STOP Intermittent Fasting If You Want to Stay Young

A lot of people probably focus on the short-term effects of things. They'll do something and they'll see what happens, you know, a month or two later. And they try to extrapolate that into the rest of someone's life, but it doesn't work like that. If you look at 100 years of data, the only intervention to make mice and rats constantly longer live is protein restriction. High animal protein intake have a major increase in diabetes, also a major increase in overweight and obesity. If you have high tour activity, this tends to keep the system in a pro-growth modality, but also pro-age. A lot of people like to hear about eat a lot of this or avoid that. And in most cases, it's having to get it exactly right growth hormone. It's clearly the most powerful that there is. When that becomes important, that's a little tricky. As you make those anything, they're going to disrupt this equilibrium. Very sophisticated equilibrium that the human body has built after billions of years of evolution. 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This is his second time on the show, and he's a professor of gerontology and biological sciences. And director of the longevity institute at USC, which is a pretty good pedigree for someone who's going to talk about longevity, and what happens if you don't eat every now and then, or maybe you do eat, but you just eat the right things. Fulter, welcome back to the show. Thank you. Good to be here. All right. You spent your whole career studying aging, and thank you for that, by the way. If you had to explain the biggest thing that people still get wrong about aging, what would you start with? Probably focus on the short-term effects of things, right? So they'll do something, and they'll see what happens, you know, a month or two later. And they extrapolate, or they try to extrapolate that into the rest of someone's life, but it doesn't work like that, right? You could have something that is extremely effective, short-term, maybe even for years. I think probably GLP1 drugs are one of those examples. And then, you know, eventually, it can still help you, but it might help you a lot less than something else, right? So, you know, again, GLP1, you could look at it as an anti-aging drug, or you're beginning to look at it as anti-aging drug. But then you have to say, I will compare to something else that maybe is much more effective. So, yeah, so I think that's probably the, my number one complaint, yeah. What's more effective than GLP1s for longevity? So, I think that if you look at what I call the longevity diet, right? So, but even if you just look at the Mediterranean diet. So now we know that for GLP1, there's a reduced risk for cardiovascular disease, long-term, right? So, somebody could say, okay, now you have the weight loss, you also have the reduced. That's what everybody's saying, right? You have reduced risk for cardiovascular disease, so it's very good. But then you compare with just the Mediterranean diet. And the Mediterranean diet is two to three times more effective, you know, against cardiovascular disease. And so in the Mediterranean, it's probably not the ideal in an anti-aging intervention. It's a good one, but I don't think it will compare with what I call the longevity diet, which has, say, fasting, mimicking diet, 12-hour time restricting, intervening at the exercise, and the sleep, and all of that, right? So, yeah, so that's probably much, much more powerful and not necessarily not feasible, right? So, a lot of people will say, well, it's too many things. Yes, there's a lot of things, but not that big of a change compared to what people normally do, right? And that's why we're talking, for example, fasting, mimicking diet. And I'm assuming we're going to talk about that three times a year. Now we're testing it in Italy once every three months for the first time. Actually, we're almost done with that large clinical trial. So, what happens if you do this? Only three or four times a year versus once a month, which is what the previous trials were focused on. And for listeners who didn't catch the last time you're on the show, and Prolon is a company that you help to start that does the fasting mimicking diet. So, you basically get a box of food that you can eat, but you're still getting the effects of a fast while you're eating it. I just did a Prolon fast recently. I did it online with a bunch of people because it's easier than fasting for five days to just eat nothing. So, the compliance is a lot higher with something like the fasting mimicking diet. What does it work, though? Why does it work? Well, probably lots of reasons, right, and one of them, so we published a series of papers in both mice, rats, and people. And so, in mice, we were seeing what we call multi-systemic regeneration. So, you see effects in the pancreas, in the gut, in the nervous system, in rats, we just published in kidney. So, in some cases, is the increase of stem cells. So, the fasting mimicking diet increases circulating stem cells or local stem cells. And in some other cases, is reprogramming cells. So, it's turning on what's called Yamanaka factors. Sometimes, multiple Yamanaka factors. The interesting thing is it seems to be different. So, from a study to study organ to organ. So, for example, in the kidney, we saw mick being activated, nanog, and some other embryonic developmental factors. Whereas, in the pancreas, we saw, you know, opt-for socks to different reprogramming factors. And the Yamanaka factors basically have the job of bringing a cell, an old cell, back to an embryonic like state. But, whereas, when you force, let's say, Yamanaka factors, you could have good and bad, the advantage of fasting is a very coordinated, very much evolved method or system. And so, you don't have the good and bad list, maybe some bad, but we haven't seen it yet. Because, again, the great majority of organisms have undergone fasting periods in their history, or in the history of their species. So, I guess we have multiple mechanisms. I usually look at insulin levels and M-tore as being the most important reasons we had fast. Can you explain what those are for people who don't know, and what fasting does for those? Yes. So, insulin is usually reduced long-term. So, insulin is responsible for allowing glucose to come into cells, but it's also controlling fat storage. So, high insulin levels are associated with the high storage of fats. So, insulin after cycles of the fasting making diet come down, and they usually stay down. But, also, something like insulin like growth factor 1, IGF 1, it comes down acutely, but it also stays down for months after the fasting making diet is discontinued. So, yeah. So, there is reprogramming of a lot of these factors, including insulin, IGF 1, and part of the effects, at least, even the ones that I just mentioned, and reprogramming and stem cells are due to tore down regulation. So, M-tore is a kinase and enzyme that basically is involved in protein synthesis and lots of other growth, you know, recent size, let's say, of organs and cells. And so, one of the messages that blocks this reprogramming and stem cell activation is the one given by torque. So, if you have high-tore activity, this tends to keep the system in a pro-growth, pro-expansion, pro-reproduction modality, but also pro-age. If you don't have enough of this M-tore, which causes tissue growth, you can't put on muscle, though, and you don't regenerate. How do you balance that out? Yeah. So, there is a minimum that you need to activate muscle generation, let's say. And so, yeah, you need to hit the minimum. It's usually, I mean, of course, the fasting making diet is only five days every, let's say, two, three, four, six months, even. So, you have all the time in the world to do that. But let's say that you had a very low protein diet, in particular, a very low lucy metion in diet. Yes, those could bring a tore activity below a certain level, and let's say, if you were maybe below 0.7 gram per kilogram of body weight, and especially if there was mostly plan-based. So, if you have a combination of low protein and mostly plan-based, yeah, you may have a problem building new muscle, just because this levels of tore is so low that it prevents muscle synthesis. Now, you know, in the FMD, you know, trial number four or five that has looked at muscle mass, we see either very small reduction, again, compared to the GLP ones, we see lots of fat mass loss, very low limb mass loss. In some cases, even increase in limb mass loss. And so, this could be due to the activation of potentially of this PAC-7 and somebody's satellite cell, muscle stem cell activation. And so, we believe that maybe that's why, in some cases, we even see muscle increase after, for example, in this study we published together with University of Rome, and six consecutive cycles of the fasting making diet once a month. At least the estimation of muscle mass of limb body mass was an increase, a major increase after the six cycle. Now, it was done by by imperial geometry, so I don't necessarily believe that there was this as big of an increase as we saw. But even if there was a minor one, there's two very good news because it suggests that there is a targeted loss of fat, especially abdominal fat, in protection of limb mass. When people are too lean but still have adequate muscle mass, do they need a fast less? Probably, yes, right. So, somebody is, say, very low BMI, they are, well, they could still benefit from the fasting, but because we're cautioned, I would say, they should probably fast less or a lot less. And, too, we know more or a lot more about it. I mean, so the people that my colleagues study color restriction, continuous color restriction is severe, continuous color restriction, they would say that the people, the even males that go down to a BMI of 19 are very healthy. And so, they may say, well, it's okay, even if you're lean or very lean to keep fasting, but I think in our case, we are, we're ready to be cautious and say, maybe not, right? Maybe do it less. And let's wait until, you know, we have more years of reports and millions and millions of people have done this and then maybe we can make that choice. I'm kind of asking for a personal reason, like, I'm 6% body fat, right? And like, I don't want to be lower than 6% because from what I've seen, not having adequate body fat might increase your all-cause mortality risk, like, maybe should be at 8% as a guy. Maybe even higher, but I think it's probably benefits and problems, right? So, and that science is still poorly understood, you know, so why is fat? And lots of even male studies, some of the mice that are able to retain fat are the ones that do better under color restriction, right? So, if you're color restricted, you undergo this severe diet, some of the mice that perform the best are the ones that are better able at keeping some fat. So, yeah, so is it the same in people? And of course, the data is indicating that, you know, older people that have a little bit more fat reserves, they tend to do better. And so, yeah, I think what I always imagine is this equilibrium or having to get exactly right versus this idea of a lot of this and little that, right? So, a lot of people like to hear about eat a lot of this or avoid that. And in most cases is having to get it exactly right. And fat is the same way probably, right? So, although, you know, what is the perfect fat level? Well, probably changes between different ages, right? So, your age may be fine to be very low, but, you know, as you get older, it may be that a little bit more reserves are better. Through all the different biohacks and optimizations, I'm not lacking muscle, but it's very hard for me to put on fat now. And I've come from a background of being obese, I was 300 pounds. And so, all the people in my family are fat except for me. And I find it extremely hard now to put on another 2% body fat. And so, I wrote a major book on fasting. I'm certainly a fan of it. Then I do short intermittent fast, but I haven't done a longer fast other than the pro one fast recently in a while just because I'm maybe I should get a little chunkier. But it seems like the science is out on that. Yeah. And I mean, there are ways to gain some fat to then lose it again during the fasting or the fasting making diet. So, that's usually what we recommend to patients that are particularly fit. And then they gain. I've been trying to gain fat. I just don't work. I mean, I can eat 400 grams of carbs and, you know, sticks of butter. I just don't have fat. It's kind of crazy. Maybe you're in such a metabolic state that, you know, at least short term that those interventions don't work. It's an interesting conundrum because we have this kind of fetishization of, you know, having abs. And especially in women, that can be too lean. I think sometimes in guys it's too lean as well. I don't know that we have a ideal body fat, like I said, it may change over time, but I think for listeners, I'm being too lean is probably not ideal and being too fat isn't ideal, but we don't know the perfect middle. And it may vary based on your genes and your your background, you know, if you're from a part of the world where people will usually carry more fat, maybe you need more fat. Is there like doing that research? That are probably people doing it. But I haven't seen a consensus on that. Certainly, if somebody is, say, less than 60, a low body fat is probably generally good, right? Or very low body fat. I think once you get to, so in our studies, when we look at the enhanced database, after 65, the population, the US population starts losing weight, so losing weight means losing limits, but also losing fatness. And so probably that's when having low fat may contribute to the problem. Because now the fat is also reserves, energetic reserves, maybe stem cell reserves. So probably that's when it may be problematic to be extremely low fat, when things are starting to go, you know, the downward way. That makes sense. And I'm hoping that some research group comes out, maybe someone who's studying a PhD is listening right now. And yeah, optimal body fat based on what variables. Yeah, let's do that research. I think it would be helpful for a lot, like tens of millions of people. I want to talk with you about protein. And when I wrote my big longevity book, I'd, you know, thousands of papers and things. And it seems like 0.6 grams per pound a body weight. There's a bunch of research suggesting that, which is, you know, 1.2 grams per kilo, or thereabouts. And there's also, though, another smaller but vocal group that says, no, it should be 1 gram per pound, or 2.2 grams per kilo. I've tried both. And man, my markers are better and my energy is better, my body composition is better when I do the 2.2 grams per kilo. And I'm trying to compare that with your recommendations, which are substantially lower protein than what I've found works. And it seems like there's these, these kind of two spikes of data around these. And there's a bigger spike that says 0.6. And you're even below that. So how do we make sense of the optimal amount of protein for humans? I think, I think we're going back to what I was saying earlier, right? Acute effects versus how do you make it to 110 healthy. And so, you know, if you look at a hundred years of data, and maybe we talked about a few years ago, when I was on, if you look at a hundred years of data, maybe the only intervention with that color restriction to make mice and rats constantly longer live is protein restriction, right? Or methane restriction. You can do protein restriction, you can do methane restriction, or you can do color restriction. But that's really hard to do it any other way, right? Without color, especially with that color restriction. So if you look at the monkeys, they lived the longer the longest or there were and color restriction in the Wisconsin study, you know, they had the 25% reduction of color, but including proteins. And if you look at the harbor data on, you know, a protein intake and diseases, you know, one of the studies by Franco, a few years ago, showed that, you know, this is the physician and nurse study indicating that those that have high animal protein intake have a major increase in diabetes. And with that, also a major increase in overweight and obesity. So, and then if you look at their cardiovascular epidemiological studies, pretty consider one just came out. I think a week ago, high protein intake associated with a major increase in cardiovascular deaths. If you look at, you know, I was having a conversation with Dan but in a few days ago, and I say, then you turn the world and, you know, looking for people that live long. Did you ever meet a long live population that had a very high protein diet? And he's like, no, I don't, I don't know, I don't recall a single one. What about Hong Kong? Like Hong Kong, they eat more meat than anywhere else on the planet and they have a well blue zone there just without the beans. It seems like I always like to find the outliers because then they tell us that our hypothesis has room for corner cases, right? Because that is a big red meat eating population. Right, right. I mean, we don't have any causality type studies, right? So, we definitely don't have causality that's fine, I'm asking. This is why I described the epidemiological data, including our own, right, looking at enhance a major increase in cancer and major increasing in overall mortality. But then the Swedish studies, the Harvard studies, and the Mao studies, the red studies, the centenary studies, the genetic, you know, the little people in Ecuador that we follow, well, we guess where they have the mutation in the growth hormone receptor. So they're very low IGF1 and, you know, clearly protected in the mice, right? The mice that are growth hormone receptor deficient or the mice that are growth hormone deficient. 30 years of work by John Kupchik and Andre Barkey. And those are the mice that have the record longevity extension, right? And where do they have the mutation in the protein path? In the protein amino acid pathway. So it's like, they were consistently and constantly on a very low protein diet. Okinawan's record longevity in Japanese historically traditional Japanese diet. Japanese have been number one in life expectancy for 25 years now. Right. Japanese have always had one of the lowest protein intake and 50/50 plant animal, right? So low protein intake and lots of plant based proteins which have very low essential amino acids. So I think you have all of this, you cannot argue with Hong Kong, right? I mean, you could say, "Hey, what if?" But you have now 100 years of data and you need another 100 years of similar data to counterbalance that. And we can not just pick a study or two and say, you know, especially Hong Kong where it's not like, you know, we follow them for 30 years and and we now know that the proteins are contributing to their, you know, high life expectancy. So they may be, they may be like they could have been even longer lived or healthier if they had the the same healthcare system and everything the same, but a low protein diet, right? So Yeah, it's, it's a good understanding. I just said a two-hour show with Dan who's just a wonderful human being. And so I, I don't play the, you know, take down. I'm just genuinely curious and I'm always saying, well, if I can find one example, but you're saying that the Hong Kong example isn't, isn't strong enough from a data perspective to, to take action on it. It just, it might be a counterpoint, but we're not sure yet. Is that a good way to put it? No, we're pretty sure that we shouldn't use it as, as an example. I think we should use the five pillars, you know, epidemiology, clinical studies, you know, the mouse studies, the red studies, the monkey studies, yeah, all of it, right? The centenary and studies, you know, the mediterranean diet, traditional mediterranean diet, guess what? Fairly low protein, you know, two to one plan based, the traditional one and the mother one is, is, is different. But so again, low, I mean, as, and by the way, I think we eventually, very soon, we should stop, we're going to publish a few papers and this, we should probably stop talking about proteins, right? Because it's really relevant, uh, we'll, we'll protein. Because you can, three, four, five falls difference in amino acids between two different sources of protein, right? So, so then, and I know we need application, we're going to need the application because people are going, are going crazy already as is. So, I should be made easy, but I think it's really about, I mean, you know, acids, right? So, how much, what is the amino acid profile in the diet of someone and, you know, and, and then, you know, make, they can make decisions based on too much of one or more, amino acids that are contributing to aging or they're contributing to frailty if they're, if there are deficient, yeah. There's another variable for protein that the people don't oftentimes talk about in just a common Instagram influencer world. It's the rate of absorption. So, even if you have a certain amino acid profile, if it takes six hours for your body to absorb it versus two hours to absorb it, there's a peak of amino acid availability in the body that's probably important. So, like, slower proteins do something different than fast proteins. Do you have any, uh, any opinions on that? Um, I think that the opinion will be more about the timing probably with, uh, we're working out, right? So, if somebody was trying to build muscle, then, um, you will probably want to time it. And there's lots of papers we cover some of them and, you know, indicating different timings and different quantities of proteins being, um, you know, so the one I quoted some years ago, but I have not updated it was, you know, 30 grams of good quality proteins will maximize the, uh, muscle synthesis if time correctly with the workout. So, also, and there was many in my book, uh, but, uh, yes, I think soon enough, it probably be good to, uh, to, you know, put it all together and, and, and see, if there is any changes compared to what I, I had proposed, uh, back a few years ago. But, yeah, so I think that that, because, uh, other than that, I think the body is, uh, is pretty good that, uh, you know, absorbing, uh, what it needs. I mean, unless there are gastrointestinal issues and they utilize in it, uh, for, for the purpose of protecting the, the muscle and, and the, and the bone density. I saw a couple studies recently showing that it doesn't look like there's an upper limit to the amount of protein we can absorb. They were doing 100 grams per meal and finding that the body was making use of it. Is there any, any case to centralize in all your protein to one meal in a day versus spreading it out? I think that in general, probably, again, going back to the 30 grams, if somebody has a goal of, of muscle growth, uh, probably good to have at least that level. I think it was leucine had to be, uh, so high. And I think it was because leucine affects on tour. And so you have to meet those otherwise probably the synthesis is limited. But in general, I would, I would, I mean, of course, I recommend 0.8 grams per kilogram of body weight as many, uh, medical associations around the world are fine with. So, so it's fairly low. But, you know, I, I agree that, you know, if you look at, for example, southern Italians and Italians in general, they were more frail, they were longer lived more frail compared to central and northern Europeans, right? So probably is telling you about trade-offs, right? And so, and then I'm, and I'm sure I mean, there's data indicating the Japanese were more frail compared to lots of other countries, least traditionally. So they, they, they live very long, but they did give up some things. And, and so again, we need to find that that balance that reduces cancer, reduces cardiovascular disease. And, uh, and reduces obesity and diabetes. And at the same time, it, it, it optimizes, uh, strength and function in an age-specific manner, right? So, yeah. So we're about to publish several papers on that. And, uh, but they're not all, yeah, so, so, you know, hopefully six months from now, we'll, we'll, um, we'll be able to sort of say more about exactly, you know, what is the way that you orchestrate, you know, longevity, disease prevention, function, and strength? Yeah. Wow. I, we'll come back on when those come out, because I'd love to go deep with you on it. Um, what is the, the best amount of total losing per day if you want to live a long time? Yeah. Yeah. I, yeah. I'm in red to calculate it. But, you know, Lucene is, is fairly low in, in legumes and, and lots of other plain-based, uh, protein sources. And so the, the, the, to live long, and there's data, you know, where Lucene restriction makes, um, mice live longer. And, uh, and, you know, if you look at the traditional kinawan, they had 39 grams of proteins per day, at least according to some of the, the traditional kinawan diet papers. So, 39 grams of all plain-based proteins, right? We had this, the, the, the, the zokinawan's had such a, a long lifespan and health, you know, had a ridiculously low amount of amino acids, including Lucene. So, so, yeah, so, I think that, um, again, probably, very low levels are promoting high levels of protection against aging in diseases, but also promoting frailty. And so, and so, Lucene would probably, uh, eventually have to be those based on, again, age, what age, what muscle mass you have, and what risk do you have of developing one of a number of diseases for which high levels of this amino acid could be a risk. Your face is the first thing people see, and you can work out clean, but if you still look older than you feel, especially if you're a guy, you're not maximizing your potential. Your skin is a signal of how well you're really taking care of yourself. And if it looks inflamed or tired or just old, that's what people are going to notice, even if you're doing your best to eat well. The good news is there's a company called Keldera Lab that's here to fix that for you. This isn't your girlfriend's 20-step routine. It's skin care designed specifically for men, which means it has to be simple and effective and backed by science, but not too much work. After using Keldera Lab products, 100% of men said their skin looks smoother and healthier, and 97% said they had improved hydration and texture, and 93% reported a more youthful appearance. Keldera Lab has spent years developing and testing each of their formulas with leading cosmetic chemists, so you can tell it actually works. 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So if you're not taking over your skin because it's just been too much work, now you have a solution calderalab.com/dave. Haging doesn't start with low power or how many calories you eat, even how much exercise. It starts inside your mitochondria. These tiny engines inside yourselves make energy, and as you get older, they naturally slow down, unless you do something. When they slow down, recovery takes longer, your strength goes down, and your power fades, no matter how well you eat, or how well you train. Might appear by timeline addresses this at the source. It's the only form of uralithin A that human clinical trials support, and it works by promoting a natural process that scientists call mitophagy. This is where your body gets rid of old damaged mitochondria and recycles them into new, healthy ones, and I've written two books about mitophagy. The result from mitopure is noticeably more energy, stronger muscles, and better resilience, and your workouts start working again. I'm light and spent more than 15 years researching mitopure, and now they offer it in a gummy without any BS, and it's really delicious. The gummies are sugar-free, NSF certified, and clean label project verified, which is really important if you care about purity and living a long time. Mitopure delivers the exact dose that scientists used in human trials. I've used mitopure for over five years because having healthy mitochondria is a huge part of my longevity strategy. Mitopure belongs in your longevity sack too. If you want to support cellular energy where it actually starts, give mitopure gummies a shot. Go to timeline.com/dave and get 20% off. That's timeline.com/dave. Is there a way to block losing? So if I want to eat a steak, but I don't want all the losing, what can I take with it so I don't have to pay the cost of the steak if there is one? Well, we've been working on that with John Coptic, right? So John is the Ohio university professor who came up with Sunday Coptic Visumant, and Pig Visumant is an FDA approved drug for acromegaly, right? So excess crotormone. And so John and I, for a number of years, I've been trying to start up a company where we will focus on, let's say, oral crotormone receptor inhibitor. So this is the same crotormone receptor that is blocked in this very long live mice and the people in Ecuador that are, you know, don't develop disease or develop disease, a lot less than anybody else. So I think that's probably the best way also because there's all these data coming from all these directions and very consistent. So blocking the crotormone receptor. Now, you know, the FDA is not that interested in aging. And so investors are now very interested in aging, but that's a drug that was pat as not being funded yet. So we'll see, right? We'll keep on trying. But yeah, I think if you think about safety and efficacy, that is probably the best way to go. That's interesting. About two weeks ago, I interviewed the new head of the FDA and we talked about aging and longevity. And I was blown away. I mean, he seemed very committed to pulling out the stops and not taking 10 years to come out with new substances and embracing longevity. So, and this is in front of an audience of 500 people. So I was actually pretty excited. So I'm hoping they become more friendly real quick here, at least for the next few years. Are you seeing any any benefits? Not just friendly to longevity, but friendly to a much quicker and less expensive system of getting things approved, right? So, for example, we're working on cocktails or drugs for cancer that we combine with the fasting making diet. And it's really not a path to go forward with the FDA approval. So the week can go fast and we can have these technologies used to treat cancer patients. So I think that it'd be nice if the FDA begins to look at what's beneficial to patients. You know, regularly, and of course, more than what's beneficial to drug companies that are trying to get monopolies and sometimes on drugs that are out there, right? So I don't think the system right now is set up for, let's say, the cancer patient or the diabetes patient. It's more set up. And well, yeah, the drug company puts a lot of money into it and then the FDA process is so expensive, it's so difficult that nobody wants to even, I mean, unless you have a sure thing, you don't want to, nobody wants to touch that. And now we approach, for example, the FDA with the fasting making diet. And they were very nice, but you know, they already 16 ingredients in the fasting making diet. So the discussion was like, well, maybe you can have seven, right? And we've got from 60 to seven. So the FDA is not set up for big changes. So hopefully, hopefully the lop and up to these changes because they're badly needed. Yeah. They are, for sure. The National Institutes of Aging, similar historically, they were in favor of aging, not trying to stop it. So maybe, maybe they'll change their tune. Let's talk about cyclical keto. A lot of listeners will go into ketosis for a brief period of time or they take ketone supplements. What does a fasting mimicking cycle with Prolon give them that they're not getting from intermittent fasting and, you know, an 18-hour fasting window? I think that the main thing is this coordinated three billion-year-old process, right? So the body during fasting shrinks a little bit, not very much, but shrinks. And even in our clinical trial, we showed that the people, you know, based on MRIs, we see organs becoming smaller. And then they re-expand, right? So if you look at our mouse and red data, they indicate they're probably also in people, especially when we saw very similar results in mice than we saw in rats. We gave a good idea that this is probably conserved. And so, yeah, in this five days, the system shrinks. And at that point, the stem cells, the ammonica factors, the autophagy, and by the way, autophagy in a recent study, which I think is not published, it took about five days to see markers of autophagy, right? And this is also consistent with other work that was done before. So it takes a long time for lots of cells in the human body to activate these self-eating processes, right? So, yeah, so you want to allow enough time so that things break down and then the system decides, okay, activate the stem cell, reprogram, lots of different cells that may be damaged, it then begin the process of re-expanding, right? And that's in the next five days or seven days, and by the way, if you look at rats and mice, if you do, when you do refeeding, you see these ammonica factors go up at the end of the diet, let's say on day four or five of the diet, right? And then, and they, one refeeding, you see many of the embryonic developmental genes still up, but sometimes you see them after three days and maybe even later than that, right? So, there is a process post-refeding that in some cases, it could last weeks. Yeah, so this is just, you know, a brief description of why you, I mean, you can biohack your way to it, and that has some effects, but this coordinated, really beautiful response that is fast in every feeding. It's start to match with anything else that I, you know, I always challenge people and I'll challenge you with the, you know, give me an intervention that will cause more changes in the human body than a long-term fasting and refeeding, right? Oh, you and I are both pretty firmly in the fasting camp. I've, I wrote the first major book on intermittent fasting and a second book because people were doing it wrong, so I think it's the most powerful other than maybe getting your circadian biology working. I think having bright light in the morning and having actual darkness at night and eating before it gets dark, maybe as important as fasting, other than that, it couldn't come close. Yeah, you know, but I was talking about actual molecular changes, right? So, if you, you took a cell, cells of a human body and you disrupt the circadian rhythms, or you, you run day five, or the fasting making diet, and then you refeed, you see, man, you know, I mean, I don't know that anybody's ever done that, but I'll bet money. You see, many more changes in the, I mean, everything after five days of fasting is revolutionized in the human body. Now, it disrupts the circadian rhythm. Yeah, there are some changes, but not you would not have a revolution of your gene expression, let's say, in the brain, in the liver, in the, in the gut and everywhere else, you know. Not in five days. If you did it for six months, you might see similar magnitude changes again. I'm just guessing, but it, it's so broad, broad spread the more I look into it, the more I'm like, wow, you know, PMC and all the things that are activated, even by UVA and UVB, like there, there's a lot going on in the mitochondria that has chromophores that I just think we're, we're starting to understand that better than we have, but I'm with you. If you, if I have five days, going on, a good prolon fast is the fastest thing you could possibly do with everything we know, including peptides and everything. By the way, I agree completely because we recommend FMD, say three or four times, a year, and then 12 hours of time rest of the evening per day, right? So this is part of the longevity diet. And so I absolutely, I mean, aligning with the circadian rhythms is very, very important. It's funny. I just personally have experimented with the lower protein things and it, I almost wonder if there's a genetic thing. I'm, I'm bask, but like 28% or something and bask is the land of rabbis. So there, there could be a genetic thing. Have you explored whether your ancestry affects the amount of protein or specific amino acids that you need in order to maintain your health? I have not explored them, but when you look at, for example, the Harvard studies, you know, 120,000 doctors and nurses, you know, it's probably all kinds of genetic backgrounds, right? So, I would say overall, it's probably pretty consistent, but yeah, there could be, there could be people that need another level of proteins and amino acids to reach their goals. So, and it would make sense, so it would make sense that the different people may come from different histories and with different needs and, yeah, but, but say overall seems to be fairly consistent when you look at, you know, epidemiology or, or any other type of, of, you know, pillar. I'm seeing kind of a breakdown of some epidemiology over the past five years as personalization gets bigger and bigger because, you know, you have the middle of the curve and you're designing, you know, 80% of people are above this part of the curve, but if you're one of the 20% of people that's on either edge, the stuff that's supposed to work doesn't work for you. And, you know, we're finding 20 different things beyond MTHFR issues and things like that where it's getting to be more and more and more personalized, where we might say, well, this, you know, your average for this part of your biology and then this other part isn't average. So, for instance, in a folic acid metabolism is a classical one. So I'm, I'm guessing that with AI over the next five years will be to the point where we can say, you should be based on your genetics and maybe based on your current state, you should do a prolonged fast every month or every six months, right? Or you need, we're already doing this, you need more of this nutrient less of that nutrient where if you look at a population of million people, you don't have any granularity to be able to pull those people out, but when you look at pathways, we're getting better and better. Are you hopeful on that front where personalization is going to move in? Yeah, no, I agree completely. I think AI is going to, it's going to do it fairly soon and we're working on that and lots of people are working on that. And, yeah, so we're combining everything we know with, with what AI can do to personalize it, absolutely. So I have foundation clinics and, I mean, in the foundation clinic, historically, we've done one, one person at a time, one professional at a time, but that's why we, in the foundation, we have physicians and we have the PhDs, right? And that's the job the PhD to do the AI work. The PhD will have more time and they can sit there and they can start thinking about you, right? Well, we did this and it's not working, you know? And so for example, we do the longevity diet. It's like pescatarian, low protein and, you know, mostly vegan diet. And some people, you put them on it and they lose a lot of weight and they do great. And some people, you put them on it, nothing happens, right? And then a year later, but then you put them on it, nothing happens. Then you start the FMD and that all locks the insulin resistance and so then it starts working, right? So I think the toolkit, we have five or six different things and with this, and we personalize, we are pretty successful with most people in trying to achieve the things that we want to achieve. But yeah, AI is just going to probably do a much better job than than even we can do with lots of scientists and physicians. Yeah, it's getting better and better as long as we have an understanding. Another question that I've been just wanting to ask you, ever since our last interview, I've become more and more convinced that oxalate is a driver of systemic inflammation, which drives aging and a meaningful number of people because there's abundant studies showing direct mitochondrial harm from oxalate in foods. And when I look at a lot of the plant-based diets, things like black beans are just full of it and beats and some of these other things, do you have any perspective on oxalate and whether we need to limit that? I think that that's where I will go to the pillars, right? And say, you know, if you look at study after study, after study, you will see these ingredients and the legumes coming, you know, at the very top or among the top of the foods associated with life expectancy increase. Yeah, so I would say that, you know, something that could look bad, I mean, there's data on all of oil, right? Because in inflammation and so, but, you know, overall, I think that the overall effect is very positive, positive or very positive. Now, could it be that something even better? Yes, maybe it could be that if you eliminate certain food that have, you know, one of many potentially toxic molecules, you could do better, but then what would you miss? Right? So now you're removing a problem and maybe you're introducing a bigger problem. Yeah, so that's why I think that we have to focus on the multi-pillar system and say, if this ingredient, so I really like, for example, Harvard's Franco's latest study, looking at how do you get to seven or 75 healthy with no diseases, right? And, you know, and what are the foods that get you there? And what are the type of diets that are associated with an increased ability to get to get to seven or 75 cognitively and overall healthy. And, yeah, so I think a lot of the studies point to the same vegetables. You know, sometimes the fruits are there, sometimes they're not as high. So absolutely, fruits and vegetables can have inflammatory effects, but I think you have to personalize there. And that's what, again, what we do in the foundation, so we have these diets that basically get rid of any inflammatory component. And some people, you know, and gluten plus many, many, a hundred more ingredients. And we just exclude them all, right? And a lot of the people, when we do that, they feel they do a lot better. But it's a, it's a, it's a, it's not a small percentage of the population, but I would say it's, you know, maybe one in five, one in four, one in five, that for whom we have to remove lots of ingredients that, then inflammatory or, you know, they cause problems or sometimes severe problems here. It's interesting because we can metabolize about 200 milligrams of oxalate depending on your gut bacteria and some other metabolic pathways. But some of the western superfood diets have people on a gram a day. And it does, you know, contribute to kidney stones and things. And when, you know, early we talked about, well, maybe it's not the meat. It's the amino acids in the meat. And if you're looking at, say, lentils, the white color lentils are very low in oxalate, almost as low as white rice. Right. So there's a car they got some protein in them. If you're not sensitive electens, no big deal. But if you switch to like navy beans or pinto beans, those are very high in oxalate, where you're getting, you know, a hundred milligrams half your total daily amount in a single serving. So it's like, maybe we should recommend the right lentils the same way we recommend the right amino acids for people. And it's just level of personalization and it's kind of harm minimization that is a part of this conversation because I'm not a carnivore. But I do eat a lot of red meat because my markers improve when I do it. And I feel like crap when I don't. But I also maybe a neanderthal. So like, I'm just an end of one. And so we're saying how to make population of the recommendations. Then how do we tune them for people? And I'm my predictions that we're going to figure out more and more about oxalate. But it's mostly because we paid attention before 1950 and then kind of stopped paying attention. So absolutely. Right. So eventually some of these could end up being toxic. But it could also be that, you know, lots of people, they start on legumes, they feel terrible for two or three months. And then they start feeling really well. So, yeah, you know, so is the redistribution or rebuilding the microbiota with that, you know, bring it down to a level that is non toxic or could it be that in fact that that oxalate is stimulating certain responses that are, you know, more beneficial than than bad in the long run. Right. So this is why you need the multi-pillar because you don't want to say, well, oxalate causes this problem acutely and so it's bad. You want to say, well, let's look at people that have been eating that pinto beans for 30 years. Are they all dead of, you know, colorectal cancer or maybe are they protected from colorectal cancer? Right. So, so, you know, our meat is, you know, about our meat season. So there's a lot of complex responses that the body goes through. But this is why we always say, stick with your among the foods of the longevity diet, what I call the longevity diet, which also learns from Harvard and from lots of other people, pick the ones that your grandparents used to eat all the time and they always be very good with. Yeah. So it's basically saying, if your grandparents never ate pinto beans, you know, don't start having a ton of, and this is also the recommendation in the foundation clinics, you know, don't all of a sudden because it's part of the longevity diet. Start, you know, get rid of everything you do and start eating, you know, beans six times a week because you may have a problem, right? So, yeah. That's your dating life, if nothing else. At least for the first couple months, yeah. Going back to fasting, is there a point where fasting starts to break things and how do people know if they're fasting too much? Well, I think fasting, I don't know if we talk about this the last time, but I hate the word fasting, right? Because I always say, it's not eating. Is eating good for you or is it bad for you? It's a pointless, right? So I think we need to move from fasting to exactly what we're talking about for whom, right? So like FDA, right? So you have a medicine, what's the dose, who takes it? When you take it, otherwise, we're probably going to do more damage than good, right? So because people hear that word and say, well, it must be good, you know, I could do three weeks, I could do two weeks, I could do one day. So yeah, so then, you know, for example, we know that if you fast for long enough, your body goes into a more of a hypermetabolic or a tristymal, right? And so, and so if you enter the modality, that could last a long, long time, right? And so we know this from the carestition studies in humans and lots of other studies. So this is why, for example, we pick five days with a fasting-making diet and now I mean, beside the fact that water only would be very tough, but also the fasting-making diet, for example, in mice, when we compare the fasting-making diet with water-only fasting, water-only fasting increased the leakiness of the gut, and the fasting-making diet not, right? So, but the point is that we, the length, but also the composition, has to be tested in mice and, you know, different organisms, and then in people, randomized trials, and then at a certain point, I think the medical community is going to say, "This looks good," or, "No, this does not look good." Yeah, so I hope we can have that to avoid fasting disappearing. So a fasting comes around every 50 years, and this appears after a few years, because people are damaged by it, doing it wrong, right? And then, and then doing it too much, and doing it too long, and, and, and, and so a bit the same as people start taking their own drugs, say, "You know, I come up with my own, my own medicine, and, you know, I, I think I understand it enough, so I can decide what drugs I should take and, and what kind of dose, right? Yeah, you could do that, but most people are going to be hurt by it. I'm not saying I've charged GPT, right? I mean, in probably five years, right? In five years, I don't want to offend any doctors, but I mean, five or six years, you know, maybe that that's going to get, you get to get a better response. I don't know, yeah. You wouldn't be the first high-end medical professor who has said that AI is doing better than doctors real soon now on, at least some things. So, yeah, it, it seems like we're heading in that direction. Not better than all doctors. It's just better than average. Yeah, we just, some of these are going to be possible. I don't know, I think, but yeah, no, I don't, I'm not saying that that's what's going to be, but AI, in fact, in fact, is using a multi-pillar system, right? So AI, I mean, at least eventually, it's going to get trained to say, I'm not just going to look at epidemiological studies. I'm going to look at all, right? And then, and then put it all together into a, a recommendation that keeps all of it in, in, in consideration, right? So, that's why I think eventually is going to be more powerful than, you know, the individual, each focusing on, I'm an epidemiologist and I'm, you know, I'm an endocrinologist and I'm a PhD. So, in each, with an opinion, right? So, yeah, at some point, of course, we're not there yet because the sophistication is not there and where do you learn, right? How do you pick, how do you pick the good studies and, and, and separate them from the bad ones where I saw? Yeah. So, I think doctors and, and scientists can do a better job now, but for all long, I don't know. I have a question for you. You're probably one of the few people who could really answer this because you worked on IGF1, MTOR, PKA, and other longevity pathways, not just one. Can you stack rank them from most important to least important for longevity? Yeah, I would say most important, I would go up to the master regular grotormone, right? Grotormone receptor and grotormone because that's very, very consistent. Now, the complication is, is a important lifelong or is it important during development because it just switches you to modality B, the long live modality. So, it's clearly the most powerful that there is, right? But, you know, when, when that becomes important, that's a little tricky. Now, if you, if you look at studies then that start a, advance ages, at least in mice, then TOR seems to be the most promising because the studies on TOR started a fairly long, old, in fairly old mice and they still work and they still make a tremendous difference in the mice, longevity and health, right? So, TOR seems to be the enverpomizing and another repomizing is the drug because the repomizing also causes hyperglycemia and lots of other problems. You see, finding a way to, to modulate it in an optimal way. And, of course, you know, the fascinating thing that modulates all of it, the grotormone and the IGF1, the TOR, and the PKA. But, yes, I would say number one grotormone receptor modulation and number two TOR. And, you know, insulin and IGF1 and TOR are all regulated by grotormone, grotormone receptor. So, I think all of them are important. Like, you know, high insulin, high IGF1, high TOR. You probably want to have low levels, but also you want to have, so we always, so if you think about fasting, right? You have low all these, but then when people repeat, they'll have high levels of all these, right? So, I think we've underestimated the alternation of low and high, right? And, and so, low, it protects you, it gets rid of maybe out of new cells and maybe of cancer cells or pre-cancer cells and lots of other things, but then high is, is there to rebuild maybe part of the immune system, right? It's rebuild muscle and et cetera, et cetera. So, yeah. So, these grot factors have to, so, so this idea of restricting and blocking all the time is probably not the right one. It's probably better to alternate times of, of low levels in times of rebuilding. I certainly believe that about Amtore. It should be chronically low and occasionally elevated so that you have regrowth, right? So, it, it makes a lot of sense. And you said something really important that people miss about fasting. If you fast for five days on water, the gut bacteria start eating the lining of your gut and you get leaky gut, which can cause allergies. And it certainly lets lipopolysaccharide toxins come in that cause brain fog and systemic dysregulation. And one of the reasons I like Perlon and the fasting mimicking diet concept is that I, at my first book, I wrote about something I called protein fasting. And it was, you can have a thousand calories a day with no protein. It goes under 10 grams of protein. And you pretty much get the effects, but you've commercialized it and tested it in such a way going down the fasting mimicking diet that you're not creating the, the leakage in the gut, which is why, I think it's much more sustainable to do a Perlon fast multiple times per year because it's much less aggressive on the GI tract than just having a water only fast or something like that. Do you have concerns about people who are doing water fasts for multi days, multiple times a year because of this? Yeah, I mean, not just because of this, because of hypertension, because of hypoglycemia, because of the difficulties in, you know, I've done it once and I still remember every day of it. Yeah, so I think that's, there's lots of issues. That doesn't mean that I can, you know, help a lot of people and a lot of people have been doing it even for religious reasons and they do great on it. So I don't want to go against it, but really, you know, the FMD is, we think of it as a drug made of food. And it's got lots of things like glycerol, for example, glycerol is there to protect muscle and to protect from, you know, to have a gluconeogenesis ingredient, right? That can feed the muscle when, you know, can substitute, I mean, as it comes from the muscle, when the body is trying to make new glucose. So, so I think that that's the idea of the FMD is trying to have the prebiotic components is trying to match the longevity diets of the world, like, you know, the blue zones and and what people, some of the areas of the other world have been the healthiest. I mean, there was my idea from the beginning, let's take the healthiest ingredients that you can think of, and then match them with the fasting mimicking properties, and then add things like glycerol to it that can can improve it even more, right? So, yeah, so that was, that was the idea. I absolutely love it that you're talking about glycerol. And most people, even in the influencer health community, are unaware of this, but there are studies that show like that taking glycerol can have an effect similar to taking creatine on cognitive function and mitochondria output. It's really good for hydrating cells as well. So, I love that if they're actually have added instantized glycerol to electrolytes, you know, just put a little bit in, in a, in a glass of water, the only problem is if you get too much of it, it gives you GI upset pretty quickly. So, you're using the appropriate dose, I haven't seen that from Prolon, and that's like a, it's going to make people's brains work better when they're on the fasting mimicking diet, and it's, it's just unacknowledged to the space. It is a fasting response molecule, right? So, glycerol will go up as you fast for, of course, from breaking down triglycerides. So, that was also the reason for putting in there. It wasn't, you know, biohacking supplement. It was more like consistent with the fasting response. What would the, the human body have in relatively high levels during fasting and glycerol is one of those molecules, right? So, so, yeah. So, I think that, that's a way I approach the, the development of the fasting mimicking diet. And by the way, I give everything to charity. I don't take a penny from, from El Nucho, the company, the, the, the sales, the, the product, and even my shares will all be donated to charity. So, just to make sure that people don't think that I'm here advertising for, for, for a product. Walter, you're, you're working for the good guys. And so, Dan butler, by the way, is that there's some people in the carnivore community who just hating on Dan, and he's, he's a true believer in longevity. And it's just a great human being. And the fact that we don't all agree on everything, it doesn't matter. But I, I have no, no questions about your motives. You've been studying this for 30 years because you care. And thank you for that. Like you've, you've moved, moved the, the knowledge forward. What's your take on creating? I'm always worried about supplements and, you know, because I always, in my book years ago, I talk about vitamin C, right? And, and say, well, of course, you know, Linus, Pauling, and many, many people have talked about vitamin C. But, but I'm afraid that, you know, creatine and, and vitamin C and lots of other molecules, they are going to do good and bad. And, but the main thing is they're going to disrupt this equilibrium, right? So, this is very sophisticated equilibrium that the human body is as built, you know, with, after billions of years of evolution. It's so now as you make those anything, of course, it's going to have maybe a very powerful effect for whatever it is that that it does. But then what happens to this equilibrium, right? What happens to everything in a step that, you know, so, so if you think about a hybrid car, right? And it has been designed a certain way to alternate between using the combustion and the electric engines. And so, it's so, you know, what happens if you put it, if you try to force it together, right? Well, I could maybe go faster for a while, right? And you get a lot of benefits, but, but then what, right? It wasn't designed for that, right? So, so, yes, you add in mega doses of molecules, you could have very beneficial effects. But then you're pushing the system in direction. And GLP1 is another example, right? And are you pushing this, look at going receptor agonist, receptor with an agonist? And, you know, you keep pushing and pushing and pushing in a to a receptor or a receptor that is now, it was never stimulated like that, right? None in combination with all this food that is coming in and all this, this, you know, molecules that are normally not associated with high levels of GLP1. So, yeah, so what happens that after two years of that mixture, this mismatch between a drug and what the body normally did when GLP1 was, in fact, elevated. And, you know, and how long is normally GLP1 elevated for? And, you know, and what does it coordinate with when it's elevated, right? So, we think like that, you know, and it doesn't mean that there could be exceptions where, hey, it just happens to be good, right? Okay, then then I, we say, okay, okay, show me the mice live longer, right? And creating, creating does not make mice live longer. I'm pretty sure it's been tested by the intervention program in mice and show me the rats who live in longer and show me the epidemiology. If you don't see this up, I mean, clearly positive in each, say, maybe not in all five pillars, but say three pillars out of five, say, hey, if you give creating into a mouse, it consistently lives longer. Okay, so it's a good start, right? And, you know, epidemiology is like 30, there's meta-analysis on creating levels and, you know, longevity, extension, or life expectancy. That would be another good one. Yeah, so if those come up, then I'll say, okay, that looks interesting here. The idea of equilibrium is something I've really struggled with because I recognize that there is such a thing, but we've already disrupted it. I was in Dubai last week. I'll be in Paris tomorrow. I'm sitting under LED lights. I'm surrounded by microplastics and endocrine disruptors. And, you know, all sorts of things that create disequilibrium, unnatural EMFs, glyphosate and food, you know, ultra-price, like there's a lot of stuff out there. So, part of my go with biohacking, say, well, if you're not in equilibrium because you're not living in the forest the way we evolve to, how do you use selective interventions to bring yourself back to equilibrium with the environment that we live in versus the one that we evolved in. And it's, you know, delicate dance. So, I also seek equilibrium. I also know that, you know, if I can increase hydration in the brain and my cognitive function goes up, even if I don't extend my life, if I'm smarter, more focused and more awake, and it's not going to shorten my life, I'm totally okay with that. So, there's something in the middle and it's just my hope that as we get better at doing RNA testing, so we can see what's actually going on in there and we start just getting better and better data that pretty soon we'll be able to say, yeah, creatine that was a fad, or maybe it wasn't, but we'll actually know instead of guessing. Pillars, right? So, pillars are, you can test it, right? So, we are bombarded by all these chemicals and devices and problems, but okay, why don't we see, so are the mice, right? The mice probably have microplastics and there are also lots of, lots of bad things even in the lab, but yeah, why don't we see that, right? Why don't we see consistently, right? So, if the mega dose did something, you start, you should start seeing it over and over and over, right? For longevity, it agreed, it just were not measuring like the mouse's subjective well-being. Oh, you can measure the ability to focus necessarily, right? You can measure the well-being, you can have quality of life testing, a lot of epidemiological studies have that, right? So, and the Harvard and Montreal study, I was referring to earlier, they were not even looking at longevity, they were looking at, can you get to 70 or 75 healthy, right? We cognitive function and, and yeah, so, and what was in there, they came up, you know, it was vegetables, it was nuts, it was, so, and they made a big difference, right? So, there was maybe 10 different things that you shouldn't do, at 10 different things that you should do. And that's one pillar, I mean, so I would say, yeah, if creating, if creating builds that type of, that type of data behind it, then, you know, and maybe it is effective, but there is good data, not for longevity, but in mice, it reduced anxiety like behavior, creatine, had antidepressant-like effects, enhanced cognitive performance in mice, in multiple studies, and it also increased exploratory interest. None of those are longevity, but all of those are useful for humans, so I'm like, okay, if it's not going to make me live less, it's not going to give me cancer, like, there's that, I don't like the word "health span," I think it's kind of dumb, like, I would like to extend life, not just be healthy and diet a normal age, but I also want to have full energy and vibrance, and that's one of the motivations behind biohacking, but the fastest thing you can do is restore equilibrium, but it's got to be equilibrium matching the life you're living, and it goes in a different direction than longevity, but I think longevity is the final goal. I just don't want to feel like crap and live twice as long as I'm trying to solve for that. It doesn't go along, right? So, meaning that if something that is making the mice healthier, like growth or more receptor knockout, it's also, it's making them long-lived and making them healthier all the way, right? And more vigorous and better memory, and so it usually goes along, functions, strength, and longevity. They're very closely connected, and you know, the argument would be, well, look at what this mutation, where the mutation is, that is making the biggest impact on healthy lifespan is growth hormone, the same growth hormone that people inject for short-term impact on unhealthy and longevity, right? And you're saying having a lower, lower growth hormone over time, extent life. Yeah, I'm not saying it. I'm saying this was 100 years of data in years. Yeah, you know, and yeah, you're saying it back by the science, because you generally only say things back by science is in my experience of you. This is the same growth hormone that people take for short-term effects, which have a lot of the features that you just described for creating, right? So a lot of people, you know, will have great benefits, shorter, right? So the question is, you know, we already know from Acromagalix, the very high levels of growth, and they die very young, with lots of problems, right? So and same thing for the mice and the rats. So, so, yeah, so I think that we have to be careful, right? Because short-term effects and long-term, you know, consequences are very, very different. So we, you know, ideally, you want to have both. You want to have short-term effects, and then you want to have the support of all the data indicating that you're going to live longer, and you're going to prevent cancer and lots of other diseases. And sometimes we just have to take a flyer. Like I think I'm there with creatine in part because getting Alzheimer's and Parkinson's is bad news. And even in mice, there are studies showing that creatine protects the dopaminergic neurons in the brain over time. So if I can lower my Alzheimer's and Parkinson's risk, it's probably good for longevity. But I could be wrong. And it's not knowing. And then just kind of making a bet. And then tracking your numbers over three years. No, that was a dumb bet. And then going in other direction, not everyone's going to do that. But the people who are curious about this are probably going to do that. And hopefully we share enough of that with AI and on Reddit and everywhere else that it starts to bubble up into something that maybe you'll study in the lab, not necessarily at creatine, but just any of the things where people are doing things that seem stupid, but they seem to be getting results and we scratch our heads and go, man, we should test that. I'm hopeful that more things will pop out just from looking at not epidemiology, but from looking at a massive, massive data set that has enough data behind it that we can personalize it. Like, oh, only people with this gene does that work for it. But I'm actually feeling like we're right on the cusp of like the golden age of personalized longevity where the things that you've found with the fascinating and making diet, I think they're foundational and that there's going to be other little tweaks that become more and more not just backed by science, but backed by science for you, but not for your wife or your best friend because they're just not the same. Do you think we're close to that? Yes, I think we're very close, right? And I think it's a combination as we were saying earlier of AI and the right group of people, right? Because as you know, with anything, you have, I always say, you know, if you're going to get surgery, you're going to look at, you know, what university this surgeon has graduated from and, you know, I mean, years of residence. I mean, residency, where did they do it or she do it, et cetera, et cetera. And so I think that AI is the same way, meaning like, you have to pick the best of the best, right? And lots of people each with different expertise. And if you do that and combine it with AI, I think it's going to be very powerful, but I think the filtering is going to be needed of all the junk, right? Because if you insert a lot of bad, bad information AI, at least right now doesn't seem to be doing very good at bouncing it. And so, but yes, once that the good group of people gets together with AI, and then the personalization is very close, right? Because the ability to process the information is going to be, you know, a million times faster than many groups can imagine. I'm similarly hopeful. And it's an exciting time, even just getting daily heart rate variability changes and all. I'm stoked. And without the mechanistic pathways that you've been pioneering, we just don't understand, don't understand it. I want to ask you one more question about growth hormone here. Is there a case for suppressing growth hormone in people in order to live longer? I think there is a case for suppressing it in those that have high levels of it, right? Or not high levels of growth hormone, but high levels of the growth axis, right? Growth hormone insulin IGF1 tour. So if somebody is consistently and constantly in this pro-growth mode, because you know, the neurons, for example, and the mice live long, they have very high growth hormone and very low IGF1 because the growth hormone receptor doesn't work, right? So, so that's probably very good, but what's not good is very high growth hormone high insulin IGF1 tour. And yeah, so in that group, which is probably maybe half of the people that are relatively young in the United States, yeah, they probably would benefit. Now, you know, we don't know. I mean, nobody's done that test, but I mean, I wouldn't be surprised if eventually we look at IGF1 as we look at cholesterol right now. We say we brought a meta analysis on that where we said, well, between 120 and 160 seems to be ideal for mortality and people that are much lower, they do poorly and people that have higher, they do poorly. So yeah, so then the possibility would be a check your growth factors level levels. And then if you have 280, yes, maybe you want to bring it back to lesser 160. It makes good sense. So we want to have it at the level where we have enough muscle and we're not, you know, losing our brains, but not too low and not too high, right? And so equilibrium yet again. Vulter, your work is fascinating and it's groundbreaking. And I think your innovation with the fasting mimicking diet is absolutely worthy because a lot of people, they're just not going to do a five-day fast for a long period, over and over for a long period of time. It is burdensome. And this is an option and you've shown with really clean science that this works, why it works, how it's put together. So this is a really good innovation. I'm glad you did it. And I'm still not certain that I'm going to go down to 0.36 grams of protein per pound of body weight. I think I would blow away and not feel so good. But I recognize that that might work really well for some people and not for others. And I'm happy to play with my levels to see what works. And I'm truly grateful that you're just open-minded and asking questions and and sharing the science. So what you're doing for hopefully another hundred years, hopefully, yeah. And if you do lower your protein in that way, I would love to know what happens, right? Is there a major impact on your muscle or anything else, right? So yeah, that would be interesting. I think if I can find a time when I'm not going to be on an airplane in like for a month or something, I would do that with the amount of travel that I'm doing now. I know that if I lower the protein, my cognitive function goes just not it's not a good thing. But I also have very weird biology compared to most people. But I'll play with it and I will share the results with you. I know without everyone else too, if I if I radically cut my protein for a long period of time and nothing bad happens, that'd be amazing. So give me six months to find the window. In the meantime, I'll just eat some prolone occasionally. That sounds good. All right, thank you, my friends. See you next time on the Human Upgrade Podcast. The Human Upgrade, Formalable Approved Radio, was created and is hosted by Dave Asprey. The information contained in this podcast is provided for informational purposes only and is not intended for the purposes of diagnosing, treating, curing or preventing any disease. Before using any products referenced on the podcast, consult with your healthcare provider, carefully read all labels and heat all directions and cautions that accompany the products. 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