Health Longevity Secrets
A podcast to transform your health and longevity with evidence-based lifestyle modifications and other tools to prevent and even reverse the most disruptive diseases. We feature topics including longevity, fasting, ketosis, biohacking, Alzheimer’s disease, heart disease, stroke, cancer, consciousness, and much more so that you can find out the latest proven methods to optimize your life. It’s a mix of interviews, special co-hosts, and solo shows that you’re not going to want to miss. Hit subscribe and get ready to change your life. HLS is hosted by Robert Lufkin MD, a physician/medical school professor and New York Times Bestselling author focusing on the applied science of health and longevity through lifestyle and other tools in order to cultivate consciousness, and live life to the fullest .
'Envision a world of love, abundance, and generosity'.
Health Longevity Secrets
Is Rapamycin the Best Longevity Drug? with Dr Rick Cohen
Dive into the fascinating world of longevity research as we explore rapamycin, potentially the most powerful anti-aging pharmaceutical currently known. Dr. Rick Cohen, longevity physician with over 25 years of experience, reveals how this natural molecule discovered on Easter Island targets a fundamental cellular pathway called mTOR that acts as our body's metabolic switch between growth and repair.
This episode is sponsored by Gatlan who makes rapamycin that we will be discussing available in their program. I am an advisor to Gatlan but I only advise companies that I believe in and would use for myself and my family.
The conversation uncovers the remarkable story behind rapamycin's discovery - how it sat forgotten in a researcher's freezer for years before its life-extending properties were recognized. Dr. Rick explains that mTOR has been conserved through billions of years of evolution precisely because it's so critical to survival, sensing nutrient availability and telling cells whether to grow or repair themselves.
What makes this discussion particularly valuable is Dr. Rick's practical approach to using rapamycin as a metabolic health tool rather than a miracle drug. He shares insights on proper dosing strategies, emphasizing the importance of cycling between periods of mTOR suppression and activation to mimic natural patterns our bodies evolved with. This cycling approach - perhaps taking rapamycin for a few months, then taking a month off for anabolic growth through strength training - may be key to optimizing its benefits.
The breadth of rapamycin's benefits is truly remarkable - from hair regrowth and skin rejuvenation to improvements in hearing, fertility, and protection against diseases ranging from Alzheimer's to atherosclerosis. This suggests rapamycin isn't just treating symptoms but addressing a fundamental mechanism of aging itself.
Ready to understand how this single pathway could influence every aspect of how we age? Listen now to discover why balancing growth and repair cycles might be the key to extending your healthspan and potentially your healthspan and potentially your lifespan.
https://www.gatlan.com/
Lies I Taught In Medical School : Free sample chapter- https://www.robertlufkinmd.com/lies/
Complete Metabolic Heart Scan (LUFKIN20 for 20% off) https://www.innerscopic.com/
Fasting Mimicking Diet (20% off) https://prolonlife.com/Lufkin
At home blood testing (20% off) https://siphoxhealth.com/lufkin
Mimio Health (LUFKIN for 15% off) https://mimiohealth.sjv.io/c/5810114/2745519/30611
Web: https://robertlufkinmd.com/
X: https://x.com/robertlufkinmd
Youtube: https://www.youtube.com/robertLufkinmd
Instagram: https://www.instagram.com/robertlufkinmd/
LinkedIn: https://www.linkedin.com/in/robertlufkinmd/
TikTok: https://www.tiktok.com/@robertlufkin
Threads: https://www.threads.net/@robertlufkinmd
Facebook: ...
Hey, welcome back to the event. Our guest today will be speaking about, arguably, what is the most powerful anti-aging pharmaceutical currently known, and one of my favorite topics, which is rapamycin, and we'll also be touching on some other ones. You're going to learn what the strengths and weaknesses of these various pharmacological approaches are to longevity when you stay to the end. Our presenter for this discussion is Dr Rick Cohen. He's a longevity physician with over 25 years experience in functional and performance medicine. Rick has both a personal and professional passion for a long, youthfully resilient life. He's the chief medical advisor to HealthSpan and he's the founder of Ignite Longevity, a longevity consulting and age reversal strategizing company. Let's go ahead and jump on in, hey Rick. Thanks for joining us today, hey Rick thanks for joining us today, super.
Speaker 2:I'm excited to be here and share some hopefully new information or new insights into this topic.
Speaker 1:I'm so excited to talk about one of my favorite topics and you're an expert in the area, so I can't wait to learn things from you and let me, maybe let's start just a basic question what is mTOR and?
Speaker 2:why is it so important and going to be so fundamental to our conversations? Got it Right. So, for anyone new to this space or field, right, mtor is the mechanism target of rapamycin, and I don't know if you want to get into this story, because I'm sure they've heard it before.
Speaker 1:Sure, could, yeah tell them if they.
Speaker 2:I don't think we we've talked about it on this program yet, so yeah, so so it it turned out and there's there's actually a great um podcast on uh about the story of, of of the the discovery of rapamycin. But it was discovered on Easter Island and there were some scientists that were going to Easter Island before the airport was installed, so it was like this primitive, 2,000 miles out in the Pacific Ocean, one of the most isolated locations in the world. The story, as far as I know, is that they were also curious what was in the soil, because people walked in the soil and never got tetanus, even though there were lots of horses. So there's something in the soil that they thought was interesting and they wanted to go get samples and within the samples it was discovered there was this antifungal, that the bacteria existed. It was a mycin which was eventually targeted rapamycin and for rapanui, which is the name of Easter Island. So rapamycin was uncovered and it had this unique antifungal property which we'll shorten the story had a also immune modulating property, but that wasn't discovered. And the cool, the interesting part of the story was this sample was part of I don't remember the companies, but it was one scientist who was working on the project.
Speaker 2:The project got sort of canned when a company was sold so they took it home and they kept it in their ice cream freezer for 10 years or 15 years. The company was repurchased and he was hired and they said hey, what other projects do you have? He goes oh wait, I have this in my freezer. So he took it out and at that point they discovered lots of activity. Have this in my freezer? So we took it out and at that point they discovered lots of activity. Not only that this molecule had this immune modulating property, but, as the name mtor was, they actually found a mechanism for cellular energy sensing that they named after the molecule they found on rapamycin. So it was like a reverse, reverse, um you know naming project. So it's crazy how little. I mean. This is only the 90s, right like you go back and I was med school in the 80s, no one knew any of this stuff.
Speaker 1:Like you know, we were taught just you know, even to to your book.
Speaker 2:So so they have this molecule which was used for um transplants. So they they knew if they use it in a higher amount of dosing it had an effect on something called mTOR2, which is another variant of this phosphokinase enzyme called mTOR. It was used to sort of prevent the body from attacking immunologically this transplanted organs. In the, I guess, early 2000s there was a trial called the intervention ITP right which uses three different locations and they test mice and they look at different molecules. Well, it turns out that rapamycin to this day has the strongest positive effect on lifespan in mice. We can leave it at that because it can go on and lots of people can talk about that deeply. But that gives the broader picture.
Speaker 2:But the interesting thing to this, you know, other than the story which has so many twists to it and the podcast is Radiolab, that's the one that. So Radiolab has a really fun story about it is that this mechanism, target of rapamycin, is something that's been maintained throughout, you know, hundreds of thousands of years, you know from worms to humans. So evolution has not changed this particular mechanism, these particular enzymes. Well, there are, there are a few out there like that, that certain proteins, certain hormones that haven't changed very much. But when evolution doesn't change something, you got to perk your ears up and go hmm, it's probably quite important. So mTOR senses energy, it senses nutrients, you know in simple terms. And at that point it tells the cell to grow. You know, it tells the cell to multiply or to get bigger or to be do all the different variety of tasks. You know. Obviously it's not a complete on and off.
Speaker 2:There's there's a modulation there but it's, it's get bigger, you know it's, it's get stronger. The problem with m mtor is um, it can be triggered by too many calories. So if you look at the simple solution, the simple way to think about this and going right up your alley, robert, is too many calories in today's world eating all the time. Go back and look at the 1980 New York Yankees, look at the just you know I give you the numbers like the average baseball player was six feet 185, and now they're 6'2" 220. But just look at them.
Speaker 1:It's like they look like high school kids.
Speaker 2:It's quite impressive to see the size of people. Why did that happen? Mtor right, so we're driving mTOR. But the problem is, if you continually to drive mTOR without taking your foot off the pedal, the cells eventually hit a stage where they can't grow anymore and they, they, they modulate into these other stages of cellular function and eventually become harmful cells to the body and they reach.
Speaker 2:There's a theory by michael blagosquoni, who is a researcher, is a cancer researcher who started in the early 2000s, has a whole series of papers, so if anyone's really interested in reading a non-science I mean, but he's also very much philosophical, I enjoy his reading. So he has a theory called hyperfunction and basically a lot of our diseases that we experience are due to this mTOR constantly being on. As it turns out, there's another side to mTOR. It's called another phosphokinase, adenosine, monophosphokinase, ampk, which balances mTOR, and that's triggered when we're without calories. And when you trigger AMPK and you shut down mTOR, the body begins to sort of clean itself out. Right, you can't just party all the time. You need to clean the house and reset and that's what the cell needs to do.
Speaker 2:As well as this foundational sensing, signaling, cellular health um mechanism is critical to why we're in this epidemic of metabolic health. Right, and once you understand that, you can understand perhaps how the body needs to cycle on and off it. It sort of begins to understand oh, intermittent fasting Okay, that's where that fits in. Or you know, um, going hard and resting and recovering. The body likes to be challenged. It likes, it likes on off states. It doesn't like doing the same thing all the time.
Speaker 1:So I don't know if that covers. No okay, let me see if I understand that. So there's this metabolic switch called mTOR that's conserved over billions of years, all the way from yeast to human beings, and the fact that it's conserved means it's really, really important. It's almost like a survival switch that goes on to grow or off to repair, or autophagy, and and, and then there's a molecule called rapamycin, a drug that will turn mtor from the growth side growth state to the repair state. So it turns mtor down.
Speaker 2:um yeah, and yeah, you say it is a drug, but it's a natural molecule it's a natural molecule. It's a natural molecule that's been made into a pharmaceutical agent. Whatever right, but it's a nuance. But yeah, it's a natural molecule. It hasn't been synthesized.
Speaker 1:Good yeah, good point. And then AMP kinase is another kinase that actually is linked to mTOR and their beneficial effects of AMP kinase being turned on versus beneficial effects of mTOR being turned off. Does rapamycin affect AMP kinase directly or is it through mTOR?
Speaker 2:Yeah, it's primarily. Rapamycin is primarily targeted to mTOR and, just to sort of a slight switch, there's two mTOR, two main mTOR you know isoenzymes. There's two mTOR, two main mTOR you know isoenzymes mTOR1 and mTOR2. Mtor1 is the one that has the primarily beneficial effects of tamping down. Mtor2 is the one that you wanted to tamp down if you wanted that immune modulation or immune suppressing effect. The problem, but the challenge with rapamycin is dosing so that you're primarily suppressing mTOR1, but not over suppressing mTOR2, because then you get into the issue of immune suppressing.
Speaker 2:The difference in, you know, in how rapamycin is used for metabolic health and that's how I like to point out rapamycin. It's got this longevity drug. It's a metabolic health. If you think about rapamycin is in the same basket and by improving metabolic health, guess what? You improve health span and maybe improve. Add some of some years. It's hard to say right, we don't have that data yet. In rice, in mice it does, but mice die of cancer. So cancer for the most part is a metabolic disease. So by reducing or improving metabolic health now we're allowing these you know mice to live longer. Um nuances that we need to further understand.
Speaker 2:But think of rapamycin as a metabolic health and to people I say it's like it's a metabolic health tool to have in your basket right, and not everyone may need it, and that's so, and it's another important point that I see is like oh, rapamycin, is this longevity drug right? It's out there, I'm gonna take it. Yes, yeah, but understand how you're using it and what you're using it. So you know, if you see very enthusiastic people using rapamycin, well, they're fasting and there's strength training and they're they're, they're low protein and they're doing all these things which are already suppressing mTOR. And then they're taking polyphenols. You know berberine green tea. You know there's mango. There's just a whole cacophony of polyphenols that trigger AMPK. So what are they're? Just? They're suppressing the body, and the extreme example of that would be if you go back and look at the old biosphere labs and someone can search. You know Roy Wolford, ucla guy, right, I don't know.
Speaker 1:I met him once while he was still alive. Yeah.
Speaker 2:Yeah, so when he came out of that biosphere.
Speaker 2:After two years of super low calories he did not look very good. He did not look healthy. You know extreme calorie restriction Immune system was not strong too, so he over suppressed mTOR. We want to not suppress mTOR all the time. We need to have a better regulation of mTOR. So if people have eaten too many calories and as they get older and the cells are reaching this gerosynescent to senescent state, we need to sort of slow that process or tamp that process down.
Speaker 2:So, using rapamycin in a pulsed way and even a more sophisticated way, using it in a cycled way, you know where, depending on age, depending on goals, depending on needs, you know someone may take rapamycin for two or three months, right, and focus on just maintaining, and then for one month like I'm going to get anabolic right, come off of rapamycin and then really focus on strength training, eating more calories. That's okay, right, for that month. You're not going to cause some sensitivity and it resets the body. And now you cycle back through. So that's sort of one of the things that we're working on. The challenge is in the space. So we know rapamycin, you know work or some, you know advise company with. You know 3000 people using rapamycin and you know, working with groups and forums, that people take rapamycin.
Speaker 2:It's very clear, and even my personal experience, that rapamycin is a very powerful or powerful beneficial, you know, for metabolic health, right, and I'm hoping that some of the studies are able to show that signal. The problem is everyone is different and everyone's dosing and everyone's lifestyle is different. So the trick is how do we determine who needs rapamycin, what's the best dose for them, and then how to monitor the effects, right, because the first thought is, well, you don't want to have anything harmful, so you don't want to take too much, that you're not suppressing mTOR2. So I personally prefer going every two weeks. I'd rather pulse it, have a higher dose and then give the body more time to recover. Seems to work well and I'm giving little mini cycles as well as right, so you're cycling through and you're not shutting down all the time. Could be proven wrong, but just intuitively, from what I see, that makes more sense.
Speaker 2:So you're alleviating some of that mTOR2 effect, the other sort of cool thing to do is if you look at some of the fasting research through Victor Longo and looking at the AMPK research, those seem to affect mTOR2 as well. They upregulate mTOR two. So there may be a way and we're working on that too is to synergize rapamycin and then bring in a short little fast or perhaps bring in some polyphenols like dihydroperbarine and, and you could then orformin just for a few days later in the cycle to perhaps kick mTOR2 back into gear. And we're looking at people who one of the not really side effects, but one of the things that some people see perhaps if mTOR2 is overly stimulated, is their lipids or their glucose may go up a little bit. So for those people, especially those who come in already with a problem, we're actually beginning to add that up front and to see if we get less of that metabolic unwanted effect per se. Then I mean the other.
Speaker 2:The other thing is how to determine how much you need, right. How do we know how much rapamycin? It's not like this person, right? We have an influencer driven world. So sometimes people want to take something because there's an educator and I will never tell you that you need six milligrams and I will tell you, if I take six milligrams, do not take what I take, because I'm taking it for me and actually for my example. My wife takes it. She takes eight to 10 milligrams every two weeks. Well, twice a month I take three milligrams or two milligrams. It's not good, right I? I can't quite figure that out quite yet.
Speaker 1:So I mean, isn't the six milligrams uh based on, uh, basically misha blog lasconi based on joan mannix paper, where they did six milligrams or eight milligrams or something, and then, you know, other influencers talk about it, and for no good reason, I mean for a while no, good reason misha was taking 10 or 20.
Speaker 1:You know because at one point I know. And so how do you, how do you know that's? To get to that question how do we know when it's too much or too little as far as rapamycin goes like, how do you, how do you modulate the dose? How do you know when it's good?
Speaker 2:and is it so? So let's start with yeah. So I guess the first is like if you're seeing metabolic dysfunction, right, the whole idea is to become metabolically healthy, right? So for me, if rapamycin is not improving your metabolic health and whatever markers that we want to look whether it's serum chemistry or visceral fat or power output on a cycle, we work with athletes, so it has to have a metabolic improvement. It means it has to be improving mitochondrial function, and if it's not improving mitochondrial function in some way, then we're not achieving what we want. Yeah, yeah.
Speaker 1:And one thing I liked about rapamycin, with Alan Green reporting it himself, but, like with Matt Kaperlein with the Dog Aging Project, they were seeing ejection fraction changes in the heart as a really like, wow, significant thing. Are you looking at anything like that?
Speaker 2:Not currently. I'm trying to work with a lab there's a lab in Germany that has the technology to actually look at the electron transport chain so we actually be able to look at cytochrome 1, 4, four and five through a blood spot and actually activation of the ferroxidase enzyme in cytochrome four, which is the copper iron driven, which then goes to five, which is magnesium atp. So so that'll give us a better set. It's still a lab, right, and labs are useful, but they have variants. But it gives us a sense of and it hopefully can give us some good ideas that people can understand where they are.
Speaker 2:But labs are take a while to process, so that you know they lag. So they're better for checking in periodically. So how can we and I'm very much like as a background, as an engineer looking at, how can we look at things phenotypically right, how do we look at our body? And now we have the ability of using some devices. Perhaps that can guide us. And do you remember broda barnes? Do you ever study Broda Barnes? Unsuspecting illness, hypothyroidism? Oh, I know the name.
Speaker 1:Yeah, yeah, yeah.
Speaker 2:Yeah, you know. So he was the sort of family doctor in the 60s, 50s, 60s that you know would have people check their body temperature with a thermometer, right, and he determined that was one of his ways, along with old time doctoring looking at people and their skin, their facial structure and their eyebrows and the hair and their legs and the thickness, you know, the viscosity and some other markers. He didn't need blood tests, right? He could very easily say that someone is, I think we would say in his world, hyper hypothyroidism, right, and he would give people natural thyroid and they would do much better and their temperatures would improve. It may not have been direct thyroid, it may not be a glandular thyroid problem.
Speaker 2:At the time it may have been sort of processing, which you know we now understand is is even more nuanced, but it was very clear, you know, when you paid attention to certain markers. So if mTOR and this is theory based on reading, based on we're still working to it, we're going to work this out. If our goal is to achieve this fluctuating state, what does the body do when it's in a fasting mode? Right? Are there things we can look at that would say that we're in a state where the body's in a more autophagy mode. Right Circadian temperature is one um. You know, you can look at metabolic gases. You know carbon dioxide oxygen. You can look at deep, deep sleep staging.
Speaker 1:Those are the three that so there's those three, because ketosis itself wouldn't uh, wouldn't be an indicator that you're in autophagy, because you could be in ketosis, potentially with mTOR turned on. That's why fasting is an added benefit to a ketogenic diet. It's not enough just to be on a ketogenic diet, you need to do periodic fasting also, right?
Speaker 2:Yeah, so one of the things you know looking at working on so I did there's a company and one could check their temperatures. And if you go to forums and you talk to people who are, you know, who are more motivated, you know they'll check their temperatures and they can see the temperature go down. But it's actually more more than go down. Like a healthy circadian temperature is higher in the morning and lower at night, so there should be again in the body some fluctuation. So I'd really like to start looking at that.
Speaker 2:And there's came across a device out of Switzerland that they were using for triathletes and it's a it measures sort of heat transfer, it's patch, but it measures core temperature. So you can actually wear that and track your temperature throughout the week. And they use that for sleep staging as well. Wow, and then I'm trying right, right. And then if you can marry it with a good sleep staging device, which most of the wearables now are not right Like or just not good for deep sleep, so I would really like to be able to pick up deep sleep. Now that's going to vary more, right, like deep sleep and HRV, but if we see trends, so if someone's on a long-term plan and you're trending the right direction, then you're doing something right.
Speaker 2:Right, if you're trending the wrong direction and you click 30-day moving averages. You're not, and we need to pay attention to that. The problem for a lot of people is they do 10 things at once, right, and you don't know what's working. You don't know if a and b are canceling each other out, so, um, hey, what's the name of that company?
Speaker 1:for our hackers out there in the audience. You remember the name of that, is it do they sell to consumers, also for?
Speaker 2:this so the portable core, yeah, core temp, okay, cool temp. And the, the medical, it's out of switch. One is called green tag g-r-e-e-n-t-e-g. Oh cool, you actually have one right right here.
Speaker 1:Oh nice, very very interesting.
Speaker 2:They started that's used for cyclists and triathletes. They actually try and train them to get heat adapted. So they use. They use the circadian temperature with certain training modalities, but I think there's. I know, because if you look at circadian temperature and some of the research there is, there is a link to that, for sure and interesting and it came out recently. Like you know, current current population base body temperature is lower. Like if you go back from 100 to 120 years, you know the nations has now a lower body temperature than they did and that shouldn't be. So they said we got it wrong. Did we get it wrong? Excuse me, did we get it wrong or has our metabolic health changed right? Wow?
Speaker 2:wow and it's one of these things that you shaped so you could be. Um, if you're like I said, if you're hypothyroid right, and we'll just say hypothyroid your mitochondria are not producing enough energy and temperature, you're going to have a lower body temperature. If you get a healthy metabolic system, your temperature is going to go up. But if you look at research, lower body temperature, you know, seems to be a good thing, but only if you're intentionally cycling through that right. So it wouldn't be a good thing to have a low body temperature in a metabolically unhealthy state, where it's okay to have a lower temperature spread periodically if you're intentionally doing it, because then you're in a hormetic state and that the body likes right.
Speaker 1:Well, um, what one question I want to shift to, to get to before we run out of time, is, uh the well, the mtor. Um, it's this powerful signaling molecule and their benefits to being both on and off, and we want to cycle through it. In the modern diet, modern lifestyle, is turning mTOR on all the way, which is bad and driving chronic diseases and metabolic disease as well. So we can turn mTOR down, as we've talked about with rapamycin. What do you think the role lifestyle plays in turning down mTOR by? You know, obviously, manipulating nutrition, so it'd be low carb and maybe certain protein, certain amino acids maybe, but a low carb, ketogenic diet could turn mTOR down, depending on how you do it, or other things. So what is the role of lifestyle and rapamycin? Is it both one or the other? What are the advantages? How do you look at that?
Speaker 2:Clearly, lifestyle is important and you know sort of low carb, low calorie, lower calorie, because you can push protein and fat too high as well and still be keto and be driving mTOR. So you can do that and I think it's a bit unclear. But my take is mTOR driven through strength training is not the same. Again, if we think if you put on metabolic health lenses right, not mTOR, longevity research on rodents, like what do we want? We want to be metabolically healthy and if you then sort of back off of that, the things that you do that are going to make you metabolically healthy should not then be overdriving mTOR. I'm just not going to, you know, I just don't believe that's the case because phenotypically those responses someone's insulin sensitive, they're lean, they don't have visceral fat, they have energy. You know they're not overdriving mTOR. Now, if you take a bodybuilder or someone who's trying to put on 40, yeah, they're going to be overdriving mTOR to achieve a particular kind of effect. So you need to be careful and you know there's nuances within the diet but whatever it takes to achieve that metabolic health, you know, and however we look at it, whether it's circadian temperature or visceral fat, you know really quite impressed with how much of an issue that is, you know, from inflammatory and also the. The other big piece which I didn't mention is iron, copper dysregulation. So rapamycin actually can play a role in preventing iron from, you know, depositing in the liver and actually improving copper into the mitochondria. They used it with tubularosclerosis and there's paper that talks about one of its effects is driving copper into the mitochondria, which would then play a role with this mitochondrial effect. Iron, which the majority of our population is overloaded, is anabolic. Iron is an mTOR trigger. So if we exist in an iron overloaded state we're chronically driving mTOR.
Speaker 2:Daphyroxamine, an iron chelator, is an AMPK activator which I find like totally fascinating that that was just another drug randomly found that was supposed to be used as an antibiotic. They were trying to find SIBA in the fifties, something that would stop bacteria from growing, and they knew whole iron out bacteria parasites don't grow right the body needs. So they were looking at and they couldn't get defroxamine to work well as an iron as an antibiotic. But it was the first iron chelator. We don't lose men and women in menopause don't lose iron any longer. Ever. You know I should we used to.
Speaker 2:You know how we got iron out of our body. It's crazy when I saw this, um, like right, we don't unless you were bleeding from injury, helmets, hookworms, we had this synergistic effect. You know, obviously too much was not good, but if we were already always infected, you know sort of the epic. You know the pandemic for thousands of years is we had hookworms and helmets and they drained iron and I haven't seen a paper and I, I would bet you know, based that are the hemoglobin levels that we think for men now were much lower. You know, just like uric acid, right, let's say your, the normal uric acid was like three.
Speaker 1:You know, under your three and a half 100 years ago. Interesting that's fascinating.
Speaker 2:Yeah, it's like whoa it? That was a blow my mind when I I came across that. So keeping iron um down is really important within the mTOR world and that's not a piece that is regularly discussed, you know. So when I work with people's donate blood, um, it's a good thing and there's some metrics to there's some nuances to it, but just donate blood every two to three months, it it's a. It's going to be beneficial to your health in a number of different ways.
Speaker 1:We're almost out of time here. I have one other one question. I was recently reviewing literature on rapamycin and you know I looked at the phenotypes of aging and obviously it was cherry picking literature. But you could find studies where rapamycin gives, given the mice it, it makes the hair grow it. It changes gray hair into black. You give it to humans on the skin, it restores the collagen and reverses wrinkles and aging. With periodontal disease, it slows, reverses that with hearing loss. Hearing loss it corrects age-related hearing loss in the animal model. With menopause, it actually increases fertility and delays menopause in animals. And then you look at the diseases. There's FDA indications for atherosclerosis, where rapamycin-coated stents actually stop that, cancer, and Alzheimer's disease. There's animals. What's going on here? All these different processes? What is it about rapamycin? That affects every single phenotype of aging and all the chronic diseases. What's the underlying principle there?
Speaker 2:I just hang my hat on the name too. If there's some other nuances, I hang my hat on the main two. You know, if there's some other nuances, right, I hang my hat on if it's adjusting mTOR, that's the biggest one right.
Speaker 2:That's the elephant in the room. And the other thing, if it's affecting iron regulation, that's my other big elephant in the room. If there's some other subtle pathways, you know and perhaps it's you know autophagy as well, so it's having a role in the cells are able to clear out. I would say that's probably my guess. I don't know. What do you think?
Speaker 1:Yeah, no, that makes perfect sense. Well, I think this has been a wonderful conversation. I think we need to do another one of these. I want to get you back on the program and on the podcast and we could talk some more, because there's so many things we haven't gotten into, but maybe you could tell people in our audience how they could follow you on social media or your website and find out more information about you.
Speaker 2:Yeah, right now, personally, it's just rick at ignite longevitycom. I'm working on a we can talk more about another time with a group of other physicians to do more. N equals one true age reversal. You know, within, within the paradigm of, instead of testing a molecule to see if that molecule is effective on a thousand people, is working with individual people and use the tools that we have in our basket to sequence and synergize, because age, or sort of call it resilience is, is a symphony of different pieces and the medical field is really dominated by individual instruments and not an orchestra, because you can't. You can't study it and it's really quite hard to combine multiple factors together because it takes a little work.
Speaker 2:So, through that, I have a company that I started a number of years ago, pure Clean Performance. Some really high quality beet juice based products for nitric oxide and essential amino acids, or fundamino is quite good. So if anyone wants to maintain a good protein status, you know, using an essential amino acid which is 99% absorbed, um, you know, virtually no calories, it's a quite easy way to do it. Everything that we have there we designed sort of for our family, um, for our local community of athletes, because that that company was driven by performance athletes and then sort of athletes, because that that company was driven by performance athletes and then sort of it's. It's changed a little bit over the time for health and and well-being. So that's it for now. But yeah, the the consortium will be coming and that's well. Yeah, I'm spending most of my time I want to.
Speaker 1:I think we can devote a whole session to that. Uh, I want to get you back.
Speaker 2:Yeah, it's a complete paradigm shift.
Speaker 1:Yeah, yeah, and do that. That's it. That's, that's awesome. Well, well, thanks so much, rick, for spending time with us today and thanks, thanks for all the exciting work you're doing. It's, it's been, it's been fun yeah, it's really fun.
Speaker 1:It's a big puzzle so many fascinating things about rapamycin and mtor and its effect on metabolic disease, and things we're just beginning to to understand. Uh, I want to thank uh rick cohen for joining us today and and sharing dr cohen's amazing knowledge with us all. Remember that Dr Cohen is giving us a bonus to our VIP Pass members. If you still haven't claimed your VIP Pass to access the recordings, transcripts, mp3s and must-have bonus package, you can get it now by clicking the button on this page to upgrade before it's too late. Remember that when the event's over, the recordings and all the bonuses go away. So make sure you climb your VIP pass before it's too late.