It’s one thing to hear the physicians talking about rapamycin for longevity. But today we get to hear for from one of the citizen scientists who is taking it himself. Our guest today is Gregg Davison, a student of longevity science.
It began for him over six years ago when a news article making intriguing claims came to his attention. The series of scientific studies radically extended mouse lives up to 25% longer, all due to a drug, a drug that Gregg subsequently takes. Gregg studies have grown and today he speaks regularly about why and how we age and how a drug may be able to do for humans what it does for other species that has been administered to Gregg has a Bachelor of Science in Biology from the University of Utah. He has worked in the gurney cellular lab on the Human Genome Project, and also as a paramedic in the greater Salt Lake area for over 10 years. Before we start the episode, if you liked what you hear, please consider supporting the work we do as well as joining us on your personal health longevity journey. You can do both by becoming a member of our community. The benefits include a private messaging area, live QA sessions, weekly premier videos, product discounts, free giveaways, and much more. You can join for as little as $1 per month, and the first month is free. See the link in the show notes for more information.
- 00:15 – Introduction to Gregg Davison
- 01:55 – Rapamycin
- 04:09 – Damage to DNA
- 05:06 – Reactive Oxidative Species
- 05:29 – Piper Functionality
- 07:50 – Energy Sensing Pathway
- 10:14 – Synaptic Cells
- 12:40 – Senescence
- 14:55 – Biological Clocks
- 18:54 – Master Nutrient Sensing Pathway
- 22:40 – mTor
- 33:21 – Lipids
- 39:27 – Phenotypes of Aging
- 44:07 – Lithium
#rapamycin #cell #longevity #senescence #aging #drug #negligiblesenescence #lithium #immune system #metformin
#robertlufkinmd #drlufkin #robertlufkin #healthlongevitysecrets
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Robert Lufkin 00:00
Welcome back to the health longevity Secret show and I’m your host, Dr. Robert Lufkin. It’s one thing to hear the physicians talking about rapamycin for longevity. But today we get to hear for from one of the citizen scientists who is taking it himself. Our guest today is Gregg Davison, a student of longevity science. It began for him over six years ago when a news article making intriguing claims came to his attention. The series of scientific studies radically extended mouse lives up to 25% longer, all due to a drug, a drug that Greg subsequently takes. Greg studies have grown and today he speaks regularly about why and how we age and how a drug may be able to do for humans what it does for other species that has been administered to Greg has a Bachelor of Science in Biology from the University of Utah. He has worked in the gurney cellular lab on the Human Genome Project, and also as a paramedic in the greater Salt Lake area for over 10 years. Before we start the episode, if you liked what you hear, please consider supporting the work we do as well as joining us on your personal health longevity journey. You can do both by becoming a member of our community. The benefits include a private messaging area, live QA sessions, weekly premier videos, product discounts, free giveaways, and much more. You can join for as little as $1 per month, and the first month is free. See the link in the show notes for more information. And now, please enjoy this conversation with Greg Davison. Hey, Greg, welcome to the show.
Gregg Davison 01:47
Thank you, Robert. It’s wonderful to be here.
Robert Lufkin 01:50
I’m so excited about talking with you today about one of my favorite subjects rapa myosin and and all the all the fascinating things you’ve you’ve learned about and that you’re doing with yourself as a citizen scientists. But maybe before we do that, let’s just take a moment like like we’d like to do and set the stage and tell. Tell us a little bit about how you came to be interested in this fascinating area.
Gregg Davison 02:18
I gotta say it all has to do with a very interestingly named gentleman named Blaga Sconnie. But six years ago, I saw a news article that caught my attention. I didn’t believe it. At first, it sounded obscure and strange. I couldn’t pronounce the gentleman’s name. I’d never heard of the drug. But the outcomes, this study this, what he was talking about the collection of scientific studies to scientific work, spoke for itself. This drug was extending the lives of mice 15 to 25 27%, long. Across the board, study after study after study. It’s the numbers which really drove my interest. And then from there, it was down the Mousehole. I’m just intrigued by the science I’m, I’m intrigued by the theories. And they’ve driven they’ve been very exciting to study it. And I’ve been talking to anybody who will listen to me about it.
Robert Lufkin 03:30
That’s great. Well, maybe before we, before we talk specifically about the drug itself, let’s maybe set the tone and talk a little bit just in general terms about longevity and theories of aging. What’s your, what’s your philosophy on it? What what is longevity? And what’s what’s really changing about it?
Gregg Davison 03:52
I think it wouldn’t be fair, if I didn’t tell you that when I was studying biology at the University of Utah, I was told a terribly convincing story. And that story is is that aging is the collection of damage to DNA, mitochondrial DNA, because specifically, of reactive oxidative species that were created at the metabolism in ourselves, that is like lightning in a bottle in so many ways, creates damage to the fragile DNA that becomes inherited, sell to sell through mitosis over time.
Robert Lufkin 04:34
I have to admit, I’ve, I know that story and my day job is a professor at at medical school. And I actually taught taught that when people ask, you know, that’s, that’s the standard answer that so many people here across the board so why is that not? Why is how is that changed?
Gregg Davison 04:59
It is change because it doesn’t stand up to scientific rigor when these reactive, reactive oxidative species are removed through antioxidants, we’ve all heard of those bad things happen. Less outcomes in long, big animals don’t live very long. They get sick, even people, it can be dangerous and toxic. Wagga Sconnie is theory of Piper functionality, which is this notion that cells, principally because they’re rate limited, they can only divide so many times, once he gets to two, he gets four through my talk mitotic process driven by the energy and growth sensing pathways of the cell, a pathway that’s going on 2 billion years old, and drives this process in is vital for health and life. But at a certain point in time, maturity, it starts to drag on the system, because these cells can only divide so many times that’s been observed with skin cells. 50s, the number of people talk about is actually a little bit lower, a little bit higher and changes during our course of our lives. But when that number limits, the cells persists on a fraction of time, just maybe one in 1000, maybe one in a million, but as a 32 to 37 billion cell organism, it happens enough. And those cells persist, they become synaptic or old, and go through a process where they start benign and become terribly dangerous. As Dr. Greene says, they start to send out a witch’s brew of chemical signaling that spreads dysfunction at a cellular level, to their neighbors, that tissue and organ dysfunction, we start to see slowly as the disease process that just gets worse over time as the synaptic cell burden, the old cell burden persists and gets worse.
Robert Lufkin 07:09
Right. So let’s let let me let me rewind that a little bit and amplify a couple of things you’ve said about first of all, you mentioned important nutrient sensing process that is going to be fundamental when we talk about rapamycin and the way it works. Can you elaborate a little bit on that, on that process, and that on that enzyme, what it is and and expand on that a little bit? It seems that
Gregg Davison 07:44
every organism on the planet that has more than one cell has this energy sensing pathway, which when it senses glucose, insulin, in in humans, human growth hormone and some other things, says to the cell, grow, grow, grow. This is so widespread in life, plants, habit, fungus, habit, yeast has it all animals have it. That it tells us getting from the one cell that we start as have given us to from our mother and our Father, to the 32 to 37 trillion cell organism that we are. It’s the most important job one of the most important jobs on the planet. And that’s why this mechanism in our cells, is so ancient, and so persistent.
Robert Lufkin 08:43
Now, it sounds like the command to grow it some points in our life would be valuable. So when in this, this sensing protein sends off the growth signal. So when when is it? When is it helpful? And when is it non helpful? It seems like it could be in both situations.
Gregg Davison 09:08
I think it’s important to think about this growth pathway, the chief amongst him as vital and important all the time. Certainly during our growth phase from that one cell all the way up to maturity, say 20 years or 20 years of age plus or minus a few. And it’s not that we ever want to turn off these growth pathways, chief among them being the one that rapamycin effects, but we certainly want to bring its level of activity down down to the point where there’s a balance, balance where we need our rapidly growing cells of our immune system to stay vibrant and rapidly growing, but not really any more much higher than that level.
Robert Lufkin 10:00
Yeah, fascinating. So what what are the implications of this, then what? What can we learn from this?
Gregg Davison 10:09
I think what we can learn from this is that the old cells, the synaptic cells, are either the direct cause of the diseases of aging, or secondary to it. I’ll just give you an example athlos sclerotic plaques, heart disease. They occur, this plaque occurs with the formation of a foam cell that migrates to the inside of the artery and begins to accumulate the plaque. It’s the dysfunction of the foam cell that’s directly related to the sin synaptic cell, the old cell. Bone weakening, but very much a two by two process. One cell builds bone, one cell takes a down osteoblast osteoclast dysfunction in this system spread by these old cells creates a weakening of thinning of the bone throughout our entire bodies, this dis easing process Blaga Sconnie says I’m gonna I’m gonna paraphrase and he says it like this. We can look at a person and think of their aging as a collection of their disease state. I would maybe like to frame it just a little bit different. I think we can look at the synoptic cell burden, the burden that these old cells are putting on our tissues, organs and body as a dis easing process. And that leaves us open to think about aging as something different than dis easing. We won’t get there until we have enough people go through this process. Like naked mole rats do the very long live Rodin with a negligible senescent burden.
Robert Lufkin 12:02
Yeah, you mentioned important concept there negligible signal senescence, and that’s a it’s easy for me to say negligible senescence, and that is one of the arguments against longevity being a an accumulation of DNA mutations, gradual wear and tear gradually over time, maybe just expand a little on Negligible Senescence, and why that’s such a powerful concept for people thinking about longevity, and they could roll with rats.
Gregg Davison 12:33
Oh, my Toastmasters group is so terrified of naked mole rats. Your strange little beasts. We I think we can think of senescence as the catch bucket for many, many of the theories of aging that came before. For example, if you have DNA mutations in the mitochondria or in the cellular DNA, you will end up with a senescence cell, hopefully, versus maybe a cancerous cell. But the senescence starts to catch a big burden of the stress cells, the damaged cells that just aged in rate rate limited out cells. So the senescence cell burden. Can you repeat the question I got lost on the side,
Robert Lufkin 13:18
No problem, just the the idea of negligible senescence, where people they basically don’t age until the end, and they don’t become senescent until the end, and then they just suddenly they hit a wall and it all drops off, which sort of goes against the theory of of aging just being an accumulation of wear and tear, but but it makes it rather like something’s program going on there. Like the naked mole rats, right? They have negligible senescence, I think you said
Gregg Davison 13:49
They do. A particularly the Queen female lives so dramatically long, the equivalent of 1000 human years. How do they do it? Negligible Senescence, and a very stable epigenome. It’s quite possible that we can think in advance the theory by thinking of displeasing as senescence and aging at an epigenetic level. Here’s the thing about epigenetics. There’s only one real known disorder associated with it. And that’s an obscure hearing disease. That doesn’t mean though, that it’s not playing a part in the way our cells are expressing themselves, the kinds of proteins that are making, how they’re behaving, how they’re responding to stress and what have you. But the disease state that disorders that’s being driven by the big gorilla in the room or mouth, big mouse in the room, and that’s the senescent burden.
Robert Lufkin 14:52
Yeah, yeah. It’s that’s fascinating in the whole epigenetics the the idea of these biological clocks To measure biological age by looking at the epigenome are, are fascinating and and even some of the, some of the approaches of reprogramming the epigenome with Yamanaka factors are really
Gregg Davison 15:13
Better than you. I can’t pronounce that you said that so much. With the risk factor being the formation of Blastomyces, being able to drive a cell from senescence all the way back to pluripotent, it’s at the beginning of stem cell, or to do it less recent 2017 study with mice drove the epigenome back, but not fully intermittently. And the mice that had that fact those factors applied live 19% longer.
Robert Lufkin 15:50
Yeah, yeah, it’s a fascinating area for research and development. And But now Now, this, this process going to senescence and this master nutrient system, how does wrap up what is rapamycin? And how does that fit into the whole thing?
Gregg Davison 16:10
Oh, rapamycin is both blessed and cursed at the same time. It’s blessed because it’s an amazing drug. It’s cursed because it’s off patent. It’s cheap. And it’s produced in multiple countries around the world. And what that means is when I say it’s cheap, you’re not going to see a commercial about anything to do with rapamycin. You the average person knows more about Restless Leg Syndrome than they do about what rapamycin is, rapamycin, I like to think of it as a lock in a key to this energy sensing the chief energy sensing control pathway in our cells. It has a one to one target. It has no toxicity levels. And it does it has a 54 and a half hour halflife. So it tends to persist. So by locking it down benefits are or are seen for hours and days afterwards.
Robert Lufkin 17:19
Yeah, it’s fascinating. You hit on, there’s so many things there. But one thing I want to underscore is the the idea that rapamycin, unlike most other drugs that we prescribe, and we take for things, has a very, very narrow target, it basically fits in this one protein. And that may explain why there’s very relatively few side effects off target effects other than the effects on this protein. So that that’s going to be very useful when we talk about using the drug. Because we don’t have to necessarily worry about many other effects, the effects are going to be the effects of this one master controller, but at least we know it’s narrow or on that.
Gregg Davison 18:05
Yes, it’s a very, very understandable and prescribed method. Its mechanism of action is well understood, well studied. In fact, it led to the discovery of this method mechanism. In 1990. The drug found its own pathway, at least to human knowledge. Before we had no idea science didn’t know about this process. And let’s let it out of the bag. It’s called mTOR. It used to stand for mammalian target of rapamycin. But it’s since been discovered that this protein exists in all basically all life with more than one cell. And it’s moved its name is shifted to a mechanistic target of rapamycin.
Robert Lufkin 18:50
I mean, it’s amazing to think that this master nutrient sensing pathway that controls all our metabolism and survival in every eukaryotic cell, every cell, like you say, from single celled organisms up to humans, wasn’t even discovered until the 90s. And the only reason it was discovered was because in the 1960s, this drug rapamycin was discovered and this master controller is the target of rapamycin
Gregg Davison 19:22
in the discovery story, and the initial years of development of the drug, I think it could be a lifetime mini series covered on Easter Island, pulled out of the dirt. Because an intriguing and I don’t know the name of I can’t recall the name of the gentleman who discovered it. But he saw something in the ground that triggered his intuition is his instincts. He took a sample and sure enough, you found this bacteria that could inhibit the growth of have yeast and kill it not heard it. Just stop it from growing any closer.
Robert Lufkin 20:09
And why did they call it rapamycin? What what how did that name get started?
Gregg Davison 20:15
rapa is the site of course rapamycin is the I believe we call it the scientific name. You can’t actually buy a drug for human use called rapamycin. But the scientific name is rapamycin rapa stands for is the first part of the name for the indigenous name for Easter Island, Rapa Nui. So it really, it ties it back. It’s, it’s quite mysterious. And then it had a can only be described as the most dramatic development story. At one point in time, when the company that originally was developing, it had isolated from the bacteria was going through a merger and acquisition, the lab team was ordered to destroy the samples. And then they couldn’t do it. So they took it back to their own house, stored it in a refrigerator. It’s like it’s like a real, it’s a real dramatic story.
Robert Lufkin 21:13
facet fascinating. So so how did rapa myosin come from being a something that works on fungus to what it is today?
Gregg Davison 21:27
Oh, wow. I don’t actually know the details. But it went from what was obviously an antifungal treatment to being something that can poison the immune system, our immune system as well as the ubiquitous mice in the lab, it does it the exact same way that it keeps the yeast away and the fungus away. It stops the fast growing cells in you and me, our fast growing cells are our immune system cells. So our immune system cells, like our neutrophils, only live three to five days. They’re a very important part of our immune system. I like to think of them. They have a lot of functions, but I like to think of them as the hooligans of the immune system. They’re in the bar drinking and they have the team shirt on. And if somebody comes in the bar with the other team shirt, they bum rush them and throw them out. That’s sort of what they do in our bodies, although they don’t wear team jerseys.
Robert Lufkin 22:35
So that rapamycin inhibits this, this, this protein called mTOR. Which when mTOR works, it stimulates growth. So rapamycin turns down growth and slows the growth of fungus and slows the growth of other things, and also the immune system in us. So how does that how does that benefit longevity, then?
Gregg Davison 23:04
It truly it doesn’t if we’re going to take it to the way that we would need to stop our immune system so that we can accept an organ transplant from somebody else. We’re really not barking on the tree of longevity there, we’re really just trying to survive and improve our quality of life for the remaining days or months or years that we have left organ transplants a kind of a you know, it’s a it’s a last ditch effort to save human life. When we flip the switch on it though, and we go from taking a lot of rapamycin, frequently to taking some rapamycin, infrequently. All of a sudden we slow down the rate limiting clock for growing cells, so the cell may be experiencing insulin, the cell may be experiencing glucose, but its growth pathway is turned down because of the rapamycin. So we have less of these turnovers. Therefore we have the less of a creation of the old cells, the synaptic cells. But rapamycin does at least one other thing too. it quiets down the old cells, because the old cells start fairly benign, they start without much problem. They’re normal. They perform normally, but driven by their energy sensing and growth pathway. They start to change over time, and they change from being normal to being fatter, flatter, and dangerous to their neighbors and themselves. So rapamycin quiets that old cell process as well. So the burden on our bodies or tissues in our body is reduced from both sides of that equation.
Robert Lufkin 25:00
Let me just before we get into that, let me clarify one thing before we just touched on was that was the transplant immune suppression and transplants just to be clear for our audience. The rapamycin is actually FDA approved for humans and it’s regularly prescribed. But the indication, as you mentioned, Greg was for one of the indications is for immune suppression for transplanted organs like kidneys and all and that they suppress the immune function. But as you say, for that particular application, the rapamycin is given on a daily dose to maintain a certain a certain level. And I guess when we, when we get into the dosing patterns, we can talk about how rapamycin for longevity is a different dose there as well.
Gregg Davison 25:53
I like to explain it two different ways. One is with aspirin, and one’s with alcohol, I talk about aspirin, taking a small dose of aspirin, like a baby aspirin, for mature adults, has shown to extend life, reduce heart disease, and reduce colorectal and esophageal cancers. If you were to take a regular size aspirin every day, you would be in very high risk of death, within a matter of days from a bleeding disorder from bleeding. So the dosage and the frequency are very important for for targeting drugs. Alcohol is maybe even more understandable. I think we understand that a glass of wine with dinner can be beneficial and helpful for our life or digestion and even possibly, for long living a little bit longer. Drinking a glass of wine an hour is definitely something that would cause a different effect.
Robert Lufkin 26:58
So the black rusconi papers really got you thinking about this and then the subsequent things that you read confirm this and what were the what were the next steps you took, what was the process? Like? How did you find a physician that would that would prescribe this because although it is FDA approved, rapamycin still requires a doctor’s prescription in the United States to get from the pharmacy, for sure.
Gregg Davison 27:28
I think what really got me going was a 2017 study from the National Institutes of Health that dealt with the way 70 year olds, seven year old folks responded to the flu shot. The way the cohort who received the rapamycin had no side effects, and the massive benefit they received to me, if that didn’t turn the understanding that there was massive benefit here. It was going to be on me. And I was already aware of a physician named Dr. Greene practicing out of New York State. At that point in time, a few weeks later, I reached out to him via email and asked if he would be my prescribing doc. He said he would love to this was right around when he had about 200 250 patients. But I would have to go to New York to go and see him and that seemed very and he recommended I speak to a physician or or somebody like that a practitioner locally in Utah to attempt to get prescribed here in Utah. And I gotta tell you, I did I spoke to my physician, multiple physicians I really run ran into a brick wall. I did not run it find any Doc’s who were willing to prescribe rapamycin to me. Fact I got the strangest look under the sun, like there are better ways to hurt yourself kind of look. I found a wellness clinic in my hometown that was doing stem cell work that had a non prescribing health care provider. I think he has a master’s in Chinese medicine. And he’s a really wise guy and he does a lot of podcasts where he was talking about mTOR I reached out to them because I know they had a prescribing network and physician type services. And I was able to after a lot of a lot of arm twisting and pushing to get the prescription for rapamycin that way
Robert Lufkin 29:31
for for your own in this process this decision process for yourself. What were you weighing as the risks to yourself versus the benefits that in making this decision? What what was going through your head?
Gregg Davison 29:47
rapamycin has a lot of scary risks associated with it in the literature. Everything from organ failure to strange bleeding to even death. I was convinced by reading Dr. Greene’s assessment of both his for himself as patient one. And his few 100 patients who had been treating now for I think for about three years, two and a half to three years that absolutely none of that was observed that by changing the dosing schedule from daily to weekly or every 10 days or whatever have you completely changes some of the outcomes of the side effects that he talked about the the side effects being possibly soreness of the tongue, which I experienced both the first and third times I took rapamycin, I ended up with a kind of a hotspot on my tongue. Six to 10 hours after I took the drug, it was enough to wake me up at night of not enough to keep me up. And by the time I woke up in the morning, it was gone. It was kind of a very interesting experience. I that that was three years ago, I haven’t experienced it since. And then also for me, one of the risk factors has been increased in lipid levels. I don’t know if we’re probably going to talk about that later, Robert, but that was sort of obscene as the main risk factors. I left one out, and it was possibly taking too much rapamycin, and driving down the white blood cell count in your body called the neutrophils. I was able to do a simple blood test. Three months after I started taking rapamycin and observe that the dosage for me had no change in the neutrophil level.
Robert Lufkin 31:35
Yeah, before we talk about neutrophils, and lipids, if you want, how did you? How did you with your physician work out the dose? What was the what was your strategy there? And how did you approach that
Gregg Davison 31:51
went off the scientific literature and much of the scientific literature looks to prescribe mice to milk point 02 milligrams per kilogram of mouse. We translated that into some body weight and came up with an idea. Looked at Dr. Greene’s prescribing data and just kind of kind of threw a dart at the wall and came up with a number. For me it was six milligrams.
Robert Lufkin 32:16
And did you did you ramp up to six milligrams? Or did you start just start with six milligrams? Cold Turkey? Sort of?
Gregg Davison 32:25
I did ramp up. I started to four and then six.
Robert Lufkin 32:29
I see I see. And and then the plan is to stay at six. Is that right?
Gregg Davison 32:35
I’ve been at six milligrams weekly for the last two and a half years a little bit more.
Robert Lufkin 32:39
And maybe talk about the the lipids and any of those effects. Do you you mentioned you check your labs for the white blood cells? How often do you do that?
Gregg Davison 32:55
I did it. The first I did it for the right with intention. I did it at three months. And then my regular annual physical was about six months after that. So other than that, I’ve simply been checking that in a CDC blood test once a year, and it’s been very stable.
Robert Lufkin 33:14
And how about lipids? What is the issue with lipids and rapamycin
Gregg Davison 33:20
lipids, it’s observed in some of the animal models, not necessarily humans, but in some of the animal models that lipids can become dis regular can elevate with long term use of rapamycin. And I have indeed seen that with myself. Nothing crazy. I went from being and this took over two years actually. But at around that two year mark I observed in just my normal annual blood test that my lipid levels had gone up from the like 190 to 240. And also my cholesterol level elevated just a little bit.
Robert Lufkin 34:00
Okay, and so it was across the board for triglycerides and LDL, everything. Everything went up.
Gregg Davison 34:07
Just to look yes, everything just a little bit. Yeah. And
Robert Lufkin 34:12
well, we can we’ll talk a little bit at the end about other things you do in your life as far as lifestyle and everything in diets and how that may may have affected it. But so those were the side effects then that you were that you were alert for. And you mentioned that the tongue the little they the app, this ulcers that sometime can can occur. They went away. What about the the other side? What about? How do you know it’s working? Yeah. How do you know? What’s the positive side? How do you know that six milligrams a week is the right dose.
Gregg Davison 34:52
Great, great question. I don’t know that some people really feel benefit of that reduction. Have this senescence cell, the burden that they’re experiencing, whether that’s in their kidneys, or maybe in how they’re urinating at night, or some other functions that are bothering atherosclerosis. For me, I didn’t have any of those burdens. So I didn’t observe any benefits directly. And I still don’t, which is probably a good thing right from the prescription. So the question isn’t, should I be taking less? The question is, Should I take more? I haven’t felt that there’s a real benefit to taking more, although in the animal studies, it is shown that more in series does tend to drive better results. So I don’t have a great answer for you on I know that less isn’t, isn’t going to be better. But the question is, would more be better? And I don’t know if a higher dose makes any sense for me.
Robert Lufkin 35:55
Yeah. And this, of course, we’re all we’re all facing the same thing. This is really the earliest stages of these of these breakthrough, potentially breakthrough longevity drugs. And the problem is, as, as we’ve discussed, we don’t really have any endpoints to monitor it effectively, to know how it’s working. You know, it’s not enough to say check back in 20 years, and I’ll let you know, it’s like,
Gregg Davison 36:21
I can give you an anecdotal story, because I just recently had a death in my family. And I traveled along with my brother, who’s a few years older than me to go spend time with my cousins who lost their mom. And my cousins are right around my age as well. We were sitting around a table, and this is now going on close to three years of being on rapamycin. And although I have younger cousins, there were some pretty profound responses, the way I look compared to the way they look, ranging from age 47 to 5052 years of age. So I don’t I don’t know what that means. We’re all very related, have similar lifestyles, but it is what it is.
Robert Lufkin 37:04
Yeah, I mean, in the effects of the rapamycin and it’s been dramatic in in all body systems, including the skins so and so it’s not unreasonable to think about seeing manifesting as skin changes as as well as the other changes, but but like you say, the it’s an issue with dose that there are very few side effects on one, which is good news. But on the bad news, or the challenge is that there aren’t really markers that it’s working either. So, you know, we don’t know whether the dose is too low or too high in some, some some huge, you know, human individuals who are using it or even advocating going as high as 20 milligrams twice, once every two weeks, in order to allow blood brain barrier delivery cross the blood brain barrier. And, and of course, there’s the whole issue of bioavailability and how much we absorb it and different people may absorb it at different rates. And you know, six milligrams a week for you maybe may deliver a different dose than six milligrams for me, even assuming, you know, body weights are the same in everything. So it’s, we have so much to learn with this. And we’re all just kind of, you know, exploring as we go here. This is
Gregg Davison 38:23
sort of been classically observed, even through this standard way the drug has been used historically, to suppress the immune system. If you read the literature, it doesn’t deal with weight and people it deals with volume. So I don’t know if you take your patient who’s about to get somebody’s liver or I’m sorry, kidney and submerge them in a tank to figure out their volume or if you just estimate it, but I think even for standard administration purposes for organ suppression of immune suppression, there’s some real challenges to getting rapamycin the right dosage.
Robert Lufkin 38:57
Yeah, yeah, there’s, there’s so many so many things we don’t know the answer to but like, like you’ve mentioned, there’s so many really encouraging things about rapamycin and I just want to underscore a couple one is that rapamycin it not only slows down aging in the animal models, but it actually reverses them for certain certain phenotypes of aging, which is which is interesting, and it’s so it actually can roll back age for myocardial fibrosis and, and other aging things. And then the other point is that for if you think about a longevity drug, oftentimes you might have to administer it for the whole lifetime of the animal but from from the interventions testing program, due to a way one of their experiments was set up, they had the interesting results where rapamycin was delivered to the equivalent of 60 to 70 year old mice, and the effects still took place. In other words, they the mice didn’t start taking rapamycin until they were already elderly, and they still got effects of it, which was pretty remarkable. Which means it could be applied to a human, you know, extrapolating mice to humans, etc, with all the caveats there. But you could have an effect and even older humans that started taking it at that point.
Gregg Davison 40:28
I’ve got another one for you. That’s maybe a little on the reverse side of that. Recent study results rapamycin was given to juvenile mice in a single dose, it reconfigured their growth pathways in a certain way that led particularly in male mice living 12% 50% longer I can’t remember the exact number a single dose to use. Now, of course, that would you know, that has no business in human medicine, or practice but it just maybe speaks to this very interesting nature of rapamycin.
Robert Lufkin 41:02
Yeah, yeah, I mean, one way that people conceptualize of rapamycin as mimicking calorie restriction as this protein and then growth and all and one thing that is consistently seen with calorie restriction animal models is the animals are smaller in size when they have it their whole life. So again, just hypothesizing here like like you say, we may not want to give rapamycin before age 25 or so until the growth growing up is completed. And then after that point, when you’re growing you’re no longer growing up but you’re growing old you know as Blake was Tony says in his model, which is very compelling Yes, so I on rapamycin do you do many of your colleagues take it if you do have a rapamycin community there of users? Are you the are you the point of the spear and
Gregg Davison 42:04
I am I am the point of the spear. But I have a handful of local folks here in my hometown Park City who have heard me speak that are really ready to go and and under the care of a physician and get on rapamycin.
Robert Lufkin 42:23
Yeah, it’s very it is this is very exciting times and and you’ve emphasized senescence as part of your view of longevity and the important role it plays and certainly that, you know, the literature supports that. And rapamycin is a powerful senolytics. In other words, killing senescent cells through activating autophagy by turning down mTOR and all Do you do you? In addition to rapamycin, have you looked at specifically taking other drugs to enhance destroy destroying senescence or other Santa lytic drugs as they’re called?
Gregg Davison 43:06
No, not yet. I just think for me locally, it would it’s not that I wouldn’t. But I think in particular, we’re probably talking about a keratin and dinar strutted. Did I pronounce that right? Which is a
Robert Lufkin 43:24
de sac? Yeah. Yeah. Renounce it all different ways. Yeah.
Gregg Davison 43:30
Powerful cancer drug, which will, is proven, highly successful at targeting senescence cells, at least one tissue type, and assisting the body in removing them, encouraging the removal of these old burdensome cells. I know that’s I don’t think my local physician group would be into that at all. That might be a bridge too far for at least for now. Although Dr. Green is doing it and is shown safe administration for, you know, months, if not years. So that’s very encouraging. One other thing I take highly specific towards longevity is a supplement that lithium, I take a micro dose of lithium every day, basically, because lithium makes cells tough. When a cell is stressed, either from sunlight, or energy production, or chemical cells that have lithium stay healthy and viable. And cells that don’t have lithium, either go through a self destruction process, or end up as synthetic cells. So lithium helps reduce that synaptic cell burden as well, not by quieting down senescence cells, but by reducing the number that are produced over time. And population studies in Japan have shown that people with groundwater that have higher levels of lithium have a reduction in all cause cause mortality. Love that word all cause mortality. Just a great catch basin of of health and longevity, all cause mortality is reduced with higher levels of lithium. It’s dirt cheap and easy to get very safe to take.
Robert Lufkin 45:16
Interesting. Yeah, we’ve heard some other people talk about lithium as well. Back to synapse senolytics. And those we were Alan, Dr. Alan Green has been on this program, we’ve talked about baton and as you say, he’s he, in addition to using rapamycin is using senolytics in this practice, but unlike rapamycin, which, as you say, is relatively inexpensive, the de sac nib is crazy expensive and unless you get it formulated yourself, it’s it’s it’s really price for EBIT IV. But hopefully that that will change. And I think Dr. Green has a source for it, or he has a way that that it’s, it’s affordable through a compounding pharmacy that he has a relationship with, but But yeah, there’s many different things to look at down the road. And as as someone who’s taken a deep look at longevity and really consider these for for yourself and all the possibilities. What else do you do for your own life, if you don’t mind sharing your own lifestyle choices as far as diet fasting, exercise, what other supplements do you take.
Gregg Davison 46:36
And once again, I love this idea of all cause mortality. If you can look at these behaviors, diets, or practices that get you on the right side of all cause mortality, you’re doing really well for yourself. So the first is, you know, we’ve known for going since 1996, we really know that an active lifestyle is it’s better to be active, and smoking cigarettes, then sitting on the couch and not smoking cigarettes, if that’s a fair way to say it. So right so I live in active likes lifestyle, and I think we can describe an active lifestyle today, as 7000 steps are the new 10,010 minutes of HIIT training just for me personally 10 minutes of any kind of physical action, which hits head is intense, is what you need for your kind of check that box. So I enjoy that gives me energy throughout the day. And I would encourage you to but it helps to live in Park City, Utah, where out my back door is a trail where I can see coyotes and moose and deer and hike up to an Olympic Park. I know not 300 days a year. I’m not sure everybody can do that. But I think you can find it somewhere in your life. Another thing I do is I intermittently fast most days, so I try not to eat anything after eight o’clock at night. And then I don’t eat anything besides green tea in the morning until about 1045 1111 30. I’m not super strict about it. But it’s a nice long window that I just I’m not putting anything down my mouth, letting my gut relax and not do its job to get some recovery time.
Robert Lufkin 48:29
And how about nutritional choices? Are there any foods that you that you include or don’t include in your diet?
Gregg Davison 48:38
I’m a real omnivore, I kind of will eat it all. I try to eat a plant based diet. But you know, I definitely eat plenty of meat products. My wife and I have tried to do a Monday meatless Day, which has been a lot of fun because we enjoy cooking together. It’s something we do together to talk about it, we plan it so that’s fun. But it’s not really something so that I’ve brought into my lifestyle. On advice of my my physician, I’m taking fish oil to help counteract some of the increases in lipids. I’m not exactly sure how that works, but it’s been observed.
Robert Lufkin 49:17
And then as far as other other medications, Metformin. Some people take that for longevity.
Gregg Davison 49:27
And I can see why Metformin. If it’s cheaper than dirt, you can probably get it from your dock without the look, if you ask for rapamycin, you’re gonna have to explain what rapamycin is to your doc, you’re not going to have to with metformin, and it’s very, very tolerable even for at low doses for people who aren’t diabetic. So it’s a great drug and there’s a UK study which shows that being diabetic and taking Metformin is a better outcome than not having diabetes. That’s amazing. One of the thing I do regularly as a practice is I donate blood. And I have a very low blood storage of iron called ferritin.
Robert Lufkin 50:13
Yeah, that’s it’s another thing that other people have been using. Well, this this has been so great today, Greg, maybe we’re going to be sharing in the shownotes, the articles we talked about and references. We’re also going to have your YouTube channel and your website in there. But for people who are listening to this presentation as a podcast and don’t have access to the shownotes maybe you could just tell us right now, what those are and how they can access them. Oh,
Gregg Davison 50:45
the website is longevity, SCI sci.com and the YouTube channel is longevity science explained where I just do a deep dive on cool scientific, very nerdy studies and try to D nerd them and make them kind of fun to with ideas on how you can maybe benefit from this cutting edge and rapidly growing science.
Robert Lufkin 51:11
I love it. This has been so much fun today Greg I really appreciate you taking the time to spend an hour with us and share all the all the great things you’re doing with your own choices in your life and, and work with rapamycin. Thank you so much.
Gregg Davison 51:30
Thank you, Robert. It’s been so much fun. I really appreciate the opportunity.
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