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The Rich Roll Podcast
Fasting For Longevity: Valter Longo, PhD Shares Cutting-Edge Fasting Science & Optimal Nutrition Protocols For Lifespan Extension & Disease Prevention
02:03:27
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- [00:01]
Rich Roll
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- [01:38]
Dr. Valter Longo
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- [01:41]
Rich Roll
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- [03:02]
Dr. Valter Longo
It's a very undisciplined world. If you look at Europe, 60% of people are overweight or obese and the United States is 75%. If you can make somebody younger, they will live longer, they will be much healthier. Of course you can make somebody live 10 times longer, but could you make them 50% longer? Right, so I think it's possible. Right, so from 80 to 120.
- [03:24]
Rich Roll
Returning for his third appearance on the podcast, I'm very pleased to welcome back Dr. Valter Longo, a pioneering research scientist in the field of longevity, fasting and age related disease. Named One of the 50 most influential people in healthcare by Time magazine, Dr. Longo is both the director of the Longevity Institute at USC where he is also a professor of gerontology and biological sciences, as well as the the director of the longevity and cancer program at the Institute of Molecular Oncology in Milan, Italy.
- [03:58]
Dr. Valter Longo
Fasting, mimicking diet plus chemo immunotherapy, hormone therapy, kinase inhibitor. I mean, the potential is huge in all the different cancers and in all the different stages.
- [04:10]
Rich Roll
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.
- [04:54]
Dr. Valter Longo
What do you eat every day is going to have a huge impact on your health span and lifespan. What is it about these diets that is so protective?
- [05:07]
Rich Roll
Valter, thank you for returning to the podcast. It's been between like two and a half and three years since we last sat down to talk. We reconnected at that Google conference recently where you were on a panel with Rhonda Patrick and Peter Diamandis, who both have been on the podcast recently. So you're completing the triumph for it. Yeah. Here to kind of dive deep into longevity science, fasting. We're going to talk about the impact of the fasting mimicking diet on cancer specifically, which is the subject of your new book, Fasting Cancer. But before we get into all of this, I think it would be valuable to just spend a minute or two, discussing what has transpired in the last 24 hours. So today is January 23rd, when we're recording this. We're on day four of the Trump administration. And just yesterday, there was a freeze on NIH grant review panels. There was an article in science.org about this. So there's a little bit of a mild panic among scientists who depend upon grant funding, 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, an interruption in billions of dollars in research funding. So, as a scientist who runs a lab, I suspect you are potentially impacted by this and just wanted to see kind of where you stand and what your thoughts are on this.
- [06:50]
Dr. Valter Longo
Yeah, well, we're very worried, of course. I just submitted a grant to the NIH, and this is a $15 million grant as a major grant for my lab at USC. And we depend on that. Right. So we depend on these NIH funds to do research. And my group has helped maybe 50 universities and hospital do clinical trials. Without the NIH research, none of those will have happened in our trials, I think, are particularly relevant because they're not on drugs. Right. So there are trials on. And 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. Right. So obviously there's reform needed at the nih, and I think most of the NIH people will say the same. Right. Certainly blocking the NIH process is. Is a big problem.
- [07:51]
Rich Roll
Yeah. I think they are responsible for something like $47 billion in allocations. And I think, you know, it's kind of important to understand that not all research is 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, etc. It goes well beyond kind of what I think perhaps people might imagine in terms of its scope and depth.
- [08:25]
Dr. Valter Longo
Yes. And I think a lot of people may think that it's just about basic science. Right. But in fact, the NIH funds a lot of clinical trials, and some of these clinical trials could have a. Almost final impact on whether an intervention gets used or not by people eventually. Right. So in some cases, they may even fund trials that are going to be FDA approved. So, yes. So basic research, it fuels the translational science or translational science and then translational science that fuels clinical trials and treatments. And I think that with that the NIH will be a drastic problem, especially for those diseases or problems where the big pharma don't want to invest. So, like rare diseases and diseases that are not that profitable. So that's where the NIH steps in and funds research and clinical work to treat it.
- [09:27]
Rich Roll
Yeah, well, interesting times indeed in which we live. But we were both lucky enough to avoid our homes being impacted by the recent fires, although there's fires still burning right now. So it's a very, you know, 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?
- [10:17]
Dr. Valter Longo
Yeah. So I will say that at least in my opinion now the more clear evidence for fasting is in the time restricted eating domain. So the daily fasting, and I think we discussed it before, but I stick with the 12 hours of fasting and 12 hours of feeding per day. And there's new data indicating that in fact maybe the problem of skipping breakfast and doing 16 hours of fasting and skipping breakfast may not be about skipping breakfast, but maybe about the 16 hours. Right. So we don't know, but certainly that's a possibility. And So I think 12 hours is a much safer way to go. And not as effective, of course, as 16 hours of fasting every day, but still effective. And so I think Satchin Panda and I will agree. And they say 11 to 12 hours daily time restricted period. So, you know, eat for 11 hours or 12 and fast for 13 hours or 12.
- [11:20]
Rich Roll
My understanding, correct me if I'm wrong, is, is that we still need more research to really drill down on 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, this seems to be the window that is the safest and most predictable in terms of outcomes.
- [11:54]
Dr. Valter Longo
Yeah, the easiest, safest. No 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 I think it's a good compromise and I think something that everybody should do that's also consistent not just with the epidemiological data, the clinical trials, also consistent with what centenarians have been doing for 100 years or more. So yeah, so I think that the 12 hours is one, and then I've always argued against the alternate day fasting, the 5, 2, and not because they're not effective, but again, they're very demanding. Right. So not eating every other day, it's going to be something that very few people will ever be able to do. And then you get into again the territory of are there side effects caused by not eating every other day or not eating for two days a week. So I would say in general, I just don't see a big future, at least not for the general population. Some people can do it. We'll see about the efficacy and the safety. But I think that in general, I will say that at least I'm not enthusiastic about either alternate day fasting or two days a week of fasting. Then of course I'm enthusiastic about the fasting making diet. So in addition to the time I said e eating daily than 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, have been using it for all kinds of diseases from diabetes, pre diabetes, cancer, Alzheimer's, autoimmunities, et cetera, et cetera.
- [14:02]
Rich Roll
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 been just fasting. Correct. Do I say that accurately?
- [14:24]
Dr. Valter Longo
Yeah, that's accurate. So then that was first developed in mice. And so we use certain markers to make sure that there is a fasting response equivalent to that of water only fasting. And then the same was done in people. And again, we're looking for certain factors in the blood that would show that, in fact that that person has responded as it would if it was not eating at all.
- [14:50]
Rich Roll
Before we move on from time restricted eating in this 12 hour window, you know, to, 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 8 in the morning and you go to bed at 9 or 10 at night, like there's literally only an hour or two in which you're not meant to be eating.
- [15:08]
Dr. Valter Longo
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, it's a very undisciplined world. And so that's very important to also say not just what will be most effective but will be easiest for people, realistic for people. And so I think that 12 hours, a lot of people say that's not fasting at all. Well, it is fasting because now on average, and this is work by Panda, people were eating for about 15 hours a day. Right. So yeah. So people all over the world like to eat for long periods every day. Yeah. So then somebody may start at 6:00am and end at 11:30pm Right. And so that, you know, the three, four, five hour restriction can make a big difference. It can make a big difference not just in reducing calories because you have less opportunities, but also in metabolic switches. They may make it make energy expenditure higher, let's say. Right. And also help people sleep. So those are some of the things that are emerging in mouse and human studies.
- [16:23]
Rich Roll
If people are eating on average 15 hours a day, is there evidence or is anybody kind of looking at the co founding factor of the impingement on sleep that would be impacting deleterious health outcomes? Because if you're eating for that many hours, you're probably staying up late and not getting the eight hours that you should be getting or seven hours.
- [16:45]
Dr. Valter Longo
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. So that's consistent.
- [17:10]
Rich Roll
That's still the hardest thing for me. It's really difficult for me to go to sleep when I don't have a full stomach or am feeling hungry at night, it's just a mountain I still have not mastered.
- [17:23]
Dr. Valter Longo
Yeah. And I think it's important. You know, the foundation clinics, we. Everybody's got a different method, right. So I think it's important. So for example, it's better to eat a light dinner, but I have a very big dinner. Right. So. Because I would be unhappy having a big lunch and a small dinner. So to me it works for me, it works. And so I think it's okay. I sleep well 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 suggesting that you're going to live 10 years shorter because of that. Right. So if you're sleeping well, that's probably okay. And okay compromise.
- [18:12]
Rich Roll
I do notice though, if I overdo it in terms of volume and hour of the evening, I'll generally wake up around 2 or 3 in the morning. And when I was wearing a CGM, I would notice these spikes and these drops that would occur over the course of the evening that don't happen when I eat earlier or reduce the volume.
- [18:32]
Dr. Valter Longo
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 if somebody's not affected by it by eating later is probably okay until that becomes a problem. Right. So I think that's a good way to look at it. And of course you have to know that it's a problem. But you know, not sleeping well, most people will know even without a bracelet or.
- [19:02]
Rich Roll
Yeah, you don't, you'll know. Yeah, you don't need any kind of like data feedback to know whether you're sleeping well 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 kind of describe your research and kind of the thesis of the work that you do.
- [19:38]
Dr. Valter Longo
Yes. So that's, 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 very difficult for people to do and potentially giving problems and solutions. Right. So, so then the fasting mimicking diet was about can we get the same effects as this phenomenal effects that calorie restriction has been demonstrated to have in monkeys and lots of different animals and in people without the problems. Right. So that was the idea. Like maybe you do 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 fast mimicking 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. And so in fact we have a number of papers that are going to 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 pescetarian diet. How do these affect aging, longevity, age related diseases and also frailty and strength. Right. So that's another big part of my laboratory. What do you eat every day? So let's move away from words like Mediterranean diet or Okinawa diet and just move into what is it about these diets that is so protective? Is it the protein? Is it the type of protein? Right. So for example, you could say high protein, low protein and I will argue it's irrelevant. Right. Because you can have a five to tenfold difference in certain amino acids with the same level of proteins. If you eat legumes versus you eat. And sometimes you can have that between different plant based sources. You can have a five fold difference of certain essential amino acids between two different plant based sources. I think we probably need to move away from also same protein levels. Right. They move into amino acid profiles. Anyways. It's just, I think the pillar number two of my work is, you know, what do you eat every day is going to have a huge impact on your health span and lifespan. And so what is it that you should change among all the things that you eat. And how do you personalize it? Right, Because I always say you can have eggplants and be very healthy, or you can have eggplants and be miserable because they happen to cause an inflammatory response in you. Right. So yeah, two people, maybe even brothers and sisters, 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. So not just we don't look at diet in a vacuum. We look at diet, whether it's fasting or eating, as how does it affect the genes that regulate the aging process? How does that affect IGF1, growth hormone, growth hormone receptor? How does it affect Torb, Ras and all these genes, these networks that are now clearly, and we talked about in the past, a simple organism. We can manipulate these genes and if we combine fasting with genetic mutation, we make simple organism live 10 times times longer. Right. So we're trying to bring that to people. So, you know, of course you cannot going to make somebody live 10 times longer, but could you make them 50% longer? Right. So I think it's possible. Right, so from 80 to 120 that is possible. And yeah, and I think all of this has to be understood very well and put together in a way that will cause the benefits without the problems, you know, or without generating new problems.
- [24:03]
Rich Roll
It's so complicated. There are general principles and yet there's diversity. To your point about the eggplant that you have to address. And I think what's interesting about your work is that, and maybe what's somewhat unusual about you, as somebody who is a research scientist, is that you are thinking about how you balance your discoveries around efficaciousness with sustainability and adherence in the general population. It's one thing to look under a microscope, have a discovery, 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?
- [24:48]
Dr. Valter Longo
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, just once a month without changing their diet. And that's a very important thing. Right. So we don't change our diet, we don't change our 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, so that's what we're trying to do. Say, can we standardize this, you know, 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 so University of Leiden or the University of Heidelberg did the first trial a couple years ago and showed impressive, impressive effects on A1C, but also on reduction of drug use. And then Leiden repeated and got the same results. And so I think, yes, this is 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 rats with kidney damage and then in people with kidney disease. Right. But in people, of course, we don't get to see what happens, but in rats we get to see what happens. And it's really remarkable. So we damage 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 mimicking diet. And you see that. So there is a very precise architecture, let's say three dimensional, and that is completely destroyed by this toxin that we give the rats. Right. Then we start the fasting diet cycles and you see everything going back to where it was almost like a magic intervention. So it's not really the fasting mimicking diet that is doing anything. Right. It is the rat that always. And people are the same, that always had programs that are able to be triggered by fasting to turn on regenerative and developmental like programs. So the same genes that are used when the organ, when the kidneys are.
- [27:35]
Rich Roll
First generated in a baby, like pluripotent stem cell generation. Is that what you're talking about?
- [27:42]
Dr. Valter Longo
Yes. So the cells are being reprogrammed into some of these reprogramming factors, Yamanaka factors, also known as Yamanaka factors, are turned on. And you see that every organ is turning on different ones. Right. So in some cases you see October four being turned on. In some cases you see myc. So different organs use different ones, but they all have the same thing in common. They turn on these many genes that are involved in organ generation, and then that's how they can go from this very disrupted state back to the previous healthy states. So they know exactly what to turn on to get back to fix the problem. So yeah, so then that's the power of these fasting making diets. So turning on the ability of the body to fix itself. And so now, 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 like gut, we are clearly seeing it in animal studies. And now there are many a number of trials that will test it in, in clinical trials.
- [28:58]
Rich Roll
You know, what is your understanding of the, you know, kind of mechanistic landscape here? How much of this can be attributed simply to caloric restriction? How much to the timing window and how much to the, you know, kind of macro composition of the FMD or whatever kind of fasting diet that one.
- [29:20]
Dr. Valter Longo
Is on the eating window? None, because we don't use eating window in the FMD diet. So people can eat for 18 hours a day if they want to. So that's in that case, I'm not saying that that's not beneficial, as we discussed earlier, but not in this case. Calorie restriction, probably none, because Vermont eat mice, rats, and probably people, they eat about the same amount. So they overeat anything they didn't eat during the, the FMD five days. So they have 25, 26 days to even overeat a little bit. And this is what we see very clearly in animal models that per month, rats that receive the fasting Mickey diet eat the same level of calories as the control as those on the control diet. Yeah, so I think it's mostly signaling. Some of it seems to be stem cell activation. So for example, in the blood we see an increase in what's called LTHSCs, hematopoietic stem cells. So in the blood it seems to be stem cell driven. In lots of other organs, the gut, the kidney and some other tissues, it seems to be reprogramming, right, what 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 excess food, you want to put it away. If it's winter and you don't have any food or food that is scarce anywhere, I start using those reserves that's the other big effect of the fasting making diet is unlocking that. But very importantly, and I don't remember if we talked about it before, without getting the organism into a thrifty mode, because if you go long enough, now we know from calorie restriction studies and lots of human studies that eventually if you starve or restrict the system of a human body for long enough, it'll go into an energy saving mode. And so you want to trigger this metabolic switch from the fat storage to the fat burning, but don't get into the thrifty mode, which now is going to try to save anything that it can. So lower energy expenditure and save it because the system is worried about running out of fuel. Right? So it's very tricky, right? And this is why the five days of the fasting vegan diet and then go back because. And that's why also eating is probably important, right? So you're eating but you're restricting for five days. And the message is, okay, get out of the energy saving mode, burn the fat and we see the ketone bodies go up and the fat burning clearly going up. But don't enter this energy saving mode because we're okay, we're not going to starve.
- [32:36]
Rich Roll
Right? So from a layperson's perspective, that would mean an emergency state in which the body is essentially saying like slow the metabolism down, like we got to 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.
- [32:52]
Dr. Valter Longo
Yes. And that 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 going to starve to death. And so for a couple of 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 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 lack that makes them just hungry all the time and with low energy expenditure, so making it impossible.
- [34:00]
Rich Roll
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, etc. And are in that state where now they'll say like, it doesn't matter what I do, I can't, I can't lose weight, 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, etc. 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?
- [34:44]
Dr. Valter Longo
Yeah. So I mean, so the Create Cures foundation that I started has dietitians that are specialized in this. It's a nonprofit that's here in Los Angeles, but they can follow anybody anywhere. We usually apply four things we applied the longevity diet, it's pescatarian, low protein, mostly plant based diet, the fasting mimicking diet, and the 12 altimeters, the eating and then the exercise. Right. And, and this, a combination of this. And some people say I don't want to do the fasting making diet, and some people say I don't want to do the longevity diet. But most people say, okay, I can do three out of four or two out of four. 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. A lot of times we try to minimize the changes, right. We really focus on not giving you, here's a diet that you should have. It's more, well, what do you, what is your diet and what are, 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 discussed it before, if you start doing this yo, yo, then you're in trouble, right? And 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 lose it and regain it. That's what the great majority of people do.
- [36:27]
Rich Roll
We're brought to you today by Go Brewing. I gotta say, it's been really fantastic to see this explosion of the alcohol free lifestyle and the many incredible beverage options now available to meet that growing demand. But the suds that have my attention are Go as in Go Brewing, a new company that crafts non alcoholic beverages that perfectly align with intentional living. After testing thousands of batches in their modern brewery and lab, they've created drinks that aren't just delicious, but are also free from added sugars and all unnecessary additives. Go Brewing's hard work is paying off. After launching an only 2023, they've already earned gold and silver medals at the Best of Craft Beer Awards. Their lineup includes their popular Double IPA and Sours, all produced in small batches with carefully selected hops. The beverages are made with natural ingredients, honoring traditional styles while providing a healthier alternative. And I must say their can designs are pretty next level. Each one is like a piece of art you can drink from and will feel right at home with even your less than dry compadres. So whether you're exploring alcohol free options or simply looking for a better beverage Choice, check out gobrewing.com and use code RICHROLL for 15% off your first purchase. So I recently revamped my home gym and I did it with some amazing products by NordicTrack and I got to tell you, I'm really blown away by the quality of their machines. This is a company that that for 50 years have been leaders in at home fitness equipment and my setup includes the amazing commercial X32i treadmill. And part of what makes it amazing is that it goes up to an insane 40% incline as well as a 6% decline. So imagine a workout where you put the treadmill at 40% and start marching up. It's unreal. I also have the S27i Studio bike with a 20% incline and a negative 10% decline as well as the smooth quiet RW900 rower. So cycling between the three of these products has just been amazing for my fitness. But what really brings these machines to Life is the iFit Pro membership. They have a new AI coach that helps you set goals, create personalized workout plans and it kind of acts like this amazing accountability partner all through texting with iFit, I also get to follow my world class trainer pals and past podcast guests, people like Tommy Ribs and Knox Robinson. And the machines actually automatically adjust to match the trainer's intensity and IFIT learns my preferences over time. It even reads my heart rate and adjusts intensity to keep me in the right zone at the right time, completely removing any guesswork from every single workout. NordicTrack, together with iFit, offer a personalized fitness experience for body, heart and mind with thousands of workouts including strength, yoga, pilates and mindfulness. So stop stalling your progress with NordicTrack and iFit. Just press Start and let the trainers and tech do the rest. Head on over to nordatrack.com richroll to experience personalized fitness. It's one thing to talk about fasting in the context of weight loss. I mean, let's be honest, that's probably what gets most people interested in this world to begin with. Another thing to talk about it in the context of chronic lifestyle disease prevention. But certainly, you know, 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?
- [40:45]
Dr. Valter Longo
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 you know, the mice would get chemotherapy and there would be dramatic or drastic negative effects, of course, on the immune system and the white blood cells and they will come down and stay down. And this is a problem that a lot of cancer patients have. Right. And so then we started doing the fasting, making diet cycle or the fasting cycle. Back then we were not just 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. Right. And so we said, how is it possible they come down? So the fasting was not protecting the lowering of the white blood cells, it was just making them come back up to normal within a couple months. Right. And so it turned out to be, it was stem cells. Right. So the FMD cycles were turning on the bone marrow stem cells and the bone marrow stem cells. It took a couple of months to regenerate healthy white blood cells and repopulate the normal immune system. Right. So really remarkable effect. And then we had a follow up paper with the pancreas where we completely damaged the pancreas in animals, so completely blocked insulin production by the pancreas permanently. And then we started the FMD cycles. And then you see that again, these two Yamanaka factors being turned on in the pancreatic cells, in the beta cells of the pancreas. And then after a couple of weeks, insulin would get back to normal. And so this was showing that the pancreas can fix itself and can go back to normal insulin production. So essentially treating type 1 diabetes. Right. And so those are the two papers that I think, one stem cells and the other one reprogramming in a very sophisticated way. So I'm always entertained by the sort of pharmaceutical point of view that drugs are sophisticated and what could nutrition possibly do? Right. And instead I think you see evidence for nutrition starting something that is so sophisticated and it's so old. Right. It's billions of years old and has evolved for the process of, for the purpose of fixing lots of things in a way that it would be unimaginable with any cocktail or drugs or intervention that you could think of. For now. Right. Maybe 20 years from now we'll have artificial intelligence driven repair systems and it'll be another world. But I think that it's going to 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.
- [44:02]
Rich Roll
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. Like.
- [44:22]
Dr. Valter Longo
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 alternate day fasting, showing that the Opposite of what we have shown for long term fasting by using everyday fasting. So they gave chemotherapy and then they cycled normal food fasting, normal food 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 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.
- [45:56]
Rich Roll
Yeah. 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, how much we can read into these animal studies in terms of their applicability to human biology.
- [46:20]
Dr. Valter Longo
I think that, I mean, of course, so we, we're running trials, right? By we, I mean lots of universities and a lot of, a lot of these trials are independent of us, meaning we just help them do the trial. So a lot of them have been demonstrated now in the clinic, like diabetes type 2 and there are a number of clinical papers on cancer. And so most likely the mechanisms are similar. Right. So we've shown it in mice, we've shown it in rats, and now we've seen the effects on our human disease. Likely it's the same mechanism, but we don't know. Right. So for example, the paper we just published on kidney damage in the rat, 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. It's called a randomized crossover trial. Right. So first six patient and then a control diet, and then the control diet group goes into the fmd. Right. And in both cases, remarkable effect on what's called proteinuria. Saw the protein in the urine as evidence of kidney damage. Right. So not only the proteinuria was reduced. Right. After three fasting, mimicking diet cycles in the kidney disease patients, but a year later, and the great majority of them still maintained that benefit. Right. And interestingly, when we look at these mesenchymal stem cells in the blood, kidney, mesenchymal stem cells, so they're like Progenitor cells for kidney regeneration, they tripled in the blood of patients. Right. So we don't know. Right. Is it, are they being released to go to the kidneys, are they being released in the bloodstream to go to the kidney and fix the problem, or are they increasing the kidney and leaked in the blood? But it's really remarkable because you see a threefold increase in these progenitor cells that are clearly mostly used to repair kidney damage or generate kidney tissue. In a lot of the trials, we see something very much consistent with what we see in the animal work. And of course, proving it is more, much more complicated. But in some cases women, I 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 we know how it works in mice. Do we need to prove the mechanisms in humans? No, we just need to prove that it works. It is feasible and. But yes, it would be nice eventually to show that, you know, for example, Harvard is interested in looking at pancreatic in the type 2 patients, looking at whether beta cell regeneration process that we've shown in mice is also occurring in the type 2 diabetes patients that are receiving fasting, making diet cycles. So there are ways I think to look into is reprogramming, stem cell based regeneration, etc. Are happening in people. It just takes a lot longer.
- [49:45]
Rich Roll
What is the receptivity in the traditional medical community amongst general practitioners or nutritionists and dietitians with respect to the work that you do, fasting in general, the fasting, mimicking diet? Because when you, you know, we could talk about longevity all day long and you know, are we going to live to 120? But meanwhile, like something like between 30 and 40% of Americans are suffering from type 2 diabetes or are pre diabetic. Obesity rates are through the roof. Childhood obesity rates are through the roof. Heart disease is our number one. 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 kind of death sentence that visits millions of people unnecessarily every year.
- [50:48]
Dr. Valter Longo
Yeah. And I think the two things are very much connected. 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 it's better to intervene on aging than intervene on obesity. Right. So even obesity compare is dwarfed by the effects of 30 years of aging on any of these diseases. Right. Meaning it's very small effect. Of course it's got a big effect, but it's very small compared to aging at least 30 years of age. So let's say that you could make people 30 years younger. That's, that'd be the best way to go, just make him younger and they can even be overweight. But of course the best way to go would be to do both. And this is what the fasting making diet, 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 a very coordinated, it's very different than blocking an agonist, a GLP1 receptor agonist. This is very coordinated response. And so there is not really a theoretical reason why there should be problems. Right. And again, we don't see, in fact in mice we see bone density increase compared to the control. So if you take mice middle age and we give them the FMD all life long and we look at bone density, it's higher than in the controls. Right. 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, in fact we did a trial with women with breast cancer and even after many cycles of the fmd, if they had a good healthy Mediterranean diet in between, they actually increased lean body mass. Right. The muscle absolute weight increased and also the muscle function was increased. So this is by a what's called impedentiometry method. So we don't know that part, we don't know how carefully was measured. But certainly in general there seem to be protection of muscle mass in these women even after many cycles of the fasting Migi diet. So that's very important to get the reverse the adiposity. So the fat storage probably reduce the inflammation. And we clearly see these anti inflammatory effects of the fasting Mickey diet go after the aging process. So, for example IGF1 and all these aging markers factors are reduced and they reduce long term. You don't just see the insulin like growth factor 1 being reduced temporarily and then go back up leptin and IGF1. They are reduced long term. And this is shown many trials, right? So, yeah, so it's going after the adiposity, it's going after the aging acceleration or their aging rate. And it's doing so because it's guided. Right. And we developed a lot of this with those problems in mind. Is not affecting the healthy tissues, including bone and muscle.
- [54:30]
Rich Roll
Is there a use case for somebody who is severely obese to go on a GLP1 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 of. They don't have the hunger pangs that they normally would have. And because you know 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, is that like a good way to go? Like if somebody's really like in a, you know, like a really acute unhealthy state?
- [55:17]
Dr. Valter Longo
Yeah, no, in my mind that's option B. Right. In my mind, option A. And I hope that eventually the government will also understand that we need professionals that are specialized in nutrition and they know what to do and they know how to do this carefully. And this probably involves molecular biologists, physicians and dietitians. Right. That team and maybe psychologists. 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 that would be the way this should be done. The way we do it at the Curious foundation is take your time, take a couple years and take the patient by the hand and say, okay, we're going to 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. Bakarin in Brazil who's been doing exactly what you just said. Right. So she gives liraglutide, which is a short. It's a GLP1 agonist less than the new versions. Right. And so she combines the fasting, mimicking diet with the liraglutide. And then eventually she gets the patient off liraglutide 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.
- [57:12]
Rich Roll
The liraglutide is like a lower dose or less intense version of Ozempic or.
- [57:18]
Dr. Valter Longo
It'S a shorter lasting something that I think you have to give every day to the patient. Right. So the half life is much shorter. It means that, that there is also less concerns because of course these GLP1 agonists are causing insulin production. Right. And the fasting vegan diet cause insulin sensitization. So it means that it makes insulin work better. So now if you increase the insulin on one side and you make insulin work better, a lot better on the other side, you could have a problem because now you could get the blood sugar level very low. Right. Very quickly. And so, yeah, that's why 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 1 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. 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, 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 there was a very, very good to think of the worst, right? Think of the worst when you're combining drugs and fasting. This is why option A, I like it much more because we don't see muscle loss. And it's also, I just wrote an article on this, is that we are more and more underestimating the importance of the effort. Right. So the effort of doing it like you did it, it's hard. I understand you cannot maybe do it on your own, but you get the professionals around you, they're helping you put the effort in.
- [59:27]
Rich Roll
And people don't want to hear that. Valter.
- [59:29]
Dr. Valter Longo
Yeah, no, I understand that, but people have to hear that because, you know, I wrote in the article, I talked about exercise and now in the 50s, nobody exercised. And then some, I forget, the doctor came around and said, you know, people should exercise every day. And people didn't know what that was, what is that? Why? And, and I remember I read some of his interviews in the 60s, and people were like, oh, people are gonna die if they're gonna exercise this much every day. Right? And then eventually the health of the world, you know, hey, that's tough, right? That's much tougher than what I'm talking about to have to exercise regularly. Right. But people do it. So I think that that's really the solution also mentally, psychologically. In that article that I wrote, I said, of course you cannot tell everybody, do 50 miles a week of exercise or running, 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 than when they exercise.
- [60:39]
Rich Roll
So yeah, I think it's a broader conversation around our relationship with discomfort. Right. And you know, all good things are on the other side of the, you know, kind of uncomfortable things that you're avoiding, whether it's food, nutrition, exercise, or any other goal that you set for yourself. But the byproduct of kind of grappling with that is well beyond like achieving the goal that you've 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 and your own life, but like how you think about the decisions that you make, food, exercise, et cetera. But you know, the people you surround yourself with, everything and all of that, you know, all of those things are fundamental to well being.
- [61:32]
Dr. Valter Longo
Yeah, but I agree with you. Let's say 50, maybe 60% of the population is not going to accept that short term. I think for exercise, it took decades for the US and then the world, because this followed all over the world, right. This was, I think, an American idea. It took decades, maybe 20 or 30 years to have a significant portion of the population actually saying I'm going to go jogging, I'm going to go and take a bike and $50k. So I think that, that before that happens, yes, we need to have methods that are maybe including drugs for some, for a percentage, but certainly methods like the fmd. And that's what I was saying earlier. We were testing it in southern Italy in one of the worst areas of either one of the worst or the worst in Europe. Right? Yeah.
- [62:24]
Rich Roll
We think of Italy as sort of this giant blue zone, but it's not really that.
- [62:29]
Dr. Valter Longo
Not at all. I mean, if you look at Calabria and Campania. Yeah. So Calabria and Campania have surpassed the United States as far as overweight portion in children. Right. So it's a big problem. And so the way we addressed it was, what about if we give an FMD for five days every three months? And everybody thought it's crazy, never gonna work. We haven't published it yet, but let's say that it's looking good so far. Right. So that's cool. So, yeah. So now it gets down to very little. Right. The five days, every 90 days that you have to dedicate to this. A program in a box, essentially a medicine in a box. Yeah.
- [63:08]
Rich Roll
Since we last spoke, I would say that there's been an explosion in interest in healthspan 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, sort of the sophistication of scanning equipment, all of the these developments that are making healthspan extension more and more plausible. And I think among this group of people, you share there's many things, principles, ideas that you share in common. There are differences as well. And I think one of the key ones with respect to diet is this emphasis on protein. So somebody like Peter Attia, Rhonda Patrick, they're always pushing protein, talking about the importance of protein, particularly 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 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.
- [64:43]
Dr. Valter Longo
It's entirely Vegan?
- [64:44]
Rich Roll
What's that? Entirely vegan. All right. I mean, you know, I've heard you talk about fish, you know, two or three times a week. Right. On the longevity diet. Right. So maybe kind of state your case or your perspective on this controversial macronutrient.
- [64:59]
Dr. Valter Longo
Yeah. So first let's take out the fmd, the fasting making diet. Because it's just five days, let's say.
- [65:05]
Rich Roll
Sure, Longevity diet, sorry, three times a year.
- [65:08]
Dr. Valter Longo
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 go zero protein, no effect whatsoever on your muscle. Right? No effect. And we've shown this clinically in 10 different trials. In fact, in a new trial, we're actually showing 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. 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 is a big problem when we are using like a one or two pillar system to look at things. Right. So let's say epidemiology. A lot of people love to use epidemiology, studies of big population. But even if you look at it, epidemiology, we've done that. And we've done that, you know, in a study publishing 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 but sufficient proteins. And then in our own paper, and we were the first one publishing on that, the 65 was the switch moment. Right. So 65, we did not see, so people reporting a low protein diet where there was overall mortality or was cancer mortality. People reporting a low protein 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, 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 Giovannucci in 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 is not even clear what the meaning of protein is anymore. Meaning that it's irrelevant because it's really about 20amino acids. Right. So we should be talking about amino acid level and amino acid patterns. And that probably explains. So, meaning that probably it's very clear that a low but sufficient amino acid intake is what you want up to a certain age. And by the way, the age should be biological age, it should not be chronological. So it could be 65 to somebody, but it could be 45 to somebody else and 72 to somebody else. So at some point, and you see the population weight, instead of going up, it comes down. Right. That's the point where we see this switch in mortality prediction. Yeah. So then it's about amino acids and again, epidemiology is one pillar. But then you have clinical studies, you have basic research. So how do you make a mouse live longer? Well, over and over and over and over for almost 50 years. Low protein, low methionine diet. Right. Just, you know, in rats, in mice and no matter who did it. And so, yeah, so then that's like another pillar. And then the centenarians, whether you look at okinawa, had a 9% protein diet, right. And for the longest time had record longevity. So I will encourage my colleagues to, you know, just expand from one pillar science to, you know, five pillar, and the fifth is complex system. But let's say even if you just go for four pillars, and if you go for four pillars, you see the devil is in the detail. It's about amino acids and it's about having sufficient and 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 that if you can make somebody younger, they will live longer, they will be much healthier. And again, there is a 10 to 30 fold difference between obesity and aging and 30 years of aging as a risk factor for Alzheimer's, cancer, cardiovascular disease, diabetes, etc. So. 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. Right. So the Ecuadorians have growth hormone receptor deficiency and that's the protein pathway. Right. So either mice, mice that have a growth hormone receptor or growth hormone deficiency are the ones that live the longest. They live 40% longer with the lowest disease profile. Right. This has been known John Kapczyk, Andre Barkey work for decades now, surprisingly, in yeast, the tenfold lifespan extension comes from the protein pathway, mostly from the protein pathway. So you block the protein pathway and the yeast now are reprogrammed to live 10 times longer. And then our work in Ecuador with people, sure enough, people that have growth hormone receptor deficiency are protected in spite of a terrible diet, are protected from diabetes, they're protected from cancer, they're protected from cognitive decline. They seem to have. And we brought them to LA to do a functional MRI test and their 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 we're lower or much lower in the pathway, the response to protein intake is blocked. The most damning part is the Harvard study showing a 40% increase in three different studies in this, Franco's work, three different studies, 40% increase in the diabetes risk in subjects eating high protein diet. Right. Compared to the lowest, I think it was quintile. So lowest quintile versus the highest quintile, those that were in the highest quintile protein intake in three different studies, almost identical results, right? So, yeah, so I think that it's really hard to imagine how you could conclude from all of these studies, and we were talking about hundreds and hundreds of studies that a high protein diet is good for you. I mean, it should be sufficient and was sufficient plus muscle training. Right? That's very important. And a lot of studies indicate that the protein intake you need per meal is very low. It's around 30 grams per training session. Right. If you have 30 grams of good quality protein with enough leucine and that stimulates TOR activation, you're going to get maximized effects on muscle building. And that's probably, I mean, and you could do, say even if you did it twice a day, you'd still be in a, you know, 60 grams, you'd still be in a relatively normal to low a protein diet.
- [72:59]
Rich Roll
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 weightly, you know, regardless of age, if they're like in the gym and you know, do like the negative implications of a higher protein diet would be abated by that very active person.
- [73:24]
Dr. Valter Longo
Yeah, not necessarily.
- [73:26]
Rich Roll
No.
- [73:26]
Dr. Valter Longo
No, not necessarily, no. Because the growth factor 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 want to maximize, reduce the aging rate and while increasing the functionality. So we're about to publish a couple of papers on that in mice, but also using the Harvard databases. And so. Yeah, I cannot discuss it, but certainly it's very consistent with what I'm saying. Right. The data is that first of all you need to really understand mechanism. How is each amino acid affecting which genes, which are affecting what processes. For example, if 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, that reprogramming factor, it seems like if you want to stop that process, high protein, and it makes sense. Right.
- [74:52]
Rich Roll
And does it matter if it's animal versus plant?
- [74:54]
Dr. Valter Longo
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 of if it was a 20, 30% difference between let's say legumes and red meat, you could say, okay, 20, 30%. I mean legumes and let's say soy or legume and seeds. Seeds and nuts. Right. So seeds and nuts. The amino acid profile between a seed protein, a nut protein and a legume is huge. Right. Then it's even bigger if you got red meat or even white meat. Right. And sometimes it's up to tenfold. 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 that amino acid may be the one that is making the big difference.
- [75:52]
Rich Roll
Yeah, I understand. And it's complicated. It's always more complicated than you think it's going to be. Right?
- [75:57]
Dr. Valter Longo
Yeah. But it's not complicated in terms of how you implement it. Right. So if you have a mostly plant based diet. 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 a low protein intake and then it's all legumes, you're going to have a problem. Right.
- [76:31]
Rich Roll
Because you're missing essential amino acids. Because you're 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, you know, 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 just, it's never really been an issue for me.
- [77:12]
Dr. Valter Longo
Right, right. But some people, let's say, you know, the Okinawans, you know, historically, and the southern Italians, and maybe this is why they were so long lived. Right. But they were very frail. That's interesting. Right. So if you look at southern Italy, the same regions that have record longevity because they used to have mostly legume diets, you know, yeah, the seeds and the nuts were there, but not in the type of quantities that. So the legumes were very much available and the rest of it was maybe less available. And not surprisingly, you see a frailty level that is almost twice as high as central and northern Europe. Right. So a lot of the Mediterranean countries are very frail, long lived, but frail. So I think that in your case, you probably had the muscle training and all of that and enough variety, but to a lot of people it could become a problem. Right. So if you say five times a week, your proteins are all coming from legumes, then they might not be so easy. If it's low road and mostly from legumes, then it might be difficult to keep the muscle mass.
- [78:37]
Rich Roll
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- [81:06]
Dr. Valter Longo
Yes.
- [81:07]
Rich Roll
And his blueprint protocol?
- [81:09]
Dr. Valter Longo
Yeah, I mean I don't know the blueprint protocol. I know the 100 supplements.
- [81:15]
Rich Roll
Lots of supplements. Basically putting a lot of time and resources and energy into trying to crack wide open this anti aging equation. But part of it entails his diet, which is a entirely plant based diet limited to 2,250 calories. I think something like that. It's very dialed in. His last meal of the day is at 11am so this is a fasting protocol. I think he goes to bed around 8:30 or 9 at night. He eats within, I don't know, 30 minutes of waking up in the morning, probably around 6am or something like that. And I think he has three meals throughout the day, small meals. Have you looked at this? Do you have thoughts on kind of what he's doing here? Yeah, all those biomarkers seem to be fantastic.
- [82:04]
Dr. Valter Longo
Yeah, yeah. Well the short term effects may be completely irrelevant compared to the long term effects. Right. So a good example is let's say the Breakfast Keepers. Right, The Breakfast Keepers, you know, if you look at short term they might be actually very beneficial. Right. And now people argue that the Breakfast Keeper have a worse lifestyle and all that. But let's say that new clinical data suggests that it's not just, it's not that. Right. If you start eating later you're going to have problems but it may be difficult to see what's going to happen 20 years later. Right. And you're going to get surprised. And the ketogenic diet could be another example. Right. So if you look at the ketogenic diet, very beneficial. Very. It makes you, you know, impressive results. But in the long run, people on a low carb diet and there's lots of Harvard studies, they live shorter or much shorter, much higher mortality, especially if it's low carb, mostly animal based diet. Right. So yeah, So I would say that, that when you enter a lot of territories, the 100 supplements and eating within three hour window each one of them is a gamble, is a big gamble. Right. And then if you put four or five together now it's a very bad gamble. Right. So you're exiting the territory of the five pillars in multiple ways. Right. So these centenarians eat in four hours and. No. Is there any data from mice? Yes, there is some data from mice that show that that's beneficial or potentially eating within a smaller window is beneficial. So you have mixed data in lots of things that is doing. But a lot of it I think is going to be negative. Right. So it's going to be. Or not done before. Right. So could it be positive? Yes, but it could also be negative or very negative. And so the surprise could come after 25 years and it could be a big surprise. Right. It could be a big surprise that now that is causing a big problem. People don't realize you just need like for example, ketogenic diet. Well, everybody talks about the ketogenic diet and cancer as a positive thing and it can be. Right. And there's a lot of animal studies now, some clinical trials that are suggesting. This is also in my book, that are suggesting that the ketogenic diet can be beneficial. But people don't talk about the cancers that are fed by ketone bodies. Right. Some cancers, they grow much faster. And there are 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 not 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, I just looked it up the other day and in Italy, drugs just. In Italy, drugs kill about 40,000 people every year. Drugs, right. Drug. Drug interaction.
- [85:24]
Rich Roll
Not like recreational drug use. No, no, no. Drug.
- [85:28]
Dr. Valter Longo
Prescription drug. Prescription drugs is 40,000 people a year. And in the US it's a huge number. I don't remember. I just looked up the Italian number for some reason and not the US but it's a huge number. Right. So you combine lots of drugs, they start interacting in ways that you cannot predict. And so now if you take 10 supplements, 20 supplements, 30 supplements, the higher the number, the more certainty, almost certainty, that it's going to cause a problem. It might take one year, five years, 10 years, but sooner or later that's going to cause a problem.
- [86:01]
Rich Roll
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. And we don't know, even AI wouldn't.
- [86:15]
Dr. Valter Longo
Be able to handle it for at least 20 or 30 years. They're so complex that you would need 20 or 30 years of data fed into AI to say, okay, now the only AI understands that maybe that's going to cause a problem. But yeah, so right now we're very far away being able to handle. Because you need big data, right?
- [86:39]
Rich Roll
So how is the selenium that you're taking interacting with kind of the mega dosing of vitamin D for example, or something like.
- [86:48]
Dr. Valter Longo
Yeah, because then the two are going to change the host metabolism or the host response and now the new host response. So it's not just how the two interact, it's how the two change the body. And now the two plus the body change, affect the third one that you're going to 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 supplements, now you have a recipe for disaster, maybe iron overload. Because now you just have added the third supplement that is making the ferritin work less. Well, for example, I see.
- [87:27]
Rich Roll
If you were counsel to Brian Johnson, what would your advice be? 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.
- [87:42]
Dr. Valter Longo
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 will add personalization. Right. So you will want to know everything about him and personalize all of it to him.
- [88:00]
Rich Roll
I think you 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 every day.
- [88:12]
Dr. Valter Longo
If that was the case, you wouldn't be eating in three or four hour window. Right. I think he's underestimating the uncertainty of doing something that nobody's ever done before. Right. If you just think about the short term effects and this is the overestimation everybody's making, you have diagnostics and you think that because, you know, so I had big experts in the field tell me, you know, I have extremely low fat, you know, like 5% fat. Well, well, data suggests that if you have a little bit higher fat levels, you may live longer. Right. So short term you could say I have 5% fat, I'm going to live forever. But the data is actually showing that those that live forever might be more in the BMI 25 range, right? Yeah. So then that's this acute response and this idea that if you have a very low fat that makes you very healthy is misguided. Right. Because that's not the case if you're trying to get to 110 healthy. And I don't mean just 110 frail like the southern Italians or maybe the okinawans, I mean 110 healthy. So then you have to have the five pillars or more than five pillars, and those speak very, very clearly. Right. So then on top of the five pillars, then you need the diagnostics. Right. Then you need to say, okay, I'm using the five pillars. I came up with all these things and now my cholesterol is still very High. Right. Well, okay, that's not enough. Then we need to intervene and make sure that cholesterol goes back to normal. And so, yeah, So I would say that again, if you look at the longevity records, it comes from mutations that do lots of weird things, like growth hormone receptor knockout. Right. It makes mice and people very short. Right. So. 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.
- [90:21]
Rich Roll
Speaking of people who are short, I came across that CNN article about Laren 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.
- [90:42]
Dr. Valter Longo
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 short term, you probably conclude that they are younger or they're functioning better, let's say. Right. But the mouse and the human data suggest exactly the opposite. Right? So the little people, it's like if you inject them with growth hormone, they'll have absolutely no effect. Right.
- [91:22]
Rich Roll
Because the receptors don't.
- [91:24]
Dr. Valter Longo
They're missing the receptor. You have the key, but you don't have the keyhole, so. Worthless key. Right. And so those mice and people that have the blockade in the growth hormone pathway are the one that by far are doing the best. Right? By far. I mean, if you look at, you know, mice, there is nothing that even comes close to this growth hormone and growth hormone receptor. And that's nice because. Because it can be that the mice are lacking growth hormone or lacking the growth hormone receptor. Either way, they have record longevity and record health. And this has been shown. We work with these mice, but lots of laboratories, so there's really no doubt about it. Right. So, yeah, so that's why this genetics data is so important. And it's part of the, you know, I put it in the centenary and the people that have lived with that change for. For 100 years. So now we have the data both for the Larones, but also for the Okinawans and for the centenarians of southern Italy or Loma Linda.
- [92:28]
Rich Roll
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.
- [92:57]
Dr. Valter Longo
I mean differently 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, say stage three, stage four, the ones that are in trouble, a lot of the clinical studies are now showing that it seems to have a big effect, right. Making the whatever, especially chemotherapy thus far better, right. So one of the nicest ones that I mentioned in the book is that triple negative breast cancer, very aggressive women with metastatic cancer. The fasting Mickey diet now is nearly doubling overall survival. In the first study by Vernieri and colleagues and then they just published a follow up paper which is not in the book, showing either chemotherapy alone, chemotherapy plus fasting mimicking diet or chemotherapy plus fasting mimicking diet plus metformin. And again nearly a doubling compared to the the expected survival of what's called pcr, complete pathologic response. These are just a few trials, but there is lots of them that are indicating that the fasting making diet is making survival better, making also the pathological response better. So if you look at the masses, the cancer masses after the treatment, they seem to have less active cancer cells. Now, now there's also an argument and this is why we say be careful, as I mentioned earlier, if you misuse it, let's say you say all fasting is good and so I'm going to get chemo and then I'm going to refeed at the same time. That could cause problems and not solution. And the other thing is fasting, mimicking diet has a very powerful effect, a 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, right? So in the early stages of the disease, right? So we don't know enough about it, we really haven't seen that. But I would say if it's early stage and the treatment is likely to be very effective, stick with just the treatment and don't try anything else. Maybe the longevity diet, maybe the 12 hour time restricted eating and this is what we do in the clinics, we say it's early stage and you have a 98% chance of being cured by it. Just leave it alone now. It could be that it will have helped you a lot, even in those early stages, but it could be that there's something that we don't know yet. 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.
- [95:55]
Rich Roll
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 that traditional therapy, that is chemotherapy in conjunction with a fasting, mimicking diet seems to have a beneficial effect that outweighs chemotherapy alone.
- [96:26]
Dr. Valter Longo
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. They're showing hormone therapy, for example. Right. Hormone therapy. So pulbociclib fulvastan. This is in mice, Right. And we also had the clinical trial, but in mice is very conclusive. You use the standard of care, pulbosiclib and full restraint 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. Right. You had the fasting, miking 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. The animal data is remarkable and really almost surprisingly, and it's not just my data, it's now a lot of labs that are looking at it. For example, in mice we published two papers and some Spanish groups have done the same immunotherapy. Mice does almost in some of these models for like say breast cancer and even melanoma does very little. And the fasting, mimicking diet alone does more than immunotherapy. Right. So I would say the potential is huge in all the different cancers and in all the different stages. But because there is a system and the system should be respected and we don't know yet, we haven't tested it for a lot of clinically, we haven't tested mice. We tested it, but not clinically, you know, that needs to be done before somebody. And this is why my comment about definitely if you're stage four and nothing else is working, yes, go for it. Right. Because the animal data is phenomenal. But if you're stage one and you already know that. You know, what's been done for 20 years is working very well, then I don't think you want to 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.
- [98:42]
Rich Roll
I think that you're very kind of circumspect in the way that you talk about, in the way that you just did throughout the book. Like, hey, listen, I'm not here to tell you this is some panacea. Here's what we're seeing right now. Here's what I'd like to see. Here's some resources, research that still needs to get done. I'm not telling you to not, you know, pursue every traditional therapeutic modality there is. I'm just saying, you know, 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.
- [99:18]
Dr. Valter Longo
Right, right. But in some cases, the clinical trial, like for triple negative breast cancer. Right. And even for hormone therapy, I mean, for triple negative breast cancer, you're starting to see randomized trials showing a big difference from what you expect or from what the control arm has. And this is in patients. So, yeah, for those, I would say probably talk to your oncologist and say, hey, what about these three or four papers? It's looking good.
- [99:49]
Rich Roll
How up to speed are the oncologists in this field?
- [99:53]
Dr. Valter Longo
Some are up to speed and a lot of them are not. And a lot of them are going to wait for an FD FDA approval, which may or may not come. Right. So some of these, it's very expensive, hundreds of millions of dollars to get an FDA approval. The FDA looks at fasting. Migraine diet is very complicated. So we talk to the fda, and to make it feasible or to make it appropriate for the FDA, you probably need to take the 60 ingredients or so in the fasting making diet and make it into six or seven, which would make it very difficult to do and very difficult for the patient. Right. So it may or may not end up in FDA approval. And so I think the way to go is for the oncologist to be informed and to follow. And it's going to be a point where there's going to be enough trials and there is enough standardization of the diet that the oncologist could say, hey, this has been tested in seven or eight trials. It looks very good, and I'm going.
- [100:55]
Rich Roll
To recommend it is breast Cancer, the form of cancer in which you're seeing the most kind of optimistic positive indications.
- [101:03]
Dr. Valter Longo
No, in the animal studies, it's working very well with all kinds of cancers.
- [101:08]
Rich Roll
In humans though.
- [101:09]
Dr. Valter Longo
Yeah. In humans. Is breast cancer just being tested a lot more? It's not that we tested the others and it didn't work. It's more that we know this disease better. Well, there 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 in breast cancer or immunotherapy in breast cancer. But now that we're starting, they're starting our trials on colorectal cancer. We finished one on prostate cancer. Eventually, hopefully we'll have a lot more. But there just hasn't been that many trials in any other cancer other than breast cancer.
- [102:04]
Rich Roll
There's one randomized study that you talk about in the book with respect to breast cancer. 131 patients showed very promising results in the context of the fasting mimicking diet being kind of woven into their treatment protocol. 90 to 100% tumor free masses were seen in only 8% of patients who completed chemotherapy without any FMD, 29% with one cycle of the fasting mimicking diet, 33% with three or four cycles, and 53% with all chemotherapy cycles combined with a fasting mimicking diet. I mean that 131 patients, not the biggest population, but not insignificant either. Like that's a considerable result.
- [102:56]
Dr. Valter Longo
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 that that's too early because that trial was in women that were to receive the surgery. So early stage, about to receive surgery. So I think that, you know, we'll see, but it falls into the category of too early to try it until there's more clinical data. Right. But whereas in the metastatic setting where we see the same exact results with, with the, the very similar to what you just described. But now in patients that are, have metastatic cancer. Yeah. Then I think that that's a very different scenario. It's working very well and that's where we've seen the overall survival difference, at least in the early trials. So I'm more optimistic and excited about, about the metastatic one than the early one because the early one in that trial is not enough to make conclusions about Long term survival. And 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 that definitely a wild card. I will call it that, a wild card for any cancer patients. You know, of course, after a discussion with the oncologist, for any cancer patient that is in this situation where this is not working, right. And then the oncologist says, you know, doesn't look good.
- [105:06]
Rich Roll
That's it, you know, two to six months. And there's not much more.
- [105:10]
Dr. Valter Longo
Not just that it can be stage four, you know, three to four years, but it's not working very well. And we're concerned. Right. So, yeah, that's the. If the oncologist comes back with, okay, this didn't work, but we have this, and this could work extremely well. Right. And we're very confident, okay, then try that. But at the point where the oncologist comes back and say, there's really nothing left, and yeah, you could still live seven or eight years, but we just don't have anything right now, that's when I would definitely talk to them. This is what the clinic, the foundation clinics do. Working with the oncologist and saying, okay, this is a good time to give it a shot. Right. And see what happens. Hey, and 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 Vernieri, published five cases of stage four colorectal lung cancer. And in fact, the lung cancer patient.
- [106:13]
Rich Roll
Yeah, Maggie Jones. I mean, that was like the most impactful story in the book, I think.
- [106:18]
Dr. Valter Longo
No, Maggie. Yeah, but then in the Vernieri, I didn't talk about it a lot, but in the Vernieri study that is published in European, I think, Cancer Journal, there's 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, there'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 four going into remission. Right? And so, yeah, so they were so surprised that they decided to publish a paper saying, okay, we don't know, it could be a crazy coincidence. But that's a little strange, right, that we're seeing all these essentially. I don't know if I want to call it that sentence, but certainly, you know, there's not much hope left, right? And then, you know, seeing in one case, I think it was the colorectal, the cancer came back after three or four years, but there was already and then the same treatment and the same result. So, yeah, so I think the hope that there is something that could make a big difference, right? That's, I think what we got right now and hopefully we'll have the demonstration of it in big clinical trial.
- [107:40]
Rich Roll
You know, from a mechanistic point of view, the way you describe it in the most basic sort of layperson 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 cells in the same way they impact cancer cells. And through autophagy, like they can kind of, you know, kind of regenerate themselves. Regenerate healthy cells. Is that, is that.
- [108:21]
Dr. Valter Longo
Yeah, I think the, 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, hey, I gotta get it from the bloodstream, right? So if you just do fasting or fasting, milking diet, they're not happy, you know, but it's. 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, it'll have the slowing down effect of cycles of chemotherapy. But then when you combine it with chemo and we combine it then with immunotherapy, when you combine it with Hormone therapy, et cetera, et cetera. That's where you see in a lot of cases, we actually can drive the cancer down to zero or really stop, stop its growth for a very long time. So I think, yeah, the cancer cells are confused. And now we have this technology that I talk about in the book, which is we call starvation escape pathways blockade. So basically we use technology to say, okay, I starve the system with the fasting making diet, but then I take the cancer cells and I look at how they rewire using this RNA seq technology. So I can show, oh, 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 I just block it. Right. And that's really. And we publish has got incredible effects. Right. So alone that, yeah, delays a little bit, then we identify the escape pathways and we block it and tumor comes down and stays down either for a long time or permanently.
- [110:37]
Rich Roll
So what is the message that you're trying to convey in this book? 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, so who's the reader for this and what is it that you want people to kind of get from it?
- [110:58]
Dr. Valter Longo
Yeah, well, first of all, everybody in the cancer prevention settings, right. So treat aging, prevent cancer. And that could have a remarkable, whether it's the fasting making diet or the longevity diet or the time restricted eating or the other things that are in there. So prevent cancer. Then if you're unlucky enough and you get cancer at the beginning, you can still do lots of things like longevity diet, time restricted eating different. Right. So now time restricted eating, we go to 14 hours from 12 if you are a cancer patient. Right. So we increase it to 14 hours. And longevity diet, we have to work on making sure that you don't lose muscle, your immune system doesn't get weaker. And so that's everyday diet. Then the fasting, mimicking 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 would say just do the longevity diet and time restricted eating and do lots of other things that we talk about in the book, but that's it. You know, if you are metastatic or the oncologist say 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.
- [112:27]
Rich Roll
What is your sense of the impact that AI is having or will soon have on your specific field of study?
- [112:35]
Dr. Valter Longo
Yeah, I mean, what I just said. I think eventually AI will make that process of identifying the escape pathways and the drugs very quickly, almost immediately. And I'm not talking about 20 years, I'm talking about two or three years. So in two or three years, I think we can probably, if we had enough money now, if the NIH is shut down, maybe we won't. But I think in two or three years of enough funding, we'll be able to use AI to very quickly get to the escape pathways. And so then the idea will be I use the FMD as a wild card and I use the AI to tell me what the other drugs are. And then I use fda. Already FDA approved drugs block it. Right. And so it's a little bit of a science fiction world. I call them cancer antibiotics. Right. So, yeah, so I see that with enough funding in the next 10 years, we might have this sophistication to say kind of like 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 finding, this could happen in the next 10 years where, you know, you get your cancer antibiotics, you have very low toxicity, kind of like FMD plus plus plus very low toxicity drugs that you can just take. And let's see if the cancer goes away. And you know, if it doesn't go away, then we'll try something else. But yeah, I think that's clearly theoretically, but also using the animal data, this is very close, right? But yeah, so sometimes it could be very close. Three years, it could be very close 30 years. You know, it's hard to know, but I think with the right funding, it could be within 10 years.
- [114:16]
Rich Roll
And outside of the cancer context, are you among the techno optimists in terms of how AI is going to impact healthspan extension in a wide variety of ways, kind of beyond your area of expertise specifically?
- [114:33]
Dr. Valter Longo
Yeah, I'm very scared of AI, so I don't like it at all. All.
- [114:37]
Rich Roll
Well, here's Sorry to interrupt, but I'll just say one thing. I've said this before on the podcast but like, you know, I've had Yuval know a Harari on the podcast and he's, you know, 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.
- [115:00]
Dr. Valter Longo
Yeah, yeah. Very scary, right? Very scary. Yeah. You know, I think to see how scary it is, you have to look at evolution. Systems evolve and it doesn't really matter whether that system happens to be derived from single cells or from a programmer. That's the 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 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? Right. So that's what sets the stage for it's just a matter of time before it's going to evolve. Right. And it's going to find its way. And the question is, what way is it going to find? Well, if you look at the past dinosaurs and all kinds of organisms, you can see that some of the evolution could end up in the wrong place for humanity as an antagonist. So yeah, that's what I'm worried about. Of course I agree with all the benefits. I just talked about one but it's not something that we couldn't do computationally anyways. So I think that, I mean, I don't know, maybe there's nothing we can do. Right. We cannot block AI so I think we could regulate it. Right. And begin regulated in a planet wide manner. So that's probably the thing that we need to do very quickly. That would be my suggestion as somebody that works 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. Imagine generating a dinosaur and thinking about how much money you're going to make in Jurassic Park.
- [117:16]
Rich Roll
Well, this is happening. The woolly mammoth is underway. That company just raised like some crazy amount of money and like it's going to. That's what. That is what is happening.
- [117:26]
Dr. Valter Longo
Yeah. Yep. We have more problems than AI then I guess. But yeah, so I think that we, I Don't understand. I mean, maybe it's just obsession with making money that is driving this irrational exuberance that has very little worst case scenarios. Right. You know, what's the worst case scenario? Well, if the worst case scenario is really bad for human beings, then probably not a good idea to not regulate it. Right?
- [117:59]
Rich Roll
We talk about regulating it, but not really. I mean, I think there are a lot of smart people who are thinking deeply about this, but the momentum behind this just moving forward is too great at this point. And I think, yes, 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 going to keep doing the thing and we'll like deal with the circumstances in the aftermath and yeah, we'll give lip service, we better be careful, but we're bowling forward no matter what. And that's what I see happening. And I think in the short term, like certainly there's incredible implications 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 is something to celebrate. But there is the larger looming existential questions that are a little bit harder to kind of grapple with and determine solutions. But I think we lack the adequate humility to really respect the gravity of what we're doing. And I think we think we might know what the implications are, but I don't think we really do at all.
- [119:28]
Dr. Valter Longo
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 probably rather not be in, right? Somebody goes crazy, it just wipes out the entire planet. Planet. So this is much worse, right? I mean, compared to the AI, I think the danger of nuclear power is very small. Right. That's why it's particularly surprising that we don't see it for how powerful it can be. And it will be. I mean, it's not. It can be, it will be what happens then, Right. So I don't know if we went back and you know, in the nuclear science we had made the same choices. If we had a choice at some point back in the past, 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. There's a lot of benefits, but maybe, maybe it wasn't worth having those benefits available to us considering where we are right now. Yeah. So in AI, I think it takes it to another level.
- [120:46]
Rich Roll
Well, we're going to 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 going to have a baby soon. Yeah, yeah, yeah. So you're probably thinking about things more philosophically.
- [121:03]
Dr. Valter Longo
Yeah. That's what makes me worry. Right? Oh, yeah.
- [121:06]
Rich Roll
Yeah. Well, I appreciate the work that you do. It's a service to humanity and I just want to acknowledge you for that service and appreciate you coming here and sharing with us. And you're always welcome here. The new book is Fasting Cancer and if people want to learn more about your work, specifically Valter, where should they go in addition to checking. Yeah.
- [121:28]
Dr. Valter Longo
Instagram, I think. Professor Valter Longo on Instagram and also the Create Cures foundation. That's, you know, createcurious.org I think. Yeah.
- [121:39]
Rich Roll
Excellent.
- [121:39]
Dr. Valter Longo
Thank you. Thanks a lot, Rich. Great talking. Cheers. Peace.
- [122:02]
Rich Roll
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@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@meals.richroll.com if you'd like to support the podcast, the easiest and most impactful thing you can do is to subscribe to the show on Apple Podcasts, on Spotify and on YouTube and leave a review and or comment. This show just wouldn't be possible without the help of our amazing sponsors who keep this podcast running wild and free. To check out all their amazing offers, head to richroll.com sponsors and sharing the show or your favorite episode with friends or on social media is of course awesome and very helpful. And finally, for podcast updates, special offers on books, the meal planner and other subjects, please subscribe to our newsletter, which you can find on the footer of any page@richroll.com Today's show was produced and engineered by Jason Cameolo. The video video edition of the podcast was created by Blake Curtis with assistance by our creative director, Dan Drake, portraits by Davey Greenberg, graphic and social media assets courtesy of Daniel Solis. And thank you Georgia Whaley for copywriting and website management and of course Our theme music was created by Tyler Pyatt, Trapper Pyatt and Harry Mathis. Appreciate the love, love the support. See you back here soon.
- [123:41]
Dr. Valter Longo
Peace plants.
- [123:43]
Rich Roll
Namaste.