogenesis is when an egg is fertilised, there's—begins to build an organism, and then once that organism is built, then those cells just play a specific role to do their job within their organ.
But by cancer cells begin to go back and re-express those embryonic genes, and when you look at an early embryo, the cells look like cancer cells. They’re extraordinarily glycolytic. They're evading the immune system. They're dividing like crazy. So it's really a recapitulation of biological programs that we already have within us.
How do you tell genes to behave within the collective? One of the things is oxygen. That's an extraordinarily powerful signal to cells to be in the collective. The other is avoid any sort of chronic irritants over time. Don't smoke and things like that. Then, just mind the microenvironment of your body, which is giving it the right food, exercising.
It's designed to do that. Every time you do that, it brings down those inflammatory processes, and so forth. So the soil in his model is just as important as the seed of cancer. Whereas before, we always focused on the seed, what is going wrong in that one cell to cause it to turn into cancer, and we didn't really focus on the soil.
Lisa: That is just such a beautiful analogy, and it sums up basically the approach so nicely, That's why I'd love to get Dr Jason on too, because I think, yeah, these sorts of insights. He's a nephrologist for those who don't know who we're talking about. He's the author of The Cancer Code, another fantastic book.
Travis, you've been absolutely amazing today. I can honestly talk to you for hours, and I'd love to go into the nitty-gritty of stuff that—all around the ketones and all that sort of thing. But is there anything that you think we haven't covered off on this conversation that would be really beneficial or anything that you're wri