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

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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 cannot make somebody live 10 times longer, but could you make him 50 % longer?

I think it's possible, so from 80 to 120.

Returning for his third appearance on the podcast, I'm very pleased to welcome back, Dr. Walter 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 I'm the director of the Longevity Institute at USC, where he's 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.

Fast -emimicking 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 health span and lifespan.

What is it about this diet that is so protective?

Voltar, 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 Diamandas who both have been on the podcast recently.

So you're completing the triumph, right?

Yeah, 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.

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, whose 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 in 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 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 from my lab at USC.

And we depend on that, right?

So, we depend on this NIH funds to do research. And my group has helped maybe 50 universities and hospitals do clinical trials.

Without the NIH research, none of those will have happened.

And 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 diet.

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.

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 it's kind of important to understand that not all research is pharma funded and foundations only go 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 this is 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 going to be FDA approved.

So, yeah. 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 the DNA -HA would be a drastic problem, especially for those diseases or problems is where the big pharma don't want to invest. So 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 was a very interesting time here in Los Angeles.

Anyway, because it's been a couple 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 will say that at least in my opinion now, the more clear evidence for fasting is in the time rest of the eating domain, you know, so that the daily fasting and I think we discussed 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 or 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 is 16 hours of fasting every day, but it's still effective.

And so I think Sachin Pandey and I will agree on the say 11 to 12 hours daily time restricted media.

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 is, this seems to be the window that is the safest and most predictable in terms of outcomes.

Yeah, the easiest, safest, nor physician will ever argue that that's a bad idea.

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.

It's also consistent not just with the epidemiological data, the clinical trials, also consistent with what centenarians have been doing for 100 years or more.

So yeah, so I think that the 12 virus is one.

And then, I've always argued against the alternate day fasting, the 5 -2, and not because they're not effective, but again, they're very demanding, 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 the territory of....

Are there side effects caused by not eating every other day or not eating for two days a week.

So I will 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 are enthusiastic about either alternative fasting or two days a week of fasting.

Of course, I'm enthusiastic about the fasting making diet.

So in addition to the time where they're eating daily, then the cycles of the fasting making diet.

And so this is a plant -based low calorie, low sugar, low protein, high plant -based fats.

The program that we've been testing, we and many universities have asked to test it, I've been using it for all kinds of diseases from diabetes, prediabetes, cancer, Alzheimer's, autoimmunities, 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 kind of menu that physiologically mimics what the body would experience had it and just fasting.

Correct, is that, do I say that accurately?

Yeah, that's accurate, so then there was it 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 he would if it was not eaten at all.

Before we move on from time -restricted eating in this 12 -hour window, 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, there's literally only an hour or two in which you're not meant to be eating.

Right, yeah. And that's 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 what will be easiest for people, realistic for people.

And so I think that 12 hours a lot of people say that's not fasting at all.

Well, it is fasting because now on average, and this is work by Panda, that 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 so many of it started at 6 a .m. and ended at 11, 30 p .m. And so, the three, four, or five hour 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, is they may make energy expenditure higher, let's say, 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 not getting the eight hours that you should be getting or seven hours?

Yeah, so Satchin 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.

and 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 I'm feeling hungry at night.

It's just a mountain I still have not mastered.

Yeah, and I think it's important, you know, 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'll 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 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.

that 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 in these drops that would occur over the course of the evening that don't happen when I eat earlier or reduce the volume.

Right. And as you get older, they might get worse, right?

So then yes, the recommendation stays, eat earlier and eat within 12 hours.

And then, you know, if somebody's 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 not sleeping well, most people will know or even without a bracelet.

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 you know, 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 in your own words describe 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 my former mentor was one of the pioneers of calorie restriction, which is just, 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 a 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 there was the idea, maybe you do this 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 fasting diet, meat -meek 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.

So in fact, we have a number of papers are gonna be published in the next year or two, which is about what if you eat a normal diet you know, so we've been talking about Mediterranean diet and 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 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?

So, for example, you could say high protein, low protein.

And I will argue, it's irrelevant because you can have a five to tenfold difference in certain amino acids with the same level of proteins.

If you eat legumes versus, and sometimes you can have that between different plant -based sources, right?

You can have a fivefold difference of essential amino acids between two different plant -based sources.

Or I think we probably need to move away from also same protein levels, right?

Then move into amino acid profiles.

Anyways, it's just, I think the pillar number two of my work is, what you eat every day it's 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 know 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, 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 another 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 with its fasting or eating as how does it affect the genes that regulate the aging process, how does that affect IGF -1 growth hormone, growth hormone receptor and does affect Tor, you know, Ras and all these genes, these networks that are, that are now clearly, and we talked about in the past, and 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, you know, of course you're gonna make somebody live 10 times longer, but could you make him 50 % longer?

Right? 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, you know, there are general principles and yet there are, you know, there's diversity to your point about the eggplant that you have to address.

Yes, 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 want to 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. Yeah, 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 it really never happened, right?

So that's what we're trying to do.

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 were very confident and and so University of Leiden, where the University of Heidelberg did the first trial a couple of years ago and showed impressive, impressive effects, an A1C, but also on reduction of drug use.

And then Leiden repeated and got the same results.

And so, so I think yes, these are feasible ways to bring people back to a functional state from a disease state to a functional state.

And I think that a lot of that has to do with molecular mechanisms that are much more sophisticated than people may imagine.

So for example, we just published in collaboration with Laura Perrin at a children's hospital.

We published 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 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 on and off in the different cells of the kidney.

And then we start the fasting making diet and you see that, so there's a very precise architecture, let's say, right?

Three -dimension, and then they can completely destroy by this toxin that we give to rats, right?

Then we start the fasting making diet cycles.

and you see everything going back to the, to where it was.

Almost like a magic intervention.

So it's not really the fasting mimikin diet that is doing anything, right?

It is the rats 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 kidneys are first generated in a baby.

Like pluripotent stem cell generation.

Is that what you're talking about?

Yes, so the cells are being reprogrammed into some of these reprogramming factors, the 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 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 these very disruptive state back to the previous healthy state.

So they know exactly what to turn on to fix the problem.

So yeah. So then that's the power of this fasting making diets.

So turning on the ability of the body to fix itself.

And so now, you know, 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 gut, we are clearly seeing it in animal studies, and now there are many number of trials that will test it in clinical trials here.

What is your understanding of the 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 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, right?

So that's, in that case, I'm not saying that that's not beneficial as we discussed earlier, but not in this case.

Calr assisting, probably none because per month it mice rats And probably people, they eat about the same amount, so they overeat anything, they didn't eat during the FMD 5 -days, so they have 25 to 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 meat in diet, eat same level of calories as the control, as it does on the control diet.

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 LTHCCs, emotopated stem cells.

So in the blood, it seems to be stem cell driven in lots of other organs, the gut, the kidney, and in 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 it's probably metabolic.

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 access food, you want to 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, we're not 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 will 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?

This is why the five days of the fasting -making diet and then go back, 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 are 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 going to get our next meal and everything kind of goes into low power mode.

Yes, in the 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 years I'll keep you in this energy saving mode, and then we'll see 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 a very few clinics that are dealing with people that are overweight and obese understand this.

And so, without this understanding and intervening, it's 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 they create curious foundation that I started, has dieticians that are specializing 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, this pescetarian, low protein, mostly plant -based diet, the fasting and making diet, and the 12 Alzheimer's, the eating, and then the exercise, right.

And this, a combination of these, and some people say, I don't wanna do the fasting making diet.

And so people say, I don't wanna do the longevity diet.

But you know, most people will 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 what do you, what is your diet?

and what are the problems that you're having?

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've 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 rather than losing and regaining.

that's what the great majority of people do here.

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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 kind of 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've been 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 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 fast food making that cycle 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 the immune cells would come back up only in the mice that were giving chemotherapy plus fasting cycles.

And so we said, is that 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 that took a couple of months to regenerate healthy white blood cells and repopulate the normal immune system, so really remarkable effect.

And then we had a followup paper with the pancreas where we completely damaged the pancreas in animals, So completely black insulin production by the pancreas, permanently.

And then we started the FMD cycles, and then you see that again this two yamana 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, you know, showing that the pancreas can fix itself and can go back to normal insulin production, you know, so essentially treating type one diabetes, right?

And so those are the two papers that I think one stem cells and the other one of reprogramming in a very sophisticated way, right?

So I'm always entertained by, you know, the sort of pharmaceutical point of view with that you know, drugs are sophisticated and what could nutrition possibly do, right?

And instead I think you see evidence is for nutrition starting something that is so sophisticated and it's so old, it's billions of years old and it's 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, maybe 20, 30 years from now, we'll have artificial intelligence driven repair systems and it'd be another world, but I think that it's gonna be hard for a while to beat that extremely sophisticated, 3 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't understand mechanisms, you could cause problems, right?

It's very powerful.

And so if you don't understand how it works, then you could 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 refeed 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 the alternate day fasting showing that the opposite of what we have shown for long -term fasting by using 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 cardiotoxicity went up instead of down, right?

So there are 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 we're running trials, right?

By we, I mean, lots of universities in 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, you know, there are a number of papers on, uh, clinical papers on cancer.

Um, and so, um, most likely the mechanisms are similar, right?

So we've shown it in mice, we showing in rats, uh, and now we've seen the effects and now 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.

Mouse and rat, 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.

So first six patients, and then we 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 not only the proteinuria was reduced right after Tris fasting maybe in diacycline in the kidney disease patients, but a year later, and the great majority of them still maintain that benefit, right?

And interestingly, when we look at these mesenchymal stem cells in the blood, kidney mesenchymal cells, so they're like progenitor cells for kidney regeneration, they tripled in the blood of patients.

So we don't know, 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 leaking the blood?

but it's really remarkable because you see a threefold increase in this progenitor cells that are clearly mostly used to repair kidney damage or generate kidney tissue.

So in a lot of the trials, we see something very much consistent with what we see in the 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 the effect of the FMD and reversing diabetes it'd be nice in humans so so we know how it works in mice do we need to prove the mechanism humans no we just need to prove that that works it is feasible and but yes, it'll be nice eventually to show that, you know, 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 in the type two diabetes patients that are receiving fasting making that cycles.

So there are ways I think to look into who 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 gonna live to 120, But meanwhile, like something like between 30 and 40 % of Americans are suffering from type two diabetes or are pre -diabetic, obesity rates are through the roof, childhood obesity rates are through the roof, heart disease is our number one.

Like 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, you know, kind of death sentence that visits, you know, millions of people unnecessarily every, every year.

Yeah. And I think the, 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 want to intervene on one thing, is better to intervene in aging than intervene in obesity, right?

So even obesity compared is dwarfed by the effects of 30 years of aging on any of these diseases, right?

I mean, 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, you know, the best way to go would be to do both, right?

And this is what the, you know, the fasting, making that, the longevity diet do.

And by the way, unlike what we see with the GLP1 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 very coordinated.

It's very different, right, than blocking an agonist, a GLP1 receptor agonist. This is a 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 age and we're given the FMD all lifelong and we look at bone density is higher than in the controls, so that means that maybe there is even 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 increase lean body mass, right?

The muscle absolute weight increased and also the muscle function was increased.

So, this is, you know, by what's called impudentiometry methods.

So we don't know, you know, that part, we don't know how carefully was measured, but certainly in general, now they seem to be protection of muscle mass in these women even after many cycles of the fasting -making diet.

So that's very important to get the reverse, the hadeposity, so the fat storage, probably reduce the inflammation.

And we clearly see these anti -inflammatory effects of the fasting -making diet go after the aging process.

So for example, IGF -1 and all these aging markers are reduced, and they're reduced longterm.

You don't just see the insulin microfactor one being reduced temporarily and then go back up.

Laptin and IGF -1 they're reduced longterm.

And this is shown many trials, right?

So yeah, so it's going after the adiposity, it's going after the aging acceleration or the aging rate and is doing so because is guided, right?

And we developed a lot of this with those problems in mind is 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 easy to do that.

they're not kind of, they don't have the hunger pains that they normally would have. And because your house is on fire, you got to 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's really like in a really acute unhealthy state.

Yeah, in my mind, that's option B, right?

In my mind, option A, and I hope that, you know, 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, these probably involve molecular biologists, physicians and dieticians, right?

That team and maybe psychologists, 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 this should be done.

Like the way we do it, at the site Curious Foundation, is take your time, take a couple 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's just saying.

So she gives Lyroglutide, which is a short, it's a GLP1 agonist that less than the new versions, right?

And so she combines the fasting and baking diet with the Liragglutide.

And then eventually she gets the patient off Liragglutide and keeps them on the, yeah.

So the hunger 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 said, 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 lyric lutide is like a lower dose or less intense version of Ozempic or some of the lutide.

Right, yeah. And it's a shorter lasting song that I think you have to give every day to the patient, right?

So the health life is much shorter.

It means that there is also less concerns because of course, these GLB -1 agonists are causing insulin production, right?

And in the fasting, making diet cause insulin sensitization.

So that 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 can have a problem because now you could get the blood sugar level very low, right, very quickly.

And so yeah, that's why a 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.

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.

But sure enough, we ended up in that situation.

At least with one child.

And so, yeah, so that was very good to think of the worst. 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.

So the effort of doing it, like you did, it's hard. I understand you cannot maybe do it on your own, but you've got the professionals around you they're helping you.

You put the effort in and people don't wanna hear that.

Volter. I understand that, but people have to hear that because I wrote in the article, I talked about exercise and now in the fifties, nobody exercise.

And then so 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 sixties and people were like, oh, people are gonna die if they're gonna exercise this much every day.

And then eventually the half of the world, you know, and 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, you know, in that article that I wrote, I said, you know, of course you can not tell everybody do 50 miles a week of exercise or running, right?

Nobody's going to do it.

but if you make it reasonable, let's say 150 minutes and that's what people do now.

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 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 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 well -being.

And that spills over into like, not just your external outlook on the world in 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 well -being.

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 U .S. and then the world, because this followed all over the world, right?

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 going to go jogging.

I'm going to go and take a bike and do, you know, 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 percentage, but certainly methods like the FMD.

And that's what I was saying earlier, we're testing it in southern Italy.

One of the worst areas of...

One of the worst are the worst in Europe, right?

Yeah, we think of Italy as sort of this giant blue zone, but it's not really that.

Not at all. I mean, if you look at Calabrian Campania, yeah, so Calabrian Campania have surpassed the the United States as far as overweight portion in children right so it's a bit it's a big problem and so the way we address that was what about if we given FMD for five days every three months and everybody thought it's crazy never gonna work we haven't published yet but let's say that it's looking good so far right so that's cool 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 It's essentially a medicine in a box.

Since we last spoke, I would say that there's been an explosion in interest in a health span extension, longevity medicine, 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 in sort of the sophistication of scanning equipment, like all of these developments that are making health span extension, you know, more and more plausible.

And I think, you know, 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 Attia, 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 in the other direction.

You know, 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 pescatarian.

What's entirely vegan?

What's not entirely vegan, right?

I mean, I've heard you talk about fish two or three times a week 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 I should have. 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, this is 15 days in a year.

So even if you got zero protein, it will have no effect whatsoever on your muscle, right?

No effect. And we've shown this clinically in 10 different trials.

infected in a new trial, we're actually showing increase in 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, right?

So yeah, so I think that it's 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 in a study published in JAMA with Harvard. We've done it on 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 and 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 on low protein diet, whether it was an overall mortality or was cancer mortality, people reporting a low death, or very low protein diet did the best up to age 65.

And then did not do so well after 65.

So if an 80 -year -old said, if 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 Giovanni Nucci and the JAMA Paper, I think that he showed or we showed because I was a co -author, 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 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 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, right.

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 immortality prediction.

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 metionine diet, right?

Just in rats, in mice, and no matter who did it.

So yes, so then that's another pillar.

And then the centenarians, whether you look at Okinawa had the 9 % protein diet, right?

And for the longest time had record longevity.

So I would encourage my colleagues to just expand from one pillar science to five pillar and the 50 is complex system.

But I say even if you just go for four pillars and if you go for four pillars, you see the devil is in the video.

It's about amino acids.

And it's about having sufficient and protect the immune system, protect the muscle, protect the bones, but reduce as much as possible the aging rate, because again, what dominates is aging.

So 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, right?

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.

So either mice. Mice that have a growth hormone receptor or growth hormone deficiency are the ones that live the longest, that live 40 % longer with the lowest disease profile.

This has been known, John Kupchick, Andrei Barki, worked 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 the limit 10 times longer.

And then our work in Ecuador with people, sure enough, people that have grown to a more receptive efficiency are protected in spite of a terrible diet.

Are protected from diabetes, 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 under brain.

They had the function of a much younger person cognitively.

And now we just publish on a neutral to positive effect on cardiovascular disease, which really surprised us that the plaques were lower or much lower in the pathway.

pathway that responds to protein intake is blocked.

The most damning part is the Harvard study showing a 40 % increase in three different studies, and this is Frank whose work, three different studies, 40 % increase in the diabetes risk in subjects eating high -protein diet, compared to the lowest, I think it was quintile.

So at 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.

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 going to get maximized effects on muscle building.

And that's probably all.

I mean, and you could do say, even if you did it twice a day, you still be in, 60 grams, because you still been a relatively normal to low a 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 the negative implications of a higher protein diet would be abated by that very active person, yeah.

Not necessarily. No. No, not necessary, 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, you know, increasing the functionality, you know, so we're about to publish a couple of papers on that in mice and, but also using the hardware databases.

And so yeah, I cannot discuss it but certainly it's very consistent what I'm saying, right?

The data is that, you 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 both of those, 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.

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 2030 % difference between let's say legumes and red meat, you could 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 nut protein and a legume is huge, right?

Then it's even bigger if you go 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 100 grams of protein which are providing 10 % or 20 % of that amino acid.

And the 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 going to be, right?

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, seeds 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 low protein intake and then it's all legumes, you're gonna have a problem, right?

Because you're missing essential amino acids.

Yeah, and if you follow.

So I'm missing on one thing, yeah.

I mean, I think people, when I said complicated, I meant like, you know the sort of physiological pathways and you know, 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 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 Italy, the same regions that have record longevity, because they used to have mostly legumes.

Yeah, the seeds and the nuts were there, but not in the type of quantities that the...

so the legumes were 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 by 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, So it could become a problem, so if you say five times a week, your proteins are all coming from the legumes, then they might not be so easy to if it's low protein, and mostly from legumes, then it may be difficult to keep the muscle mass.

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Are you familiar with this guy, Brian Johnson?

Yes. And his blueprint protocol?

I don't know the blueprint protocol.

I know the hundred supplements and all that.

Lots of supplements.

Basically put 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 dunno, 30 minutes of waking up in the morning, probably around 6 AM 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?

All those biomarkers seem to be fantastic.

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 it 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 suggest that it's not just that, it's not that, right?

If you start eating later, you're gonna have a problem.

But it may be difficult to see what's gonna happen 20 years later, and you're gonna get surprised.

In the ketogenic diet, it could be another example.

So if you look at the ketogenic diet, very beneficial, it makes you impressive results, but in the long run, people are in 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 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, a big gamble, right?

And then you should 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 these centenarians eat, you know, 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 is 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, you know, 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, a 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, You know, 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 is some cancers whose incidence goes up tenfold 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 now within the domains of what's been tested for 100 years and all you need is one of let's say 100 supplements or even 10 supplements.

People don't realize, and 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.

No, no, no. You described drug 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 now 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.

We don't know. Even AI wouldn't be able to handle it for the next, for at least 20 or 30 years.

Yeah. The so complex that you will need 20 or 30 years of data fed into AI to say, okay, there's now the only AI understands that maybe that's going to cause a problem.

But yeah. So right now, we're very far away with being able to handle, because you need big data, right?

Right, so how is the, you know, the selenium that you're taking interacting with, you know, 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 responds.

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 or 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 And now you have a recipe for disaster, maybe iron overload, because now you just have it added the third supplement that is making the ferritin work less well, right?

I see. You know, if you were counseled 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 timers the eating, the fasting, making diet, the longevity diet, I would 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 on.

What you wouldn't say every day.

If that was the case, you wouldn't be eating in three or four hour window.

I think he's underestimating the uncertainty of doing something that nobody's ever done before.

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, you know, data suggest that if you have a little bit higher fat levels, you may live longer, right?

So short term you could say, you know, IF5 % 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 be get to 110 healthy.

And I don't mean just 110 frail like the Southern Italians or maybe the Okinawans, 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 the 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 makes 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 Laron 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 what I was saying, people are now, millions of people around the world are using growth hormone injections to become younger, right?

And so if you look at them, uh, short term, you probably conclude that they are younger, uh, or they're functioning better, let's say.

Right? And so, but the mouse and the human data suggest exactly the opposite, right?

So that the little people, uh, it's like if you inject them with growth hormone, they'll have absolutely no effect.

Right. Because their receptors don't.

Their receptors don't.

We 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 ones 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, record health.

And this has been shown.

We work with these mice, but lots of laboratory, so there's really no doubt about it, right?

So that's why this genetics data is so important and it's part of the, I put it in the centenarian, the people that have lived with that change for 100 years, right?

So now we have the data, both for the La Ronge but also for the Okinawans and for the centenarians of Southern Italy 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 100 different diseases, maybe a thousand different treatments.

So I would say that in general, especially for those that have advanced stage cancer, I 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.

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 done in the book, showing either chemotherapy alone, chemotherapy, plus fasting -making diet, or chemotherapy plus fasting -making 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, you know, making survival better, are making also the pathological response better.

So if you look at the cases, the cancer cases after the treatment, they seem to have a less active cancer cells.

Now, there's also an argument and this is why we say, be careful as I mentioned earlier, like, if you misuse it, let's say you say all fasting is good and so I'm gonna go with chemo and then I'm gonna refeed at the same time that could cause problems and not solution.

And the other thing is fasting mimicking diet is a very powerful effect on stem cells.

And so 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.

So in the early stages of the disease.

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 timer study 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, you know, 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, then it's just overwhelming with all kinds of cancer, you know, colorectal, lung, and breast, and name it, right?

And 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's showing hormone therapy, for example, right?

Hormone therapy, so pulbocyclic, fulvostan, this is in mice, right?

And we also had the clinical trial but in mice it's very conclusive.

Use the standard of care, pulvosiclib and fulvestrant.

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 fasting, making diet, cycles.

And now you see, the tumor going the opposite direction until it goes to zero, right?

So it's just over and over and over.

It says the animal data is remarkable and really, almost surprisingly, and it's not just my data, there's now a lot of labs that are looking at it.

It's just remar - 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 breast cancer and even melanoma does very little.

And the first immuno diet alone that's more than immunotherapy, right?

So, I will 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 it.

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 it's nothing else is working, go for it, right?

Because this animal data is phenomenal.

But if you're stage one, and you already know that, and you know, 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, you know, 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 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 for triple negative breast cancer, And even for hormone therapy, I mean, for triple negative breast cancer, you starting to see randomized trials showing a big difference, right?

From what you expect or from what the control arm has, right, 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?

You know, it's looking good.

how up to speed are the oncologists, you know, in this field?

Some are up to speed, and a lot of them are not, right?

So a lot of them are gonna wait for an FDA approval, which, you know, may or may not come, right?

It's very expensive, you know, hundreds of millions of dollars to get an FDA approval.

The FDA looks at fasting in the diet, it's very complicated.

So we've told to the FDA to make it feasible or to make probably for the FDA, you probably need to you know, 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 you know, 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 it's gonna be a point where there's gonna be enough trials then and there's enough standardization of the diet that the oncologist could say, hey, this is been tested in, you know, 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, it's working very well with all kinds of cancers.

In humans, though? Yeah.

In humans, is breast cancer just been 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 is 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 they're starting our trials on colorectal cancer and we finished one on prostate cancer, eventually, hopefully we'll have a lot more, but yeah, there just hasn't been them 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.

or 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, at 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 and that that's too early cause that trial was in women that were to receive the surgery.

So early stage about to receive surgery.

So I think that we'll see but it falls into the category of too early to try it until there's more clinical data, right?

Whereas in the metastatic setting, where we've seen the same exact results with the very similar to what you just described, by now, in patients that have metastatic cancer, yeah, then I think that that's a very different scenario is 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 Then the early one, because the early one in their trial, it's not enough to make conclusions about long term survival.

And so it's very, very early before surgery.

So yeah, I don't know.

I don't want to make that category of breast cancer patients too excited about, 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 there definitely a wild card, I will call it that, a wild card for any cancer patients.

You know, of course after the discussion with the oncologist, for any cancer patient and that is in the situation where this is not working.

And then the oncologist says, you know, doesn't look good.

That's it. Two to six months and there's not much more.

And not just that, it could be stage four, you know, three to four years but it's not working very well and we're concerned.

So yeah, that's the, if the oncologist comes back with, okay, this isn't work but we have this and this could work extremely well.

Right? And we're really 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 clinic, the foundation clinics to the working with the oncologist and saying, okay, this is a good time to give it a shot, right?

So, and see what happens there.

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 I've got - 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 a lot, But in the Vernieri study that's published in European Cancer Journal, there was 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 you know, the oncologist thought, yeah, that's nothing we can do.

You know, 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, because they say, we never seen five patients out of a single trial with stage IV going to remission, right?

And so they were so surprised 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 are seeing all these essentially, I don't know if I want to call it that sentence, but certainly, yeah, there is not much hope, laugh, 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 thing for what we got right now.

And you know, hopefully we'll have the demonstration of it in big clinical trials.

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 you 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 them.

So regenerate healthy cells.

Is that. Yeah, I think the normal cells have been trained for 3 billion years, right?

So they know exactly what to do for bacteria.

If you starve them, they know exactly what to do.

Yeast and all organisms on earth.

Most organisms on earth, by the way, are in starvation, are starving right now, right?

If you look at microorganisms, 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 they gotta get it from the bloodstream, right?

So if you just do fasting or fasting, making 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 fasting making diet cycles they'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 what you see.

In a lot of cases, we actually can drive the cancer down to zero or really stop it, stop its growth for a very, 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 called starvation escape path with blockade.

So basically we use technology to say, okay, I start the system with the fasting, making that.

But then I take the cancer cells and they 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 going to take basically, and then just block it, right?

And that's really we publish it's got incredible effects, right?

So So Alone does, yeah, delays a little bit.

Then we identify the escape pathways and we block it and two more comes down and stays down, you know, either for a long time or permanently.

Yeah. So what is the message that you're trying to convey in this book?

Like, because there is a sort of caution like, okay, don't get too excited.

I'm talking about a very specific set of circumstances in which kind of what I understand would apply.

So, who's the reader for this and what is it that you want people to kind of get from it?

Well, first of all, everybody in the cancer prevention settings, right?

So treat aging, prevent cancer And that could have a remarkable, you know, whether it's a fasting making diet or the longevity diet or the time -restricted eating or the, you know, all the things that are in there.

So prevent cancer. Then if you're unlucky enough and you get cancer, you know, at the beginning you could still do lots of things like longevity diet, time -restricted eating, different, right.

So now with time -restricted eating, we've got 14 hours from 12.

If you are a cancer patient, right?

So we increased 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 the everyday diet.

Then the fasting and making diet is only, I think, for patients that need to do it, right?

So if you're early stage and everything is, you know, you're having low levels of side effects and everything is smooth, I will say just do the longevity diet and dimersteep to the 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 path within the drugs very quickly, almost immediately, right?

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, will be able to use AI to very quickly get to the escape pathways, you know?

And so the idea would be, I used the FMD as a wildcard and I use the AI to tell me what the other drugs are and then I use already FDA -approved drugs to block it, right?

And so it's a little bit of a science fiction world, you know, I call them cancer antibiotics, right?

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

So I think, and maybe I'm optimistic with the time, but I think with the right funding this could happen in the next 10 years where you get your cancer antibiotics.

A very low toxicity, kind of like FMD plus, plus, plus.

Very low toxicity drugs that you can just take and let's see if a 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, sometimes it could be very close.

Three years, it could be very close, 30 years.

You know, it's hard to know, but I think, you know, 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 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.

Sorry to interrupt, but I just wanna say one thing.

I've said this before on the podcast, but like I've had, you've all know Harare on the podcast and he's sounding the alarm about like, you know, the sort of end of democratic systems and humanity at large, but we were both at the Google Zeitgeist conference and it's just, you know, Pollyanna all day long in terms of like how amazing it's going to be.

Yeah, yeah, it's very scary, right?

Yeah, you know, 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, you know, 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.

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, where can it end up?

So that's what sets a stage for it's just a matter of time before it's gonna evolve, right?

And it's gonna find its way and the question is what way is it gonna find?

Well, if you look at the past, right, then dinosaurs and all kinds of organism, you could see that some of the evolution could end up in the wrong place for humanity, right?

and is a 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 can have block AI, so I think we could regulate, right, and begin regulate in a planet -wide manner.

So, that's probably the thing that we need to do very quickly.

That would be my suggestion is somebody that works on 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, right?

that, you know, imagine generating a dinosaur and thinking about how much money you're gonna make in Jurassic Park, right?

And - Well, this is happening.

The wooly mammoth is underway.

That company just raised some crazy amount of money and like, that's what is happening.

Yep, we have more problems than AI I guess.

But yeah, so I think that we, I don't understand.

And I mean, maybe it's just this 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 regulated, right?

We talk about regulating it, but not really.

You know, 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, you know, 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 bullying 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 for this that are going to benefit humankind, specifically in 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, you know, is something to celebrate, but there is the kind of larger looming existential, questions that are a little bit, you know, 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 are in a situation that we've 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 a 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.

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.

So in AI, I think it's...

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?

So I'm a little - You're probably thinking about things more philosophically.

Yeah, that's what makes me worry, right?

So, yeah. Well, I appreciate the work that you do.

It's a service to humanity.

And I just wanna acknowledge, you know, 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, Voltr, or where should they go in addition to checking out your work?

Yeah, Instagram. I think, Professor Walter Longo on Instagram and also the Create Cures Foundation.

That's, you know, createcures .org I think.

Yeah, excellent. Thanks a lot Rich. Great talking to you.

Thanks. That's it for today, thank you for listening.

I truly hope you enjoyed the conversation.

To learn more about today's guest, 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, Voicing Change, and The Plant Power Way, as well as the Plant Power Meal Planner at meals .richroll .com.

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Peace. Plants. Namaste.

Babes,

[장수 과학의 선구자 발터 롱고 박사와 함께하는 단식 모방 식단과 질병 예방]-[Fasting For Longevity: Valter Longo, PhD Shares Cutting-Edge Fasting Science & Optimal Nutrition Protocols For Lifespan Extension & Disease Prevention]

📋 Summary

장수와 질병 예방을 위한 과학적 접근

1. 12시간 시간 제한 섭식(Time-Restricted Eating)

2. 단식 모방 식단(Fasting Mimicking Diet, FMD)

3. 장수 식단(The Longevity Diet)과 단백질에 대한 오해

4. 암 치료와 단식의 결합

결론: 지속 가능한 변화의 중요성

🎯Key Sentences

📝Key Phrases

📖 Transcript