The Rich Roll Podcast - Fasting For Longevity: Valter Longo, PhD Shares Cutting-Edge Fasting Science & Optimal Nutrition Protocols For Lifespan Extension & Disease Prevention

Episode Date: February 10, 2025

Dr. Valter Longo is a pioneering longevity researcher, Director of the USC Longevity Institute, and one of TIME’s 50 most influential people in healthcare. This conversation explores his groundbreaking Fasting Mimicking Diet and its profound implications for aging, disease treatment, and longevity. From cancer therapy to diabetes reversal, Valter reveals how therapeutic fasting could transform modern medicine. Along the way, Valter challenges my long-held assumptions about protein intake and sleep. His research offers hope for extending human healthspan, and this conversation is illuminating at every turn. Enjoy! Show notes + MORE Watch on YouTube Newsletter Sign-Up Today’s Sponsors:  Seed: Use code RICHROLL25 to get 25% off your first month 👉https://bit.ly/seedxrrp2025 Squarespace: Use code RichRoll to save 10% off 👉https://bit.ly/squarespace2025 Go Brewing: Use the code Rich Roll for 15% OFF  👉gobrewing.com  iFit: Use the code RICHROLL to get 10% off any purchase of $999+ 👉 nordictrack.com/RICHROLL LMNT: Get a FREE LMNT sample pack for just $5 shipping 👉 drinkLMNT.com/RICHROLL BetterHelp: Use the code RICHROLL to get 10% off your first month 👉BetterHelp.com/richroll Check out all of the amazing discounts from our Sponsors 👉 richroll.com/sponsors Find out more about Voicing Change Media at voicingchange.media and follow us @voicingchange

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It's a very undisciplined world. If you look at Europe, 60% of people are overweight or obese, and the United States is 75%. If you can make somebody younger, they will live longer, they will be much healthier. Of course, you can make somebody live 10 times longer, but could you make him 50% longer? Right? So I think it's possible, right? So from 80 to 120.

Returning for his third appearance on the podcast, I'm very pleased to welcome back Dr. Valter Longo, a pioneering research scientist in the field of longevity, fasting, and age-related disease. Named one of the 50 most influential people in healthcare by Time Magazine, Dr. Longo is both the director of the Longevity Institute at USC, where he is also a professor

of gerontology and biological sciences, as well as the director of the Longevity and Cancer Program at the Institute of Molecular Oncology in Milan, Italy. Fasting mimicking diet plus chemo, immunotherapy, hormone therapy, kinase inhibitor. I mean, the potential is huge in all the different cancers and in all the different stages. In this conversation, we parse longevity science from myths. We talk about the most important habits to consider to keep aging and disease at bay, the optimal way to fast,

and what Dr. Longo's research reveals about the impact of fasting on our biological clock, on lifestyle disease generally, and on the prevention and treatment of various types of cancer, which is also the subject of his latest book, Fasting Cancer. Dr. Longo is truly at the cutting edge of a field that is rapidly rewriting the rules on how to live longer and more vitally. It's incredible stuff. And my hope is that this conversation will leave you rethinking your non-ideal nutrition habits and empowered to make better ones.

What you eat every day is going to have a huge impact on your healthspan and lifespan. What is it about these diets that is so protective? Walter, thank you for returning to the podcast. It's been between like two and a half and three years since we last sat down to talk. We reconnected at that Google conference recently where you were on a panel with Rhonda Patrick and Peter Diamandis, who both have been on the podcast recently.

So you're completing the triumph right here to kind of dive deep into longevity science, fasting. We're gonna talk about the impact of the fasting mimicking diet on cancer specifically, which is the subject of your new book, Fasting Cancer. But before we get into all of this, I think it would be valuable to just spend a minute or two discussing what has transpired in the last 24 hours.

So today is January 23rd. When we're recording this, we're on day four of the Trump administration. And just yesterday, there was a freeze on NIH grant review panels. There was an article in Science.org about this. So there's a little bit of a mild panic among scientists who depend upon grant funding, who studies are under the umbrella of the NIH, which is an enormous institution, I think

something like 300,000 people, 2,500 institutions underneath that. And it perhaps is a momentary pause. Certainly I would imagine there's bloat in this bureaucracy that is worthy of review, but at the same time, an interruption in billions of dollars in research funding. So as a scientist who runs a lab, I suspect you are potentially impacted by this and just wanted to see, you know,

kind of where you stand and what your thoughts are on this. Yeah. Well, we're very worried, of course. I just submitted a grant to the NIH, and this is a $15 million grant. It's a major grant for my lab at USC, and we depend on that, right? So we depend on these NIH funds to do research

and my group has helped maybe 50 universities and hospitals do clinical trials. And we study NIH research, none of those will have happened. In our trials, I think are particularly relevant because they're not on drugs, right? So there are trials on fasting, fasting-mimicking diets and longevity diets. So things that are either free or inexpensive

in those, particularly those, depend almost completely on the NIH and sometimes on some foundation funding, but mostly on the NIH, right? So obviously there's reform needed at the NIH. And I think most of the NIH people will say the same, right? Certainly blocking the NIH process is a big problem. Yeah, I think they are responsible for something

like $47 billion in allocations. And I think, you know, it's kind of important to understand that not all research is, you know, pharma funded and foundations only go, you know, so far, right, like in terms of how we underwrite critical research, not just in terms of clinical trials, but all manner of research to find new cures to diseases, et cetera, it goes well beyond kind of what I think

perhaps people might imagine in terms of its scope and depth. Yes, and I think a lot of people maybe think that it might imagine in terms of its scope and depth. Yes, and I think a lot of people maybe think that it's just about basic science, right? But in fact, the NIH funds a lot of clinical trials and some of these clinical trials could have a almost final impact on whether an intervention gets used or not

by people eventually, right? So in some cases, they may even fund trials that are gonna be FDA approved. So yes, so it's basic research that fuels the translational science or translational science, and then translational science that fuels clinical trials and treatments.

And I think that with that DNAH will be a drastic problem, especially for those diseases or problems where the big pharma don't wanna invest, right? So like rare diseases and diseases that are not that profitable. So that's where the NIH steps in and funds research and clinical work to treat it.

Yeah. Well, interesting times indeed in which we live, but we were both lucky enough to avoid our homes being impacted by the recent fires, although there's fires still burning right now. So it's a very interesting time here in Los Angeles. Anyway, because it's been a couple of years since you've been here,

I thought it would be great to kind of catch us up on the latest findings with respect to fasting, the fasting mimicking diet, which is your kind of like focus, intermittent fasting, time restricted eating. There's a lot of confusion out here around that. Last time you were on, we kind of canvassed all of these, but a lot has happened in the intervening kind of period in which we last sat down. So kind of where are we and what's got you kind of excited

or what's giving us greater clarity about the impact of this science? Yeah, so I would say that, at least in my opinion now, the more clear evidence for fasting is in the time rest to the eating domain, you know, so that the daily fasting. And I think we discussed it before, but I stick with the 12 hours of fasting

and 12 hours of feeding per day. And there's new data indicating that in fact, maybe the problem of skipping breakfast and doing 16 hours of fasting and skipping breakfast may not be about skipping breakfast, but maybe about the 16 hours, right? So we don't know, but certainly that's a possibility. And so I think 12 hours is a much safer way to go.

And that is effective, of course, there's 16 hours of fasting every day, but it's still effective. And so I think Sachin Pandey and I will agree on this 11 to 12 hours daily time-restricted period. So, you know, eat for 11 hours or 12 and fast for 13 hours or 12. My understanding, correct me if I'm wrong, is that we still need more research to really drill down on, you know, the efficacy of these specific windows. But as of right now, like it's sort of a safe bet, like this 12 on 12 off seems to be the one that kind of works for all purposes.

Whereas others may have benefits or deleterious impacts that we're still trying to better understand. But as of right now, like this seems to be the window that is the safest and most predictable in terms of outcomes. Yeah, the easiest, safest, no physician will ever argue that that's a bad idea. And really and really not a single paper saying that this is not safe or that is not effective or at least partially effective in preventing and treating a number of diseases. So yeah, so I think it's a good compromise and I think something that everybody should do.

That's also consistent, not just with the epidemiological data, the clinical trials, also consistent, not just with the epidemiological data, the clinical trials, also consistent with what centenarians have been doing for a hundred years or more. So, yeah, so I think that the 12 hours is one. And then I've always argued against the alternate day fasting, the five, two, and not because they're not effective,

but again, they're very demanding, right? So not eating every other day, it's gonna be something that very few people will ever be able to do. And then you get into the, again, the territory of are there side effects caused by not eating every other day or not eating for two days a week.

So I would say in general, I just don't see a big future, at least not for the general population, right? Some people can do it. We'll see about the efficacy and the safety. But I think that in general, I will say that at least I'm not enthusiastic about either alternate day fasting or two days a week of

fasting. Then of course, I'm enthusiastic about the fasting-making diet. So in addition to the time we're sitting, eating daily, then the cycles of the fasting-making diet. And so this is a plant-based, you know, low calorie, low sugar, low protein, high plant-based fats. That program that we've been testing, we and many universities have asked to test it, have been using it for all kinds of diseases

from diabetes, pre-diabetes, cancer, Alzheimer's, auto-immunities, et cetera, et cetera. For people that didn't listen to our previous episode, the fasting mimicking diet is essentially a way of eating a calorie restricted diet with a very specific, you know, kind of menu that physiologically mimics what the body would experience had it been just fasting. Correct, is that, do I say that accurately?

Yeah, that's accurate. So then that was first developed in mice. And so we use certain markers to make sure that there is a fasting response equivalent to that of water only fasting. And then the same was done in people. And again, we're looking for certain factors in the blood that would show that in fact,

that that person has responded as it would if it was not eating at all. Before we move on from time restricted eating in this 12 hour window, you know, to restrict your eating to a 12 hour period isn't really fasting at all. It's sort of like if you get up at eight in the morning and you go to bed at nine or 10 at night,

like there's literally only an hour or two in which you're not meant to be eating. Right, yeah. And this is very important, right? Because if you look at Europe, 60% of people are overweight or obese and the United States is 75%. So we're in a world, I think,

and this is not just Europe and the US, it's the whole world with few exceptions. So it's a very undisciplined world. And so that's very important to also say not just what will be most effective, but will be easiest for people, realistic for people. And so I think that 12 hours, a lot of people will say, that's not fasting at all.

Well, it is fasting because now on average, and this is work by Panda, people were eating for about 15 hours a day, right? So yeah, so people all over the world like to eat for long periods every day. Yeah, so then somebody may start at 6 a.m. and end at 11, 30 p.m. Right.

And so that, you know, the three, four, five hour restriction can make a big difference. It can make a big difference, not just in reducing calories because you have less opportunities, of our restriction can make a big difference. It can make a big difference, not just in reducing calories because you have less opportunities, but also in metabolic switches, they may make energy expenditure higher, let's say, right?

And also help people sleep. So those are some of the things that are emerging in mouse and human studies. If people are eating on average 15 hours a day, is there evidence or is anybody kind of looking at the co-founding factor of the impingement on sleep that would be impacting deleterious health outcomes? Because if you're eating for that many hours,

you're probably staying up late and not getting, you know, this the eight hours that you should be getting or seven hours. Yeah, so Sachin Panda published on that and showed that in fact, when they reduced the eating window from 14 hours and above, if I remember correctly, to less than 11 hours, there was an improvement in sleeping quality.

So yes, so that seems to be the case. And I've always been also preaching, not eating for the last three hours before you go to sleep. So that's consistent. That's still the hardest thing for me. It's really difficult for me to go to sleep when I don't have a full stomach or am feeling hungry at night. It's just a mountain I still have not mastered.

Yeah, and I think it's important, the foundation clinics, everybody's got a different method, right? So I think it's important. So for example, it's better to eat a light dinner, but I have a very big dinner, right? So because I would be unhappy having a big lunch and a small dinner.

So to me it works, for me it works. And so I think it's okay. I sleep well and or pretty well, unless I'm traveling like I just did. But yeah, if you eat late and that's a big deal to someone, but that doesn't really affect you negatively. I don't think there is too much data was suggesting that you're gonna live 10 years shorter

because of that, right? So if you're sleeping well, that's probably okay. And okay, compromise. I do notice though, if I overdo it in terms of volume and hour of the evening, I'll generally wake up around two or three in the morning. And when I was wearing a CGM, I would notice these spikes and these drops that would occur, you know,

over the course of the evening that don't happen when I eat earlier or like reduce the volume. Right, and as you get older, they make it worse, right? So, yeah, so then, yes, the recommendation stays, eat earlier and eat within 12 hours. And then, you know, if somebody is not affected by eating later, it's probably okay until that becomes a problem, right?

So I think that's a good way to look at it. And of course you have to know that it's a problem, but you know, not sleeping well, most people will know even without a bracelet or- Yeah, you'll know, yeah. You don't need any kind of like data feedback to know whether you're sleeping or not, honestly. Before we kind of even go further,

perhaps we should just take a minute and set the table a little bit. Your expertise is on nutrition and its impact on longevity and disease prevention and to some degree, disease treatment through the lens of fasting. So maybe, you know, in your own words, kind of describe, you know, your research

and kind of the thesis of the work that you do. Yes, so that's the, let's say 50% of what we do is what you just described. So the fasting-making diet and the origin of that is in something called calorie restriction, which we talked about in the past. And the fact that, you know, my former mentor was one of the pioneers of calorie restriction,

which is just, you know, what happens in a normal person that has a normal diet, if you reduce the calories by 20, 25%. In my observation that that was just not feasible and not very difficult for people to do and potentially giving problems and solutions, right? So then the fasting-making diet was about, can we get the same effects as this phenomenal effects

that calorie restriction has been demonstrated to have in monkeys and lots of different animals and in people without the problems, right? So that was the idea. Like maybe you do these five days once a month and maybe you do it as little as every three or four months. And that's what we're actually testing now in Southern Italy on a big cohort.

Yeah, so the fascinating that making diet is that and we can talk about it. Then we're working on what I call the longevity diet. And that's a big part. Yeah, so the fascinating that me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, me, ketogenic diet. And so we just tested them all, right? So in mice and now we're testing a lot of these diets

and we're comparing them, you know? So what if you can compare a vegan diet and a ketogenic diet and what I call the longevity diet, which is a pescatarian diet. How do these affect aging, longevity, age-related diseases and also frailty and strength, right? So that's another big part of my laboratory. What do you eat every day?

So let's move away from words like Mediterranean diet or Okinawa diet and just move into what is it about these diets that is so protective? Is it the protein? Is it the type of protein, right? So for example, you can say high protein, low protein, and I will argue it's irrelevant, right? Because you can have a five to 10-fold difference

in certain amino acids with the same level of proteins. If you eat legumes versus you eat, and sometimes you can have that between different plant-based sources, right? You can have a five-fold difference of, I mean, certain essential amino acids between two different plant-based sources. I think we probably need to move away from also same

protein in levels, right? They move into amino acid profiles. Anyways, it's just, I think the pillar number two of my work is, you know, what do you eat every day is gonna have a huge impact on your health span and lifespan. And so what is it that you should change among all the things that you eat

and how do you personalize it, right? Because I always say, you can have eggplants and be very healthy, or you can have eggplants and be miserable because they happen to cause an inflammatory response in you, right? So, yeah, two people, maybe even brothers and you, right? So, yeah, two people, you know, maybe even brothers and sisters, right? One could be having eggplant all day and one could be very much sensitive to it.

So, yeah, so then the everyday, I think diet is a very important thing. And the third one is genetics, right? So not just we don't look at diet in a vacuum, we look at diet, whether it's fasting or eating as how does it affect the genes that regulate the aging process? How does it affect IGF-1, growth hormone,

growth hormone receptor? How does it affect TOR, you know, RAS and all these genes, these networks that are now clearly, and we talked about in the past, a simple organism, we can manipulate these genes, these networks that are now clearly, and we talked about in the past, a simple organism, we can manipulate these genes. And if we combine fasting with genetic mutation, we make simple organism live 10 times longer, right? So we're trying to bring that to people.

So, of course you can make somebody live 10 times longer, but could you make him 50% longer, right? So I think it's possible, right? So from 80 to 120, that is possible. And yeah, and I think all of this has to be understood very well and put together in a way that will cause the benefits without the problems, or without generating new problems.

It's so complicated. There are general principles and yet there are, there's diversity to your point about the eggplant that you have to address. And I think what's interesting about your work is that, and maybe what's somewhat unusual about you as somebody who is a research scientist is that you are thinking about

how you balance your discoveries around efficaciousness with sustainability and adherence in the general population. It's one thing to look under a microscope, have a discovery and extrapolate from that into some sort of principle, but how can that be translated into something that the average person can take and use sustain that will benefit them over time.

Yes, and I think that we wanna take it all the way to disease cures, not just treatment cures, right? So now, for example, with diabetes, we now have three or four trials, all of them showing a 50 to 70% regression of the disease. And then- On the FMD. On the FMD, just once a month without changing their diet.

And that's a very important thing, right? So we don't change your diet, we don't change your lifestyle. And we're saying, so, you know, for thousands of years, people have been talking about food as medicine, right? But then really never happened, right? So that's what we're trying to do is say, can we standardize this vegan-based medicine

and then use it to, in some cases, even cure diseases? And so diabetes, I think, is definitely one of the ones where we're very confident. And so University of Leiden, where the University of Heidelberg did the first trial a couple of years ago, and showed impressive, impressive effects on A1C, but also on reduction of drug use.

And then Leiden repeated and got the same results. And so I think, yes, this is a feasible ways to bring people back to a functional state from a disease state to a functional state from a disease state to a functional state. And I think that, you know, a lot of that has to do with molecular mechanisms that are much more sophisticated than people, you know, may imagine. So for example, we just published in collaboration with Laura Perrin at a children's hospital, we publish on the use of the FMD in kidney, in rats with kidney damage,

and then in people with kidney disease, right? But in people, of course, we don't get to see what happens, but in rats, we get to see what happens. And it's really remarkable. So we damaged the kidney, and you see a complete disruption of the gene expression. So our genes are turned down and off in the different cells of the kidney.

And then we start the fasting-making diet. And you see that, so there is a very precise architecture, let's say, right, three-dimensional. And that's completely destroyed by this toxin that we give the rats, right? Then we start the fasting-making diet cycles. And you see everything going back to where it was, right? Almost like a magic intervention.

So it's not really the fasting, mimicking diet that is doing anything, right? It is the rat that are always, and people are the same, that always had programs that are able to be triggered by fasting to turn on regenerative and developmental like programs. So the same genes that are used when the organ, when the kidneys are first generated in a baby.

Like pluripotent stem cell generation, is that what you're talking about? Yes, yes. So the cells are being reprogrammed into some of these reprogramming factors. Yamanaka factors, also known as Yamanaka factors are turned on. And you see that every organ

is turning on different ones, right? So in some cases you see OCT4 being turned on. In some cases you see MIC. So different organs use different ones, but they all have the same thing in common. They turn on these many genes that are involved in organ generation. And then that's how they can go from this very disrupted state back to the previous healthy states.

So they know exactly what to turn on to fix the problem. So yeah, so then that's the power of these fasting-making diets. So turning on the ability of the body to fix itself. And so now, diabetes, we're seeing it. We're seeing now with kidney disease, we are now seeing it with, I mean, at least this is in humans and animals, but for some other like gut,

we are clearly seeing it in animal studies. And now there are many, a number of trials that will test that in clinical trials. What is your understanding of the, you know, kind of mechanistic landscape here? How much of this can be attributed simply to caloric restriction? How much to the timing window

and how much to the kind of macro composition of the FMD or whatever kind of fasting diet that one is on? The eating window, none, because we don't use eating window in the FMD diet so people can eat for 18 hours a day if they want to. So that's in that case, I'm not saying that that's not beneficial as we discussed earlier, but not in this case.

Calor restriction, probably none, because per month in mice, rats, and probably people, they eat about the same amount. So they overeat anything they didn't eat during the FMD five days, right? So they have 25, 26 days to even overeat a little bit. And this is what we see very clearly in animal models that per month, rats, they receive the fasting-making diet, eat the same level of calories as the control, as the controlled diet.

Yeah, so I think it's mostly signaling, some of it seems to be stem cell activation. So for example, in the blood, we see an increase in what's called LTHS, hematopoietic stem cells. So in the blood, it seems to be stem cell driven. In lots of other organs, the gut, the kidney, and some other tissues, it seems to be reprogramming, right?

Which we just discussed. So I think that on one side is the stem cell reprogramming mechanisms, and on the other side is probably metabolic switches. What does that mean? It means that people and all kinds of organisms, they can be in a fat storing mode or energy storing mode or in an energy burning mode.

So if it's summer and you have plenty of food, you have excess food, you wanna put it away, right? And if it's winter and you don't have any food or food that is scarce, then you will start using those reserves. That's the other big effect of the fasting-making diet is unlocking that. But very importantly,

and I don't remember if we talked about it before, without getting the organism into a thrifty mode, right? So, because if you go long enough, now we know from calorie restriction studies and lots of human studies that eventually, if you starve or restrict the system of a human body for long enough, it'll go into a energy saving mode. And so you wanna trigger this metabolic switch

from the fat storage to the fat burning, but don't get into the thrifty mode, which now is gonna try to save anything that it can. So lower energy expenditure and save it because the system is worried about running out of fuel. Right, so it's very tricky, right? And this is why the five days of the fasting vegan diet and then go back because,

and that's why also eating is probably important, right? So you're eating, but you're restricting for five days. And the message is, okay, get out of the energy saving mode, burn the fat and we see the ketone bodies go up and the fat burning clearly going up, but don't enter this energy saving mode because we're okay, we're not gonna starve. Right, so from a lay person's perspective,

that would mean an emergency state in which the body is essentially saying, like slow the metabolism down, like we gotta conserve everything because we don't know when we're gonna get our next meal and everything kind of goes into low power mode. Yes, and then low power mode could last years, right? This is why sometimes you hear people saying,

I don't know what happened, I'm not eating anything and I cannot lose weight, right? And this is a big problem, right? And this is what people understand, the devil is in the detail. If you get into that, it could be epigenetically regulated. What does it mean? It means that the DNA can get modified

to impose this thrifty mode, right? Impose that energy expenditure should be the lowest, as low as possible, because that's my biggest problem, that you're gonna starve to death. And so for a couple of years, I'll keep you in this energy saving mode, and then we'll see if things are consistently better,

maybe I'll get you out of it, right? So yeah, so I think that a lot of that is happening, and very few clinics that are dealing with people that are overweight and obese understand this. And so without this understanding and intervening is very difficult to get the person out of this potentially epigenetic luck that makes them just hungry all the time

and with low energy expenditure. So making it impossible. Yeah, I think that's a sort of common but under discussed thing that happens with people who are sort of chronically overweight and they've gone on a lot of extreme diets over the years and restricted their eating, et cetera, and are in that state where now they'll say,

like, it doesn't matter what I do, I can't lose weight, it doesn't matter how much I exercise and I'm doing all the right things. And I'm kind of in this place where I just, you know, maintain the same overweight status forever. My energy levels are low, et cetera, all of that. So for somebody who is experiencing that, or is listening to this and is relating to that,

what is that long road out of that? Like, how do they, you know, where should they kind of direct their attention to, you know, claw out of that hole? Yeah, so, I mean, so the Cure Cures Foundation that I started has dieticians that are specialized in this. It's a nonprofit that's here in Los Angeles, but they can follow anybody anywhere.

We usually apply four things. We apply the longevity diet, it's pescetarian, low protein, mostly plant-based diet, the fasting-making diet and the 12-hour time rest of the eating and then the exercise, right? And this, a combination of this, and some people say, I don't wanna do the fasting-making diet.

And some people say, I don't wanna do the longevity diet. But most people say, okay, I can do three out of four or two out of four. And I would say that it takes about one to two years to get somebody back to where they need to be and just comfortable with this new diet. And a lot of times we try to minimize the changes, right? We really focus on not giving you,

here's a diet that you should have. It's more, well, what is your diet? And what are the problems that you should have. It's more, what is your diet? And what are the problems that you have? Can we change this? And can we minimize the changes that you have as long as you think you can keep them for the rest of your life, right? So that's really the important thing because,

and I'm sure we discussed it before, if you start doing this yo-yo, then you're in trouble, right? Then it's worse than having done anything at all, right? So it's better to just keep the weight and keep the problems, right? Rather than lose it and regain it. That's what the great majority of people do, yeah. ["Go Brewing!" theme music plays.]

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including strength, yoga, Pilates, and mindfulness. So stop stalling your progress. With NordaTrack and iFit, just press start and let the trainers and tech do the rest. Head on over to nordictrack.com slash richroll to experience personalized fitness. It's one thing to talk about fasting in the context of weight loss. I mean, let's be honest, that's probably what gets most people interested in this world

to begin with. Another thing to talk about it in the context of chronic lifestyle disease prevention, but certainly if it helps you to lose weight, then you're at a lower risk for being afflicted by many of those diseases. And then another thing altogether to talk about disease reversal, which you already sort of touched on. What was the lightning bolt moment for you

where you began to see like, oh my Lord, like this actually has an impact on reversing conditions that people have, like serious conditions? Well, of course we'd be working on cancer for a long time, but as far as multi-system regeneration, I think the first one was our work on chemotherapy and the immune system, right? And the blood and the immune system.

So, you know, the mice would get chemotherapy and there would be dramatic or drastic negative effects, of course, on the immune system and the white blood cells and they will come down and stay down. And this is a problem that a lot of cancer patients have, right? It's all, then we started doing the fasting making diacycle or the fasting cycle.

Back then we were not, it was more than 10 years ago. We were not even working with the FMD. We were working with just water only fasting in mice. And we saw that the stem cell, we saw the white blood cells, so that the immune cells will come back up only in the mice that were giving chemotherapy plus fasting cycles, right?

And so we say this, how is it possible? They come down, so the fasting was not protecting the lowering of the white blood cells. It was just making them come back up to normal within a couple of months. And so it turned out to be, it was stem cells. So the FMD cycles were turning on the bone marrow stem cells and the bone marrow stem cells,

it took a couple of months to regenerate healthy white blood cells and repopulate the normal immune system, right? So really remarkable effect. And then we had a follow-up paper with the pancreas where we completely damaged the pancreas in animals, so completely blocked insulin production by the pancreas permanently.

And then we started the FMD cycles. And then you see that again, this two Yamanaka factors being turned on in the pancreatic cells, in the beta cells of the pancreas. And then after a couple of weeks, insulin will get back to normal. And so this was showing that the pancreas can fix itself and can go back to normal insulin production.

So essentially treating type one diabetes. And so those are the two papers that I think one stem cells and the other one reprogramming in a very sophisticated way. So I'm always entertained by the sort of pharmaceutical point of view that drugs are sophisticated and what nutrition possibly do, right? And instead, I think you see evidence for nutrition

starting something that is so sophisticated and it's so old, right? It's billions of years old and has evolved for the process of, for the purpose of fixing lots of things in a way that it would be unimaginable with any cocktail or drugs or intervention that you could think of for now, right?

Maybe 20, 30 years from now, we'll have artificial intelligence driven repair systems and it'll be another world. But I think that it's gonna be hard for a while to beat that extremely sophisticated, three billion year old system that has the job of identifying a problem and coming up with a solution.

Yeah, it's been designed through evolution over so many years to work in a way that the blunt instrumentation of pharmaceuticals can't, like they're directed at one thing very bluntly, and then there's all sorts of downstream implications and side effects from that, that you don't see with the nutrition intervention, right? Well, you can see it with the nutrition intervention

if you misapply, right? If you don, you can see it with the nutrition intervention if you miss apply, right? If you don't understand mechanisms, you could cause problems, right? It's very powerful. And so if you don't understand how it works, then you can do a lot of damage. I'll give you an example. There was a paper recently.

So for the longest time, we've been saying, if you give chemotherapy to a mouse or a person, don't re-feed the mouse or the person while the chemotherapy is still high in the system, right? Because the refeeding means the growth factors go way up and now you have a very quick proliferation of cells while there's a lot of chemotherapy in the system, right? And so a year ago, somebody published an intermittent fasting

like I think it was was alternate day fasting showing that the opposite of what we have shown for long-term fasting by using, you know, everyday fasting. So they give chemotherapy and then they cycled normal food fasting, normal foods fasting. So now you have high levels of chemotherapy together with the refeeding.

It's a very bad combination, right? And as we had predicted, the cardio toxicity's a very bad combination, right? And as we had predicted, the cardio toxicity went up instead of down, right? So the two different methods of fasting, one causes really remarkable protection of the heart, the other one causes remarkable damage to the heart, and both of them are called fasting. So this is why it's very important to standardize it,

make food as medicine, test it very carefully, understand the mechanism. And then, and only then it would beat, I think, lots of drug-based approaches. Some of the remarkable study results come from rats and mice. You talked about the kidney and the pancreas, et cetera. How much of that can we sort of extrapolate to apply to humans?

Obviously you can't study humans in the same way. Like I'm always confused about, you know, how much we can read into these animal studies in terms of their applicability to human biology. I think that, I mean, of course, so we're running trials, right? We, I mean, lots of universities and a lot of these trials are independent of us,

meaning we just help them do the trial. But so a lot of them have been demonstrated now in the clinic, like diabetes type two, and there are a number of papers, clinical papers on cancer. And so most likely the mechanisms are similar, right? So we've shown in mice, we've shown in rats, and now we've seen the effects on our human disease,

likely it's the same mechanism, but we don't know, right? So for example, the paper we just published on kidney damage in the rat and mouse and mice and rats. So very powerful, the FMD cycles in fixing the damage. But then in people, it was a small trial, but it was six patients and then seven patients in is called a randomized crossover trial, right? So first six patient and then we had control diet.

And then the control diet group goes into the FMD, right? And in both cases, remarkable effect on what's called proteinuria. So the protein in the urine is evidence of kidney damage, right? So, and not only the proteinuria was reduced right after three fasting immune diacyclics in the kidney disease patients,

but a year later, and the great majority of them still maintain that benefit. And interestingly, when we look at these mesenchymal stem cells in the blood, kidney mesenchymal stem cells, so they're like progenitor cells for kidney regeneration, they tripled in the blood of patients. So we don't know, right?

Is it, are they being released to go to the kidneys? Are they being released in the bloodstream to go to the kidney and fix the problem? Or are they increasing the kidney and leaked in the blood? But it's really remarkable because you see a threefold increase in these progenitor cells that are clearly mostly used to repair kidney damage or generate kidney tissue, right?

So yeah, so in a lot of the trials, we see something very much consistent with what we see in the animal work. And of course, proving it, it's more, much more complicated, but in some cases we may not need to prove it, right? So right now, do we need to prove, you know, the effect of the FMD and reversing diabetes? It'd be nice in humans, so we know how it works in mice.

Do we need to prove the mechanism in humans? No, we just need to prove that it works. It is feasible. And, but yes, it will be nice eventually to show that, for example, Harvard is interested in looking at pancreatic in the type two patients, looking at whether beta cell regeneration process that we've shown in mice is also occurring in the patient

and the type two diabetes patients that are receiving fast and making type cycles. So there are ways I think to look into is reprogramming stem cell based regeneration, et cetera, happening in people. It just takes a lot longer. What is the receptivity in the traditional medical community amongst general practitioners or nutritionists

and dieticians with respect to the work that you do, fasting in general, the fasting mimicking diet, because when you, you know, we could talk about longevity all day long and, you know, are we going to live to 120? But meanwhile, something like between 30 and 40% of Americans are suffering from type 2 diabetes or are pre-diabetic, obesity rates are through the roof,

childhood obesity rates are through the roof, heart disease is our number one. This is what's killing people, right? And this is kind of where everybody should be focused in terms of constructing a lifestyle to avoid these chronic lifestyle ailments. And your work and everything you talk about in your books, et cetera,

seems to say pretty clearly and loudly like that this is a way out of that, kind of death sentence that visits, millions of people unnecessarily every year. Yeah, and I think the two things are very much connected, right? So if you look at the major risk factors for diabetes, cancer, Alzheimer,

and cardiovascular disease is aging, right? So if you just wanna intervene on one thing, it's better to intervene on aging than intervene on obesity, right? So if you just wanna intervene on one thing, it's better to intervene on aging than intervene on obesity, right? So even obesity compare is dwarfed by the effects of 30 years of aging on any of these diseases, right? Meaning it's very small effect. Of course it's got a big effect.

So, but it's very small compared to age, at least 30 years of age, right? So let's say that you could make people 30 years younger, that'd be the best way to go, right? Just make them younger and they can even be overweight, right? But of course, the best way to go would be to do both, right? And this is what the fasting making diet, the longevity diet do.

And by the way, unlike what we see with the GLP-1 agonist, so far, when we don't use drugs, we don't see lean body mass loss. It's very clear trial after trial after trial, no lean body mass loss. We just don't see the bad thus far, right? Of course, yeah, you could say, when you have millions of people,

maybe we'll start seeing some bad, but it's a very coordinated, it's very different, right? Than blocking an agonist, a GLP-1 receptor agonist. This is very coordinated response. And so there is not really a theoretical reason why there should be problems, right? And again, we don't see, in fact, in mice, we see bone density increase compared to the control.

So if you think mice middle-aged and we give them the FMD all lifelong, and we look at bone density, it's higher than in the controls, right? So that means that maybe there is even, you know, bone regenerative, we don't know. I mean, I'm not claiming that there is, but there may be. But certainly in both mice and humans,

we don't see muscle loss after even many cycles. And in fact, we did the trial with women with breast cancer and even after many cycles of the FMD, if they had a good, healthy Mediterranean diet in between, they actually increased lean body mass, right? The muscle absolute weight increased and also the muscle function was increased. So this is, you know, by a,

what's called impedance geometry method. So we don't know, you know, that part, we don't know how carefully was measured, but certainly in general, there seemed to be protection of muscle mass in these women, even after many cycles of the fasting-migraine diet. So that's very important to get the reverse, the adipocities, so the fat storage,

probably reduce the inflammation. And we clearly see these anti-inflammatory effects of the fasting and making diet, go after the aging process. So for example, IGF-1 and all this aging markers are reduced and they're reduced long-term. You don't just see the insulin like factor one being reduced temporarily and then go back up.

Laptin and IGF-1, they are reduced long-term. And this is shown many trials, right? So yeah, so it's going after the adiposity, it's going after the aging acceleration or their aging rate and it's doing so because it's guided, right? And we developed a lot of this with that, those problems in mind,

it's not affecting the healthy tissues, including bone and muscle. Is there a use case for somebody who is severely obese to go on a GLP-1 and during that period of time, adopt the FMD until it becomes rote? Like it becomes like easy to do that. They're not, you know, kind of, they don't have the hunger pangs

that they normally would have. And because, you know, your house is on fire, you gotta put the fire out before you can do anything else, right? Like to take a person through that for however many months and then wean them off of it and then kind of monitor their adherence on a longevity diet.

Like in your mind, is that like a good way to go? Like if somebody is really like in a, like a really acute unhealthy state. Yeah, no, in my mind, that's option B, right? In my mind, option A, and I hope that, eventually the government will also understand that we need professionals that are specialized in nutrition and they know what to do

and they know how to do this carefully. And, you know, this probably involve molecular biologists, physicians and dieticians, right? That team and maybe psychologist, right? None of this is reimbursed, or just the doctor part is reimbursed, but even the doctor part, not clear that it's reimbursed

for giving nutritional and lifestyle advices, right? So I would say, you know, that would be the way that should be done, the way we do it at the CREQEURs Foundation is take your time, take a couple of years, and, you know, take the patient by the hand and say, okay, we're gonna get there, don't worry about it. We'll address the hunger, we'll address all of it, right?

It's a 360 approach and we'll get you there. There's no hurry, we'll get you there. In the absence of this, yes. So there is, for example, a physician in Dr. Bakker in Brazil who's been doing exactly what she just said. So she gives Lira Glutide, which is a short, it's a GLP-1 agonist that less than the new versions.

And so she combines the fast imidium indide with the Lira Glutide, and then eventually she gets the patient off liraglutide and keeps them on the, and yeah. So the hunger is, was her main problem. And she said, well, I just have an easier time with the patient by combining, because then at some point the patient say, okay, I don't need the drug anymore, I'm good.

And I can see the effects of the FMD. And I'm just, then I continue with the FMD. And the lyrical glutide is like a lower dose or less intense version of Ozempic or Cymric glutide. It's a shorter lasting Sunday that I think you have to give every day to the patient. So the health life is much shorter. It means that there is also less concerns

because of course these GLP-1 agonists are causing insulin production, right? And the fasting-migraine diet cause insulin sensitization. So it means that it makes insulin work better. So now if you increase the insulin on one side and you make insulin work better, a lot better on the other side, you could have a problem because now you could get the blood sugar level very low,

right, very quickly. And so, yeah, that's why continuous glucose monitor would be a very good idea. And a physician that really paying attention because for example, we've done a trial on type one diabetes in children in Italy. This was the first use of the FMD in children. And we were very concerned about justice, right?

Insulin injection and FMD. And the fact that maybe the nurses would not expect that the child all of a sudden with the same level of insulin would be much more responsive in controlling glucose. And so we saw problems, you know, luckily we were prepared and everybody was wearing continuous glucose monitors, but we caught it on time.

But we had some issues, even though I was very paranoid at the beginning, but they were not taking me very seriously. It's like, ah, don't worry about it. We do this all the time. And, but sure enough, we ended up in that situation at least with one child. And so, yeah, so that was a very, very good to think of the worst, right?

Think of the worst. When you're combining drugs and fasting, this is why option A, I like it much more because we don't see muscle loss. And it's also, I just wrote an article on this, is that we are more and more underestimating the importance of the effort, right? So the effort of doing it, like you did it, it's hard.

I understand you can maybe do it on your own, but you got the professionals around you, they're helping you put the effort in. And- People don't wanna hear that, Walter. Yeah, no, I understand that. But people have to hear that because, in the article I talked about exercise

and now in the 50s, nobody exercise. And then I forget the doctor came around and said, people should exercise every day and people didn't know what that was. What is that? And I remember I read some of these interviews in the 60s and people were like, oh, people are gonna die if they're gonna exercise this much every day.

And then eventually the health of the world, hey, that's tough, right? That's much tougher than what I'm talking about to have to exercise regularly, right? But people do it. So I think that that's really the solution. Also mentally, psychologically, in that article that I wrote, I said,

of course you cannot tell everybody do 50 miles a week of exercise or running, right? Nobody's gonna do it. But if you make it reasonable, let's say 150 minutes, and that's what people do now, but if you make it reasonable, let's say 150 minutes, and that's what people do now, right? In Europe and the United States, 150 minutes a week, a lot of people do it. It's not easy, but people manage,

and I think it makes them happier, right? Then when they exercise, so. Yeah, I think it's a broader conversation around our relationship with discomfort, right? And you know, all good things are on the other side of the, you know, kind of uncomfortable things that you're avoiding, whether it's food, nutrition, exercise, or any other goal that you set for yourself. But the byproduct of kind of grappling with that is well beyond like achieving the goal

that you set for yourself because you've made this investment in yourself. You did the hard thing, you feel good about yourself and suddenly you're more emotionally connected with your own wellbeing. And that spills over into like, not just your external outlook on the world and your own life, but like how you think about the decisions that you make, food, exercise, et cetera.

But, you know, the people you surround yourself with everything. And all of those things are fundamental to wellbeing. Yeah, but I agree with you. Let's say 50, maybe 60% of the population is not gonna accept that shorter, right? I think for exercise, it took decades for the US and then the world, because this followed all over the world, right?

It was, I think, an American idea. It took decades, maybe 20 or 30 years to have a significant portion of the population actually saying, I'm gonna go jogging. I'm gonna go and take a bike and do 50K. So yeah, so I think that, you know, before that happens, yes, we need to have methods that are maybe including drugs for some, for a percentage, but certainly methods like, you know, the FMD. And that's what I was saying earlier, we were testing it in Southern Italy,

one of the worst areas of the, one of the worst or the worst in Europe, right? Yeah, we think of Italy as sort of this, you know, giant blue zone, but it's not really that. Not at all. I mean, if you look at Calabria and Campania. Yeah, so Calabria and Campania have surpassed the United States as far as overweight portion in children, right?

So it's a big problem. And so the way we addressed it was, what about if we give an FMD for five days every three months and everybody thought it's crazy, it never gonna work. We haven't published it yet, but let's say that it's looking good so far, right? So, yeah, so now it gets down to very little, right? The five days, every 90 days that you have to dedicate

to this program in a box, essentially, a medicine in a box. Yeah. Since we last spoke, I would say that there's been an explosion in interest in health span extension, longevity medicine, you know, this field in which you've invested your career and have been in for many, many years, a lot of energy right now.

And everybody has their own kind of specific lane, whether it's AI technology, sort of the sophistication of scanning equipment, like all of these developments that are making healthspan extension more and more plausible. And I think among this group of people you share, there's many things, principles, ideas that you share in common.

There are differences as well. And I think one of the key ones with respect to diet is this emphasis on protein. So somebody like, you know, Peter Atiyah, Rhonda Patrick, they're always pushing protein, talking about the importance of protein, particularly, you know, after a certain age, certainly after age 65,

when you really need to be eating more protein than you might think to maintain your muscle mass. And, you know, the kind of critical role that muscle mass plays in terms of how you're aging up. Your fasting mimicking diet and much of what you speak about kind of goes you're aging up. Your fasting mimicking diet and much of what you speak about kind of goes in the other direction. Maybe it's different when you reach a certain age,

but at least on the FMD, this is a pretty low protein protocol and it's not entirely vegan. It can be entirely vegan or pescetarian. Oh, it's entirely vegan. What's that? Entirely vegan, right. I mean, I've heard you talk about fish, two or three times a week.

No, but that's the way they die, right? On the longevity diet, right. So maybe kind of state your case or your perspective on this controversial macronutrient. Yeah, so first let's take out the FMD, the fasting-making diet, because it's just five days. Sure, longevity diet, sorry. Three times a year, and so it's completely irrelevant.

So sometimes I've heard that argument that maybe Peter made it, but I don't understand it, because we're saying, you know, this is 15 days in a year. So even if you go zero protein, it will have no effect whatsoever on your muscle, right? No effect, and we've shown this clinically in 10 different trials. In fact, in a new trial, we're actually showing increasing muscle mass

after six cycles of the fasting making diet, right? And even not just relative, but absolute lean body mass, right? So that's clinically demonstrated to be false. If anybody's saying the FMD is causing reduction of muscle mass, it's the opposite, right? So far it's the opposite. The only time we see some lean body mass loss

is in combination, in the diabetes trials, in combination with drugs. That's the only time so far we've seen lean body mass loss. Then the longevity diet is very different. What about every day? So yeah, so I think that it is a big problem when we are using like a one or two pillar system to look at things, right?

So let's say epidemiology, a lot of people love to use epidemiology. Studies of big population, but even if you look at epidemiology, we've done that. And we've done that, you know, in a study published in JAMA with Harvard, we've done it in our own study. It's pretty clear that you don't need a lot of proteins, right? And it's pretty clear from many, many studies that the people that do the best are mostly

vegan, low by sufficient proteins. And then in our own paper, and we were the first one publishing on that, the 65 was the switch moment, right? So 65, we did not see, so people reporting a low protein diet, whether it was overall mortality or was cancer mortality, people that are reporting a low protein

or a very low protein diet did the best up to age 65 and then did not do so well after 60. So if an 80 year old said, I have a very low protein diet, it did not do very well either for cancer or for overall mortality. So, and then the Harvard study with Giovanucci in the JAMA paper, I think that he showed or we showed, because I was a coder, that plant-based protein, high animal protein was not good, but high plant-based

protein was associated with improvements, right? And that's where the devil in the detail comes in, because there can be such a big difference, as I mentioned earlier, in amino acid levels, in the plant-based proteins versus the animal-based protein that it's not even clear what the meaning of protein is anymore, meaning that it's irrelevant because it's really about 20 amino acids, right?

So we should be talking about amino acid level and amino acid patterns. And that probably explains. So meaning that probably it's very clear that a low but sufficient amino acid intake is what you want up to a certain age. And by the way, the age should be biological age. It should not be chronological.

So it could be 65 to somebody, but it could be 45 to somebody else and 72 to somebody else. So at some point, and you see the population wait, instead of going up, it comes down, right? That's the point where we see this switch in mortality prediction. Yeah, so then it's about amino acids.

And again, epidemiology is one pillar, but then you have clinical studies, you have basic research. So how do you make a mouse live longer? Well, over and over and over and over for almost 50 years, low protein, low methionine diet, right? Just, you know, in rats, in mice, and no matter who did it.

And so, yeah, so then that's like another pillar. And then the centenarians, whether you look at Okinawa had a 9% protein diet, right? And for the longest time, had record longevity. So I would encourage my colleagues to, you know, just expand from one pillar science to, you know, five pillar and the 50 is complex system. But let's say, even if you just go for four pillars, and if you go for four pillars,

you see the devil is in the detail. It's about amino acids and it's about having sufficient and protecting immune system, protect the muscle, protect the bones, but reduce as much as possible the aging rate, because again, what dominates is aging. So that if you can make somebody younger, they will live longer, they will be much healthier. And again, there is a 10 to 30 fold difference between obesity and aging and 30 years of aging as a risk factor for Alzheimer, cancer, cardiovascular disease, diabetes, et cetera.

So yeah, it's about aging. The proteins are driving the growth factor, which are clearly at the center of the aging process in all organisms. And this is why our work with the Ecuadorians come in. So the Ecuadorians have growth hormone receptor deficiency, and that's the protein pathway, right? So either mice, mice that have a growth hormone receptor

or growth hormone deficiency are the ones that live the longest, live 40% longer with the lowest disease profile, right? This has been known John Kopchick, Andrej Barki work for decades. Now, surprisingly in yeast, the 10-fold lifespan extension comes from the protein pathway, mostly from the protein pathway.

So you block the protein pathway and the yeast now are reprogrammed to live 10 times longer. And then our work in Ecuador with people, sure enough, people that have growth hormone receptor deficiency are protected in spite of a terrible diet, are protected from diabetes,

they're protected from cancer, they're protected from cancer, they're protected from cognitive decline, they seem to have, and we brought them to LA to do a functional MRI test on their brain, they had the function of a much younger person, cognitively, and now we just published on a neutral to positive effect on cardiovascular disease, which really surprised us that the plaques were lower or much lower in the pathway

that response to protein intake is blocked, right? The most damning part is the Harvard study showing a 40% increase in three different studies. In this, Frank Kuh's work, three different studies, 40% increase in the diabetes risk in subjects eating high protein diet, right? Compared to the lowest, I think it was quintiles, the lowest quintile versus the highest quintile.

Those that were in the highest quintile protein intake in three different studies, almost identical results, right? So, yeah, so I think that it's really hard to imagine how you could conclude from all of these studies. And we were talking about hundreds and hundreds of studies that a high protein diet is good for you. I mean, it should be sufficient and was sufficient plus muscle training, right?

That's very important. And a lot of studies indicate that the protein intake you need per meal is very low. It's around 30 grams per training session, right? If you have 30 grams of good quality protein with enough leucine and that stimulates tore activation, you're gonna get maximized effects on muscle building.

And that's probably, I mean, and you could do, say, even if you did it twice a day, you still be in 60 grams, you still be in a relatively normal to low protein diet. But beyond that is not to your benefit for reasons related to growth factor. I would presume that that would be offset for somebody who is extremely active weightless, regardless of age, if they're like in the gym and do like the negative implications of a higher protein diet would be abated

by that very active person. Yeah. Not necessarily. No. Not necessarily, no. No, not necessarily, no, because the growth factor, it could accelerate or is known to accelerate the aging process independently. So your active lifestyle could certainly help you in other ways live longer, but you're still,

if you're accelerating your aging, your pro-aging pathways, that still can cause damage, right? That is still driving a faster aging rate in all your organs. Yeah, and then the exercise helps and maybe they could cancel out, but that's not what you want, right? You wanna maximize, reduce the aging rate

and while increasing the functionality. So we're about to publish a couple of papers on that in mice but also in using the Harvard databases. And so, yeah, I cannot discuss it, but certainly it's very consistent what I'm saying, right? The data is that, first know, first of all, you need to really understand mechanism, how is each amino acid affecting which genes,

which are affecting what processes. For example, we talk about stem cells and we talk about reprogramming, we see protein as the major blocker of the Botadose, right? Stem cell activation or self renewal and reprogramming the Yamanaka factor, the reprogramming factor. It seems like if you wanna stop that process,

high protein and it makes sense, right? And does it matter if it's animal versus plant? Yes, because it's about amino acids. That's why I think eventually, I think very soon we should begin to move away from even using the word protein intake because it's completely irrelevant, right? Because if it was a 20, 30% difference between, let's say legumes and red meat, you can say, okay,

23%, I mean legumes and let's say soy, right? Or legume and seeds, seeds and nuts, right? So seeds and nuts, the amino acid profile between a seed protein and not protein and a legume is huge, right? Then it's even bigger if you got red meat or even white meat, right? And sometimes it's up to 10 fold.

So that's when it's irrelevant because you could have a hundred grams of protein which are providing 10% or 20% of that amino acid. And that amino acid may be the one that is making the big difference. Yeah, I understand. And it's complicated. It's always more complicated

than you think it's gonna be, right? Yeah. But it doesn't, it's not complicated in terms of are you implement, right? So if you have a mostly plant-based diet, you just need to, and this is what I preach, let's say that you're a vegan, then you should mix about a third, a third, a third plant,

I mean legumes, seed and nuts, right? If you have that, then you're good to go, right? So, you know, practically it's very simple, right? But if you only have legumes and you have already, so if you have a low protein intake, and then it's all legumes, you're gonna have a problem. Because you're missing essential amino acids. It's so low.

Because you're focusing on one thing. Yeah, I mean, I think people, when I said complicated, I meant like, you know, the sort of physiological pathways and the science of it. I mean, the practicalities of it, as somebody who's been plant-based, I've been plant-based for a very long time. Like people think that it's this complicated,

time-consuming thing. But if you're just kind of grazing on a wide variety of plant foods, it really takes care of itself. Like evolution has sort of figured it out. Like I've just never really had a problem with this and have been confused by people who seem to kind of obsess on protein intake. Like it's just, it's never really been an issue for me.

Right, right. But some people, let's say, you know, the Okinawans, you know, historically and the Southern Italians, and maybe this is why they were so long lived, right? But they were very frail. That's interesting, right? So if you look at Southern Italians, and maybe this is why they were so long lived, right? But they were very frail, that's interesting, right? So if you look at Southern Italy, the same regions that have record longevity because they used to have mostly legume diets, you know?

Yeah, the seeds and the nuts were there, but not in the type of quantities that, so the legumes were very much available and the rest of it was maybe less available. And not surprisingly, you see a frailty level that is almost twice as high as central and Northern Europe, right? So a lot of the Mediterranean countries are very frail,

long lived, but frail. So I think that, in your case, you probably had, the muscle training and all of that and enough variety, but to a lot of people, it could become a problem, right? So if you say five times a week, your proteins are all coming from legumes, then they might not be so easy to, if it's low protein and mostly from legumes,

then it might be difficult to keep the muscle mass. Yeah. Yeah. Yeah. Yeah. Yeah. Yeah. Yeah.

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You know, one of the things that I've learned over the years about therapy is that it's not all about crisis management or just about facing and working through your shortcomings. It is that of course. It's helped me through all of my darkest, lowest and most desperate moments. But therapy actually really shines

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And his blueprint protocol? Yeah. I mean, I don't know the blueprint protocol. I know the hundred supplements and all that. Lots of supplements, basically putting a lot of time and resources and energy into trying to crack wide open this anti-aging equation. But part of it entails his diet, which is a entirely plant-based diet,

limited to 2,250 calories, I think, something like that. It's very dialed in. His last meal of the day is at 11 a.m. So this is a fasting protocol. I think he goes to bed around 8.30 or nine at night. He eats within, I don't know, 30 minutes of waking up in the morning, probably around 6 a.m. or something like that.

And I think he has three meals throughout the day, small meals. Have you looked at this? Do you have thoughts on kind of what he's doing here? Yeah. All his biomarkers seem to be fantastic. Yeah, yeah. Well, the short-term effects

may be completely irrelevant compared to the long-term effects, right? So a good example is, let's say the breakfast keepers, right? The breakfast keepers, if you look at short-term, they may be actually very beneficial, right? And people argue that the breakfast keeper have a worse lifestyle and all that, but let's say that new clinical data suggests

that it's not just that, it's not that, right? If you start eating later, you're gonna have problems, but it may be difficult to see what's gonna happen 20 years later, right? And you're gonna get surprised. And the ketogenic diet, it could be years later, right? And you're gonna get surprised. And the ketogenic diet, it could be another example, right? So if you look at the ketogenic diet, very beneficial, very, it makes you impressive results.

But in the long run, people on a low carb diet, and there's lots of Harvard studies, they live shorter or much shorter, much higher mortality, especially if it's low carb, mostly animal-based diet, right? So yeah, so I would say that when you enter a lot of territories, the 100 supplements and eating within three hour window,

each one of them is a gamble, is a big gamble, right? And then you should put four or five together, now it's a very bad gamble, it is a big gamble, right? And then if you put four or five together, now it's a very bad gamble, right? So you're exiting the territory of the five pillars in multiple ways, right? So the centenarians eat in four hours and no, is there any data from mice? Yes, there is some data from mice that show that

that's beneficial or potentially eating within a smaller window is beneficial. So you have mixed data in lots of things that he's doing, but a lot of it, I think is gonna be negative, right? So it's gonna be, or not done before, right? So could it be positive? Yes, but it could also be negative or very negative. And so the surprise could come after 25 years

and it could be a big surprise, right? It could be a big surprise. And now that is causing a big problem. If people don't realize you just need, like for example, ketogenic diet. Well, everybody talks about the ketogenic diet and cancer as a positive thing. And it can be, right?

And there's a lot of animal studies now, some clinical trials that are suggesting, this is also in my book, that are suggesting that the ketogenic diet can be beneficial. But people don't talk about the cancers that are fed by ketone bodies, right? There's some cancers that grow much faster.

And there's some cancers whose incidence goes up 10 fold in people that have a high ketone body level, right? So yeah, so then very healthy short term, not so healthy for lifespan, and now associated with a much higher level of certain cancers, right? So this could be the surprise, right? Now all of a sudden, whatever you're doing

that is not, you is not within the domains of what's been tested for a hundred years. And all you need is one of, let's say a hundred supplements or even already 10 supplements. People don't realize, I just looked it up the other day. And in Italy, drugs, just in Italy, drugs kill about 40,000 people every year. Drugs, right?

Drug-drug interaction. Not like recreational drugs you see. No, no, no. Prescribed drug. Prescription drugs. Prescription drugs. It's 40,000 people a year. And in the US, it's a huge number.

I don't remember. I just looked up the Italian number for some reason and not the US, but it's a huge number, right? So you combine lots of drugs. They start interacting in ways that you cannot predict. And so now if you take 10 supplements, 20 supplements, 30 supplements, the higher the number, the more certainty, almost certainty

that it's gonna cause a problem. It might take one year, five years, 10 years, but sooner or later, that's gonna cause a problem. For every additional supplement that you add into your routine, the complexity of how all of these things are interacting with each other, kind of increases exponentially, basically, is what you're saying.

Even AI. And we don't know. Even AI wouldn't be able to handle it for at least 20 or 30 years. That's so complex that you would need 20 or 30 years of data fed into AI to say, okay, this now the only AI understands that maybe that's gonna cause a problem. But yeah, so right now we're very far away

we've been able to handle because you need big data, right? So you need- How is the selenium that you're taking interacting with kind of the mega dosing of vitamin D for example, or something like that. Yeah. And because then the two are gonna change the host metabolism or the host response.

And now the new host response, so it's not just how the two interact, is how the two change the body, and now the two plus the body change affect the third one that you're gonna add, right? And our react. So now all of a sudden, let's say your ferritin goes up, right?

And now if you have a high ferritin and now you add some other supplement, now you have a recipe for disaster, maybe iron overload, because now you just have added the third supplement that is making the ferritin work less well, for example. I see. You know, if you were counsel to Brian Johnson, you know, what would your advice be?

I mean, I know I'm setting you up a little bit because you would have to know everything that he's doing, but kind of from a bird's eye view, general principle perspective. Well, I mean, of course, I mean, the only thing that I will add to all the things that we discussed before, so time-restricted eating, the fasting-making diet, the longevity diet,

I will add personalization, right? So you will wanna know everything about him and personalize all of it to him. I think he would say that he probably has that dialed in. Like, I think he experimented with lots of different eating stuff with a big team of people who are weighing in and taking his blood markers like every day. If that wasn't the case,

he wouldn't be eating in three or four hour window, right? I think he's underestimating the uncertainty of doing something that nobody's ever done before, right? If you just think about the short term effects, and this is the overestimation that nobody's ever done before, right? If you just think about the short-term effects, and this is the overestimation everybody's making, you have diagnostics and you think that because, so I had big experts in the field tell me, I have extremely low fat, like 5% fat.

Well, data suggests that if you have a little bit higher fat levels, you may live longer, right? So short term, you could say, you know, I have 5% fat, I'm gonna live forever. But the data is actually showing that those that live forever may be more in the BMI 25 range, right? Yeah, so then that's this acute response and this idea that, you know, if you have a very low fat,

that makes you very healthy is misguided, right? Because that's not the case if you're trying to get to 110 healthy. And I don't mean just 110 frail, like the Southern Italians or maybe the ocean ones, I mean 110 healthy. So then, you know, you have to have the five pillars or more than five pillars.

And those speak very, very clearly, right? And so then on top of the five pillars, then you need the diagnostics, right? Then you need to say, okay, I'm using the five pillars. I came up with all these things and now my cholesterol is still very high, right? Well, okay, that's not enough then. We need to intervene and make sure

that cholesterol goes back to normal. And so, yeah, so I would say that, again, if you look at the longevity records, it comes from mutations that do lots of weird things like growth hormone receptor knockout, right? It make mice and people very short, right? So it's very counterintuitive, let's say, because a lot of people inject themselves

with testosterone or growth hormone to live longer. And yet clearly after a hundred years of research, high growth hormone is making mice and probably people live the shortest. Right. Speaking of people who are short, I came across that CNN article about Lahren syndrome and people who are genetically very small, like four feet and under, who really don't get

lifestyle disease or cancer or heart disease as readily as we do. And I know you've done some work with this community, right? Yeah. So this is what I was just talking about, right? So the growth hormone, the little people that you're referring to have a mutation in the growth hormone receptor, right? So this is why I was saying, people are now a lot, millions of people around the world

are using growth hormone injections to become younger, right? And so if you look at them short term, you probably conclude that they are younger or they're functioning better, let's say, right? And so, but the mouse and the human data suggest exactly the opposite, right? So the little people, it's like, if you inject them with growth hormone,

they'll have absolutely no effect, right? Because the receptors don't. They're missing the receptors. You have the key, but you don't have the keyhole. So worthless key, right? And so those mice and people that have the blockade in the growth hormone pathway are the one that by far are doing the best, right?

By far. I mean, if you look at, you know, mice, there is nothing that even comes close to this growth hormone and growth hormone receptor. And that's nice because it can be that the mice are lacking growth hormone or lacking the growth hormone receptor. Either way, they have record longevity and record health.

And this has been shown, you know, we work with these mice, but lots of laboratories. So there's really no doubt about it, right? So yeah, so that's why this genetics data is so important and it's part of the, you know, I put it in the centenarian, you know, the people that have lived with that change for a hundred years, right? So now we have the data both for the Larones,

but also for the Okinawans and for the centenarians of Southern Italy or Loma Linda. So your research and your latest book, Fasting Cancer, appear to support the thesis that the fasting-mimicking diet in conjunction with traditional treatments for cancer seem to have a beneficial impact in terms of recovery and remission rates in general, right? Within the context of a very complicated field.

I mean, different from diabetes, cancer is really a hundred different diseases, maybe a thousand different treatments. So I would say that in general, especially for those that have advanced stage cancer, let's say stage three, stage four, the ones that are in trouble, a lot of the clinical studies are now showing

that it seems to have a big effect, right? Making the whatever, especially chemotherapy thus far better, right? So, and one of the nicest ones that I mentioned in the book is the triple negative breast cancer, very aggressive, women with metastatic cancer. The fasting-making diet now is nearly doubling overall survival in the first study by Vernieri

and colleagues. And then they just published a follow-up paper, which is not in the book showing either chemotherapy alone, chemotherapy plus fast imidium mucin diet or chemotherapy plus fast imidium mucin diet plus metformin. And again, nearly a doubling compared to the expected survival of what's called PCR, complete pathologic response.

These are just a few trials, but there's lots of them that are indicating that the fasting-making diet is making survival better, making also the pathological response better. So if you look at the masses, the cancer masses after the treatment, they seem to have less active cancer cells. Now, you know, there's also an argument

and this is why we say be careful. As I mentioned earlier, like, you know, if you misuse it let's say you say, oh fasting, all fasting is good. And so I'm going to get a chemo and then I'm going to refeed at the same time that could cause problems and not solution. And the other thing is, you know, fasting mimicking diet is a very powerful effect

on stem cells. And so, you know, we've looked at cancer stem cells and we've shown that in breast cancer it reduces cancer stem cells, but others have indicated that in some cases it could increase cancer stem cells, right? So in the early stages of the disease, right? So we don't know enough about it.

We really haven't seen that, but I would say if it's early stage and the treatment is likely to be very effective, stick with just the treatment and don't try anything else. Maybe the longevity diet, maybe the 12 hour timers to the eating. And this is what we do in the clinics. We say it's early stage and you have a 98% chance

of being cured by it, just leave it alone. Now, it could be that it will have helped you a lot, even in these early stages, but it could be that there's something that we don't know yet. And so I know people think we're paranoid, but I think it's a good way to look at it, and unfortunately a lot of people don't look at it that way. So essentially, it's going to be case dependent, depending upon what type of cancer and how

advanced that cancer is. More advanced cancers and certain types of cancers seem to indicate that traditional therapy, i.e. chemotherapy in conjunction with a fasting mimicking diet seems to have a beneficial effect that outweighs chemotherapy alone. Well, I mean, if you look at the animal studies, right, the effect that outweighs chemotherapy alone?

Well, I mean, if you look at the animal studies, right, then it's just overwhelming with all kinds of cancer, colorectal, lung and breast and name it, right? Then fasting-mimicking diet plus chemo, immunotherapy, hormone therapy, kinase inhibitor, I mean, just phenomenal effects, right? And I mean, turning cancers that are clearly, so we published a paper a few years ago that showing hormone therapy, for example, right?

Hormone therapy, so palbosuclip, full vestrant, this is in mice, right? And we also had the clinical trial, but in mice is very conclusive. You use the standard of care, palbosuclip and full vestrant. And the tumor is the clinical trial, but in mice is very conclusive. You use the standard of care, palbociclib and full vestrant. And the tumor is kept in check, just like it is in people for a while.

And then it starts adapting and it starts growing. You had the fast in making diacycles. And now you see the tumor going in the opposite direction until it goes to zero. So it's just over and over. The animal data is remarkable and really almost surprisingly, and it's not over and over. It says the animal data is remarkable and really almost surprisingly, and it's not just my data,

it's now a lot of labs that are looking at it. It's just remarkable. For example, in mice we published two papers and some Spanish groups have done the same. Immunotherapy in mice does almost, in some of these models for like say breast cancer and even melanoma, that's very little. And the fasting-mimicking diet alone

does more than immunotherapy, right? So I would say the potential is huge in all the different cancers and in all the different stages. But because there is a system and the system should be respected, and we don't know yet, we haven't tested it for a lot of clinically,

we haven't tested mice, we tested it, but not clinically. That needs to be done before somebody. And this is why my comment about definitely, if you're stage four and nothing else is working, yeah, go for it, right? Because the animal data is phenomenal. But if you're stage one and you already know that what's been done for 20 years is working very well,

then I don't think you wanna take a chance, right? Stick with the standard of care and then God forbid, you get to the next level, then yes, then consider it. Yeah, I think that you're very kind of circumspect in the way that you talk about in the way that you just did, you know, throughout the book, like, hey, listen, I'm not like here to tell you like, this is some panacea, right?

Like, here's what we're seeing right now, here's what I'd like to see, here's some research that still needs to get done. I'm not telling you to not, you know, pursue every traditional therapeutic modality there is. I'm just saying, in my lab and in other people's research, this is what we're seeing right now. There's something interesting happening here.

I think it's worth pursuing and investigating more thoroughly. Right, right. But in some cases, the clinical trial, like for triple negative breast cancer, and even for hormone therapy, I mean, for triple negative breast cancer. And even for hormone therapy, I mean, for triple negative breast cancer, you're starting to see randomized trials showing a big difference, right?

From what you expect or from what the control arm has, right? So, and this is in patients. So yeah, for those, I would say, probably talk to your oncologist and say, hey, what about these three or four papers? It's looking good. And how up to speed are the oncologists in this field? Some are up to speed and a lot of them are not, right?

So, and a lot of them are gonna wait for an FDA approval, which may or may not come, right? So, some of these, it's very expensive, hundreds of millions of dollars to get an FDA approval. The FDA looks at fasting-making diet, it's very complicated. So we talked to the FDA to make it feasible or to make it appropriate for the FDA. You probably need to take the 60 ingredients or so

in the fasting-making diet and make it into six or seven, which will make it very difficult to do and very difficult for the patient, right? So, it may or may not end up in FDA approval. And so I think the way to go is for the oncologist to be informed and to follow. And there's gonna be a point where there's gonna be enough trials

and there is enough standardization of the diet that the oncologist could say, hey, this has been tested in seven or eight trials. It looks very good and I'm gonna recommend it. Is breast cancer the form of cancer in which you're seeing the most kind of optimistic, positive indications? No, in the animal studies is working very well

with all kinds of cancers. In humans though. Yeah, in humans is breast cancer just being tested a lot more. It's not that we tested the others and it didn't work. It's more that- We know this disease better. Well, there's more effort dedicated clinically

to breast cancer. Well, there's more effort dedicated clinically to breast cancer. So, you know, for whatever number of reasons, but there's more studies, more clinicians come to us and say, I would like to do a trial on, you know, hormone therapy and breast cancer or chemotherapy and breast cancer or immunotherapy and breast cancer. But now that we're starting,

they're starting our trials on colorectal cancer and we finished one on prostate cancer, that eventually, hopefully we'll have a lot more, but yeah, there just hasn't been in that many trials in any other cancer other than breast cancer. There's one randomized study that you talk about in the book with respect to breast cancer.

131 patients showed very promising results in the context of the fasting mimicking diet being kind of woven into their treatment protocol. 90 to 100% tumor-free masses were seen in only 8% of patients who completed chemotherapy without any FMD, 29% with one cycle of the fasting mimicking diet, 33% with three or four cycles, and 53% with all chemotherapy cycles combined

with a fasting mimicking diet. I mean, that 131 patients, not the biggest population, but not insignificant either. Like that's a considerable result. Yeah. Yeah, and this is being confirmed by the Vernieri paper that we just published very recently in cell metabolism. But I think that I like, I'm a little worried,

you know, that that's too early, because that trial was in women that were to receive that surgery. So early stage about to receive surgery. So I think that, you know, we'll see, but it falls into the category of too early to try it until there's more clinical data, right? But whereas in the metastatic setting,

where we've seen the same exact results with the very similar to what you just described, but now in patients that have metastatic cancer, yeah, then I think that that's a very different scenario. It's working very well. And that's where we see the overall survival difference, at least in the early trials. So I'm more optimistic and excited

about the metastatic one than the early one, because the early one in that trial is not enough to make conclusions about long-term survival. And so, and it's very, very early before surgery. So yeah, I don't know. I don't wanna make that category of breast cancer patients too excited about, you know, oh, I'll do this

because again, I'm worried about the cancer stem cells and other things that could be affected in different ways. Now, yeah, I don't have that worry for the metastatic because again, it's been tested now more and we see no evidence of, and we see the overall survival improvement. And so, yeah, so I think that definitely a wild card, I will call it that, a wild card for any cancer patients,

you know, of course, after a discussion with the oncologist for any cancer patient that is in this situation where this is not working, right? And then the oncologist says, you know, doesn't look good. That's it, you know, two to six months, and there's not much more we can do. And not just that, it can be stage four, you know, three to four years, but it's not working very well

and we're concerned, right? So yeah, that's the, if the oncologist comes back with, okay, this didn't work, but we have this, and this could work extremely well, right? And we're very confident, okay, then try that. But at the point where the oncologist comes back and say, there's really nothing left. And yeah, you could still live seven or eight years,

but we just don't have anything right now. That's when I would definitely talk to them. And this is what the foundation clinics do, working with the oncologists and saying, okay, this is a good time to give it a shot, right? So, and see what happens. Hey, and in the book is full of stories. And this is why I make sure that I don't make the stories

into a reality. And there's people that like, you know, Vernieri published five cases of, you know, stage four colorectal lung cancer. And in fact, the lung cancer patient that- Yeah, Maggie Jones. I mean, that was like the most impactful story in the book, I thought.

No, Maggie, yeah, but then in the Vernieri, I didn't talk about it a lot, but in the Vernieri study that is published in European, I think, cancer journal, there is five cases and one of them is lung cancer. And the person was a friend of the oncologist, right? A good friend of the oncologist. And the oncologist thought, yeah, that's nothing we can do.

Lung cancer, stage four, the person went into remission, which shocked so much all the oncologists at the Italian National Cancer Institute that they publish a paper on this. Cause they say, we never seen five patients out of a single trial with stage four going to remission, right? And so, yeah, so they were so surprised that they decided to publish a paper saying,

okay, we don't know, it could be a crazy coincidence, but that's a little strange, right? That we're seeing all these essentially, you know, I don't know if I wanna call it that sentence, but certainly, you know, there's not much hope left, right? And then, you know, seeing, in one case, I think it was the colorectal, the cancer came back after three or four years,

but there was already, and then the same treatment and the same result. So yeah, so I think the hope that there is something that could make a big difference, right? That's a thing what we got right now. And, you know, hopefully we'll have the demonstration of it in big clinical trials, you know. From a mechanistic point of view,

the way you describe it in the most basic sort of lay person manner in order that, you know, normal people can kind of understand what you're getting at is that use this analogy of cancer cells as these sort of food stealing thieves, right? The FMD is sort of an attempt to starve them. In other words, like close the grocery stores, right? That at the same time don't impact normal healthy cells in the same way they impact cancer cells.

And through autophagy, like they can kind of, you know, kind of regenerate themselves, regenerate healthy cells. Is that, is that? Yeah, I think the normal cells have been trained for 3 billion years, right? So they know exactly what to do. Bacteria, if you starve them,

they know exactly what to do. Yeast and all organisms on earth. Most of the organisms on earth, by the way, are in starvation, are starving right now, right? If you look at microorganism. So the normal cells, they know exactly what to do. The cancer cells have evolved with excess food, right? They only understand a lot of food

and they don't understand how to make their own food. They understand that, hey, I gotta get it from the bloodstream, right? So if you just do fasting or fasting-mimicking diet, they're not happy, you know, but we see over and over kind of like a cycle of chemotherapy, it's about the equivalent. So if you just do fast in making diet cycles,

it'll have the slowing down effect of cycles of chemotherapy. But then when you combine it with chemo and we combine it then with immunotherapy, when you combine it with hormone therapy, et cetera, et cetera, that's where you see, you know, in a lot of cases, we actually can drive the cancer down to zero or, you know, really stop it, you know, in a lot of cases, we actually can drive the cancer down to zero or, you know, really stop it, you know,

stop its growth for a very long time. So I think, yeah, the cancer cells are confused. And now we have this technology that I talk about in the book, which is we call starvation escape pathways, black gate, right, so basically we use technology to say, okay, I start the system with the fasting mcgindyte, but then I take the cancer cells

and I look at how they rewire using this RNA-seq technology. So I can see very rapidly and potentially now even using cells from the blood that I just collect. And so hopefully soon we'll do that in people. So I can see how they rewired and I can use drugs that are available

to block that particular highway, right? So I know what the highway you're gonna take basically, and I just block it, right? And that's really, and we publish, it's got incredible effect, right? So, so long does, yeah, delays a little bit. Then we identify the escape pathways and we publish has got incredible effect, right? So, so alone does, yeah, delays a little bit. Then we identify the escape pathways and we block it and tumor comes down and stays down, you know,

either for a long time or permanently. So what is the message that you're trying to convey in this book? Like, cause there is a sort of caution, like, okay, don't get too excited. You know, I'm talking about a very, you know, specific set of circumstances in which, you know, kind of what I understand would apply.

So, you know, who's the reader for this and what is it that you want people to kind of get from it? Yeah, well, first of all, everybody in the cancer prevention settings, right? So treat aging, prevent cancer, and that could have a remarkable, whether it's the fasting-making diet or the longevity diet or the time-restricted eating

or the other things that are in there. So prevent cancer. Then if you're unlucky enough and you get cancer, at the beginning, you can still do lots of things like longevity diet, time-restricted eating, different, right, so now time-restricted eating, we go to 14 hours from 12. If you are a cancer patient, right?

So we increase it to 14 hours. And longevity diet, we have to work on, you know, making sure that you don't lose muscle, your immune system doesn't get weaker. And so that's an everyday diet. Then the fasting-weekend diet is only, I think, for patients that need to do it. So if you're early stage and everything is, you know, you're having low levels of side effects and everything is smooth, I would say just do the longevity diet and time-restricted

eating and do lots of other things that we talk about in the book. But that's it. If you are metastatic or the oncologist says, nothing is working here, even though you're not metastatic. Yes, then I think I will consider the fasting making diet and then I will talk to the oncologist and see what he or she has to say about using it. What is your sense of the impact that AI is having or will soon have on your specific field of study?

Yeah, I mean, what I just said, I think eventually AI will make that process of identifying the escape pathways and the drugs very quickly, almost immediately. And I'm not talking about 20 years, I'm talking about two or three years. So in two or three years, I think we can probably, if we had enough money now, if the NIH is shut down, maybe we won't. But I think in two or three years of enough funding, we'll be able to use AI to very quickly

get to the escape pathways. And so the idea would be, I use the FMD as a wild card and I use the AI to tell me what the other drugs are. And then I use FDA, already FDA approved drugs to block it, right? And so it's a little bit of a science fiction world. I call them cancer antibiotics, right? So yeah, so I see that with enough funding

in the next 10 years, we might have this sophistication to say, kind of like, you know, antibiotic, you go to the doctor and say, oh, you know, you have an infection, so we'll give you this antibiotic, let's see if it works. So I think, you know,

and maybe I'm optimistic with the time, but I think, you know, with the right funding, this could happen in the next 10 years where, you know, you get your cancer antibiotics, you have very low toxicity, kind of like FMD plus plus plus, very low toxicity drugs that you can just take and let's see if the cancer goes away. And, you know, if it doesn't go away,

then we'll try something else. But yeah, I think that's clearly theoretically, but also using the animal data, this is very close, right? But yeah, so sometimes it could be very close. Three years, it could be very close, 30 years. It's hard to know, but I think with the right funding, it could be within 10 years.

And outside of the cancer context, are you among the techno optimists in terms of how AI is gonna impact impact HealthSpan Extension in a wide variety of ways, kind of beyond your area of expertise specifically? Yeah, I'm very scared of AI. So I don't like it at all. Well, here's, sorry to interrupt, but I'll just say one thing. I've said this before on the podcast, but like, I've had, you've all know,

a Harari on the podcast and he's sounding the alarm about like the sort of end of democratic systems and humanity at large. But we were both at the Google Zeitgeist Conference and it's just Pollyanna all day long in terms of like how amazing it's gonna be. Yeah, yeah, very scary, right? Very scary.

Yeah, I think to see how scary it is, you have to look at evolution, right? Systems evolve, right? And it doesn't really matter whether that system happens to be derived from single cells or from a programmer. That's a scary part that I think everybody is underestimating.

If every system can evolve, it can find its way, right? And so that's a scary part. And now for the first time ever, we have a system that evolves and is based on a program. And it can learn and eventually, you know, where can it end up? Right? So that's what sets the stage for, it's just a matter of time before it's going to evolve. And it's going to find its way. And the question is, what way is it going to find? Well, if you look at the past, right, and dinosaurs and all kinds of organisms, you can see that some of the evolution could end up

in the wrong place for humanity, right? And as an antagonist. So yeah, that's what I'm worried about. Of course, I agree with all the benefits. I just talked about one, but it's not something that we couldn't do computationally anyways, right? So I think that, I mean, I don't know, maybe there's nothing we can do, right? We cannot block AI.

So I think we could regulate it, right? And begin regulating it, you know, in a planet wide manner. So that's probably the thing that we need to do very quickly that would be my suggestion as somebody that works in evolutionary biology, we need to use its power, but also understand its power and regulate it as soon as possible.

And I don't really see any, because everybody's thinking about making money using it. Right? This is really entertaining. That imagine generating a dinosaur and thinking about how much money you're gonna make in Jurassic Park. And- Well, this is happening.

The wooly mammoth is underway. That company just raised like some crazy amount of money and like it's gonna, that is what, that is what is happening. Yeah, yep, we have more problems than AI then I guess. But yeah, so I think that we, I don't understand. I mean, maybe it's just the obsession with making money that is driving these irrational exuberance that has very little

worst case scenarios, right? What's the worst case scenario? Well, if the worst case scenario is really bad for human beings, then probably not a good idea to not regulate it, right? We talk about regulating it, but not really. I mean, I think there are a lot of smart people who are thinking deeply about this,

but the momentum behind this just moving forward is too great at this point. And I think, yes, like money is central to the whole thing, but I think beyond that, it sort of just speaks to the ingrained nature of the human animal. Like, we're nothing if not a creature that is just gonna keep doing the thing and we'll like deal with the circumstances in the aftermath.

And yeah, we'll give lip service. We better be careful, but we're bowling forward no matter what. And that's what I see happening. And I think in the short term, like certainly there's incredible implications that, you know, for this that are going to benefit humankind specifically in, in, you know, the healthcare context. I think these tools are going to be remarkable in terms

of identifying diseases at the earliest stages and figuring out ways to circumvent them and cure them and prevent them. All of that, I think, is something to celebrate, but there is the kind of larger looming existential questions that are a little bit harder to kind of grapple with and determine solutions. But I think we lack the adequate humility to really respect the gravity of what we're doing. And I think we think we might know what the implications are,

but I don't think we really do at all. Yeah, and I mean, if you look at nuclear power, right? So some of the same arguments were made. And right now we're in a situation that we probably rather not be in, right? Somebody goes crazy, it just wipes out the entire planet. So this is much worse, right? I mean, compared to the AI,

I think the danger of nuclear power is very small, right? That's why it's particularly surprising that we don't see it for how powerful it can be and it will be. I mean, it's not it can be, it will be. What happens then, right? So I don't know if we went back and in the nuclear science

where we had made the same choices if we had a choice at some point back in the past, right? I mean, I don't know right now that, everybody would like to be in a world where everything could be wiped out by just an event that goes in the wrong direction, right? So yeah, so there's a lot of benefits, but maybe it wasn't worth having those benefits available to us considering where we are right now.

Yeah, so in AI, I think it takes it to another level. Well, we're gonna find out. And since you're on a track to living between 120 and 130 years, hopefully we have it figured out so that you can live a long and fruitful life. And you're gonna have a baby soon, yeah? Yeah, yeah, yeah.

So you're probably thinking about things more philosophically. Yeah, that's what makes me worry, right? So, yeah. Yeah, well, what makes me worry, right? So, yeah. Yeah, well, I appreciate the work that you do. It's a service to humanity. And I just wanna acknowledge you for that service and appreciate you coming here and sharing with us.

And you're always welcome here. The new book is Fasting Cancer. And if people wanna learn more about your work specifically, Walter, where should they go in addition to checking out? Instagram, I think Professor Walter Longo, and Instagram, and also the Create Cures Foundation. That's createcures.org, I think.

Yeah, excellent. Thanks a lot, Rich. Great talking to you. Peace. Thanks. That's it for today. Thank you for listening. I truly hope you enjoyed the conversation. To learn more about today's guests, including links and resources related to everything discussed today, visit the episode page at richroll.com where you can find the entire podcast archive, my books, Finding Ultra, Boising Change and The Plant Power Way, as

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