The Psychology of Fighting Cancer | Dr Valter Longo

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All the cancer cells go in one direction, which is, I don't care that you're fasting me, I keep on going. And all the normal cells say, hey, I care very much about this condition. I'm going to stop. This is really probably the most powerful way to separate all cancer cells from all normal cells. We've seen a lot of people in stage 4 going into remission.

Welcome Welcome back, or welcome to the Finding Mastery Podcast, where we dive into the minds of the world's greatest thinkers and doers. I am your host, Dr. Michael Gervais. A high-performance psychologist named Michael Gervais.

Who head coach Mike McDonald and former head coach Pete Carroll brought in to work with the Seahawks.

Famous for his work with Felix Baumgartner when he jumped out of space in the Stratos Project.

Olympic athletes depend on something more than just training and talent.

They have to stay mentally tough. Today's guest is Dr. Valter Longo, professor and the director of the Longevity Institute at USC. And author of The Longevity Diet and his latest book, Fasting Cancer.

So far, we haven't seen anything that looks as promising as the dietary approach. We don't like to say too much about it because we don't want to give the impression that we know it was our treatment that did that. But certainly we've seen a lot of people going into remission.

In this conversation, we explore how small intentional habits may have a far bigger impact on long-term health than many of us realize.

I think you put it together, probably looking at maybe 20-year life expectancy difference compared to a Western sedentary lifestyle.

With that, let's jump into this week's conversation with Dr. Valter Longo.

Valter, it is great to be here with you today. I really enjoyed your book.

Oh, thank you.

Fasting Cancer. Yeah, I really enjoyed it. And the reason I enjoyed it is because, one, so many people are struggling, whether it's themselves and/or their family or an intimate loved one with cancer. It's one of the leading causes of death in the US. And you have presented a very easy-to-follow and easy-to-understand path to help, I think, reduce cancer, the onset of cancer, and actually how to work with it once you have it. Do I have those two premises correct?

Yes, it's correct. So the idea, of course, cancer and aging go together. And so by treating aging, you're also preventing cancer. And so that's one. And it was important to me to talk about exactly how you do that, what maximizes the aging treatment. And then two, once you have cancer, most people Google, what else should I do? So I go to the whatever medical center and I get the treatment, but then what do I do for lifestyle, right? What about nutrition and fasting and exercise and all of that? So surprisingly, so many cancer patients were coming to us and my foundation here in Los Angeles and saying, I don't know where to go. So then maybe 10 years ago or so, we started as a foundation to help cancer patients and then think about these integrative interventions. How do you combine— how can you be respectful of the standard of care and at the same time integrative solutions that at least have the potential of making the the side effects lower and the efficacy of the treatment higher.

At this point, are you more interested in the quality of life over time, longevity, healthspan, lifespan, those ideas, or are you more interested right now in understanding cancer and the process to help people through that?

Well, cancer I think is the number 2 cause of death in the US. So clearly whether it's cancer or cardiovascular disease or diabetes, If you wanna live to 110, you cannot have cancer, right? So you can, but we need to make sure that you don't get it. And if you do get it, you get through it, right? So that's how cancer fits in, right? So we never been a cancer lab first. We've always been thinking about cancer and cardiovascular disease, et cetera, as something that interferes with your ability to get to 110. And make it their healthier.

Why did you come up with the number 110? Where did that come from?

110 comes from two people that I follow personally. One was Salvatore Caruso in southern Italy. He made it to 110. He was the oldest man in Europe, and he was in the little village both of my parents come from. So he saw me grow up, and he was just a block away from my grandparents' and my parents' house. And the other one was Emma Morano, and Emma Morano, Got to 117 in northern Italy, and I followed her for the last 5 years of her life, and she was the oldest Italian who ever lived. And of course, it's great to think about 150 years lifespan, but I just felt that Caruso and Morano were realities, and if they made it there, then I think a lot of people can make it there. It's extremely difficult, but that's it. That's why it's so scientifically and medically a great venture because it's so difficult. It's just almost impossible to make it to 110, right? So when you look at the numbers, you're thinking, how can we possibly get this person to get there? But yeah, that's all the things that we know at work and hopefully you have a chance. Yeah.

Why did you want to study this? What first drew you into studying longevity and, you know, the quality of life?

Yeah, so I was actually a jazz performance major at University of North Texas, which is one of the great schools for jazz, believe it or not. On the second year, beginning of the second year, they told me I had to direct a marching band. And I said, there's no way I'm directing the marching band 'cause I was a rock player. I mean, I was studying jazz to play rock. And so as soon as they say that this is not an option, right, this is not optional, Then I said, I wanna study aging. So it was in my head. It always been in my head, right? I didn't think about, oh, what should I do? It was like, I'm going to the biochemistry department. And I figured if I combine chemistry and biology, that's gonna cover the ground. I say I pick biochemistry and the hardest thing that I can think of. And yeah, it was always in my mind. One of the things I speculate is that when my father, grandfather died, so Caruso was only a block away from my grandfather. They were the same age, right? But my grandfather dies 40 years before Caruso, right? Just, and so that to me was just an unbelievable thing because I thought, you know, just little things can make such a big difference, right? But I think I was in the room when he died. And so I thought, just as a 5-year-old, that probably stayed in my head as a very, you know, central problem in life, right? So I think if you see it that early, it just affected me. And so it probably, for whatever, 13, 14 years, it stayed in my head until I had the opportunity. Instead of playing, studying music, I'm gonna go study this thing that maybe is even more important than music. And I'm not, you know, I think music is very important, but just in my head, it was just, you know, I had to study aging.

Was that born out of trauma or was that just an important imprint that happened for you at a young age that sparked interest? Was it more out of that or like, or more from an inspired state?

You know, I don't think it was trauma because it didn't seem to affect me back then, but I think it just, it was a very central, it became from that moment on, like, you know, instinctively I think it became, it can't possibly be anything more important for me to do than figuring out how not to die, right? And yeah, so I think it probably is just instinct that forms when you are exposed close to it, you actually see the person die. I mean, everybody has grandparents that die, right? But if you're in the room, I think, at least in my case, it hits you in a different way where you, you see the reality of life ending, right? And, and so, so yeah, probably, yeah.

When you go back to that moment, and I'll explain in just a moment why I'm asking this set of questions, but can you go back to that moment and do you remember the room? Do you remember those elements?

Yeah, I remember everything. Yeah, I remember there was the whole family gathered together. And in fact, I put it in my first book. Alfonso, it was his name. I almost like was the doctor in the room, right? I was a 5-year-old. So, so then I say something like, can't you see he's already died? Right? So almost like in an early age, I was already thinking about that job, right? You know, that job of being a doctor or being an expert in that field. So I don't know where it came from, but even when I got to UCLA years later, My first 2 years I spent in the pathology department, right? So yes, I went to biochemistry, but then I spent, you know, 2 years in pathology department. So yeah, so to me the medical part was always very important. It wasn't about just science, you know, it was like science to, you know, get people to live to 110, right? So yeah. Okay.

Are you more interested right now in nutrition? Or are you more interested in healthy lifestyle choices?

We've always been interested in just making people live to 110, right? And so however that can be done, right? My first 10 years, all I did was genetics of aging. I didn't even do nutrition. And we discovered probably the one of the most important pro-aging pathways called TOR, siskinase, in simple organisms. But study after study of the study, was pointing, whether we studying simple organism or mice or humans, it was pointing us to nutrient signaling pathways, right? Meaning that it was all the genes that were controlling aging. So for example, growth hormone, the one genetic mutation that makes a mouse live the longest, right? It's called growth hormone receptor deficiency. With this GHRD, growth hormone receptor deficiency, The mice live 40% longer, but half of the mice never develop any disease, right?

Does the growth hormone receptor deficiency, does that mean that more growth hormone is circulating in the body?

It means that there's more growth hormone circulating in the body, but it's not working. It's almost like you have no growth hormone. In fact, the other mice that have record longevity are the growth hormone deficient mice. Right now, the pituitary is not making growth hormone, and those have almost identical phenotypes, you know, meaning they, whether they're growth hormone deficient or they're growth hormone receptor deficient, you get long longevity, extreme longevity, and extreme health, right? These mice are surprisingly healthy.

You're, you're blowing my mind because I remember when human growth hormone was kind of first the thing when I was studying it in grad school and I was like, oh my goodness, this is amazing. However, there was one Finding subscript finding that scared me, which was that it grows all cells. But at the time I remember thinking this is the elixir of youth. And what you're saying right now is when you don't have growth hormone, when the, when the mice don't have growth hormone, they're living longer.

Yeah. So now it used to be growth hormone and now it's the secretagogues, these peptides are now, they're becoming very popular. So it's the same story. So growth hormone is not bad for you. Temporarily, right? So temporarily it helps you grow and it can even help fix lots of different issues and problems. But if you're thinking about a 110-year life, right, then you have to stay as much as possible in what we call maintenance mode. There are trade-offs in evolution between, you know, the attempt to grow and the attempt to protect yourself, right? So you gotta pick, right? You cannot grow and reproduce and maximize your protection. You know, you gotta do one or the other, right?

Because the growth choices require risk and strain and—

Require a lot of energy, right? Yeah. You have to put all your energy into your offspring. Evolution doesn't care about us, right? We can, we could go, right? As long as our offsprings are doing well, evolution has done its job, right? So the force of natural selection is on making sure you reproduce. And you could argue You know, and even Darwin argued that maybe if you get out of the way, it's better, right?

Yeah.

So, so live long, not too long, and get out of the way. So then if you think about that, the growth hormone, of course, has got a temporary job. It needs to make you grow healthy and reproduce and get out, right? And that's exactly what happens, right? So it's not surprising that so many people think, wow, look at the short-term effects. But then of course what happens to you 20 years down the road? And you know, so for example, acromegaly, which is a condition where you have very high levels of growth hormone, people that have acromegaly die early. Mice that have acromegaly die early with lots of diseases and lots of problems very early, right?

They end up, I think, being like 7'6" and like—

Gigantism, yeah. So that tells you that, you know, high growth hormone. And in fact, they have IGF-1 levels. So, The growth hormone activity is measured with insulin-like growth factor 1, which is the result of having high growth hormone. So usually if they have above 300, they get a drug to block the growth hormone receptor or growth hormone release. The medical community already agrees that don't get your IGF-1, don't get your growth hormone activity too high 'cause it causes problem. But anyways, yeah, there was mice, but Then we, 20 years ago, we start following people in Ecuador that have the same mutation, the growth hormone receptor deficiency. And sure enough, we publish on them, you know, rarely having cancer, being overweight but not getting diabetes, having cognitive performance more similar to people much younger than they are. And recently, a couple years ago, we published on cardiovascular. They have less plaques, at least the one we examined. And we went down with cardiologists to determine, did they have cardiovascular disease, right? Maybe, 'cause everybody was saying, well, maybe they're protected from cognitive, they're protected from cancer, diabetes, but maybe they all die of cardiovascular disease. But in fact, they were even protected from at least cardiovascular risk factors. But my point was that growth hormone pathway is in the protein signaling pathway. Not just protein, but proteins have a central role in activating insulin-like growth factor 1, TOR, and all these genes that we described as pro-aging, right? And so I had to move to the nutrition part because it seems like nutrition was the way to control the gene to control the aging process, right?

So that's what you did with that finding. You were constantly trying to go upstream to see what had the greatest impact to make the downstream difference that you're looking for.

Yeah, so once we saw that we had people and mice and all kinds of organism living longer by having deficiency in this pathway, then the obvious thing was like, well, what happens if I manipulate the diet that controls these genes instead of needing drugs? Of course, we're also working on the drugs, but so far we haven't seen anything that looks as promising as the dietary approach. And so, you know, and later I think we're gonna talk about the fasting-mimicking diets. So then the idea has been, how can I just leave people alone but intervene instead of GLP-1 and other drugs that are going to do good and bad, intervene with, you know, dietary approaches that are much safer. Yeah, they're a little bit tougher, right? It's easier to take a pill, but they're— instead of making you not want to eat, they may make you very much happy to eat, but, you know, keep you healthy and long-lived.

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There's a lot of energy around protein and adequate consumption of protein to build muscle. And one of the unlocks for a second phase or third phase of life, meaning when you're, I don't know, past your forties or fifties, whatever phase that might be, is that if you go into that phase of life with adequate muscle, that you are set up better. You are set up better from a metabolic standpoint, from a risk of falling standpoint. And the narration there is that you need to lift heavyweights, you need to work out, you need to have, I don't know, kind of a lot of protein. And your narrative is saying, wait, hold on, I don't think you need nearly as much protein. So there's a— I know that you're aware of that friction. Can you help me understand, juxtaposed to what I just set up, how you are ringing the bell for people to make a decision for longevity?

It's good that you asked me that question because I just spent 6 months writing a review on proteins. I put together a team of like 10 people. Hundreds of papers. But the trick was not just reading the papers, right? The trick was understanding the papers. You have what we call meta-analysis, right? And some meta-analysis, and this is what gets the confusion out there, some of these studies of all studies, right? And maybe having 25, 30 studies on it, will say something like, will conclude something like higher protein intake if it's from plant-based proteins is associated with lower mortality, overall mortality, cancer mortality, et cetera, et cetera. And so I think they got distorted by influencers and a lot of people into, oh, you see, even the science is saying— so the field was based on acute effects, right? If you have a lot of proteins and you work out, you can have a small additional effect than if you just work out, right? Okay. So that was number one issue. Then this meta-analysis from top places came in and showed that— and the headline was higher protein intake. And some journalists, a lot of journalists may have gotten rid of the— and influencers may have gotten rid of the plant-based, right? And just say higher protein. When you dig into it, you see something very different, right? You see very consistently the high protein is bad for you, right? If it's animal-based, right? Very consistent, almost like no exception, right? And a lot of times you even see that in older individuals, right? Older individuals that have a high protein diet tend to do worse, right? I mean, high in the sense of 1.6, 2 grams per kilogram, as we're hearing the influencers recommend. So that's clearly bad for you. The question was, is high plant-based protein also bad for you when this paper indicated that it's not? Well, when you dig into it, you realize they never studied high plant-based protein. They studied groups that had a higher proportion of plant-based protein, but in fact had probably less amino acids compared to the lowest group, right? So anyway, long story short, high protein diet is bad for you, really bad for you. That doesn't mean that you should go down to very low protein diet. You know, you should stay with the 0.37 grams per pound or 0.8 grams per kilogram of body weight per day as recommended by most medical associations in the world. Right.

Okay. Do that again for pounds.

0.37 grams per pound. Right. So if you're a 100-pound person, that's about 40 grams of protein. If you're a 200-pound—

per day.

Per day.

Most people in the sport performance world and like you said, the influencers are saying it's not nearly enough, that it needs to be almost a one-for-one. If you weigh 100 pounds, you need about 100 grams per day.

Yeah, very dangerous, right? Very dangerous.

For what reasons?

Cancer mortality, overall mortality, cardiovascular mortality, over— gain weight, weight gain, right? It's so high protein, short-term, you get satiety and you— that's what the papers indicate.. But then in the long run, and this is Harvard, right? Study, right? In nurses and physician study. So in the long run, high animal protein diet is associated with weight gain and diabetes.

Yeah.

What about for people that are highly active, like athletes or people that are fitness-based?

I would say no difference. It's not what I will say, cuz that, that's one of the chapters in my review. So we went through it paper by paper and meta-analysis and And I will say the only exception would be for professional athletes, right? You know, for professional athletes, there seems to be a small effect on top of the, you know, the physical, the training and the exercise, small. So yeah, so I think for professional athletes, I think each athlete should look into it and say specifically for this discipline, is there an advantage or is there a disadvantage? You know, my guess is in some case you're gonna have disadvantages, But yeah, for specific type of athletes, you know, there could be a small advantage of adding, you know, so there was one paper where, you know, they were looking at the performance, you know, like muscle performance, like I think it was weightlifting or something like that. And so exercise was like 27 and adding high protein to it was plus 2.5, right? So it was either 27 or 29.5. So 27 just with the exercise.

And what is the 27? What's that?

It was like improvement in force, or I forgot now what the measure was, but the point was that most of it came from the training. And yes, so of course, if you're a professional athlete, that extra, you know, 10% is a big deal. But for most people, I would say that that's just going to get you in a danger zone, not just based on the epidemiological data that I was telling you earlier, Mice, if you look at mice, 100 years of research, the only way to extend the lifespan of a mouse, you know, in a major way, or a rat, is to either calorie restrict, so less calorie basically compared to normal, or protein restriction, right? Or methionine or branched-chain amino acid restriction, right? This is the most powerful, and now 100 labs have repeated this experiment over and over and over and over.

Even branched— chain amino acid reduction.

Branched-chain amino acid reduction or methionine reduction or protein reduction. This is not most powerful compared to diet. It's more, more powerful compared to anything, right? Just that if you look at 100 years of research in mice and rats and longevity and health, not just longevity, cancer, diabetes, neurodegeneration, and lots of issues in mice and rats. If you look at 100 years, Nothing other than calorie restriction. So low protein and low everything else beats protein restriction.

You know, you're pushing against a narrative that I've heard my whole life. So this is why I wanted to have you on. And I didn't think you were going to be this emphatic about it. I read your book and I read your position about increasing protein later in life. And I thought, wait, I can't be understanding this correctly. Reduce protein earlier in life. To the variance that you just said or the window you just said. And then you're suggesting again, like I said, to increase it later in life.

Yeah, small increase though. It's from 0.8 to say 1, right? So that, and even geriatricians seem to agree there. I mean, like if you look at, you know, good quality, let's say health plant-based, health animal-based, 1 gram per kilogram, you know, in elderly is perfectly fine, right? No need to go even in elderly in most studies. Now, you even see in the elderly, the high protein intake, higher protein intake being problematic. So, but yeah, I would say that, you know, our conclusion is 1 gram per kilogram. So going up 20% from what I said earlier after age 65, 70, and this should be a biological age, meaning like, you know, on average people in the United States, they gain weight until 65 and they start losing weight, right? And when you lose weight, that's when I think that you can make that 20%, not just increase the 20% in protein intake, but also maybe the variety, right? Are there, so for example, legumes have very low levels of methionine and also fairly low levels of branched-chain amino acids. So if you had a mostly legume-based protein diet, you might have a problem. And that's why that 20%, you know, helps, I think, in general, make sure that people that are not malnourished by, you know, having low protein and then having low amino acid type of protein that they consume.

You're gonna have a whole lot of people that are really confused right now.

And so—

Yeah, it's actually very simple. So think about, say, if you wanna be very, very safe in nourishment, think about 50/50. The best is 2:1 plant-based, animal-based, right? Proteins, right?

Okay.

So for each protein coming from an animal source, 2. So for each gram coming from an animal source, 2 grams coming from a plant-based source, right? It doesn't matter what it is. Don't worry about it. Keep the variety, right? So with legumes and seeds and nuts and cereal and, you know, whole grains and all that. And then keep that 0.8 or 0.37 grams total per pound. So if you weigh 100 pounds, 37 grams, 40 grams, I say if you weigh 200 pounds, maybe you know, 70 grams, right, or something like that.

What are some key foods that you pay attention to to make sure that you get in on a daily, weekly basis?

Well, you know, legumes are maybe a third of my protein intake, and then, you know, fish is maybe, uh, 1/4, 1/5, and then the rest of it is whole grains, nuts like almonds and walnuts, Yeah. So that's where I get most of my proteins.

No red meat, no chicken.

No, I eat chicken once a week.

Okay.

I eat chicken once a week. Yeah.

Okay.

And it may not— and it's not necessarily good, but it's fairly neutral. If you look at all the epidemiological data, chicken usually doesn't— it comes in the middle. Like, it's neither good for you or bad for you, right? It seems to be fairly neutral. So if you have it once a week, I always figure I like it and it's probably good. Having it once a week is probably okay.

Yeah. What is your position on gut health with longevity?

The health of every system is key, right? New data is suggesting that you have to worry about the one organ that goes first, right? The ages the quickest. So now you're starting to have organ-specific clocks, right? You can sort of measure how old is your liver. So if your gut is 20 years older than your chronological age. So if you're 40, but your gut age is 60, you're gonna have a problem, right? And you may end up with colorectal cancer or, you know, Crohn's or colitis. And so I think this idea is very important. It's a new idea because in the aging field, we always thought it's about, you know, your general biological age, but you could be very young and have one organ like the gut that is very old and you're still gonna have a problem, right? And my grandpa, right? So he had gastrointestinal issues. He never took care of it. And eventually after years and years and years, it turned into a cancer. And so, you know, he could have gotten an operation and, you know, just as an operation might have given him an extra 40 years of life, right? So I just wrote an article for an Italian newspaper about, you know, I always like to write about my relatives, right? And I put my uncle in there, right? And I said, you know, my aunt went to the doctor, the cardiologist with my uncle, and it was for her, right? And she's a little bit hypochondriac. And, but at the end of her visit, she was fine. She said, you know, my husband, by the way, you know, his heartbeat is very fast. And the doctor, she, can you take a look at him? And sure enough, he already had a heart attack and he didn't know, right? And then he needed a quadruple bypass. And so, hey, he was— it seemed to be very healthy and he was not, right? So he got a quadruple bypass and now 25 years later he's doing great, right? So yeah, that, you know, you could be perfect for everything else, but if your arteries are clogged up or your gut is inflamed, you got a problem right then. And it could be as simple as gluten. You know, think about celiac disease, right? Just one, just simple ingredient of one food type and it's gonna make your life miserable, right? So, so yeah. And, and you know, if you have celiac disease and you don't get rid of gluten, you're gonna have a miserable life and lots of problems.

Yeah. We had Dr. Tim Spector on who has done a bunch of research around gut health and he is saying something very similar to what you're saying. And his kind of horseshoe approach was 30 different types of plants per week of variety. Of plants. And if you're doing that, you're probably going to have a pretty healthy gut flora. Yeah, yeah, yeah. Okay, so let's— so then let's move into fasting and fasting-mimicking diets, which is a new term for me that you introduced. What do we need to understand about fasting, and is there a difference between genders across the two?

First of all, I think if you think about fasting, I always say that it doesn't mean anything, right? It's just a word like eating, right? You know, is eating good for you? And so I would say the majority of fasting practices are probably going to do damage in the long run. Right. And so why is that? Well, based on data, right? So if you look at, you know, people that fast for 16 hours, most of them skip breakfast. More the better. Breakfast skipping has been consistently associated with higher mortality, overall mortality, higher cardiovascular mortality. Now, we don't know why. But, you know, not a good start, right? So if you were doing something for your health to say, I'm going to skip breakfast, I'm healthier. And in fact, the people that skip breakfast are living shorter. Yeah. So I would say that we need to move from fasting as a word to like, exactly what is it that I'm doing and why? Right. And so we started a long time ago thinking about out of all the things that people talk about, are there some that could actually be beneficial consistently. And, you know, and how long are they gonna be and are they gonna be water-only fasting or different? So we identified, we started studying mice and say, what if the mouse, instead of having this daily intervention or restrictions, just did it once a month or twice a month for 4 or 5 days, right? So then that gave rise to the idea of periodic fasting, right? And so we introduced this idea of periodic fasting. A few people had done it before, but this didn't really exist.

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And this is different than intermittent fasting, which is what you're saying is—

Intermittent fasting is usually, let's say, you don't eat for 16 hours, you eat one day, you don't eat the next day. And yeah, so that's intermittent fasting. But essentially it takes longer for the human body or the mouse to shrink, right? And that's what you want. You don't want a major shrinking of organs and systems, but you want the human body to begin to shrink, right? And so, and it takes probably the whole 5 days. Now we're gonna go off—

5 days for senescent cells?

To begin to shrink. Shrink, right? But to shrink the body, it starts getting rid of damaged components like autophagy, right? So why? Because it has to— it hasn't eaten for 5 days and it starts looking inside for sources of food, right? And so, and, and fat is one of those, right? So you accumulate fat if you're like grizzly bear or emperor penguin, you know, when you have food, you, you eat as much as possible, accumulate it, and then you start slowly using it. And that's the same for actually cellular components, you know, the cell can start itself by a process called autophagy. But then we discovered, and that was really surprising, that stem cells are starting to become activated at the end of the diet. And something called cellular reprogramming, Yamanaka factors, you know, so these factors that have the job of making an old cell young, they also start being activated together with many different genes associated with embryonic development. So what was happening essentially? So you shrink because there's no food, right? And now when food comes back around, you have to re-expand. So we started thinking, is it possible that this re-expansion is using the same developmental genes that the mouse or the person is used when they were first born, right? And that's exactly what happens, right? So in that re-expansion phase, you're seeing the creation of a new organ, right? Of course, it's not the entire organ.. It's just, you know, component of it. But that's what we're seeing. And now the incredible thing is it also goes after the damage. It knows something is not working in this organ. So let me fix it before it start re-expanding, right? And it's really remarkably powerful because it's billions of years of evolution that have led to this extremely sophisticated. So for example, we took the pancreas of a mouse. We damage it irreversibly, right? And then they don't make insulin anymore. And then we start the fasting-mimicking diet cycles and you see that reprogramming occurring. The Yamanaka factors go up, the embryonic developmental genes, and then the pancreas goes back to making insulin, right? So it knows how to go back to its original function. And in doing so, it's becoming, you know, younger.

And you're suggesting that at 5 days, is when the autophagy process really starts to kick in. And two things are happening. One is the removal of old, decayed, decrepit cells, and the second is the rejuvenation of cells that were healthy but just a bit dormant. Is that— do I have that language correct?

Healthy, but also, and more important, the ones that are not healthy, right? So now you're taking That's why I was saying the insulin, they're no longer able to— the beta cells are no longer able to make insulin. So now the fasting mimicking diet refeeding cycles are turning them back into a healthy insulin-producing beta cell. Okay.

So it's both. Yeah. Yeah.

Okay.

I got that wrong.

Okay.

Thank you.

So describe a fasting mimicking diet as a protocol that we can all benefit from.

Yeah. So, so 15 years ago we first started doing clinical trials at USC Norris Cancer Center with young cancer patients. With water-only fasting. Nobody wanted to do the water-only fasting. And so then the government sponsored research on the fasting mimicking diet. So we said, we have enough knowledge on, you know, what is it that is triggering fasting? What is it that is blocking fasting? And so we developed a low protein, low sugar, high fat, low calorie fasting mimicking diet. And so, And that fasting-mimicking diet could have been made with any ingredients that are consistent with what I just said. But I decided that I wanted to make it with the healthiest ingredients that I could possibly think of. Like, so I combined the longevity ingredients, like the vegetables, the nuts, and, you know, the whole grains, etc., with the fasting-mimicking properties, right? And so that was a good idea. And we didn't realize that it was a good idea until we did a study in mice. On inflammatory bowel disease. And it turned out that water-only fasting was only about half as effective as the fasting-mimicking diet in repairing the damaged gut. And in fact, the water-only fasting temporarily increased gut leakiness, and the fasting-mimicking diet didn't. And then it repaired it much better, was more effective than the water-only fasting. And the reason was that the prebiotic ingredients, going back to what Spectre was saying, the prebiotic ingredients in the FMD, the fibers, et cetera, were feeding the Lactobacillus, Bifidobacteria, and other bacterial population that then helped the gut repair itself. Yeah, so I think that the fasting-mimicking diet, you know, this composition, a very healthy composition, was very good from that point of view. But also from the, behavioral, meaning training people to have a vegan diet. That was also, and maybe we didn't quite realize it until years later when we started doing trials on diabetes, prediabetes, and we're starting to see people saying, it's a slow process, but people were saying, no, I never thought I could go 5 days with vegan food and hey, I did it. And so I felt good, you know? So that was also a very interesting observation. So it's not like they revolutionize their life, they don't, but they slowly, it may take 2 or 3 years for them to say, "You know what? I'm happier eating this way," right? And also one comment we hear from a lot of people is, "I don't feel like I need, I used to maybe eat 2 pizzas in a row," And now I don't feel like that's important to me anymore. So it's like the food addictions or the relationship with food changes slowly, but it changes.

And so this fasting mimicking diet, you would suggest 3 to 4 times a year?

Yeah, I think it depends, you know, for diabetes patients, it might be once every month or every 2 months in the initial stage.

Okay.

And let's say obese diabetes in the initial stage, And then you get down and to the, in the weight and more functional. And then you can go every 2 months, every 3 months. And so now in Southern Italy, we just finished testing 500 patients every 3 months, once every 3 months. I mean, I cannot discuss the results yet, but certainly we think that that's probably, you know, a very effective, you know, once every 3 months to once every 4 months.

Okay. And then, so now let's kind of turn your gaze on cancer. And I understand your position to live a healthy life. Fasting mimicking diet is one of them. More plant-based proteins than animal proteins, reduction in overall protein. And you're suggesting that intermittent fasting is not the way to do it, but I think I read 12 to 13 hours.

No, 12 hours is very good.

Yeah.

So we, uh, FMD and 12-hour daily restriction. So 8:00 AM, 8:00 PM. Absolutely. That's like One of our first, I forgot to mention that. Yeah, but absolutely very important.

Okay. So now this is a lifestyle nutritional design to live healthier. Okay, great. Now speak to your understanding about cancer and somebody who is going through or just diagnosed with cancer, let's say. How does this relate to them?

I think I start by talking about the business of cancer, right? And why is that? Well, because the business of cancer is a very big business and it's a great business. I mean, like a lot of people are Lives are saved by immunotherapy and other very powerful drugs. But because it's so expensive, because it takes almost $1 billion to get a drug approved, it's very slow, right? If you came up with a very great idea for a cure for cancer, it may never see the— it may never happen, right? There's a filter. And cancer patients a lot of times may not get all the things that they should get. 'Cause the, you know, nobody can face that billion-dollar expense. So then you gotta think different, right? And you gotta think different without using drugs because if you use other drugs, then, you know, you get into violation. You can do it only for, with something called compassionate use. But lifestyle, you know, is allowed. Meaning like, you know, every oncologist, you have to do something. You have to eat something. You have to do something, exercise. So, You know, which is it? Yeah, so that's what my new book, Fasting Cancer, is about, is having foundations both in Europe and here in the US following thousands of patients, cancer patients, and not just cancer. We started, you know, basically helping them integrate, say, okay, you know, you're gonna go to the oncologist and the oncologist is gonna give you the treatment and great, you know, we don't of course touch that. But we are there to support that treatment as much as possible with everything we can in a personalized way, right? So then, you know, why fasting mimicking diets, right? Well, first of all, fasting, as I mentioned, is not feasible for cancer patients. Cachexia and sarcopenia and lots of problems that happen to cancer patients. They need to eat. They need to eat, right? But when you give a fasting mimicking diet to a patient, or to a mouse. I mean, in mice it's very clear. I mean, we get to look at it piece by piece, cell by cell. And so all the cancer cells go in one direction, which is, I don't care that you're fasting me, I keep on going, right? And all the normal cells say, you know, hey, I care very much about this condition. I'm gonna stop, right? And so this is really probably the most powerful way to separate all cancer cells from all normal cells. Why? It's just opposite direction, right? So now I always give the example of, you know, let's say a billion people in the desert, right? So if you take a billion people and you put 'em in the desert and you make 'em run and, you know, and they don't have, they don't have any water, what's gonna happen in 2 weeks, right? You're gonna have a billion dead people as long as they keep running. If you didn't run, you might have a shot, right? It's like you're not drinking for 2 weeks, but you're in the desert. You're sitting down. Okay, you never shut. That's what we exploit, right? Say, okay, now the cancer cells cannot stop running. And so because they keep on running, so if you take away the glucose and lots of other factors that are so important to keep running, they got a problem. But that's not enough, right? So why? Because they can steal from the rest of the body. So now you have to, okay, understand that they're running. Starve them and then hit them hard with something, which is the standard of care, right? For whatever the oncologist feels has come up. Yeah, whatever is the most, you know, whatever the oncologist says for you in this stage, I'll give you this.

Perfect.

So we work with that to say, okay, now we'll give you the wild card that makes things better, a lot better.

Okay, so cancer treatments, many of them in an attempt to kill the cancer, also damage or kill healthy cells. And what you're saying is when you starve the body just a little bit, the cells, right, or you restrict the, the glucose and the nutrients that it wants, it needs to be able to grow, it weakens those cells just a little, or makes them vulnerable, I should say. And that in and of itself opens up the treatment to be more effective. But you're still adding the traditional treatments, which is damaging the healthy cells as well. So how does your approach only target the cancer cells and not the healthy cells?

The treatment is the treatment. It's going to do damage. What we've seen, and first of all, I'm talking about mice here, and there's 20 clinical trials, human. But this is what I was saying earlier. It takes $1 billion to get through. Yeah. So the Foundation clinics are very careful at saying we don't know. What's going to happen to a patient. And usually we work more with stage 4, stage 3, stage 4, when the oncologist said, I don't have anything else. There is nothing that is going to work. So I just want to make sure that's clear. I'm not saying we don't know. The clinical trial looked very promising. For example, for triple negative breast cancer. Now you see patients in small trials, but then the FMD plus chemotherapy, surviving more or a lot more than patients with just chemotherapy. Right. That's probably the more studied. There's several trials on triple negative breast cancer, which is one of the most aggressive.

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Okay, so let's go to stage 4 brain cancer and somebody is given months to live, 6 months to live, and they refuse to take treatment, uh, traditional treatments. If they've got 6 months left, they're saying, I'm not going to go be vomiting half of them, or whatever the narrative could be for somebody. What would you suggest as an absolute baseline approach?

Yeah. First of all, we suggest— we've seen a lot of people in stage 4, you know, going into remission, right? So we suggest that— yeah, seen a lot of them, right? We don't like to, you know, say too much about it because we don't want to give the impression that we know it was our treatment that did that. We don't know, right? But certainly we've seen a lot of people going into remission, and even from stage 4. And in fact, the National Cancer Institute in Milan where they used to be skeptical about all of this, right? A few years ago, they published a paper saying, except something about exceptional responses in advanced-stage cancer patients. And so they had 5 different cancer patients that combined immunotherapy, chemotherapy, lots of their treatments with the fasting mimicking diet, and they saw 5 of them going into remission. So they thought it was so surprising that 5 in the same trial go from stage 4 to remission. That they publish a paper on it. So yeah, so I think that I would say that I would give it a shot once you get to that stage, even if you have glioma, glioblastoma, and it's a really rough prognosis that, you know, I would stick with the standard of care like temozolomide or radiation, etc., etc., and then add the fasting-mimicking diet. And then we add the ketogenic diet. And, you know, for each patient there is a— so we do time-restricted eating, We, we, and all these recommendations, by the way, are made to the oncologist, right? So we basically say to the patient, take it to your oncologist, and this is the things we recommend. So time-restricted eating, usually it's 14 hours. Then the, the fasting-mimicking diet, exercise, resistance training, and then the ketogenic diet, especially for the glioblastoma. So we rotate between fasting-mimicking diet, where we call the longevity diet, and the ketogenic diet, meaning like a very low-carb diet. And the reason is to make it as difficult as possible for these glioblastoma cells to survive.

To keep— yeah, to survive. Okay, great. And would you immediately go on a fasting mimicking diet, like right away?

Everything is personalized, right? So we look at the muscle mass, we look at the weight, we look at BMI, are they eating normally or not, and lots of things, and then make the recommendations. I mean, in the Italian Foundation, we also have physicians in-house here. Uh, the Valter Longo Foundation in Milan, we have physicians, you know, so we have physician PhDs and nutritionists here. We're, we're still, we're, we're gonna have 'em soon enough. Now we have PhDs in, and, but not physicians yet. But, but I think, you know, that, that would be the ideal to be followed by, by, uh, integrated group that knows what they're doing. And they also are respectful of the job of the oncologist. Who in the end is gonna make the, the, the decision here.

Now in your book, you walk through a handful of different cancers, like chapters, I don't know, 5 through 12, or, or approaches for each type of cancer. And is the, is it dramatically different for each type of cancer, your recommendations from a nutrition and fasting mechanism?

Yeah, dramatically different. And also stage, right? So somebody could be stage 1, more stage 1. We tell 'em don't do the fasting-mimicking diet. Age and stage and BMI and muscle mass and history and, you know, what is the chances, right? So if you have pancreatic cancer, you know, it could be early stage, but, or earlier stage, but you, you might have a 32% 5-year survival versus, you know, early stage breast cancer, you know, ER positive, we may have 97% 5-year survival. Yeah. So it's a lot of calculations of risk and benefit and yeah, so we try to bring the science to the oncologist, right? And say, hey, you know, this is all we know about all these integrative interventions, and what do you think? You know, is this something that— and most oncologists, you know, it used to be most oncologists say, no, no, don't change anything. Now it's like the other way around, right? Uh, most oncologists are saying, okay, yeah, this patient is not gonna do well with what we got, right? So go ahead, you know, I'll, I'll allow it. Yeah.

What important body of work and research you've contributed. And like I said earlier, I was really wanting to have this conversation because you are challenging many of the common narratives for healthy people, specifically around protein. I think that your research-backed approach is refreshing. I really enjoyed your book. And so— Well, thank you. Yeah, we, you know, at Finding Mastery, we've got a small team of 40-some folks and You know, we've got 3 of our, 3 of our teammates here, uh, their parents are in the thick of the fight right now. So I wanted to dig in and understand, and what a great resource your book is and obviously your foundation. Well, thanks.

Yeah.

So I don't know, hit us with 3 things that you hope all people could do to live a longer life, a better life, you know, a healthier life.

For sure.

The longevity diet, like the everyday longevity diet, which includes 12 hours of time restricted eating, right? And I think in general, it is a personalized, you know, people should do the most, right? You know, if you eat a lot of red meat, you know, try to go less red meat. That's it, right? So you don't necessarily have to, you know, abandon everything you've done before. And then, you know, the fasting-mimicking diet seems to be very powerful for so many diseases and conditions. And, you know, we're testing more and more. And so I think that list is gonna expand. And then I would say exercise, both, you know, aerobic and resistance exercise training, those are very important. Yeah, so those 3 things that I think you put it together, probably looking at maybe 20-year life expectancy difference compared to a Western sedentary lifestyle and habits.

Brilliant.

And you know, I forgot to circle back around on the gender. Are there any gender differences for the fasting mimicking diet? Or are you not finding that at this point?

We are not finding that, right? I think it's probably such a fundamental, you know, fasting response and refeeding response is such a fundamental because we see it in mice, we see it in simple organisms and it'd be strange if between a male and a female. So I think as we are now doing these 500 people and larger trials, we're gonna get to analyze everything differently and separately also. And so I think we're going to start seeing, yes, this responds better to this. And also I think with women, you know, cycle and premenopausal and postmenopausal, there is a whole, you know, effort to be put in there. Like, you know, when is the best time to do the FMD compared to the period? I mean, you know, we have ideas, but I think it'd be nice to formalize it with clinical trials. And yeah, so now we're doing doing studies on PCOS and endometriosis. And so a lot of women-specific studies. And I think those are going to help once they're done. They're going to help us also understand more specifically how we can help women both before menopause and after menopause.

Brilliant. And if you fast forward, I don't know, 3 years, do you think your protocols will be part of the mainstream treatment for cancer or do you think it's going to take a lot longer?

I think it's gonna be part of the mainstream, and I think we're working very hard with, you know, trying to get reimbursement. The fasting-mimicking diet definitely should be part of the, you know, prediabetes, diabetes, inflammatory diseases. Now Stanford has published a beautiful study on Crohn's disease and FMD, and I think many more are coming out from lots of different places. Now cancer, I think that, You know, I hope that there's more funds that, you know, we need those billions of dollars. That's the reality, right? So to take it all the way to Phase 3 FDA. Until then, you know, I think cancer is going to be the hardest one, right? Because it's so regulated and it's so hard to finish and prove it. And there's so many, it's like diabetes is one disease, cancer is 100 different diseases and 1,000 different therapies, right? So, so yeah, it's very difficult, you know, and I think immunotherapy has been a remarkable story because now it's been FDA approved for so many different uses, but it took 30 years to get there. And so with fasting, you're looking at something even harder. But, but yeah, I think it's got that potential. It's got the potential of immunotherapy in making cancer treatments work better. But we'll see.

And when somebody wants to learn more about a fasting mimicking diet, where do you wanna point them?

Yeah, of course the book, the two books, The Longevity Diet is more about prevention and living long. And the second book is Fasting Cancer. And that's just specifically, you know, with the help of many oncologists, including, you know, oncologists from MD Anderson and USC Norris Cancer Center. They had a very important role in curbing my enthusiasm, right? Sometimes like, no, no, no, no, no. You cannot say that, you know. And so it is important because, you know, one thing is to see, like you were saying earlier, right, you can see cases of people that we were talking about, they are cured all of a sudden or even going remission. But you have to say, well, you know, this happens even in the absence of fasting-mimicking diet, right? So it wasn't the FMD, was it not the FMD? And yeah, so those oncologists in the book were very important in making sure that we don't overpromise. But I think everybody agreed that, like you were, you know, we were saying earlier, you were talking about glioblastoma in 6 months, right? You know, just that hope, that idea that, yeah, what if it was you that all of a sudden you got into remission, right? And we've seen it with so many patients, could be you, right? Yeah. So I think that's a very important factor. And that was one of the major reasons to get out there. But also, you know, Of course, there are randomized clinical trials showing that, that, that it may work better. Yeah.

One of the things I love about the scientific method and scientists in particular is that we are constantly searching for the right answers, the answers that hold up in the light. And if our answers or our understandings or insights that we have right now are challenged and found to be refuted and are not holding up, then you quickly let go of them, you know, and you don't hold on. It's the, it's like the anti-scientific approach. What have you needed to unlearn that was important and foundational for you as you've been in your seat for longevity?

I think, you know, personally, I mean, I didn't take seriously the personalization early on because, you know, I was working with yeast and mice and I just thought, you know, this is gonna apply to everybody. And yeah, I have to say that, uh, I had to unlearn this, this idea that, You know, because it's conserved and because we see things that span from different, you know, they grab lots of different organisms, that's going to apply to every person. That doesn't work like that, right? So, so yeah, you have to really understand each individual, and, um, and it could be a very, very different treatment for two different individuals, you know. And also, you know, in general, the diet, right, the understanding that there could be people that in fact may need more proteins, right? They may need more animal proteins, you know, I don't know. But in general, that's not true. But, you know, maybe 3% of the people may have a genetic predisposition that makes them very sensitive to, let's say, a low-protein diet, right? So yeah, that's certainly something that I think, you know, we are appreciating more and more as we follow thousands of patients. And that's been the difference, right? Actually being there with the physicians and with the clinicians every day going through case after case after case and then being able to follow them. And you don't always have a success story that makes you think about personalization and how to solve a problem. But that also points to what the system should be, right? Which is it needs to be much more— medicine should be much more like these programs that we do together. Meaning, you know, the scientists and the physicians and the dietitians, et cetera, et cetera. It's a collaboration to not just visit you and say, okay, take this and come back in a year. It'd be more like, okay, well, let's see how this does. And then we do some reading, we come back to you and just goes back and forth until we solve your problem and then optimize your chances to make it to 110 healthier.

Dr. Valter Longo, thank you so much.

Thank you. Thank you.

Next time on Finding Mastery, we are joined by Dr. Daniel J. Siegel, Harvard-trained psychiatrist, neuroscientist, and bestselling co-author of The Whole Brain Child and No Drama Discipline. In this conversation, Dan explores why the hardest moments in parenting often reveal more about us than our children, and how understanding our own experiences may be one of the greatest gifts we can give of the next generation. From repairing after mistakes to building resilience and emotional health in our children, this episode offers a powerful framework for becoming a more present parent and a more integrated human being. Join us Wednesday, July 1st at 9:00 AM Pacific only on Finding Mastery.

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