Pharmacological approaches to longevity using drugs like rapamycin and Acarbose via targeting signaling molecules like mTOR and insulin continue to see growing support. Today we speak with Bradley S Rosen MD whose practice focuses on Living Healthier and Longer through Biogerontology.
Dr Rosen graduated with a degree in Mathematics and Statistics and an MD from the University of Florida. His residency was at Jules Stein Eye Institute at UCLA, followed by 2 Retina Fellowships at the Lions Eye Institute and the Royal Victorian Eye and Ear Hospital in Melbourne, Australia. In 2013 Dr. Rosen, M.D. joined a growing number of scientists and clinicians who are becoming increasingly interested in the fact that the hallmarks of aging themselves can and should be targeted for therapy.
@DrBradleyRosen1
Lu, Yuancheng, Benedikt Brommer, Xiao Tian, Anitha Krishnan, Margarita Meer, Chen Wang, Daniel L. Vera, et al. “Reprogramming to Recover Youthful Epigenetic Information and Restore Vision.” Nature 588, no. 7836 (December 3, 2020): 124–29. https://doi.org/10.1038/s41586-020-2975-4.
Jiang, Zhou, Juan Wang, Denise Imai, Tim Snider, Jenna Klug, Ruby Mangalindan, John Morton, et al. “Short Term Treatment with a Cocktail of Rapamycin, Acarbose and Phenylbutyrate Delays Aging Phenotypes in Mice.” Scientific Reports 12, no. 1 (December 2022): 7300. https://doi.org/10.1038/s41598-022-11229-1.
https://www.nature.com/articles/s41598-022-11229-1
Robert Lufkin 0:01
Welcome back to the health longevity Secret show and I’m your host, Dr. Robert Lufkin. Pharmacological approaches to longevity using drugs like rapamycin and a carbost via targeting signaling molecules like mTOR and insulin, continue to see growing support. Today we speak with Bradley s Rosen MD, whose practice focuses on living healthier and longer through bio gerontology. Dr. Rosen graduated with a degree in mathematics and statistics, and an MD from the University of Florida. His residency was Jules Stein Eye Institute at UCLA, followed by two retina fellowships at the Lions Eye Institute, and the Royal Victorian is near Hospital in Melbourne, Australia. In 2013, Dr. Rosen joined a growing number of scientists and clinicians who are becoming increasingly interested in the fact that the hallmarks of aging themselves can and should be targeted for therapy. And now please enjoy this conversation with Bradley s. Rosen, MD. Hi, Brad, welcome to the show.
Brad Rosen 1:18
Thank you, Rob, I’m very happy to be here. And I really appreciate the opportunity. I’ve listened to a number of your guests and your shows. And I’ve learned a lot and it’s a privilege and I’m thankful to be here. Well, I’m,
Robert Lufkin 1:34
it’s so great to have you on the on the program. And I’m so excited, I can’t wait to dive into some things with longevity and the amazing work you’re doing in that area. But before we do that, maybe we could take a moment. And just tell us a little bit about how you came to be so interested in this fascinating area.
Brad Rosen 1:59
Sure. So my background is essentially a little bit different. I think that one of the great things about this longevity, as an as an area of interest is the wide range of people that are involved. And my background is as a physician, I trained as a surgeon, I worked as a spec, essentially a retinal specialist, which made me a essentially a vascular surgeon of the eye. And I dealt with managing patients who had complications of diabetes complications of high blood pressure. Essentially, vasculopathy is of all sorts, including inflammatory disorders, lipid disorders. And over the years, I got to see with my own eyes, how these things looked inside the retina, how the blood vessels changed how the tissue surrounding the blood vessels in the retina, and the sub retinal areas changed, and also how the patient’s themselves did. Many times these were people who looked perfectly healthy on the outside and looking inside the eyes, kind of gave an insight that maybe things weren’t as healthy inside as they were outside. And looking at the various metrics, and predicting outcomes just became something that I had a strong affinity to. And I left retinal surgery in 2015. And through a combination of personal interest and interest that certain of my friends had slowly became interested in this space. It probably started when a very intelligent friend of mine, who I respect, asked me if I could prescribe him rapamycin. And I had no idea what this was, I thought that he may have lost his mind. And I started to, you know, look into the spectrum there. And I slowly realized that there’s a body of very serious scientific work looking at this problem, and I realized that once a person whose thinking allows this idea that your healthy lifespan or your health span, or the amount of years that you have your robust and healthy can be extended. It’s a very hard idea to let go of it’s it’s a compelling idea. It’s like what could I possibly do with my time with My resources, that would be a better way to spend that then to give me more time, and my friends more time and my family more time to be healthy and able to enjoy life. And I think some of the research is compelling that ageism, aging is a malleable process. We don’t have the answers yet. But I think that to view it as an unsolvable problem, is not rational at this point.
Robert Lufkin 5:38
Yeah, and as a retinal surgeon, I like as you say, I can see how you were facing daily, some of the chronic diseases that are most strongly associated with aging, things like diabetes, and vascular disease and hypertension. And all right there, right there in your space. So what what is your overall philosophy about longevity? Or aging? How does that how does that work? In your mind?
Brad Rosen 6:08
Yeah, so I think that’s a great question. I think that the answer, it’s probably a little bit dependent on which hat I’m wearing, as a as an individual. You know, I think conceptualizing and theorizing and reading this, all the studies that are out there, and all the lines of thought that are out there is, you know, it’s a pastime, it’s enjoyable. It’s fascinating, it’s inspiring, it leads you to be in touch with, you know, very impressive thinkers, some of whom you’ve interviewed, many of whom are most of whom, you know, but as a professional, as a, as a physician who’s taking care of patients. Really, I think the framework that I’m relying on is this time dependent. Increase in probability of suffering, some disabling condition, or some fatal event. And as you age, the likelihood of that, you know, rises. Unfortunately, as we get a little bit further down the path at the rate that that probability of, of, you know, failure to be resilience becomes exponential. And so I feel like the medical approach I’m trying to stay as close as I can to is men minimizing the risk of experiencing one of those age related events, and exploring some of the therapeutic agents that can help delay the rate at which, you know, one is susceptible, one loses their resilience. And so I try to combine, you know, a somewhat precautionary approach, like I’m trying to not expose people to any additional risk, what are while also trying to make available some of these newer therapies that seems to target aging, which generally have a long track record of use in health care, which regulatory agencies have looked at and have given us a fairly good handle on risk for and which, you know, as we know, we all these diseases that are age dependent, are wonderful to try and stop. But addressing the root, the root drive in the process, where you become more likely to have all these problems is going to have way bigger dividends than addressing any of the individual diseases. So to the extent that that’s true, I think I am very willing to look at a select number of agents that, you know, the preponderance of evidence supports no proof. We’re never going to get it in the space. But at the same time, there we have enough game film historically, that we’re not you know, putting people at risk that we can’t quantify in terms of long tail like you take something that’s brand new for 10 years. That’s a different story than Taking something that has a 20 year clinical history. So that’s my approach. And you know, obviously, I’m fascinated with the mTOR system and the idea of programmatic aging. I am fascinated by all the newer metabolic studies, looking at the glucose pathways, and how they impact the rate at which we age, the rate at which we experience events. And, of course, the newer modalities are what my friends and a lot of patients will ask about, I know recently, you had a very impressive guest on talking about Barrick oxygen and its role in aging. And these are fascinating topics that I’m, I’m very curious about but have yet to incorporate.
Robert Lufkin 10:56
And so just backing up a little bit, yeah, as you say, aging in itself is the is a primary risk factor for essentially all of the all of the chronic or the majority of the chronic diseases that we face. So by being able to attack aging at a basic level, then we can theoretically improve our our chances of not getting these diseases or pushing it back later. As well for those. One question you just touched on is this something that frequently comes up on a very basic level and longevity. I know back when I went to medical school, we were taught that, that aging is just the accumulation of wear and tear on our bodies kind of like, hey, my car wears out, my, my house wears out, everything wears out? Why shouldn’t my body wear out? Is that your view of aging? Or you mentioned programming also?
Brad Rosen 11:59
Yeah. So I mean, that’s another great question. And I think that’s an example of a framework that’s compelling at first glance, but the reality is when we look around us, and we see that we’re not alone as a species on this planet, and we start to inventory, what goes on in some of the other life forms that share the world with us, the rate at which we age and the rate at which other organisms age, certainly very different. But the rate at which environmental factors accumulate, and each of these agents, at least the exposure should be comparable. So it’s hard for me to say that I’m taking fewer environmental insults on a day to day basis than, say, my dog is, I think that we’re being exposed to comparable amounts of radiation, comparable amounts of metal, you know, food intake and processing pathogens, wear and tear physically on our bodies. And, you know, maybe not precisely the same and the wear and tear physically between my dog and I, but, you know, they’re not so disparate that it would explain that my pop is going to be old at 13. And I was just hitting my prime then. So there’s certainly going to be more to the story, there has to be more to the story than wear and tear. And, you know, I think that is a great example of how it is that sometimes the common sense answers, especially when it’s around a topic like aging, which I feel psychologically most people have relegated to this place of, you know, this belongs in the category of things that’s inevitable that we can’t change, I’m willing to believe it. And that is a state of mind that limits curiosity. It allows for answers to come up that aren’t, you know, that we don’t want to necessarily or don’t tend to challenge. So. Do I think wear and tear is important? Yes. But I think that to answer the problem and help our selves and our patients definitely want to look beyond that.
Robert Lufkin 14:39
Yeah, before you mentioned, you just touched on mTOR as well as glucose signaling and glucose utilization pathways. How do those What’s your thinking on how those play a role in longevity
Brad Rosen 14:59
so Oh, if if it’s okay. Before I do that, I’d like to just step back and, and reframe the way that I conceive of the approach to patients. And then within that context, I’d love to talk about both mTOR inhibition and, you know, metabolism as it pertains to insulin sensitivity and, and the light, if that’s okay,
Unknown Speaker 15:25
great. I would love it. Yeah.
Brad Rosen 15:27
Perfect. So for most patients in 2022, based on what we have available to us as tools that are proven or highly likely to be beneficial to us, what I’m trying to do is to recognize that there’s a group of patients, probably their people a little bit like us, who have reached a point in their life where they recognize that biologically, there’s a downhill trajectory ahead of us. And the question we can ask is, can we impact that in some way that benefits us. And so I think you can almost look at it simply and say, like, a 50 year old person, or a 45 year old person wants to make it to 90, and they’d like to make it to 90 robust and able to enjoy life. So if that’s the problem you’re solving for, what are the ways that you can achieve that goal. And so now you’re in, you know, you’re in a situation where you have a problem, and you can optimize for it. So you have all these risks that are going to be in, in this field, say, from age 50, to 90 or 45 to 90, there’s going to be risks that are there, and they’re going to be popping up? It seems obvious that the more of those risks we can take off the table, the higher the likelihood that we’re going to be able to get to that other side of the field intact. So how can we do that? Looking at the data on diet, looking at the data on exercise, looking at the data on sleep, can help us optimize our behavior, so that we’re giving ourselves highest probability of success, looking at the medical diseases and conditions that are most likely to impact us in that time period. And we’re fortunate, because there’s data there that tells us cardiovascular disease, cancer, neurodegenerative disease, falls, are pretty much when you sum up the variations on those the most high likelihood, risk factors to mitigate. And fortunately, a lot of those have modifiable risk? And then the last is, do you take into account the possibility that some of these putative aging medications or anti aging medications have merit and can confer some of the same benefits they’re conferring on animal models on us? And how compelling is the data? What are the risks of each one of the one of these? And can I use my inference knowing that I have to basically shy away from having randomized controlled studies to rely on which in medicine, we love to be a little bit more forward looking and offer a patient who who truly looks at this question, how do I get to 90 intact without having taken too many extra major hits? Are there Can I adopt some of these other newer medicines? And I think that the strategy really would call for assuming that you’re dealing with the right patient? And the right patient, that patient’s risk tolerance. Yes, you know, that. It’s obvious that if a anti aging medication eventually works, it’s going to be available well before it’s validated, as for sure true. And so philosophically or strategically, if you’re a person who exists in a time where that medicine has not been validated, but you want to take advantage of it definitionally you have to be willing to take a calculated risk in that in that space. And so that is pretty much the, the A to Z of what I’m offering patients. I think the biggest benefits are really a balance of all three, I think if you’re not looking at how you eat and exercise, and your sleep is doing maths,
it’s, you’re not really going to get much further. And I think if you’re not mitigating your cardiovascular risk, or you are, you know, metabolically unhealthy, there’s evidence that you are, you know, more likely to be struck down early. And then these amazing anti aging drugs that are so, you know, sexy and appealing. I think that you can look at the data, and have an intelligent conversation with intelligent patients, and come to the conclusion that on balance, because of who I am, not me personally, but who any of the patients I’m seeing are, that’s the way I want to live is by, you know, following the strategy and being maybe a little bit out in front of my skis, to position myself to be able to take advantage of the these things when they when they when they work. So that’s that. Is that Yes.
Unknown Speaker 21:33
Go ahead. Sorry.
Brad Rosen 21:36
So yeah, I mean, I can answer any questions about that, or I can I can start going into the, the, the answers about the mTOR. And the glucose, if I do feel strongly about generally both, you know, approach to medicine in general, and patients in particular take about their cardiovascular risk, I look at that as, as just this extra risk that most people have floating around that they’re unaware of, fully, at least. And are, I think most patients are more, most people are more willing to look ahead at the anti aging, the patients had seen me. But I think most of them are very, also very comfortable and satisfied. You hearing and how data and dietary exercise and cardiovascular risk management and in particular mash, because it’s, it’s it’s the case, that there’s just so much disparate and disagreeing information available to most patients have to think about them as consumers when they go on the internet.
Robert Lufkin 22:54
Yeah, I mean, the point you’re making is excellent. No matter how good these longevity drugs are, it’s it’s not a free ticket to live any lifestyle you want get poor sleep, diet out of control, and and those those other screening for those diseases is really key and cardiovascular risk. So getting all those things are key in place. Just a quick side note on the cardiovascular risk, is CT calcium score your go to test? Or is it more labs for that, to assess the risk?
Brad Rosen 23:28
So I would say that the totality of the data is the best always and more information is more personalized, better stratification of risk is better. I think, though, that if I had a patient who’s lat who had a pretty profound dyslipidemia you know, who had, you know, I don’t know what was the preferred word, and people can use a Kobe, they can use non HDL, if they really want to get in trouble, they could use LDLC. But when these levels are high, risk is high. And I would say that, especially in a person who is coming to me and saying, you know, how can I mitigate my risk? I would say that if you’re running around within a Poby level, that is, you know, above the 25th percentile, and you’re living in a nation where anywhere from 25 to 33% of us are going to be essentially taken off the board due to cardiovascular events of some sort, then you’re running around with risks that you don’t need to and if you’re coming to somebody who’s offering you a longevity strategy, who’s not mentioning that to you, they’re not doing as much you’re not getting as much as you could from the visit. That’s just my take, and I know that you I might as well be making a political statement with a comment on cholesterol. But I feel I feel like the data is overwhelming. So that’s, that’s where I
Robert Lufkin 25:12
so yeah, so that’s point well taken on that, I think so let’s say assuming we have our diet under control our exercising control our sleep, we’ve done our risk factors. We’ve done our cardiovascular risk. Now, we want to optimize longevity, what what are the what are the go to drugs that you think are the most exciting or most promising that you’re using in your practice today?
Brad Rosen 25:38
Okay, so I think that, that I’m not alone. And recognizing that the data supporting rapamycin is the strongest data of all the agents that are commonly considered. You have first of all, a plethora of longevity related data in animals, you have lifespan, extension in rodents, yeast, worms, some higher, not higher mammals, but other mammals robust longevity, and healthspan, enhancements, multiple labs, multiple investigators, multiple doses. That’s exciting. Especially when you consider the aspect of rapamycin that I think gets a good amount of attention but you know, for us, I think is particularly exciting which is you can induce our introduce rapamycin later in life and get great benefit from that. So, you know, a strategy like lifetime caloric restriction, where some of the data says, Well, if you do it later in life, you’ve missed the boat on that isn’t as exciting as as rapamycin is in that regard. So, you have the longevity data, you have a ton of individual metrics, which you always need to interpret with caution. You know, if if, if X causes Y in the lab, then the idea that you could put it into an organism and assume that y will happen reliably and because y is related to Z, you can expect z as an outcome doesn’t fully take into account that we are complex systems and the definition of a complex system is that you put in an input and you get a nonlinear output. So that said, you still want to see favorable results you still want to see favorable results in many domains which with rapamycin you do you see vascular. You see improvements in in endothelial health and the responsiveness to nitrous oxide. You see immune improvements. You see memory improvements in older animals learning improvement in older animals, you see improvement in cognitive function and Alzheimer’s models with rapamycin dose dosing. You see greater density of capillary beds and neural tissue, all of these things, I think, if they were to be found in people, if you did these things, would not be sufficient to tell you that you’re gonna get a longevity benefit, but there are the kinds of things that you would like to see. And then the limited data that we have in people, you know, seems to show enhanced adaptive immune response, increased thickness in gum tissue, reduced tendency to sarcopenia improvement in osteoarthritic metrics. So these are somewhat these are not somewhat these are exciting findings. And you’re talking about a drug that certainly is not trivial. But there’s a good amount of data on rapamycin use and at low doses, it’s generally well tolerated people will get up to saucers, which they don’t find to be overly bothersome. A subset will have a drop in their neutrophil count, which sometimes can be concerning, especially if they already have a low blood count and you look at them after a few months. To rapamycin and now they’re technically, you know, have a little or a lot of pancytopenia that is something that makes me uneasy. But most patients don’t have pancytopenia. And most patients, if you put them on rapamycin, you’ll see a somewhat of a reduction in their white blood cell count. When you think about what rapamycin is used for and what it does, in the context of immunosuppression, or immunomodulation, that’s not a big surprise. And I found that most patients tolerate the rapamycin very well. Some, again, this is anecdotal. So you know, not putting a lot of credence in it, but a sense of wellbeing, a reduced sense that the aches and pains that are associated with getting older are as bothersome a little bit better, you know, exercise or activity tolerance as a result of this, you know, not being so sore. So I would say that rapamycin is the probably top choice that I would have for a person who’s looking for an agent in it, to complement their health in anti aging. And then there’s three others that I consider as well. A car bus is usually the first one I bring up with patients because it is generally safe. It’s also I, you know, the ITP, you’re very familiar with the ITP, I would presume the listeners are mostly familiar with the ITP. But let’s just call it the gold standard for animal models of longevity. And so a carbost had positive results in the ITP, which to me makes it a better candidate than a substance that doesn’t. And you can reduce postprandial glucose peaks, you tend to then prove he glycated hemoglobin or hemoglobin anyone see. And in patients do that have done documented impaired glucose tolerance or Frank diabetes. There’s really good outcome data that shows reduction in events. And so you cannot completely extrapolate. But one way to think about diabetics is that they have abnormal sugar metabolism, but another is to look at them as a group of patients that have high event rates. So if you’re looking for agents that reduce events, that patient population is a good group to see them because you’re going to, you’re going to need a lot fewer patients to power the study to see an effect because the event rate is so high compared to normals. And so yeah, the truth is that we don’t know if in people who have no insulin resistance at all, a harvest is going to help. But there’s a fair amount of circumstantial evidence that minimizing peak glucose levels and reducing the amount of glucose herbs, simple carbohydrates that you effectively consume is going to help. So that’s an agent that I I endorse
Robert Lufkin 33:41
just one point on a carbost Excuse me, it is FDA approved for for diabetes uses the indication and it blocks carbohydrate absorption from the gut and as you say it flattened so this glucose spikes Anyway, go ahead. Yeah, yes,
Brad Rosen 33:59
no, for sure. Thank you. Thank you. I sometimes I forget where I’m at. So I appreciate that clarification always. And then, you know, it’s another anti diabetic or medicine that’s used in diabetic patients is Metformin, which gets a lot of press. I will prescribe Metformin after having a careful conversation with patients so that they understand, you know, why they’re taking it, what the potential downsides are, what the potential promise is. I think that the observational data that drew interest or Metformin that basically if you listen to near bars, slide talk, you will have an abundance of enthusiasm and excitement and I think rightfully so based on the enormity of the number of patients that have been involved in the observation studies where you’re looking at preferential survival. You’re looking at lower cancer rates and a variety of cancer subtypes that are common. You’re looking at better COVID survival on patients that are taking Metformin compared to diabetic patients that aren’t taking Metformin. And then there’s also these various animal studies that seemed to confirm the pleiotropic benefits of metformin in areas that are not that uncommon and not that unrelated to rapamycin where you have, you know, markers for vascular health and improvement Mac markers for immune health and improvement. And you clearly reduce the risk and normal patients or patients with moderately impaired glucose tolerance of becoming frankly diabetic. And I think that is another benefit. Metformin did not have a good or did not show longevity benefits in the ITP. But rapamycin plus Metformin seems to be a better longevity combination than rapamycin alone. So there’s enough there to keep Metformin in the conversation. I’m very excited to see the results of the team study. Most of the patients that I see, I counsel that if we go on the Metformin route, or we go on the rapamycin route, or we go on the route of any of these anti aging medicines, if and when data becomes available, that puts the question mark over the utility, and, most importantly, makes one wonder like, are we harming ourselves by doing this, I’ll be very quick to pivot. Because going back to the strategy, making it to 90 unscathed involves taking medicines that will give you benefit and avoiding those that will give you potential problems. So you have to be alert to this possibility. But also, I think, willing to take a bit of a chance. So then, there’s two others. One is SGS stLt. Two inhibitors as a class.
So good ICP data on can add your flows in I think is the way it’s pronounced. Kana is the way I refer to it because it’s so much easier. And, you know, these drugs basically affect the sodium glucose transport, and you can kind of think of them as offloading excess glucose in the blood when those levels start to peak. And as well as in the intestine, kind of keeping more glucose in the intestine and then then then transporting into the body. The reason that I’m really enthusiastic about the SGL T two inhibitors is because the human outcome data is just so strong. The reductions in cardiovascular events, the improvements in blood pressure, the improvements in hemoglobin a one see the benefits with respect to weight. They all argue for a positive effect here. And I think, you know, it’s for state of the art care, it’s now mandatory to treat Type Two diabetics with stLt. Two inhibitors if you’re trying to give them best care, increasingly, forward thinking doctors who are looking at patients who are at risk for heart failure or kidney failure, are utilizing stLt two inhibitors and finding benefits independent of the patient’s ability to manage manage their glucose, metabolically, so non diabetics, non insulin resistant patients getting benefits there. And the ITP being positive. So the problem with the the class of drugs is it’s a relatively expensive medicine still. And you know, it’s not obvious that most patients will get their insurance to cover it. So it’s an expense question, but I think that it’s an exciting drug to follow. And the last, I think we talked about, excuse me in our earlier conversation, was this analytic approach, which I think is going to have potentially a very promising future I really would love not only for Spry seller to satin, in particular, but for all of these medicines, from rapamycin to a karbas, to Metformin, to the stLt, to one inhibitors to sadness to have more data, but particularly with the sat nav, I wish there were more human data on its use as a senolytics to hang my hat on. But in theory, targeting senescence cells is a very appealing Avenue. And again, in animals, both in the laboratory data and in a lot of the photographs that you can see, when you see the patients animals that have been given synesthetic treatments from birth till adulthood, the differences in twin animals side by side is striking. So, with the SAT nib, you know, I, I will certainly prescribe it to a well informed patient who is highly motivated, a lot of people don’t tolerate it as well, as they tolerate all the others. They can have flu like feelings, they can be a little bit exhausted, they can spend a couple of days not feeling so great. And when I would employ it, it would be very episodic. So I think, you know, four times a year is is probably enough until or unless we have more data. You know, Spry cell is a still a chemotherapeutic agent, it’s a tyrosine kinase family drug, it’s going to have a lot of effects. So it’s not it’s not something that I will, you know, suggest to every patient.
Robert Lufkin 42:03
Yeah. So your practice that you offer is based in Los here in Los Angeles. And to be clear, it’s a it’s a medical practice, it’s not coaching or anything like that. It’s an actual medical medical practice where as you say, you prescribe these, these longevity drugs, as well as other recommendations for the patient to take care of their whole their whole self, I guess, a question, do you accept patients from outside of Los Angeles? Is there a telemedicine component to your practice that people can manage?
Brad Rosen 42:42
Yeah, thank you very much. I do take telemedicine patients, ideally, will have an in person relationship, especially with both COVID. And with the airline situation being what it is right now, that can be challenging. But I’m open to pretty much any patient who feels like the philosophy that we’ve shared and I’ve expounded on is appealing. And it’s looking for guidance in an overall context of, you know, making it to older age in as good a shape as they possibly can. And maybe in the future, we’ll be talking about an indefinite extension of life. But for now, if somebody can get, you know, 10 or 15 extra years, I think that’s amazing.
Robert Lufkin 43:43
Yeah, so much is going on in this area that it seems like every, every few weeks, there’s there’s another at least promising research study. And all it’s so fascinating in the ITP. You mentioned the interventions testing program is is a fascinating way to look at it’s some of the some of the various drugs and supplements that people talk about being applied to this, this mouse animal model in a controlled fashion, which is very exciting as well. Well, what’s the best way for people to get in touch with you Brad and find out more about your practice or join your practice, we’re going to be including it in the show notes down below. But for anybody who’s listening to this podcast, just in audio only form, maybe you could just tell them the best way to reach you and follow you on social media.
Brad Rosen 44:41
Oh, sure. Absolutely. So the website I have is mTOR MD MT LR md.com. So that would be an introduction to me and practice and what it is that I’m trying to accomplish. And a person can see if If that is sort of resonating with them, and then I have a Twitter account that is mostly focused on on this on these topics. And that’s Dr. Bradley Rosen or Dr. Bradley Rosen, MD. And I think those are the best ways to find me. You can also send an email to me at mtorr medicine@gmail.com.
Robert Lufkin 45:31
Great, well, I think we, we’ve just scratched the surface on what we will be cover, I think we need to do another session here. And I’d love to love to talk with you more and to kind of dive down into these gray areas. But I, I just want to thank you today, Brad for spending an hour with us and and sharing your experience and then the wonderful work you’re doing on longevity and making, making these these powerful, potentially life saving drugs available to patients in you know, in the right, in the right setting, of course, but thanks so much for your work, and thanks for being on the show.
Brad Rosen 46:16
No, Rob, thank you, thank you for the opportunity. And thank you also for burning, you know, doing what you’re doing with the, with their podcast, and making all this information and this whole area of thinking available to so many more people. And to the extent that you would like to have me again, I would love to be back. I think that a lot of the things that I thought about before I came on, never came up. So absolutely. And thank you.
Unknown Speaker 46:49
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