Howdy Folks. Welcome back to another round of the found. My fitness podcast, today's podcast is a spectacular round to podcast with dr. Valter Longo, if you missed the first episode featuring dr. Long go, throw your podcast player in reverse and grab that episode to also listen to you. When you get a moment that said, this bad boy is totally Standalone. So don't go anywhere just yet first, the street cred, dr. Longo is the current director of the Longevity Institute at the University of Southern California and is also the director of oncology
E and Longevity program at the Institute of molecular oncology foundation in Milan, Italy falter is in a word, a giant both himself, a Pioneer, in the field of aging and has an extremely Dynamic, and prolific publishing history. That's move the field forward. Many scientists can spend most of their career working only in one animal model. His work however is profoundly translational ranging from yeast to rodent and back to where it actually counts to the clinic. In this episode he takes us on a journey or
Edge. If you will back to where it all began with caloric, restriction, caloric, restriction has long been the focus of promising aging, research and Research into the amelioration of age-related diseases. Research and animals has shown impressive results with studies in mice and rats showing chronic caloric restriction, in able to extend the life span up to 40%, also showing the ability and some animal studies to virtually eliminate type 2, diabetes and dramatically reduce cancer incidents. Chronic caloric restriction. Perhaps unsurprisingly is not wholly without
qualities such as slowed wound, healing and a weakened immune system and other related effects, not to mention being notoriously hard to practice with long-term caloric, restrictors, ultimately, failing at reproducing. Some of the cellular signaling changes that seem to be important. But what if we could achieve some of the benefits of caloric restriction, without living a life of constant chronic deficit. That is a special question that dr. Longos research is especially poised to answer through his research into periodic prolonged fasting and more recently.
Fasting mimicking diet that has been shown to achieve many of the same effects of multiple days of water, fasting only what sets this approach apart from that of chronic caloric restriction, is that rather than undergoing constant restriction. We approach it as something. That can be cycled periodically to achieve a persistency of effects, which vaulters Research indicates can last for at least several months, after a four, or five day cycle, the utility of periodic prolonged fasting and the fasting mimicking diet fall into a few broader areas of Interest include.
Luding relevance for cancer prevention and possibly treatment as well. Via a quality known as differential, stress resistance as a tool against autoimmunity, as a whole. And as a general systemic multi tissue reset with implications for aging, or at least age-related diseases one, very large, likely contributor. To all the important effects of multi day fasting or fasting mimicking are the changes that happen to a cell signaling pathway known as the growth hormone igf-1 axis, the igf-1 axis is an extremely important pathway.
That is activated potently. When we consume essential amino acids and protein but is reduced by up to fifty percent after just a few days of fasting in humans. When this happens during fasting and animals, it is associated with a shrinking of entire organ systems, like the heart, liver and kidneys, and a breakdown of the immune system with white blood cells, rapidly being turned over and reduced by up to 40 to 50 percent Upon refeeding, A normalization of these growth signaling Pathways occurs and this causes
Has the same organ systems to really expand to their original size. This may have implications for autoimmunity. We're immune cells that when renewed from their progenitor cells have been shown in an animal model of multiple sclerosis to be restored to a naive non autoimmune State resulting in, either a reduction in clinical severity or in some cases to a complete reversal of multiple sclerosis symptoms in these animal models and there's some early evidence in humans as well. It is the sophisticated nature of this process of breakdown and Rapid rebuilding
That suggests, it might be a way of tapping into an ancient program of self-repair, mostly lost to us because of the general, abundance of food and utter lack of famine, that most of us enjoy, the temporary reduction of growth signals, may be relevant to the treatment of cancer as well. The growth hormone, igf-1, axis, and its Downstream elements, as it turns out are a hot spot from cancer, mutation to put another way cancer likes to grow and as a consequence mutations in genes, that tell the cells, not to die. And instead,
Over eight are particularly common, especially in the igf-1 receptor and some of the signaling proteins Downstream of igf-1 that also participate in growth and cellular proliferation and differentiation such as a Katie and wrath, wrath, for example, is found to be mutated in. Twenty to thirty percent of human cancers. While these mutations may be to the cancer cells advantage in a high nutrient environment, it is the low nutrient environment. In other words, the fasted environment that suppresses this so-called oncogenic signaling where things get interesting.
Dr. Longos group has found evidence that fasting May produce in cancer cells. A sensitivity to stress while actually confirming greater resilience to stress in healthy cells and tissues. This may be because the same mutations that cancer has accumulated to promote their growth. Ultimately, make them less flexible. The advantage of this should be obvious fasting may make cancer more vulnerable to standard of care treatments, while also making the side effects less severe for healthy tissues. Something still being validated but holding
Great promise. Okay, so that's just a few broad Strokes of some of the enormous potential impact of dr. Longos work and gives a great hint as to why I'm so excited about it. Additionally, we also discuss the difference between intermittent fasting, prolonged fasting, time restricted eating, the fasting mimicking diet and calorie restriction. How the shift between normal metabolism and what doctor longer refers to ketogenic mode is subject to individual variation and the type of restriction practiced how the beneficial metabolic effects, and short duration of the fasting mimicking
Diet, may help people overcome both the physiological and psychological hurdles of losing weight. How the fasting mimicking diet causes a person to temporarily lose muscle which gets restored upon refeeding, but also seems to cause a preferential loss in visceral fat rather than subcutaneous fat. This real fat is the fat that is stored in and around your major organs in the abdominal and is linked with an increased risk of a number of health problems, including type 2, diabetes, heart disease and cancer. What some of the most promising.
Young Life Span extending strategies are and how they may have the potential to improve life and old age. By reducing the prevalence of age-related diseases that actually make up what we think of as the decrepitude of old age, how massive cell death occurs during the fasting mimicking diet, but refeeding enables healthy stem cell proliferation and potential. Differentiation in the context of Aging, how the fasting mimicking diet has been shown to reset metabolism. Driving down biomarkers associated with poor metabolic Health inflammation and cardiovascular disease in humans. How short
Fast may feel to approach some of the effects of periodic, prolonged fasting, and the fasting mimicking diet by failing to achieve adequate glycogen depletion and ketogenesis some of the early but promising, pretrial, clinical anak data suggesting potential complementary roles for the ketogenic diet and the fasting mimicking diet used in conjunction with conventional treatments, like chemotherapy and radiotherapy for certain cancers like gliomas. How oncologist might approach incorporating? The fasting mimicking diet, which is still seeking further clinical validation.
Ation and approval into their patients care if they choose to dr. Longos top. Picks for assessing biological age, markers a person. Can ask their doctor to measure to gauge how well, their aging, a sneak peek at what's covered in dr. Longos new book, the longevity diet and so much more. We're almost ready to get the show started but first, hey you, yeah, you the person that's constantly finding themselves, Googling things like mtor and wrasse wanting to know everything there is to know about the growth hormone, igf-1, axis, and its Downstream.
Both giggling Pals. You are the reason we put these episodes together. You have to admit that it's pretty Niche, which is exactly why we're in a pretty special situation this podcast exist. Because people like you even exist because to everyone else none of it matters. Therefore if the stuff really hits the spot for you you should absolutely consider becoming a monthly supporter of the show. We sort of do it like NPR around here which is to say this podcast is viewer and listener supported. My goal is to make it better each and every episode and the pay what you can support from
Fans allows me to keep putting a lot of Blood Sweat and ketones into getting them out without cutting Corners, to learn more about how you can help me, keep it going through a pay, what you can pledge or the equivalent to a monthly coffee date. Head over to found my fitness.com. Ford's crowd sponsor, that's found my fitness.com. /Cr owd, SPO NSO, R crowd sponsor. Are you interested in the genetics of Longevity? If you have used, when the consumer genetic testing services, like 23andMe, you can find out if you
I have some the unique genetic polymorphisms. Research has shown might provide an edge. When aging, the good news is that, while at least part of aging, is genetic a whole lot of it, as you may learn, in this interview is environmentally influenceable that caveat aside to learn more head over to found my fitness.com. Forward slash genetics, that's found my fitness.com. Forward slash genetics, GE n. ET ICS, you'll find these polymorphisms in a report at the bottom of the page called the longevity report. Now to the podcast,
Hello everyone, I'm sitting here with dr. Valter Longo for a round two podcast. I'm pretty excited to be back. It's been a couple of years since our last discussion voltar in my mind. You're one of the leading experts in this realm of how diet and lifestyle regulate longevity particular when it comes to fasting. So there's there's been a really big interest in fast
And also in limiting food intake and limiting food intake is actually one of the probably most, I would say, reproducible interventions that's been shown to modulate the aging process across multiple organisms. So I was wondering if you could maybe describe Define and sort of describe some of the common denominators, between various modalities of limiting food intake, like colic restriction. Intermittent fasting prolonged fasting,
right?
Right. Yes, so I think that we're, at the point where we have to start, we have to stop using terms like intermittent fasting because it's it covers almost everything, right? I mean, at least in the, in the journalists mind, when they talk about intermittent fasting, it covers from two hours food, not eating to one month.
And and of course, they're completely different practices and they have completely different effects. And so I think it's important to start qualifying what it is that we're talking about. So, intermittent fasting. I guess it could be a way to include say alternate day fasting and include the What's called the fight to. So, having two days a week of a color, very restricted diet and maybe it could also include
To the one hour, one day a week of fasting of complete fast. And I think it would be fair to include those three in the intermittent fasting even though they can have very different effects. Now, of course, time restrictive, feeding is timer to the feeling which refers to let's say. Along over time, you eat per day, so 8:00 a.m. 8:00 p.m. That would be 12 hour of feeding and and 12
Hours of fasting. So and then cover restriction. Instead the mean, of course, you can say, some people use colorization to define everything that is kind of restricted. But the people in the field talk about Cairo station. When they hear car station, they think of chronic reduction of calories below the normal levels of below the level that will allow you to maintain a normal weight and so chronically. So
Do this all the time and, and then periodic prolonged fasting. Instead is what we mostly work on and it's very different and it's not intermittent in the sense that it's not something that has to happen in any type of Cycles frequent Cycles. It can be done once a year can be done 10 times a year, can be done, 20 times a year and and refers to say at least two days of fasting or longer.
Hour or two days of a fasting mimicking, diet or longer. And so, what do they have in common? I mean, some things may be in common, but they are very different interventions and they each do something different. I mean, I think and we know now from the calorie restriction field that their diet, I mean there are additional calories like that can have
About a fax and diseases diabetes, particularly but also cancer cardiovascular diseases at this is really Unbelievable Facts. I mean, the monkeys, we know that it can wipe up diabetes completely I can reduce cardiovascular disease and and cancer by 50% but the monk is either live a little bit longer or don't live longer at all. So
And this is what we and others, a few least suspected for a long time. I was a student the Royal for back in the early 90s and it was, I mean, being around character. The people it was very clear to me that this was going to have problems. But it was also very clear that this was going to have huge effects and
health. Yeah. For the, for the monkey studies that you're referring to, there were two published correct, one from the University of Madison and one from the NIH, right? And neither of them.
Kris lifespan. But they increased Health span?
No, no. There was constant. Increase lifespan. Richard weinrich was a so student the Royal for so that increased lifespan. But if you look at the Life Span, that is based on the disease dependent lifespan, so the mortality caused by Major age-related diseases, that were, there was a huge effect if you look at the overall survival. So,
Survival due to were all causes of mortality, were taken into consideration, then the, the survival curves are very close to each other.
They considered maximum lifespan. Just
one of these will be mean lifespan Min and Max, right. Okay. So small effect, they don't have maximum because I think they will have taken as some point there to stop it. So they couldn't, they couldn't really get to, you know, full-length salary to 25 years to do that. So, I think it would have been
Go to get maximum life span, but the mean lifespan was extended in Wisconsin was not extended at a DNA. Of course, the Wisconsin study had a controlled diet that was much worse than the ni a controlled diet. So the N I had somewhat of a ideal diet at least ideal monkey diet and the risk cancer didn't Wisconsin was a reasonably good model for
The the Western
diet. Oh that's interesting. Okay so so there's no really I think there was also maybe some different genetic backgrounds as well from the monkeys but
yes probably
genetic. Do you know if they in this existed in these studies? Did they see common Pathways and I want to talk about this with you genetic Pathways that are known to be modulated by Kellogg restriction where those change, for example did igf where igf-1 lowered or mtor
Yeah. Now I haven't looked at this paper in a while but almost for Sherman, do. Those were affected me in calories are cut by 30% in so they would mean 30% less proteins and 30% less sugars saw. Yes, I will assume that the both of them showed the effects and and the nutrient signaling Pathways and including tour and
igf-1. And I guess that's probably
Something that's also a common denominator between these other modalities of limiting foods, such, as the periodic prolonged fasting. I guess one of the major differences would be the shift in metabolism to when you're fasting to through beta oxidation to. Because that's is that something that's that occurs during Kellogg restriction,
the probably occurs, there's probably a minimal switch to a ketogenic mode depending on who it is and and what the restrictions
Is so it is possible that you know, chronically when you're chronically restricted. It also depends how you restricted. So for example, there are human studies where they show that because the people that are restricted, we're eating high protein, a high, vegetable protein diet and the igf-1 was not affected. So it is possible that you know, some of these individuals have a
Diet that would block entry into even a small ketogenic mode. But overall, they're probably not the relatively in a standard metabolic mode as far as Ketone bodies and fatty acids are
concerned. You said, oh, that's interesting. Cause you said the the diet was a high vegetable protein diet and I was thinking this study from, I think it was dr. Fontana's lab. That showed that people humans that are that undergo kalyug, restriction naturally.
Towards eating more protein because it's more satiating and so people that were eating a higher animal protein diet, even though they were caloric restricted. So they were eating about 30% less normal food than they normally would. They're igf-1 levels were higher because the or normal. Yeah, they weren't, they didn't go lower like they do an animal
studies until they restricted the proteins, they restricted the pro. They actually did the second study, Fontana and colleagues in the second side is the
Oh up in which they restricted the protease and then the idea
from haven't seen that one. Okay, yeah, I should definitely take a look at that but for people that are listening and kind of wondering we're talking about one of the major, right? Dietary regulars of the igf-1 pathway, which maybe you can mention a little bit about the role of igf-1 in the aging
process. Yeah. So proteins and particularly certain amino acid methionine and cysteine excetera, they regulate igf-1 levels.
And in igf-1 in simple organisms, at least the orthologs of igf-1 as well as in mammals seem to have a important role in aging. Is that clear? How much as igf-1 versus insulin versus growth hormone receptor dependent signaling, which is independent of igf-1 and Insulin, most likely it is good to more receptor.
Guatemala Guatemala, receptor. The swordmaster controllers. And igf-1 seems to be one of the one of the past the axis that regulates or accelerates aging multiple cell types.
And and from humans there are there are some cute. There's some evidence with polymorphisms and various like growth hormone.
Yeah, there's actually a lot of work with not polymorphism by mutations in the
Growth hormone receptor, something only 180 mutation, and in the people, what we knew from Mice from the work of John kaptchuk and rebar key. The mice that have either growth hormone receptor or growth hormone deficiency live longer about 40 percent longer, they also leave much healthier. There's probably, you know, I think one of the most important observations made in the Aging field you can live forty percent
Anger and yet about health or the mice, get to the end of life without any obvious pathological lesion. So they don't develop diseases and the controls. This is less than 10%. So we increase the point, I'm pointing this out, but it's a huge effect right there. I'm pointing this out, because obviously people think that, if we extend the lifespan of human life span than it's going to come with,
A lot of more problems and and instead in the mice but also in the, in our work in humans, where we, we've been following this people with go to more receptive deficiency, down in Ecuador, they're called the syndrome. They have a single goal around syndrome and so they're very much the equivalent to the mice and they, they don't have a very long lifespan. They may live a few years more than, than their relatives that
Don't have a homozygote media, your growth hormone receptor deficiency, but they're protected from cancer. They protect from diabetes and recent paper, show that they're they seem to be protected from age-dependent cognitive decline and all of these are matched by the mouse work, you know? So the makes you feel a lot more confident having the mouse data suggesting the this is concerned, the fact of having law growth hormone, of course in then low a
Flying low insulin and law tour and also writing lobe wrath. At least expression activities a little bit harder to figure out in people.
Have you measured the igf-1 levels in these people with learn syndrome is you've measured their igf-1 levels. Is that something that's achievable from doing you know, the calwork protein, restriction or the fasting, which will probably. We should probably start talking
about
Yeah, we measure the igf-1, very low and very low and the subject has like ten percent of the of the normal igf-1 circulating igf-1. Wow. Okay. Yeah. So there's extreme video, igf-1 low insulin and and also we have what we've done is we've taken the these of course we can measure in their their serum, right? But then we take in this theorem and we took human epithelial cells and we expose the human impetus LCD.
Control serum or to the serum, the runs. And then we looked at gene expression. And that showed that not only the tour was down regulated. So, was Wrath at least a gene expression wise, and in a number of other genes that there are associated with accelerated
aging and cancer. Wow. So maybe we can, I kind of took us off into the tangent here but the the
Fasting. You've done a lot of work on both doing a periodic fasting water fasting and also fasting mimicking diet which you can explain in a minute. But so I was kind of the I found it kind of interesting like the reason why you developed the fasting maybe can die. At least I read in your recent book, the longevity diet was if I'm correct because you were doing some studies on cancer patients and is
That, is that correct?
The, yes. So we we, well, first of all, for a long time, I've been had been thinking about how to get the benefits of calorie restriction, without the problems of calorie restriction. And so, there was something that I was looking for and and also I, you know, back in the days, it my graduate work, you know, we were starving yeast and bacteria, and
And we had not shown that this was very, very beneficial. So I was really, I wanted to look at the possibility that prolonged fasting will be beneficial and so dinner certain point when we discovered that, that the proto-oncogene. So the normal versions of the the ankle jeans that are so Central in cancer, they are the genes that
Control cellular protection. And so from there came the idea that maybe we discussed already in the first in the first interview but they came the idea that if you starve a system, the normal cells will become protected and the cancer cells will remain sensitive. So then you know, we started testing this in cancer patients But realize that they don't want to fast and
And then I think they give us an opportunity in the motivation to look for a fasting mimicking diet. So a diet that works as well as fasting, but allows patients to eat and and this was funded by the National Cancer Institute first and then by the nation's to an aging and so it's a, of course exploding, all these understand, all the understanding of the connection
Between the say, amino acids and tour, and igf-1, sugars, or certain sugars, and PKA actually, we've shown that as we had shown for yeast. We now shown in mammalian cells, that glucose levels are activate PKA. And so, that's part of the, that's a lot of what went into the development of a, a diet that can nourish the patient and yet,
We have facts and igf-1, a gfp P1 Ketone bodies in glucose that is equivalent to that of water only fasting.
So you basically looked at all these known genetic Pathways from your work and others that you know. So igf-1 mtor PKA rest.
Yeah, rice. I'll do arrest the main may or may not be conserved the role of rest. We didn't really see it in my mail yourselves yet. Mean, it's probably there, but we didn't see it at least in the cells that we looked.
So far, I know. Looks like igf-1 and glucose can directly feeling to PKA and igf-1 can fit into PK a so. So we think that PK is very Central, maybe handling both the protein signaling and the sugar signaling,
interesting? Yeah, that's the interesting. What do you, what are your thoughts on? And I'm going on a tangent here, I'm going to come back to it but the because you because you just mentioned this the
the role of insulin in regulating, you know, igf-1 I guess both function and also levels. So so there were some studies that I and I'm not sure if this was Fontana or who, you know, did these studies. But their say is showing that the limiting, the glucose intake was important for bioavailability of igf-1 through some of the insulin and igf-1 binding proteins like igf-1 binding protein 1 and also for regulating transcription of igf-1.
Yeah, so it's kind of
so it's all interconnected obviously, we don't know enough, you know, the association between mini insulin and igf-1 and very similar. They can interchangeably bind to the receptor each other's which I receptor with different Affinity of course. And and so yeah we our they connected. I don't know. And I'm not sure that that is very well understood but
But they're certainly connected. And in the certain link both linked to growth hormone signaling. Yeah,
yeah, I think there was another study at. This was an animal's, and this is what really piqued my interest. I'll so I'll look up the reference and send it to you. If you haven't seen it already, where I think the protein, the protein limiting, the protein intake, essential amino acids, specifically wasn't as key. If the total
The
cows were kept under a certain level in terms of activating igf-1, so that there was a sort of energy threshold where, right? If you had low enough energy, specifically from like glucose, then your protein, your instead, she let me know assets can go a little bit higher than they,
otherwise, right? And this would be consistent with our work in yeast yeast. When you have, when you look at the Aging rate is very
Clear that there is a network and it's not really a pathway. And the network is very much interconnected, you know, pki and tour and, and everything else and a, and b kinase. And, and so actually in yeast, sugar seems to dominate and the proteins seem to be second most important. So so if you remove sugar and you
Increase the protein inconsistently to watch it. We just saying that's not. So then it's not so bad, but if you have bought the sugars and protein, then you see, then you see much more, the, the protein dependent
sensitization. Yeah, it's extremely interesting. So I look up the reference to, in case you haven't seen
it. And, of course, the, in the case of East is individual, amino acids. There
is no right, and there's a wrong thing. Okay, so we went out back on a
But this is why these discussions are so interesting. But it's so you were talking about the development of the fasting mimicking diet and how you were looking at all these genetic Pathways. And also, you mentioned the Ketone bodies and and what was the last thing for
Ketone bodies and glucose and glucose. You have wondering, I give you one glucose and
Ketone and these are all these are all things that regulate cancer growth as well.
Yes they're there, they can regulate cancer. They do regulate many Cancers and in different ways, I mean Ketone bodies, you know, some will argue the heard cancer cells and but some cases actually love to use both Ketone bodies and
sugar. Yeah, there was a recent publication, I
think.
So you can actually accelerate cancer growth, we Ketone bodies but you can also hurt cancer cells. Wiki The Bodies, you know, this is why ketogenic diet, you know, I wouldn't get too, you know, confident about using ketogenic diet alone against cancer cells because of course, even fasting, a lot of cancer cells can adapt to the the change environment. So,
cancer,
It is a very it, so it's so complicated when it comes to cancer and you know it seems like a really, really have to be careful when you're trying to treat the cancer.
Yeah. And and I think that there is a lot of course interest and the ketogenic diets and cancer treatment and it's good. I think it can do. There are situations where the ketogenic diet can can hurt the cancer growth. But as for fasting, we see that you need.
To have in most cases the powerful Target intervention with the fasting. So like fastening chemo, fasting and kinase Inhibitors, you know, fasting and immunotherapy, for example. So I will assume that the ketogenic diet alone. It's going to be a complimentary intervention. So now, for example, we very interested in what happens if you do fasting, ketogenic diet,
And cancer treatment goddamn. Yeah, that I think is very promising, particularly if you do it in the sense of and we had patients that with the very aggressive phenotypes that are doing this. So they, they do the periodic fast American diet, then in between the ketogenic diet and then the keep doing the radiotherapy and particularly like gliomas, radiotherapy and chemotherapy, and it seems to be
Working are certainly very promising.
It's just an ongoing trial.
You're talking about just we ever started. I mean, we have a trials on cancer a number of Trials and can see, we don't have one on glioma yet but I know that some groups in Arizona, they are but they're mostly of just done and with the ketogenic diet but but you know, because it's so aggressive and most people, you cannot tell a glioma patient weight into the clinical trial is Israeli, right?
Because it's it's a very quick moving cancer. So in some cases we just said, look, talk go to your oncologist and ask them if they're okay. Let you follow a fasting plus ketogenic diet plus tender care. So it did just adding ketogenic diet and fast into the standard care.
Yeah. Okay. And that's so the, for the periodic fasting is that also including the fasting mimicking diet, which they can.
Yes. Oh, so the yeah, the first time we can that mean nothing?
Water only fasting, but we fmd, ketogenic diet and standard of care and the so.
So I do remember that at least with there's been a couple of studies that you were involved on with water fasting you showed in a combination with standard of care treatment? It, it seemed to be safe and also to some degree seemed to sensitize, some of the cancer cells to Deaths, and also, maybe even protect some of the normal cells, some of these blood cells.
As they weren't getting, they weren't getting neutropenia or The Silo my low toxicity. Quite as, you know, significant as people that didn't do the fast. Do you have any nine know, you've published studies on the fasting mimicking diet and animals in cancer in combination with standard of care? Is there any clinical trials that you're planning on doing with fasting mimicking diet and humans?
Yeah, no, we're doing it, right? So they're going a little bit slower than then.
Predicted in part because we didn't see coming the food aversion so patients. When you give them any food with something that is toxic, then develop a food aversion. So anything that you give them with the toxicity is now recognized as toxic also. And so now we have in to, you know, develop a number of new foods.
Terrifically to avoid the repetition. You cannot repeat anything twice essentially for. So, if somebody has eight cycles of chemotherapy, we may have to give eight different things, all respecting the formulation requirements. So, yeah, that that surprised us a little bit, so, but we already couple hundred. Patients have already been enrolled in these. Multiple randomized, clinical trials. And the good news is that there is
All the problems we have seen any problems with the fasting begin diet and cancer treatment, but it's been slower than, than expected because of these, you know, a because of course, you cannot promise. You cannot go to a patient and say, oh, this is going to make you feel better. And if you give a pill, it's much easier because there is no effort on the part of the patient with the fasting making diet. You know, if you knew it was going to be much better for
You and somebody told you, I don't think any be a problem because we see it with the with the, you know, healthy subject. But if you don't know you have cancer and then you have this food aversion all together. It makes it very tough for people. So we had about a 40% thus far compliance, and so now we need to quickly so we get to maybe
70%. Yeah. It sounds like a challenge, but if there are oncologists right now that are interested in
Using the fasting mimicking died in combination with their standard of care treatment. That is something that they can do
correct. Well, yeah, the way we've been putting it is that they can. If the patient cannot wait for the end of the clinical trials and the oncologist agrees, you know, for whatever reason that they cannot wait, then they can certainly do it.
Distended look here so they do a standard care and then the fasting making diet along with with that. Now the FDA prohibits any product or any claim related to disease, prevention or treatment for something that has not been FDA approved. So then you know I think an oncologist should be very
Careful in, in presenting it to the patient. So as to be presented as something experimental, they could be good for them or could be bad for them. And yeah, so that said, you know, of course, in mice. We have incredible result, we, and many Labs now, I've repeated this. So works very, very well. And, and so, you know, somebody can now, wait, I think, then it's fair to call her oncologist and say,
I've obviously I'm running out of options, shall we? Consider this
one? Yeah. What does it take to for? How many like clinical trials? Does it take for FDA to approve? Something is
it? The FDA is a specific process. So you have to enter, you have to file an IND application and there is a very expensive, a long process, it's not just trial, I got it. So it's you know, it's three phases Phase 1, 2 3,
And in the end you probably have between five hundred and a thousand people a dozen patients and then they made it. They make a decision based on the data whether it's approved or not the whole process usually cost about 50 million dollars. And so you know this this is what makes it complicated right, because yeah. It's not easy to justify this kind of investment.
On a diet, you know?
Yeah. So you do have evidence and this is a recent publication of yours that the fast and maybe King diet in healthy subjects. Can, it seems affect biomarkers that are related to Aging in a positive way?
Yes, aging and, and as well biomarkers for aging, as well as risk factors for diseases, right? So, so, this was a clinical trial randomized, clinical trial with three Cycles.
Of the fasting mimicking diet once a month for five days for three months, in a row. And then of course, we looked at Baseline and it was randomized crossover. So in each case, you'll have a group of controls in a group under control diet, in a group, and the first in making died in the cross over. And, yeah, the results are remarkable. I mean, first of all, if you are a healthy person with the say a healthy or
Low blood pressure. Nothing happens to you. And this is a really nice distinction with calorie restriction. For example, right there earlier we were talking about, you know, are they all going to the same place? I don't think so Sakura station, chronic it, keep driving your markers down. Right? So even if you started, I mean, if you look at Biosphere 2 and this will then confirm by Fontana and others, if you look at Biosphere 2, even people that had, at the beginning, a low blood pressure, they kept dropping. And by the end of it, they had pressure like
Five over 55 and same thing for cholesterol. Same thing for triglycerides. Almost everything is usually drop to very low levels fasting. Glucose the fast immediately said it seems as if you have a block because of 75, nothing changes, it doesn't drop it even more. If you had a fasting glucose or a hundred and six, almost in every case brings you back to normal. Hmm. This is very interesting, right? Then and also
And also very good for doctors, you know? So now we have all close to 3,000 actors just in the u.s. that are recommending. The the prolonged fasting making diet what was tested in the clinical trial. And this is a very important feature, so the three Cycles decreased in normal, people do nothing in people that had, I mean, I shouldn't say did nothing. Did not think that you can see in terms of markers because they already had
Had good levels of these markers, but in people that had elevated cholesterol, decrease cholesterol, the people that had elevated triglyceride increase triglyceride people that had the elevator igf-1, probably people seeing and a high protein diet, it dropped igf-1 and the highest people drop dramatically know came down about 60 points and people that have high fasting glucose came down. People that blood pressure there was elevated but the systolic and diastolic had
Major effects of people that have CLP systemic inflammation. In almost, every case they move back to the normal range. So it's really powerful. I think in in resetting, the system somehow that it's getting out of the, it's functional ideal state, it resets it and I think it really rejuvenates. Now we're doing, we're trying.
To calculate based on and you know, publish profiles and also methylation profiles is this rejuvenating you. And, and also A, and B after three Cycles, what is what is your risk of the for diseases in the next 10 years at Baseline? And what is your risk after three cycle? And we suspect it's going to be a drastic change. Just, you know, the if you think about is Tremont
It is just it's
whatever is in fast each one
week, five days, five days of three cycles of Five Day Festival, week in diet and then we measure it again. And of course, all these things that I just say change, but what, you know, what if we go to the databases and we plug in the numbers and we say, tell me you tell me what I what is the risk now compared to before, right? So we haven't finished that yet. But I think soon enough I just
I say that it's very the results. Look very promising, right? I have a couple of
questions. So, first, the you measure these, these biomarkers at Baseline, and then after the three Cycles, do you think if you were to have measured you measure them immediately after the third cycle or week one week? Okay. So do you
think three months? And we also measure again three
my you did. And how are they? That was my question. So what were they like three months later? Do you have to keep doing it every
yes? I mean there were about 60 percent.
And of the effects were still there. So you could tell that it was smaller, but 60% of the changes were still significant. So yeah. So this is why we say that on average, people probably need to do once every four months. And it's also important to point out that, you know, into millions of people do it. It should be and I need to do it basis, right? So if you are an athlete, you have a great diet, you know, low
Protein pescatarian and you do all the right things. You exercise Etc. You probably only need to do it once or twice a year. It's not very many people in the category, maybe like five percent of the population and then as you move to a problem state, of course then you know the minimal risk, there is associated with doing a fasting making diet is a good, is a good risk to take because of course, any drug that you take any intervention that she do.
It's going to have risks. And and so now, I think people are the, there's over 25,000 people that have done the, the fasting vegan diet. The prolonged, the same diet, they were steps to clinically. We've had very few, severe side, effect reports, right? And even the the ones that have severe side effects, you know, they they fully recovered. And there was no evidence that it was the diet that caused them, right? So,
Very good news, right? Then when you get to, this is one in the FDA. Terms will be called considered a face for when you, when you say, well, let's keep monitoring. This one sits on in the market and, and see, you know, are there people that eventually show side effects that we didn't see in the FDA trials, right? Of course, we didn't do FDA trials, but but it's also we just done Phase 1 Phase 2 and job at me skip phase 3 and now our
Phase for
you. Yeah, wow. That's that's really great. 25,000 people. That's a lot. So you were mentioning the frequency changes changes, the frequency of doing this fast American diet, may change with according to someone's health status and how what their lifestyle is. So someone that's obese or has high cholesterol, high triglycerides, High fasting, blood glucose, all these markers that you mentioned may may want to do it more frequently.
Little much more frequent. Yeah. So somebody that has those problems say, obese and multiple
Workers for disease, risk factor for disease, then once a month. So in this world of doctors have been doing so they put them on once a month and then we do monitor the changes, if it works, then you can keep it going. It doesn't mean they're going to do it once a month for their own entire life. The hope is that you slowly. And in a that's also very important, this idea, especially with obese, people will see how it works, but this idea that you can go back to your diet after
That is right. It is very mentally to people is very important. It was a struggle for five days but then leave me alone for the next 25 that I think is both potentially the mechanistic level, but also the psychological level. It could be a good way to
go. So I'll just tell you, I have a friend of mine who was morbidly overweight and he was morbidly obese. He was I think at his highest weight was about 400 pounds and had tried all sorts of types of
Diets, you know, and never could really get anything to work and the compliance was low. But then he started doing these prolonged water fast. Now, he was doing, you know, five seven days and he was doing it frequently like once a month and he's lost 200 pounds. And I think for him and he does exactly what you said. He likes food. He's he, he likes food and he likes it, he likes to eat, you know, certain
foods, it's amazing. But
he's found something that works for him where he can he just, you know, once a month, he does a five-day fast.
And then he goes back and he got his guy. Yeah, I would I would absolutely like to put you in touch with him. He's actually applying to medical school now, but he's a very smart guy. He's a lawyer. Yeah, and now he's going back to medical school because he's become very interested in obesity and all this, you know stuff.
So, yeah. So, we're ending our trial in Holland and diabetes patients, many of which are going to be obese. And yeah, so that's that's our hope that a, you know, people always ask, you know, there's a famous paper
Papers that have shown what they call the yo-yo diets right there. Shown that this can actually lower your metabolism. If you have this prolonged starvation period, it can lower your metabolism and then you tend to gain weight but in mice and humans, we're seeing really the opposite. You know, we're doing it this way. So so if you think somebody and you put them like, say two months and a very low calorie diet, then you make an exercise, there seems to be a problem, why? Because of course, they can keep doing that and then when you eventually,
Go back to a normal diet and Metabolism. Now, slow, but doing it like this, for these five days, a particular in the first in making that seem to be not doing that. So the body doesn't quite ever switch to a slower metabolism because it's so short, so, I think we'll see. But I think it may very well represent a very, very good way to, to psychologically, and also physiologically get the, the people
Help them, you know, have a long-term plan to lose
weight. For me. I would almost think that you would have the opposite effect that these yo-yo diets that people are claiming lower your metabolism. I would think, because you're spending five days and more of a fasting state or fasting, mimicking state, that you're, you're becoming more metabolically flexible because you're switching to being able to oxidize fatty acids, you know, and and, and then so you're being able to kind of switch between carbohydrate using glucose as a man.
To energy and using?
Yeah, she is switch. But what we suspect is happening in mice, we shown the per month. If you take my sin, you put on fast in making diet. They, of course, have less calories during the five-day, the four days in the case of mice. And but then their metabolism, since be speed up to the point that per month, eight, the same color. So they overeat everything, the underrate during the fight, the four days, right?
So they eat exactly the same, but they lose a lot of weight. So we suspect that what's happening is that fat burning mode keeps on going, it kind. So, they never quite. I mean, they probably get back to a relatively normal metabolism, but not quite the same. So they keep burning. They keep burning fat, a little bit to the point. I mean, we're investigating this now at the molecular level but that's where we suspect that that you know, and of course people, we saw the
Abdominal fat loss and we saw the, the weight loss and so we suspected. The same is happening. Another interesting thing which makes a lot of sense, we didn't think about it too much at the beginning, but the muscle is so almost every diet including calorie restriction. You will lose fat water and muscle, right? And almost every day it is the same way. And in this case, it's very interesting because you now,
Temporarily lose muscle. And of course, you lose abdominal fat because after a few days, this becomes your Reservoir. I mean, all the all the doesn't touch subcutaneous fat for some reason and only goes to the main Depot. They have visceral fat, so that's great news. But the muscle is also decrease, but then when you re feed the muscle is rebuilt, I mean, we have evidence for regeneration in mice, we don't know yet humans, but certainly the people go back to the normal muscle.
So now you have a specific effect on visceral fat. No effect. A man subcutaneous fat and no or very little effect and even absolute lean body mass. In fact, the relative lean body mass goes up,
right? That's yeah, because in your study, the lean body mass
relative goes up absolute either in one arm wasn't affected in one hour, which is slightly decreased so good news because because that's probably one of the very few methods.
To maintain normal lean body, mass while losing fat.
And it's and that's very important to a lot of people. I mean you don't want to lose muscle mass muscle. Mass is also very important, you know, for, for longevity. So, and that's actually a question. I was going to ask you because I wasn't sure what the mechanism was, but the shrinking of the of the organs and then sort of in the refeeding phase, the, you know, regrowing is, is kind of something I wanted to talk to you about, as well. This Rejuvenation process because you've obviously shown this
Now on several different studies both with fasting and fasting, they became diet and animals where they lose, you know, a significant amount of their or different organs, right? And and and I think that you, maybe you want to talk about this, the
yes. Oh so you might, for example, if you look at the weight of most organs, and this is, of course, was known for calorie restriction, long-term but with fasting and fasting in that is happens, much more rapidly. So, the organs will be smaller and
And, you know, at the end of the days of fasting mimicking diet, and then you re feed and of course, they go back to the normal level, right? So there is really there is this shrinking, every expanding effect. Now we don't know how much of it is cells becoming smaller versus cells. Being killed by clearly there is killing of cells. And in something, of course, we are also very interested in, is there preferential killing of the damaged cells, and we started to show that in there are
Oscar Oasis Mouse model and and also the human study there was evidence that the white blood cell level temporarily was reduced during the at the end of the fasting cycles and then went back to normal. So, yeah, so we suspected. There are these, this fast independent depletion of both intracellular components in Ornithology and in cellular components and then, you know, we should understand themselves
All to be activated and in the stem cell during the refeeding part. And that's another very important point, is the differentiates it to most of other interventions, right? All of a sudden, the even the intermittent fasting because you don't have enough time. If you do, like, even one day, barely even gets you into the ketogenic mode, right? And in, of course, if you didn't eat for one day, you wouldn't want to break down.
Too many of the components that probably having all the glycogen and having all the digestion takes, you know, 30 hours to complete the food digestion, right? In the corner. From the time, you eat to the time, the all the calories have been taken up, it takes probably over a date. So, yeah. So that's that's a very important distinction between the prolonged fasting and
Everything else including calorie restriction, which does not have the revealing moment, right? So if the rebuilding happens during refueling and you never have it, then, of course you're missing out the the the Reconstruction part which is as important as the Destruction
part in products. So many different interesting points that I kind of want to touch on. So first the the threshold between like you're mentioning the threshold between when you're, you're, you're
Actually you know getting rid of intracellular compartments through, topology clearing away protein, aggregates piece of DNA and things like that. But also in damaged mitochondria, but also the clearing away of, you know, complete cells and particularly damaged cells, which is very interesting to me. Because, as you mentioned, you've shown this now and there's two different, two different animal models for autoimmune disease. One was multiple sclerosis and the other was the think type 1
diabetes. Yeah. Ours was a now that one particularly wasn't
The not I would be immune we're doing, the autoimmune is type 1 induced by pharmacological. Induce.
Okay, so it has potential for for
but I can tell you we've now confirmed it with other autoimmune diseases. So I think it's it's going to be applicable to many autoimmune disease.
That's so this is what's so cool because I mean the you know, the potential for this this type of, you know, fasting to cause cells that are preferentially damaged to be cleared Away by
A apoptosis which makes sense. I mean, I spent six years studying apoptosis. I know a lot about it and, you know, cells that are damaged. Preferentially die. I can tell you from doing multiple moving during
development, right? Yeah. Development as well. That's the way that the good and the bad that are right.
It's also how cancer cells are primed to die as well, because cancer cells are damaged, they are mutated and completely right damaged and that maybe also why they're very sensitive to stress.
Yeah. And also I mean what's up
In there is a speculation, but we're starting to think, more, and more list. I'm starting to think more and more, is that, you know, I always say if you cut yourself, doesn't matter where you cut yourself, or if you hurt your head, the system repairs it right, remember, repairs, almost anything. And, and so, you know what, about in the the inside, you know, why is it possible that we never develop a way to fix damaged organs and very,
Systems. So we're starting to think that maybe fasting represent that opportunity to fix the inside, right? And maybe just maybe because everybody had to do it by force. They were forced to do because there's no food at some point of your month, almost unavoidably you probably were with no food and and so it because it was almost unavoidable, it was probably
One thing that, you know, I always asked to think about sleep right in his sleep. You feel so tired that you have to sleep because obviously people will have gone to sleep just on the wrong, right? But in the case of fasting because it was imposed by the environment, I suspect that maybe we never develop something that forces you to fast. And so now that we eat all the time which is completely lost this Auto Repair mode, right?
Right. This could be remarkable because imagine if we had this ability, if you have damaged liver that fixes it, if you have damaged immune cells, there are two immune the clear that and and so you never develop a defense against our community because fasting always took care of it. Now, all of a sudden you, you get rid of fasting and all these things that are start building up. Weather is insulin resistance or liver damage.
Fatty liver etc, etc. Right. So this could be really, and people always are surprised when we say no, we're publishing and all these different diseases. But if that's true then the make sense, right? Because for example, in multiple sclerosis you see on one side, it kills the immune cells, it then turns on the stem cells, then turns on the oligodendrocytes progenitor and replace, I mean, it's very soft. It's like actors at the, how does it know how to do all of this? And that's all.
All in such a sophisticated manner. So but if it was an involved process, that will make a lot of
sense. The thing that's so interesting is how the stem cells, you know, the the clearing away of these damaged cells, three apoptosis activating, these stem cells which then have to repopulate, whatever, organ or tissue. We're talking about how they actually can make normal like selling, you're talking about. In the case, at least for autoimmunity, you know, are type 1, diabetes, or multiple sclerosis, how they make theirs, their immune cells normal, you know,
Yes, so yeah, but that makes sense, right? Because if you turn on a stem cell you imagine now that the you're not going to turn on a damaged stem cell, there's got to be a selection process to pick the. So the stem cell is now of course, going to give rise to normal white blood cells. I didn't have any way to make an auto immune cell so I mean yeah so because that's happens. I think in the differentiate a shot.
Salad the corner. So you expand already differentiated. So, even I think, theoretically, they makes perfect sense that once you turn on the stem cell, the multiple systems, are you will make a healthy. Now, you can always turn that healthy cells in and do I do immune cell, but but at least initially you will make a healthy one. And and that's exactly what we see
happening. So the refeeding phase is really important for I recall, our in our last discussion, you mentioned, refeeding phase was
Important for the stem cell proliferation. So after you activate them, you want them to proliferate and continue to grow and you had mentioned if I remember correctly that igf-1 played a major role in that proliferation because it is after all a growth signal, you know.
Yeah. So there's no doubt we haven't spent too much time on it, but it's pretty obvious and that, you know, you'll need growth factors to to do that. So these also makes us think about, for example, the clinical trial that
Multiple clinical trials that we're done and igf-1 in cancer the failed. Right? And we thought well maybe they failed because the igf-1 was also needed for exam for the immune system to be built or rebuilt and in those trials, right? So so yeah. So then the generation of healthy cells is as important as the law igf-1 future generation of healthy cells. There is
GF one dependent is probably as important as the killing of damaged cells. That is low wages when dependent and they turning on of stem cells, which is also lower igf-1 dependent so
slow. I thought it was higher. I hide the turning on the stem cell not turning on the proliferation of them is high.
Igf-1. Yeah, no but the, the turning on it looks like a law now. Is this signal right to self renew? You know. Yeah. So now you have a
Population of a small population of stem cells that are just active in standing by. The improbably when igf-1 goes back up. Now, they are the ones that are pushed by your GF 1 to proliferate. And to differentiate, probably also to differentiate proliferate in French because now you you want to rapidly make new a lot of, you know, white blood cells, for example, or whatever it is. Yeah,
so that's my question about my question to you then is for the refeeding phase then,
You may, is that do you think then, for example, having some protein would be a little more important because you want protein being essential amino acids because you want a little more igf-1 activated during that specific time window? Is that something that you?
Yeah, there is no doubt that when you re feed you have to have sufficient protein to rebuild and if you don't I mean you really don't have the bricks to rebuild the whatever system you you partially broke down. So yeah, protein and also
And then I'm going to drive the igf-1. So the whole system of course is set up to the sugar and the protein is set up to give the signals to rebuild which is probably true igf-1 insulin-like and
igf-1. Excellent. So I just since we're running close to at a time here, what are your top five biomarkers that you?
Think are indicative of something that people can they're indicative of healthy, aging that people can maybe go to their, you know, clinic and measure.
Yeah. So if you, I went to the clinic, I mean if you talking to the masses and you talking about health or you talking about pure
longevity. Well, I mean, I'm talking about, you know, maybe both if there's I don't know if there are their longevity.
Markers all week that you people can do now that are
clinically available. Yeah, I think there are there are things that you can measure that the May predict your,
you're okay. So let's see. Longevity let's see what ya biological age. Let's say. Yeah
yeah. Yeah' biological age, I was certainly, you know, this is what our markers, you know, certainly igf-1, insulin glucose inflammation or systemic inflammation. So CRP
Most doctors can measure that. You could also, if you wanted to add, I mean triglyceride. And and then you could add things such as, for example, fatty liver, and these are more pathological or pathology oriented. By certainly, they can be major determinants of or certain can influence cellular functions. Like
And resistance. And so those are some of the things that I will. I want to see in the idea range of her blood pressure is another one, and yeah, then Morgan Levine. She's now a year. She has a Sheen and others have a set of markers that are taken from large population, and they seem to be predictive of biological.
And I don't some of the ones that are overlapping with the ones I said, but there are other ones that are not that I didn't list. So I people can look up her papers and also of course, you know, the methylation profile there seems to be predictive of mean, Nobody Does it now, I think to the public, but that's working. Yes, yeah, but I'm assuming the sooner,
Enough. It is going to be available, is it? Oh cool. Yeah, I
saw the let me know when it is. I'm very
interested. I so that our commercial is now, but telomere measurement at home, right? So, yeah. So now I'm assuming that soon. Enough people are at least the doctoral level, the ability to assess methylation
patterns, so cool. So you're you have a new book out called the longevity diet, which is the longevity diet.
Yeah, the longevity diet and it's divided into two sections. The First Health is all about everyday diet and in this everyday diet, I talked about five pillars of longevity. I basically say, you know, let's beasts at the decision and diet and episode of epidemiological studies, centenarian studies, basic research, focus and and Longevity clinical studies, and studies of complex systems and complex system. Being cars and planes.
It's and I always thought that it's very, very good way to remove me together with your four pillars to remove all the uncertainties and say, well what I'll do systems that we build age, you just get a fundamental understanding of, you know, about the environment and how the environment affects the complex systems. And yeah. So the First Health is that and in,
Is centenary. Mm groups, the ones that are have record longevity from around the world were really important. You know, for example, I always say to people like intergenic Diet, well, let's look at groups that have record longevity. They use the ketogenic diet, none of them, right? So that's very important to say for the safety component. Once you make a decision about what the science tells you, it's always good.
To look around the world and say our commonly use is that and if the answer is it's not used at all, you really taking a chance on this day and in the other half of the book is about the first American diet and and you know normal people the some of the things we discussed and then you know chapter on Diabetes type 1 and type 2. There is a chapter on how to immunities there is a chapter on Alzheimer's and or degeneration.
And chapter on cancer. Yeah. So it goes through all the major in a chapter and cardiovascular disease, all the major diseases and tries to, you know, mostly Based on data out there and combine it, with what we learned to to try to provide people with a complimentary intervention. So for example, if you look at diabetes,
Basically says what here's what you could do every day, but then you can introduce the periodic fathoming in diet. Of course, you're going to need your endocrinologist. To make the decision, whether this is clinical trial type of intervention or they can actually do it. Diabetes is very tricky. So I probably best be best to keep it will within a clinical trial. But, you know, some endocrinologist may be experienced enough to to fall.
Oh their own patience and allow them to do it.
That's very cool. I think that's the fascinating became diet being used as a metabolic treatment for various diseases that you're that. You just mentioned obviously many of them need to be under the care of a physician is a very promising field because you know as we're learning now metabolism, peas plays a major role in you know not only you know causing these diseases but also in the treatment and how you know some of them respond to
Yeah, and and again it's not just metabolism, really? Really, we're looking at the ability in evolved self-repair mod, right? So mean almost every disease, let's say that you have high cholesterol. What do we do? We black cholesterol synthesis, right? But is there a sophisticated not very sophisticated, right? And all in a say the great majority of the tracks, I like that. You know, if you have an autoimmune disorder, you have something that
Black's asada kind or, you know, a receptor very unsophisticated, right? So, so if there is, and I'm not sure that there is, but it looks like there is, if there is a self repair mode that goes after almost every damage system, this is much more than metabolism metabolic intervention. There is really deals with three billion years of learning how to fix a liver. You know, I mean, of course, starting with bacteria but the process of autophagy started
Extending bacteria, and are you using it? To let's say a muscle cell that is insulin resistant. Now, you may push it to undergo. A autophagy might offer gxl etcetera. And now, you just maybe resistance cell is no longer resistant, right? So, that's the power of this. I think much more than their metabolic, you know, pushing the cell into a different metabolic State. I think it pushing it into a different metabolic State while it's doing this.
This
reset, right? Reset as a great way of explaining it as the resets. Probably. What I'm most excited about is that they're they're clearing away the damaged cells and then rejuvenating or fixing, you know, fixing things. But I do I quickly want to just mention because I do recall. Now one of your studies that you at least in the clinical studies with the best American diet, I think you were trying to look whether or not there was some Stem Cell Activation and there was sort of a
Friend. You had seen mesenchymal stem cells or Trend, you know, increase in them. But are you looking is that something now, you're moving forward with and other clinical studies to look
at? Yeah. Now, yeah, we're looking at that. I mean, of course, we never took biopsies. I always feel bad about taking people's biopsies because it's very painful usually, to take light-skinned. So we had blood and it's not so easy to measure stem circulating stem cells. I mean, now techniques are getting better, right? And so I think hopefully, now we can have a better look at
the circulating one. But yeah, we're definitely going to look at I think in the trial that we're now doing the athletes. We doing a trial with athletes in the University of Bologna in Italy, I think as part of that, we have biopsies muscle my bus biopsy. And so there we should give us a better idea about least some tissue Associated stem cells, satellite cell, for
example, make so excited, I'll definitely following following your research. Thank you so much falter for the
And and you're talking about your both longevity diet. I look forward to talking to you some
more. Yeah, yeah. Thank you for all the very good
questions.
That's a wrap. Thank you so much for taking some of the time out of your day, to listen to what we discussed. And similarly, a huge thanks to dr. Valter Longo for his participation in this conversation and even more. So for the profound work, he's produced that is arguably shifted the entire landscape of the field of Aging today. We talked quite a bit about a few genes that are relevant to aging and Longevity. The igf-1 receptor, and the growth hormone receptor are some in ultimately many genes that can have some influence on longevity. There are also polymorphisms in foxo 331.
Tp53, akt1, il-6, and many more. And if you've used any of the popular consumer genetic testing services. Like 23andMe, you can find out a little bit more about them. The good news is that, while at least part of aging, is genetic a whole lot of it, as you may learn, in this interview is environmentally influenceable that doesn't make the genetics part, any less interesting. However, to learn more about that, head over to found my fitness.com, forward slash genetics. That's found my fitness.com, forward slash genetics.
And ET, ICS, you'll find these polymorphisms in a report called the longevity report found at the bottom of the page, so make sure to check that out. Hey you. Yeah, you you know who you are that crazy deep biology person. Probably rocking the earbuds and enjoying that. Sweet. Sweet podcast Pros, wanting to know everything there is to know about the growth hormone igf-1 access and its Downstream growth signaling Pals. You're the reason we put these episodes together, this podcast exist because people like you exist you Rel
Unique snowflake you because to everyone else, none of this matters. Therefore if this stuff really hits the spot for you, you should absolutely consider becoming a monthly supporter of the show to learn how you can help me. Keep it going through a pay. What you can pledge or the equivalent to a monthly coffee date. Head over to found my fitness.com, forward slash crowd sponsor. That's found my fitness.com. /Cr owd, SPO NSO, R crowd, sponsor, finally. This podcast is not meant to be medical advice, but instead,
A scientific discussion, please keep that in mind and follow good. Common sense. And consult, with the physician we're relevant, especially for the management of any kind of honest-to-god medical condition. Thank you so much for listening and I'll catch you next time.
