047-Daniel Tawfik- Rapamycin, Metformin, and Fisetin for Longevity

Rapamycin, metformin, and fisetin are all associated with improvements in markers associated with aging. We are now beginning to see them used by healthy individuals interested in longevity. Daniel Tawfik is the founder, developer, and CEO of HealthSpan. HealthSpan optimizes human performance through interventions that target cellular senescence. Healthspan was created to empower patients to regain control over the levers of aging that are at the foundation of most age-related diseases.

Daniel holds a BS degree from UCLA in molecular, cellular, and developmental biology and physics. Daniel did his graduate research at UCLA’s Protein Expression Technology Center where he studied neurometabolic disorders. 





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Robert Lufkin  0:00  
Welcome back to the health longevity secrets show and I’m your host, Dr. Robert Lufkin. rapamycin, Metformin, and ffice Sutton are all associated with improvements in markers associated with aging. We are now beginning to see the news by healthy individuals interested in promoting longevity. Daniel Tawfik is the founder, developer and CEO of health span. health span optimizes human performance through interventions that target cellular senescence. healthspan was created to empower patients to regain control over the levers of aging that are at the foundation of most age related diseases. Daniel holds a BS degree. from UCLA in Molecular Cellular and Developmental Biology and Physics. Daniel did his graduate research at UCLA protein expense expression Technology Center, where he studied neuro metabolic disorders. Before we start the episode, if you like 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 Daniel topic. Hey, Daniel, welcome to the show.

Daniel Tawfik  1:47  
Hi, Rob. Are you doing?

Robert Lufkin  1:49  
I’m so excited to have you on the program today and hear about the fascinating things you’re doing with healthspan. And these these interesting longevity drugs. But maybe before we before we dive into that, could you take a moment and just share with us how you came to be interested in in this area?

Daniel Tawfik  2:13  
Yeah, you know, there’s so there’s multiple dimensions of, of curiosity, frankly, that brought me to wanting to understand the underlying mechanisms of aging. When I was an undergrad at UCLA, I took a biology of aging course. And we learned from it like evolutionary biology perspective, or looking at salmon. And after they reproduce, they just rapidly degrade, they die. And I was curious, I was like, well, that’s just not wear and tear, right? We’re kind of taught that we have wear and tear, we have DNA damage that ultimately, tissue become dysfunctional. It’s this is this is what he has been, it seems like, based off of this example, it seems like there’s some cell programming here. And I was curious to see what what are the underlying mechanisms of this? When I was in college, I worked in a lab where we’re looking kind of at metabolic pathways that progress, chronic age related chronic diseases we’re looking at neuro degeneration specifically. And what I learned from that experience, or looking at kind of mitochondrial dysfunction in that context is that human beings have much more power over health outcomes. Then the luck of the draw kind of paradigm, we we think about this, of course, there’s genetic factors that play into health outcomes. But ultimately, it’s very empowering to know that there are interventions or lifestyle changes we can make, that can bend the curve in our favor. And so I love to geek out on the interventions that that do that right. So ultimately, the thing that made me want to make this kind of a career thing is my wife’s health. complications. So my wife, you know, this is someone who was the captain of the water polo team, she’s a super high achiever type are highly active. She had lymphoma and And she, she went through one bout of it and three years of treatment, getting chemotherapy for for lymphoma, she’s out of she, it’s, she’s in McClair for about five years, then it relapses. And then she has to do a stem cell transplant. And ultimately, you know, I had taking kind of a break from the life sciences pros been software development kind of entrepreneurial activities. I thought, well, I know all this stuff now about metabolic pathways, and in this specific case, cancer, how kind of there’s, there’s a component of metabolic ecology that can, we can kind of use to bend the curve in our favor against having getting cancer, it’s important to realize, I think this is a good way to kind of sublimate the, if I can bring something to market that allows patients to optimize healthspan through these lifecycle lifestyle interventions, and pharmaceuticals, pharmaceutical interventions, and help someone avoid the health outcome that my wife had, it would be a worthwhile pursuit. And ultimately, that was kind of the inspiration to kind of get off the sidelines, be kind of like a hobbyist, if you will, to, to make this kind of like the cause of my life. So I it’s, you know, started with curiosity, kind of wanting to geek out on underlying mechanisms of aging. And then there’s a very practical reason why we, you know, put our time and attention to building a telemedicine practice around cellular senescence. So hopefully, that gives you some idea of all the the decision making process on my end.

Robert Lufkin  7:05  
Yeah, I totally get the motivation there. And it’s very, it’s very admirable what you’re doing in it, and it’s a great area, the progress that’s being made, the discoveries in this area, is is changing so fast. So So you’re back to your concept of aging, I guess it’s, I get from it. It, in your opinion, it’s not really an accumulation of errors, but it’s a program process. So what maybe you could just share with us a little bit, what are some of the mechanisms then of these programs? How, what can we do and what’s happening that, that controls this programming?

Daniel Tawfik  7:50  
So the there’s multiple, you know, with current diseases, there’s, there’s just multiple, it’s very complex, right? So you got to have you have to pick and choose what what’s your area of focus, right. And what I’m acutely focused on is cellular senescence. And to give the listeners some background on what cellular senescence is, I cell undergoes damage, UV radiation, some kind of DNA damage that that makes it such that the body needs a way to the organism as a whole needs a way to make it such that this cell doesn’t proliferate, right? So we have cell programming to deal with damage cells. So a cell can either go through apoptosis, which is like cell suicide. It has a cell has built in program and say, Hey, there’s damage here, let’s you Radek ate this cell before it encourage more damage. There’s a second kind of evolutionary response to to cell damage, which is senescence, and that’s the arrest of proliferation of a cell. The cell still exists, but it can’t replicate. It can say in kind of like a zombie state right where it it can grow, it can exist, but it can proliferate into what would be the third outcome and the worst outcome of cell damage, which is tumorigenesis. If the cell damage cells actually replicate. So cellular senescence, the second outcome that I talked about, is a way as a protective mechanism to guard against kind of the growth of bad tissue if you will, but so you understand that senescence cells have a they have Some dividing kind of factors about them, that make them something that as we, as we age, when we accumulate more and more of them, they can cause a lot of tissue dysfunction. And that is they can’t proliferate. They can’t, they can’t replicate at all, but they can grow. They can to there’s three kinds of traits of us. And that’s itself. They exhibit Hyper Growth hypertrophy, so they can, when they’re exposed to growth factor, unlike regular cells that can’t replicate, they just enlarge, they exhibit hyperplasia, meaning they release, they can release mitogenic factors that cause adjacent cells to grow disproportionately in a way that’s not healthy for the tissue as a whole. And then lastly, they exhibit hyper functionality, B over express certain molecules. In this case, senescent cells have this, this dividing characteristic of something called the SAS. And that’s the senescence associated secretory phenotype, which is kind of a witch’s brew of kind of, very harmful molecule. So this is these are things like inflammatory molecules that cause damage to adjacent cells, mitogenic molecules that cause proliferation of adjacent cells. And so these cells, they’re, they’re growing, they’re excessively active in in producing molecules that are causing damage to the tissue as a whole, and they don’t carry out their original function, right. So you get this tissue degradation over time. And if you look at across the board, age related chronic diseases, you see senescence as a foundation, kind of theoretically as a foundation for everything. So if you look at osteoporosis, you see hyperactivity of osteo classrooms over being born.

If you look at Corrado and cites the overexpression of parents and leading to wrinkles, and we had a someone come to healthspan, the other day, interested in taking these a class of drugs called mTOR inhibitors for male pattern baldness, the the, the, the reason why is the overexpression of like androgens leading to hair loss, the and then neuro degeneration is probably the easiest to explain to the overexpression of these immune molecules that cause a autoimmune issue in neuronal cells. So the overexpression of tau proteins linked Alzheimer’s, it’s like a very glaring example of this. So senescence, as we’re young or young, we’re able to get rid of senescence cells or dispose of senescence cells at a rate that matches the rate of accumulation. But as we get older, there’s a Critical Mass Effect of where senescent cells accumulate, accumulate, accumulate at a rate that outpaces our ability to, to dispose of. And so as we get older, you see tissue degradation and dysfunction across, you know, the entire organ organism. And that, to me, is kind of a universal theory that we could I could kind of dig into and look into the interventions that kind of specifically target that. That says, Hey, let’s put some more time into kind of thinking about how do we targets in essence and kind of this kind of umbrella. deleterious dysfunctional state?

Robert Lufkin  14:29  
Yeah, before we dive too much into senescence, i i backing up just a little bit I often hear Leonard Hayflick his work in the 60s I think it was about a famously the generational limit for cell division, you know, the Hayflick limit at all, as a as a trigger for us in essence and and these things, but what you’re seeing it Is it also accumulated damage? In a sense also?

Daniel Tawfik  15:05  
It’s, it’s, it’s a so yeah, there’s there’s a kind of a normal course that leads to a senescence it. But in the exposure to damage the cell can go in these three routes, right? But we’re from evolutionary perspective, we’re really hyper protective against that third tumorigenesis state. So there’s either we apoptosis to, to like self detonate the cell, this kind of suicides date, or there’s let’s just arresting the cell cells capacity to replicate entirely. And that’s in essence as a protective mechanism against tumorigenesis. So no more proliferation. It can. The problem with a senescence cell is it still exposed to growth factor. So we see when it’s exposed to growth factor, when Tor, which we’ll talk about, it’s switched on, to kind of get in these anabolic states that grow or grow, it just gets, it has the defining characteristics of hyper growth, hyper overexpression of molecules, and then causing adjacent cells to just overly proliferative, you get kind of a tumor genesis state as well. So it’s a protective mechanism in one set when we have the cell damage, but as with many things in excess, it becomes the driver of cellular cellular dysfunction and tissue dysfunction which we which we can see as we get older right. So our tissue not being able to do its original function.

Robert Lufkin  17:05  
Now, you mentioned these the effects from the senescence the SASP. And and this other hyper functionality, hyperplasia, etc. are there are there ways we can follow that in a patient? Are there are there easy markers we can use, like CRP for C reactive protein or anything? Or what are the best senescence markers? If we had to pick something to follow senescent activity in a patient? I think this is

Daniel Tawfik  17:37  
it, these are kind of inflammatory, you would see the difference if you took it, if you took a biopsy of a young person and an elderly person, it’d be fairly easy to detect, which is which because the biopsy the older person, which is have more signs of inflammation, right? So this the SAS, we can kind of measure through proxies of inflammatory markers, right. So, you know, we have a solution where we with healthspan, what we produce is you’ll speak to one of our doctors is focused entirely on cellular senescence, and they’ll send a panel based off of their discussion with you and kind of measuring these markers of inflammation. So, tells me something you’ll talk through with your physician.

Robert Lufkin  18:41  
So, for senescence, now, there what are the what are the main drugs and Will Will, Will Will I want to get into healthspan? In a little bit, but just generally, what are the main drugs that that you look for, for for combating senescence and what are their mechanisms of how they work?

Daniel Tawfik  19:04  
Sure. So from a mechanistic perspective, it’s helpful to understand Tor. So its target of rapamycin to Tor is the switch within the cell that directs the cell to either kind of go, you know, the best way to describe it would be the easiest way to describe it would be an anabolic state, a growth state versus a catabolic state, which is a word we need to stop growing, we need to conserve energy. Oftentimes, in this catabolic state, we go through a process called autophagy, which we use cellular debris to utilize for energy. So if you have this accumulation of these this Sass, or these toxic proteins, let’s use that as an energy source. All right, so Tor is this switch within the cell, that is really its stimuli or lack of stimuli, it’s look, it’s detecting state of nutrients within the cell. So it’s primarily looking at the amount of amino acids available to sell and then through the rate through kind of mediated mitochondrial ATP to MP levels. So in a state where you’re low on nutrients, uh, you are fasting all day tours going to, you know, the simplest term sourcing to get a signal saying, Hey, we’re low on energy right now, let’s not proliferate, let’s not grow, right? Conversely, if we’re getting a lot of stimuli that says, hey, there’s a lot of amino acids, there’s a lot of ATP right? Now it’s a good time to grow, right? Like, it’s like let’s both be bullish on growing right now, then it tore will signal to the cell effect, let’s let’s it might be a good time to replicate, it might be a good time to grow, it might be a good time to over to express kind of these aggregate proteins that we talked about. So what with that being said, there’s, there’s a lot of implications to that. So one thing, before we go into the medication itself, the implications for metabolic pathways are significant, right? So on the standard American diet, if we’re constantly over feeding ourselves, we’re constantly exposing yourself to carbohydrates, you know, very calorie rich diet all the time. You’re in an anabolic state all the time. And you’re, you’re overexpressing tore continually and that has a lot of negative effects. Right? So that’s a lifestyle intervention needed think about it. What ways can we turn Tor on in certain seasons of life? And what what ways can we can we inhibit Tor to get into a catabolic state to do some kind of spring cleaning. So in terms of lifestyle, lifestyle, interventions, fasting is a way to, to signal to kind of play the the nutrient deprivation state as a lever to stop the the Tor anabolic state from from being flipped on, right. And so fasting is a great way to understand how how Tor inhibition works.

When you’re in a fasted state, you there’s the cell is basically producing less ATP. And ATP is kind of the currency of the cell to do work, essentially. And when we’re low nutrients, we produce more of this form of energy. It’s not a triphosphates of three phosphate groups, but a single phosphate or which has each phosphate group is kind of the energy source that allows the cell to do work. So when you’re in a fasted state, you’re producing more aamp kinase producing more the ratio and P the lower energy version of of this energy currency to ATP. There’s more MP, the tore through a signaling pathway says oh, there’s a lot of Andy kinase here today. Let’s turn off this proliferative hypergrowth state, right. So fasting exercise is another example of that straight these are lifestyle interventions. So that leads us into the prescription molecules that should take so Metformin is a fasting mimetic, right. I’m going to say this just to illustrate a concept. It’s it doesn’t really do the I’m going to use the word clamp. I think of it as like Metformin is a clamp on the mitochondria. It’s not a clamp on but by 100, but it reduces the output of ATP. And it signals to the to increases the output of a MP, which then mediates this inhibition of Tor and Tor It doesn’t for very practical purposes, when a MP levels are, are low, it, you know, there’s a cascade of effects here. But one of the things it’s going to do from kind of a very practical perspective, it’s going to trans look translocate blue transport channels to get more glucose into the cell, hey, we’re deprived on energy, let’s get some more glucose into the cell, right? So Metformin is a way that we can induce this, this catabolic state is a top energy state, that kind of a spring cleaning state. So but for me, it’s a cascade of effects from a metabolic. It’s going to a metabolic perspective, it’s going to lower the overall release of IGF one, which is a growth factor that causes cell growth and cellular proliferation. And it’s gonna do this cellular deep cleaning through instigating autophagy. So Metformin would be top of the list as a, an incredible safety profile. The reason why we know mechanistically, anything about Metformin is we’ve there’s tons of observational research on Metformin, with people with us an assortment of comorbidities, whether it’s diabetes or cancer, their health outcomes turn out to be better than in some cases that kind of healthy populations be looking at is observational data, folks like NIR Barzilai ly folks who really put a lot of time studying Metformin, wanting to look at the mechanistic mode of action for Metformin. Everything I just spoke about is kind of like speaks to how the form of it is first seeing that the health outcomes of metformin patients were surprisingly good even in an unhealthy patient. So Metformin is kind of the, the medication that targets senescence through kind of triggering this fasting mimetic state.

The second medication that also kind of mitigates the deleterious effects against senescence cells is rapamycin, they both fall into this category of kind of a Senate morphic they they kind of tamper they mitigate against those hyper functional kind of states that I was talking about. Metformin does this through nutrient sensing, kind of mimicking the nutrients, it’s a pathway to the mitochondria, rapamycin directly inhibits portion of the tour that controls this proliferative growth state as well. And that’s the medication that in the longevity space has the most interest because of its direct binding. So towards the target of rapamycin, and the R is, of course, the rapamycin part. So So rapamycin seems to kind of be the the rapamycin and it’s analogues that the new versions that that pharmaceutical companies are working on, seem to be having the most interest there. It’s a kind of a novel approach to targeting the mitigating the deleterious effects of senescence cells. So there’s those those two drugs which are kind of of most interest. And they really, they’re really trying to mitigate the the kind of proliferation of senescence cells and the deleterious effects of senescence cells. There’s another group of medications that the little kind of it’s it’s kind of brave new world a little bit. It’s a senolytics, which is compounds that kind of push push the senescence cells into apoptosis stay right so it’s basically trek triggering us in essence, self self detonation kind of programming. And so like the SAT nib, which is actually a chemo medication, I I’ve never taken sysadmin Dr. Greene prescribes it. Five to 10 courses, it is a combination of our interest and kind of miss analytic space to basically lead to the eradication of senescence cells, rapamycin, Metformin are kind of limiting the harmful effects of them and in and stopping the proliferation of senescence cells in literature, our folks fo are targeted towards the eradication of senescence cells.

Robert Lufkin  30:25  
I see. So yeah, a combination of both the rapamycin, the Metformin to decrease, in essence, and then the Pfizer tend to be actually analytic to, to destroy the cells that already are senescent, in a sense there. So maybe so we have these strikes. Now, I want to hear about about healthspan, about your company that makes these makes these medications available in a supervised medical setting for for patients that are curious about that. Yeah. How did that get started? And tell me more about that?

Daniel Tawfik  31:01  
Yeah. So it goes back to this experience I had with my wife and kind of trying to figure out what to do with that kind of energy and frustration. And also the curiosity component. So prior to my wife’s relapse, I was I was like, fully, but I was a geek on on these these different compounds. And these lifestyle intervention, so I would, you know, fast. over the weekends, I would do a 24 hour fast every Saturday. And sometimes I would do a three day fat once a month. But I ultimately was very curious about taking Metformin from myself, and I want to go talk to my primary care physician about taking Metformin. And so we know that Metformin is a drug that patients with diabetes take right in so I’m healthy 35 year old, and my PCP looks at me, and says, like, why would you take that forward? You’re, you have no, there’s no indication that you need to take Metformin at all. And I know I said, Well, you others these studies, and it was clear to me that one of the one of the features of our medical system is that, you know, physicians are bogged down with the day to day dealing with putting out fires, my brother’s a physician in my wife’s position. I’m surrounded by finishing my life, all my friends from molecular biology days or physicians, right. And when I would talk to them about Tor and you know, Metformin, the eyes glaze over, like, you’re talking about this stuff, again, it was clear the pipeline from the research community to the clinical community, just there’s, there’s a huge chasm because of kind of everything we talked about, about the the constraints on doctors are all that they’re responsible for, in their practices. And so, I thought to myself, Okay, this is gonna be interesting idea, there’s really not a clinical home. For these folks like myself who are interested in cellular senescence, some I call it kind of like bio hacker types, there’s, there’s not a place you can go to, or it’s very hard, at least to find a physician that’s super knowledgeable about these things. And then there’s this kind of like, overlap with the wellness community too. So you might be like a functional medicine doctor, which, which is awesome. But there’s also a kind of like, overlap with kind of holistic medicine, that is less data kind of driven. And so you might, if you’re kind of a biohacker type, you might see kind of a wellness person. So our thought my thought at the time was like, it’d be interesting to see if we can create a medical clinic that is done meta analysis of kind of what’s happening in my research community, but make it a specific focus because I truly believe in this theory, this hyper functionality, theory of aging, just targeting one thing, cellular senescence, and so I sat on the idea for quite a bit of time. I because these are, you know, starting a company, it’s you know, it’s like it’s it’s a A lot of work and it’s a it can be, you know, it can be quite challenging, you’re really kind of going to, you’re going to be dedicating a lot of time and energy into something. I said when I was like, I’m not sure how many people there are in the world, like, we then want this thing. Ultimately, my wife’s cancer relapse. And we were at City of hospital. And I had been reading Peter T. ‘s article on Metformin as kind of

manipulating the quirkiness of cancer cells, and they’re kind of robbing us consumption of glucose. And this is stuff that I knew back from my college days, but I was like, you know, if this could help one person, if we loved this clinic, it could help one person it would be worthwhile endeavor. And so I said, okay, like, it was at her city of hope. hospital room, I was like, Okay, let’s do this. And I, that’s when we put into play kind of developing the software and kind of mix and matching the vendors and all this stuff and recruiting doctors who are interested in in cellular senescence as a driver of aging. That said, Hey, let’s release healthspan.

Robert Lufkin  36:24  
And, just to be clear, this, this service is for it’s for normal, healthy people. It’s for people who want to look at longevity and anti aging. And also, you mentioned before the lifestyle things like say, I’m a patient, I’m already I’m already low carb, I’m in ketosis all the time. And I’m fast and one meal a day. So I’m, you know, I’m intermittent feeding, it can still benefit me above and beyond even when I maximize my lifestyle things potentially. Is that not correct?

Daniel Tawfik  37:00  
Yeah. And so we’re this type of patient, right? Like, we’re doing all the lifestyle intervention says, but we’re intrigued by the benefit of some of these set amorphic drugs. And so we’re providing a home for folks like us who are kind of willing to kind of expect we’re in a healthy state, we want to talk to a doctor. We want to take these medications under a doctor’s supervision and kind of put, adhere to a protocol that we had talked about this prior to the to be podcast of, you know, putting together a protocol that’s least somewhat data driven. And we can talk into the challenges around some of these off label repurposed drugs for putting protocols together, but it is a doctor supervise clinic where you know, patients from all over the country can have a telemedicine consults with a physician in their state that can ultimately discuss lifestyle interventions and if it’s appropriate, prescribe some of these mTOR inhibitors to target the deleterious effects of senescence cells.

Robert Lufkin  38:20  
Okay, so for patients who want to come to healthspan, just to be clear, they can come they don’t have to physically come to Santa Monica, California, they can it can be done remotely through telemedicine, is that correct?

Daniel Tawfik  38:33  
Yeah, it species across the country. Right now we’re just in the United States. And with the exclusion of Alaska, which has its own kind of telemedicine rules. So if you’re a patient that is intrigued by some of these, these interventions, you can talk to a doctor no matter from your own home, from your computer or your your iPhone or your mobile device, and start kind of pursuing some of these these senescent targeting protocols.

Robert Lufkin  39:13  
And the service for the patients is this. In addition is this. They these your your service specifically manages the application of these drugs for longevity, it’s not like they would still go to their primary care doctor. So this would be in addition to that, right. So it’s not a full primary care services specifically for these drugs, correct?

Daniel Tawfik  39:41  
That’s exactly right. That’s that. Thank you for clarifying that. Yeah, this is not your sort of, you’re gonna see your PCP. When you have your strep throat. This is for kind of the health band promoting kind of interventions. When you have an acute problem you’re going to go to to your local doctor, who, who will help you kind of put out that fire. This is this is for people that are specifically looking for healthspan promoting interventions.

Robert Lufkin  40:15  
And with that, I assume it’s not covered by insurance because aging is not a disease according to yet. Yeah. You know, is a

Daniel Tawfik  40:27  
problem in our in our field. It’s, I mean, so it’s all cash pay. But this is kind of opened up a conversation about, I talked about rap logs, these new, these new medications that are being produced by pharmaceutical companies. They essentially kind of mimic what rapamycin is doing. And it’s, if you look at kind of the incentive structure of so we’ve met for tickets about metformin and rapamycin have existed for decades, right? And when we look at rapamycin and metformin, conferring kind of a prophylactic benefit against these senescence driven age related chronic diseases, that’s not a that’s not there’s no clinical trial that can be done against aging there SBS specific modality that the clinical trial is kind of targeting. So it becomes very challenging to kind of make the claim that Metformin has these healthspan promoting benefits. And when I say healthspan, I’m not talking about the name of our company, we’re talking about the the amount of time in your life that you’re in a kind of a good health state or you’re not dealing with chronic chronic disease, age related chronic disease. It’s just very hard to bill insurance to for taking metformin and rapamycin. And instead, this is kind of it’s a cash pay service where Yeah, it’s kind of an elective thing for the folks who are who are coming to our clinic, I should say, our patient base are super knowledgeable about these medications. They’re probably more knowledgeable than any of us. They they face. They send us the papers on all the applications of it. They’re very interesting people. But yeah, it’s kind of like we have our tribe of folks that are very interested in senescence as a target as a as a pathway of aging. And it’s those folks that we’re seeing in our in our practice.

Robert Lufkin  42:58  
Yeah, just just one mentioned to you mentioned nearby Iris ally, who’s his one trial, I guess he’s doing the team trial with metformin. It’s, he’s trying to get trying to advance it as a disease and get the FDA recognizing it and all but it’s, it’s a long process is very, very expensive. And like you say, there’s very little incentive for drug companies to work with at least the primary rapamycin or Metformin, which are which essentially are off patent now. And and it’s, it’s both good and bad, but it’s a disincentive for them to move things forward.

Daniel Tawfik  43:37  
They’re absolutely I think there’s a lot of challenges we face as a community. And it’s one of them, it’s kind of an off label repurposing of these medications that we have to figure out. Well, then if, if there’s not an incentive to do real testing, how do we collectively test this stuff out? And maybe it is incentivizing it through the creation of these rap elog companies, rapamycin kind of analogs. But I think collectively, there’s the onus is on us to figure out how to prove safety profile and efficacy. And I think your work in the myosin registry does a lot to promote that. But yeah, it’s this is kind of what we’re the pressures that work based with.

Robert Lufkin  44:28  
Yeah, tremendous challenges but but a lot of a lot of opportunities. Well, as an expert in this space, we always like to ask, what what personal choices if you made in your your lifestyle and the drugs or supplements you take to knowing what you know about longevity?

Daniel Tawfik  44:54  
Yeah, so yeah, I would say for everyone start off with lifestyle and Pension. So like the easy do the basics first, right. And so that is for me, I like one of the the important pieces here is to understand the levers of aging of these companies the tools at your disposal to, to, you can manipulate it different seasons of life, if you will. So what I will do is, I know that I can kind of inhibit, tore through fasting, I know that if I can restrict carbohydrates, and in some cases, amino acids like leucine for periods of time, I can get into that topic each day more regularly. Now, there’s a certain point in life where I want to be more anabolic, like I’m from weightlifting, or, like I do CrossFit regularly. And sometimes I don’t want to be a more anabolic state, I want to be in a pro growth state. So I will stop taking Metformin or fast or I will, you know, sufficiently provide nutrients, right. So then kind of leaving in I will take Metformin on days that I don’t work out. And then lastly, I take rapamycin once a week, at three milligrams a week, so it’s very conservative dosage. But those are the four primary things that I do my life

Robert Lufkin  46:31  
and face it in also, do you take that? I have

Daniel Tawfik  46:35  
I am not currently taking it. I have seen Pfizer 10 And once a month at a heavy dose for like three three days, I’ll ingredients protocol for doing it, but I haven’t taken it in a while. And for no good reason. It just kind of fell off my, my habit kind of like routine.

Robert Lufkin  47:02  
Yeah, I think the challenge is that all of this space in the longevity space and and for all the drugs you’ve mentioned, are biomarkers for for successful positive outcomes we can we can always look for side effects. And you know, certainly there there’s side effects with these strokes, but would it what is your approach? Or with healthspan? In other words, what do you monitor on the positive side? Or is it? Or is it just increasing the dose to get side effects and then then pull back or is

Daniel Tawfik  47:37  
this to be completely honest, it’s something we’re still putting together kind of the laboratory kind of protocol that we have. So we will send a phlebotomist to, to your home. This is part of the service but we’re putting together a panel right now. But we also kind of less than a 10th of the problem that we have in this community is that we don’t have a real good panel for to measure autophagy and so if there’s any kind of researcher you know, we’re working on at once a wants to work on this project of like, measuring audit phagosomes like that would be really interesting everything else we just have proxies for. And then we’re also managing that we’re monitoring for side effects and hormone levels, etc. But we also more on the metabolic side who will send you a continuous glucose monitor to if that’s something that she missed you want

Robert Lufkin  48:47  
yeah, oh, this is great. Well, how can people follow you on social media Daniel will have will have links down below in the show notes. But for people who are listening to this as an audio version, maybe you could just tell us tell them the links that they can find you.

Daniel Tawfik  49:05  
Okay, cool. So I’m, I’m active on Twitter. I think that’s how we met at Dan Tawfik. That’s ta W F ik that’s primarily my social. Most of my social activities there, but you can go to my website, it’s Dan Tawfik. Calm and if you’re interested in kind of our clinical telemedicine practice, it’s get healthspan calm.

Robert Lufkin  49:35  
Great. Well, thanks so much for spending an hour with us today. It was it was it was wonderful getting to know you and also hearing about the exciting work you’re doing it health span and the possibilities for for dealing with senescence for with all these these new, amazing drugs are using.

Daniel Tawfik  49:55  
This has been a lot of fun Dr. Lofton I really appreciate it.

Unknown Speaker  50:00  
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