Can Psilocybin Slow Aging? The Study on Telomeres, Inflammation & Survival with Dr. Louise Hecker

. So when 50% of the vehicle mice had died naturally from aging, we still had 80% of the psilocybin mice were still, still alive and surviving. And not only that, they just looked better. I mean, they had better skin, they grow back hair. So bald spots grew back and hair, white hair grew back black, you know, skin looked much healthier and shinier. And if you look in the paper, you can see pictures of just this kind of thing that I couldn't quantify, but just that mice look better. And that was hard to quantify, but you know, it was certainly a real result that we could all visually see. So that made us really excited about the potential for clinical

translation. Hey there, I'm Claudia von Boeselager, a former investment banker turned entrepreneur, longevity coach, biohacker, and mother of two. Once burnt out and overwhelmed with chronic health issues, I've transformed my life and helped thousands of people do the same. I've even reduced my biological age by 17 years. Yes, I'm 26 again. Now I'm here to share the tools, strategies, and inspiration to help you live healthier, happier, and longer. On this podcast, I interview world-leading experts in health, biohacking, mindset, and performance, and share personal stories and learnings to bring you the latest

insights. Insights and

tips. Think of this as your go-to space for real talk about all things health and optimizing your life. Ready to unlock your best self? Let's dive in. This is the Longevity and Lifestyle

Podcast. My guest today is Dr. Louise Hecker, is a physician scientist and leading researcher at the intersection of aging biology, cellular senescence, and psychedelic science. Her work explores how compounds traditionally studied for mental health, including psilocybin, may influence the fundamental biological mechanisms of

aging. Dr. Hecker is a senior author on groundbreaking research published in NPJ Aging, where her team demonstrated that psilocybin's active metabolite, psilocin, can extend cellular lifespan, reduce markers of cellular senescence and oxidative stress, preserve telomere length, and increase expression of longevity-associated pathways such as

SIRT1. Her work has helped open a new scientific conversation around psychedelics as potential systemic and neuroprotective agents rather than substances acting solely on the

brain. With a background in conventional aging and translational biology, Dr. Hecker brings a rigorous evidence-based lens to a rapidly evolving field, bridging molecular science, longevity research, and the future of preventative medicine. Her work is contributing to a broader reframing of how psychedelics may one day play a role in human healthspan and aging. Please enjoy. Welcome to the Longevity and Lifestyle Podcast, Louise. I am so excited to have you with us

today. Thanks so much for having me. Excited to be

here. So your work is at the intersection of neuroscience, psychology, and psychedelic research, but what originally drew you to psilocybin as a serious area of scientific

inquiry? Yeah. Well, I had no background in this area whatsoever. Did not study psychedelics at all prior to this. And it was really just a friend of mine that just kept asking me questions about psilocybin. This is how the whole thing started. And, you know, as a scientist, I couldn't answer the questions, you know, so I decided, well, I'll just start reading and I started reading cuz I thought, well, next time I see my friend, then I'll have something interesting to, I'll be able to answer some of the questions he keeps asking me. And, and so that's kind of how it started. And when I started reading about it, I just kept on reading. I was just kind of fascinated, intrigued. I was confused. How do we know so little about this drug that is doing so much in patients? And, you know, I came across this idea that someone had put out there saying, you know, maybe psilocybin has an impact on aging. And that's one way that could help to explain these long-term effects, you know, cause people can take psilocybin and they are reporting positive impacts 5 years later, which on some levels makes no sense, right? Because it's, the drug is completely out of your system in 24 hours. So how does that work? And one idea is that maybe it's doing something to aging. And I thought, you know, I can test that. I study aging and that's That's kind of how it began. Now here I am completely changing my course, my scientific research direction, because the research just turned out to be so

exciting. So compelling. And just in case anyone's not familiar with what psilocybin is, it's essentially the compound in magic mushrooms, right? So that psychedelic experience, and obviously for a lot of people that might not be aware of the research and they hear it and they're like, oh, but you know, this is not allowed and it's illegal or it's controversial. What were some of the biggest insights that when you started reading the research that you were like, actually, I'm, you know, this is really, really compelling. Like what were those things that made you really decide to pay attention to

it? Yeah. Well, I think the first thing is that, you know, it's being used for so many different disease indications. So from lots of psychiatric disorders, like, you know, anxiety, depression, PTSD, OCD, you know, the list goes on and on, but also neurodegenerative diseases, Alzheimer's, Parkinson's, and many other things like chronic pain, anorexia. I can't think of another drug off the top of my head that works for so many different disease indications. So that was the first thing that piqued my interest. How does this one drug work for so many different disease indications? But yeah, also like we really know very little about fungi relative to, you know, let's say plants. Fungi have more genetically in common with humans than plants do. And we know so little about

them. Can you explain for people that might be like, well, how is this possible? How is a mushroom closer to a human than, than other

plants? Well, it's just kind of how things evolved, you know, in evolution and, and just genetically we're more closely related to mushrooms than plants. And yeah, like plants breathe carbon dioxide, mushrooms breathe oxygen like we do. So, you know, there are some interesting kind of similarities and things that I thought, wow, yet we know so little about fungi. There's probably a lot more to be learned here. The other thing was, is that 99% of what we know about psilocybin is really comes from because of, of course we know it's a psychedelic. So, so of course we have a lot of information about what it does in the brain. And we also have a lot of information about what it does clinically from these clinical trials that have come out showing efficacy for all these different disease indications. But we really know not much else about it. We don't really know. There's not really any studies that have rigorously evaluated what it does systemically, if it impacts other organ systems. And that was just kind of this black box of, we just don't know. And part of the reason for that is because, you know, psilocybin is a Schedule I drug. So in the government's eyes, this is the same as heroin, which makes it really challenging from a regulatory standpoint to study. So, so there are very few studies actually on psilocybin that are

published. Can you share your journey into the work and the research that you've done? And then let's talk about where you are now also. So your friend triggered the curiosity. You started reading about it. What happened next? You decided to essentially shift your focus of your research as well. So take us on that

journey. Yeah, it was really just a side project. I'm just like a curious person and that's probably why I am a scientist. And so having it pique my curiosity, I went into the lab and said, hey, let's order some psilocybin. And then I realized, whoa, it's a Schedule I drug. This is not going to be, you know, as easy. Typical project where we could start experiments next week. We have to get a DEA license. So this whole process from, you know, start to finish, uh, just to get it in our hands probably took about a year to get all the regulatory requirements taken care of and the DEA license and inspections and all the things that go along with that. So years going by, we're kind of pushing paperwork and then we're ready finally to start our first study. And the first study was a simple one. So let me back up and say that when we ingest psilocybin, it's broken down in your body, but through digestion into psilocin, which is the active metabolite of psilocybin. So what your body sees systemically is actually psilocin. And so for cell experiments, we use psilocin because again, that's what your body is seeing after ingestion. And so the first experiment was simple. It was, let's see if psilocin impacts cellular lifespan because we have these replicative senescence models, which are basically cell models that you can study cellular lifespan and cells, like people, have lifespan, and you can follow that. It's very reproducible. And so we just tried, okay, if we give silicin or vehicle, what, what happens to cellular lifespan? And that was the start. And we saw, wow, there is a dramatic improvement in cellular life extension when you treat with silicin. And not only that, it's dose dependent. And so that's kind of the first initial finding. That started leading me down, okay, what's happening inside these

cells? Can you break down what is happening with the silicin? Yeah. And in the cells

specifically? So the first thing that I did once we had that key result was to say, well, you know, look at the protein levels, what's happening inside the cell. So biochemically, and so being someone that studies aging, I just said, all right, let's pull out every marker that we have related to aging and see what's happening.. And sure enough, well, to our surprise that every single marker was rescued to some extent with psilocybin treatment. So like, for example, as, as cells age, you see an increase in cell cycle arrest markers. You see decreased DNA synthesis. You see decreased markers that regulate metabolism, cellular metabolism, you know, so cellular metabolism slowing down. So you see these kind of like age-related things. And all of these things were rescued in a dose-dependent way with, with psilocybin or psilocin. One of the main things, or one of the things that stuck out to me, because I study, happen to study oxidative stress in the context of disease and oxidative stress is something that accumulates as we age. It's also a lot of diseases you have are associated with high levels of oxidative stress. So we looked at oxidative stress levels and what we found is that even at the very low, low doses, it was a very potent regulator of decreasing oxidative stress. And to the point where at the highest doses, the oxidative stress levels were even lower than they are in young cells. And from the cellular markers, we've found that not only is it decreasing oxidative stress production, but it's boosting antioxidant responses. So you're— so psilocybin seems to be doing, hitting it from both sides on the oxidative stress angle where you're lowering the amount of oxygen produced and boosting antioxidant responses, which gives you this net effect of a low level of oxidative stress. So that was super

interesting. Is there anything that wasn't improved with the

psilocybin? That was the craziest part is that, you know, I, I was just kind of fishing at that point to say what's going on. And literally every single marker that we tested was rescued. When I saw the data, I mean, my eyes popped out of my head, literally. It was like the first round of data. And I remember my technician, Yoon, was— she loves showing me when she's got— she's like, I have good data. I love it when there's good data. She's rushing in my office, like, you're gonna like

this. What exactly is happening that this like miracle molecule, right, is able to improve all across the board? We're used to traditional medicine. You're targeting one pathway, you're targeting one area, but across the board, it's able to make all these improvements. What is happening? What, what's going on

there? Yeah. The other thing that we looked at was telomere length because telomere are the protective caps on your chromosomes and your DNA. And, and that's a very kind of a well-validated biological marker of aging. And so as we age, those telomeres shorten, leaving less protection of your DNA. And so that's one of the ways in which we can kind of characterize our biological ages by how long our telemeres are. And so in those cells that received silicin treatment, the telomere length was preserved. And so it didn't reduce like normal, like it does in normal aging, which means that the DNA has more protection. You know, in that initial study, we just kind of have like this snapshot of all of these things going on, and we're not really sure yet, and we're working on now, you know, how these things are connected. And what happens to lead to the next effect. You know, what, what is truly mediating this effect versus what's a consequence. And so that's what we're trying to kind of figure out

now. What would you love to see, or what would you hope to see, let's say, hypothetically speaking, obviously you haven't proven it

yet. It's funny, cause I, maybe I'm just like, as a scientist, I never have expectations. Like I try to not have any. Let's see the data. Yeah. That's really how I go into everything. We have ideas, which is how we decide what to try to test. But we don't know. The bottom line is we don't know. We're, we're doing all kinds of tests to look at, you know, which receptors are it's acting through because one of the things that was surprising to me, again, when I started these studies and I knew nothing about this field of science in general. It found you. Yes, it found me. And we know from the published literature that psilocybin acts on the serotonin receptor, 5-HT receptor. But that said, could it act through different receptors? And is that the receptor that is mediating these effects? And so we're doing some kind of rigorous studies where we block different receptors and trying to understand how this longevity signal is mediated with psilocybin, which again, it's never been studied. This is the first study ever. To show these, you know, dramatic systemic impacts, particularly on aging, which no one's ever shown. And so this field has just like, you know, burst open with 100,000 more questions. I think we know now that we have made this finding, we, we, we realize we have 1,000 more questions that we have not answered that we need to answer still. So yeah, so I don't know how it's going to work. Ultimately, we're testing a lot of different things. But certainly it has, has a dramatic impact systemically. So back to what I was, I got sidetracked there, but when I think of serotonin and serotonin receptors, I think of the brain. And actually what I was surprised to learn is that most cells actually express serotonin

receptors. And so, yeah, most cells

do.

Okay. 'Cause I think, ah, okay,

interesting. I didn't realize that. And so, so it actually makes sense that, you know, that it's, that it's doing something systemically because these all these systemic cells have the same receptor that it's working on in the brain. So it may work through that receptor, it may work through that other receptors, uh, to have this longevity signal. We don't know, but those are some of the things that we're looking into

now. And you need to recruit a big research team, Louise, and like be able to tackle all of these. In terms of human trials, what does that trajectory look

like? Yeah, a lot of interest has come out of the study based on the findings in the mice, which, um, maybe I should tell you about first.

Sure. Let's talk about that first and then skip onto the

wounds. So, uh, after the exciting cellular data, we decided, well, this is definitely worth testing in vivo. And so we tried to design the most realistic, uh, experiment that we could. And we had only pilot funding at the time, so we sort of knew we had like one shot here. And it, you know, part of science is is really looking at what everybody has done. So we looked at everything that had been done clinically and the doses given clinically. And we looked at everything that had been done in animals, in any published study, just to kind of get a feel of dose. And then, then part of it is a little bit of guessing. Um, you know, this study just hasn't been done before. So we tried to pick a dose that somewhat matched what has been given clinically in that it's a psychedelic dose. No one has, at least not to my knowledge, no one has ever given psilocybin repetitively long-term, and it's certainly never been done in the context of aging. So it was definitely the first of its kind study because we started with aged mice. The reason we started with aged mice is because we thought if this is doing something to impact healthspan or aging, I mean, a realistic user of this would be someone that's starting to see a lot of age-related decline, and that typically happens around 60. And that's really when you start seeing the onset of a number of age-related diseases. And so that's why we started with aged mice that were equivalent of a 60-year-old person. And we gave it to the mice once a month for approximately 10

months. And just one question, Louise, was it like a microdose for the mouse equivalent, or was it a full dose? Maybe just some context for, for

people. No, it was a, it was a hallucinogenic dose. We know that based on prior mouse studies that have shown that this dosing in this range will, will elicit hallucinogenic effects. The reason we wanted to do that is because I think clinically there's more known about the high dose psilocybin, the hallucinogenic dose compared to microdosing. There's a lot less known about microdosing than taking the high dose. And also in part because we thought, well, if there's an effect with microdosing, we don't want to miss the effect, right? If it has an effect with high dose, then we can always go back and look more at microdosing. So yeah, it was a hallucinogenic dose. We know because mice elicit a head twitch response, which is a behavioral response signaling that, suggesting they're having like hallucinogenic experience. And so we actually recorded the mice and we could see that they were having this effect. Then they, they're, the mice actually just kind of go to sleep after that. So it wasn't, it wasn't as exciting to watch as I thought it would be. But, but, uh, yes. Uh, and we gave it to them orally. So similar again to how patients are taking this in the clinic. And what we found was this dramatic improvement in survival. So when 50% of the vehicle mice had died naturally from aging, we still had 80% of the psilocybin mice were still, still alive and surviving. And not only that, they just looked better. I mean, they had better skin, they had, they grow back hair. So bald spots grew back and hair, white hair grew back black. You know, skin looked much healthier and shinier. And if you look in the paper, you can see pictures of just this kind of thing that I couldn't quantify, but just that mice looked better. That was hard to quantify, but, you know, it was certainly a real result that we could all visually— so that made us really excited about the potential for clinical

translation. That was a monthly dose, hallucinogenic dose, over what period of time was it? Did you say 6 months or 12

months? 10

months. 10

months. 10 months. Why did you pick 10 months? So we didn't really pick the time as much as our, our animal protocol allowed was for testing until any group, any group hit median survival, which is 50%. So, so when any group hit the 50%, 50% of the group died, that signals the end of our experiment. And that happened to be 10 months in when the vehicle broke hit 50% mortality. So that's when we stopped the

experiment. So appreciating that the studies haven't been done yet, but extrapolating things for the potential for humans, where do you see, and what does that trajectory look like between where you are now and where, when those studies can start happening? But where do you see this being applied then for humanity,

essentially? Yeah. Well, the good thing about this is that it has been used in so many clinical trials, right? So, we have a really good idea about its safety profile because all of the clinical trials collectively that have been done. And we know from those trials that people have these incredible impacts on all types of things, right? The good news is that, that there are dosing regimens that are safe and that we know, uh, have positive impacts for, for other things like memory and wellness and demoralization and a lot of things that are beneficial. That said, have not yet tested, and where this is what needs to be done, we really need to rigorously test what is the optimal dosing protocol for, you know, for maximal, what I would call like geroprotection. A lot more work, I think, needs to be done at the preclinical level before we can really fully understand and translate that. But because we know so much about its safety profile in patients, people are moving forward with clinical trials to evaluate this based on study protocols that are known to be safe already. So I don't, I don't know if I'm allowed to even say, but sorry, a clinical trial that's coming up that a private donor has funded. That will actually evaluate this for the first time in

patients. This is really exciting. And are you able to use any of the research? Obviously it was used under different contexts out of Johns Hopkins, Imperial College London. Obviously there's many different universities across the US now doing more research on psychedelic-assisted therapy and medicine and brain health and many different things. But is there any way to extrapolate from that data information for what you're looking to do, or it's wasn't done in the right context. And I'm speaking as a non-scientist

here. Yeah. I mean, you know, all the data that's been out there kind of in some ways contributed to, you know, this, right. But again, I, I think that no one had really had aging really in their radar experimentally because it just hasn't happened. Right. There just are no studies. So now that our paper came out, And it, I think it has really gotten people to start thinking differently and even adding different endpoints to their studies to look at things related to aging. So I know even a couple of papers that have come out since our paper was published and, you know, and we're seeing interesting results on aging markers and things like that. So people are now have this on their radar and I think are going to start, you're going to start seeing a lot more. Come out, which is really exciting, but there just haven't been anything that really helps us to understand this just yet, you know, in terms of prior

work. And do you think that there's going to be, you know, the one dose? Because obviously we're all an N of 1, we're all different the way we metabolize things, what our baseline is essentially. Do you think there's going to be sort of the one prescriptive dose or do you think it, you know, will be variant on different things? Is there a trajectory? I'm just curious what your, I don't know. Future pacing, but just curious what your thinking

is. Yeah, it's, I mean, great questions. I mean, the short answer is we don't know until we know. But I think that someone who, like me, I'm a PhD, so I am more involved in like the biological characterization of patient samples. And I think that through that type of work, we may be able to identify endotypes of patients, like people with certain baseline characteristics that may be more likely to be, you know, high responders or low responders, or, you know, better suited to take the medication, or we may find that certain patients with certain profiles are not well suited to take the medication. So I think that, you know, personalized medicine approach certainly down the road, but there's still so much to, to learn to even see that it's, 'cause right as of right now, there's no data in

humans.

Right. So the first piece is like, Does it do anything to aging in humans? I believe it will. I mean, I would bet my life on it, but we need to show that scientifically and then, and then really try to understand those patient profiles. Like even looking at who does well versus, like I said, high responders in terms of efficacy from other endpoints. Like, do they have different baseline characteristics and features that, that might help us understand how to identify and properly dose even patients moving

forward. Yeah. I'm so curious. There's obviously people out there who regularly take psilocybin. Has there been like a sort of call to, 'cause part of the interest is to see their trajectory over time. Have you, through MAPS or something, seen if there are peak candidates that are happy to come and share their N-of-1 experiments and how they're doing and measure their telomeres and things like that if they've been regularly taking psilocybin on their own

accord? Yeah. There are people out there doing, you know, Brian Johnson is a, longevity influencer, and he has publicly gone out there and done this and is measuring his biomarkers. And the data from his study is, you know, fascinating to me. But that said, you know, it's, it's tougher as a scientist to look at data from an N of 1 from patients, you know, and Bryan Johnson in particular, because he's already probably at this

level. And doing 10,000 other things at the same

time. How much of an effect are we really going to— but if he's seeing effects, it's interesting because he's already at a different baseline than most of us. Yeah, people are doing it, but there are anecdotal stories about psilocybin everywhere and all over. So I'm more interested in science of it because, you know, everybody has an opinion about psilocybin and it seems like a lot of people are very interested in it. I'm just trying to kind of focus on what we can show scientifically that will help inform people moving forward. And I guess that's the reality is that this is, even though it's a Schedule I drug, it has become legalized in a number of cities and even in states. And so people have access to it. And so I think my job is to just, you know, try to rigorously test this as best as possible and, and, and try to help provide information that can ultimately be

translated. Let's talk about that regulatory component and obviously with different compounds, right? So with ibogaine, you know, in Texas now they're funding it and a bunch of the other states as well. We've had Talia Eisenberg from Beyond Ibogaine who's doing really compelling work in his research at Stanford that even just one high-dose session of ibogaine can reverse brain aging by 1.5 years in one sitting essentially, which is just phenomenal. So they have a lot of patients or people that come between the vet vets, right, with PTSD and trauma and add— with addiction challenges, not just vets, but then you have the high performers that are like, hey, I can get more sharp by just one setting. And so what is some of the regulatory conversations, or are you already having some of those regulatory conversations to help regulators start thinking differently about this and the potential power? Because obviously it's a process and it's gonna take a while. Are these things you've already started engaging

with? Yeah, I mean, I think the fact that it's a Schedule 1 drug, I think will inherently change soon. I mean, So what, what makes something a Schedule I drug? It's potential for abuse. It's being used, or potential for addiction and abuse, being used to treat addiction. It's lack of accepted safety profile. We know it's got a great safety profile and lack of accepted medical use. It's in Phase 3 clinical trials. So pretty soon, I think just a matter of time, one of these, you know, it will get FDA approved for some indication. At that point will have a medical accepted medical use by definition. I'm, I'm like probably like everyone else just waiting for that to happen. And it seems like these kinds of things, like with marijuana, THC have, have kind of gone along this path and we're seeing a lot of changes in, you know, how that's being viewed. I think psilocybin is, you know, it's always gonna, I think, have this kind of like stigma, I guess. But I think the data and the science and what's happening in clinical trials is gonna change that to some extent until it's, it's reclassified to a different schedule, which I think will change everything. Because once that happens, that loosens these regulatory barriers that restrict us as scientists to make it much more easy to do these kinds of studies. So that's probably gonna happen. It's just a matter of time and I'm just waiting for it to

happen. If any regulators are out there, come and have a chat with Louise to, to better understand the science behind it. And I think one thing that was really compelling for me was watching the Netflix documentary. Hopefully it's still up, The Fantastic Fungi, or Fungi, where it really explains well, like where this whole war on drugs and this whole brainwashing essentially came because LSD that was, you know, already being used by psychiatrists, et cetera, in the '50s and seeing such positive results. Was just totally reclassified and this whole war of drugs came. And so, you know, we were talking offline before, Born in New York, you know, it was all about this is your brain, this is your brain on acid, and it's like the worst thing you can do. But now looking at actual scientific literature, it's actually the opposite, right? And neuroprotective and all the rest of it too. So I think that for a lot of people who are maybe suspect or suspicious and they're not looking at the research just yet, to really realize where that initial thinking comes from is actually a bit of brainwashing essentially that, that happened historically. So time for change,

right? When that happened, 1970, in fact, when it became a Schedule I drug, you can see actually just the absolute drop of all psilocybin research and funding went to nothing. Very little psilocybin research and funding, you know, for 20 years. And we had a bit of a resurgence more recently, but, you know, I think again, part of that problem is just that it's so challenging to study. It's so challenging from a regulatory standpoint. The amount of work that goes into just having it in your lab, in your possession, or being able to test on patients is tremendous compared to any other non-Schedule 1 drug. So yeah, as that changes, I think it's gonna be really exciting to see what happens with more people getting

involved. And Louise, do you see as much potential with some other compounds like the LSDs or ibogaine? Have you looked at that at all,

or? We are looking at it as we

speak. If there's— Tell, tell us about

that. What are you looking at? Oh, that are being treated with ibogaine and other analogs. So yeah, we're looking at all kinds of things because again, it's just kind of like the— our study kind of broke open the door because no one has been looking at these impacts. So we're, we're testing all types of things. We're really interested in some analogs of psilocybin that are, that are not psychedelic, that don't cross the blood-brain barrier into your brain. They will target the same things. They just can't get into the brain. And so those are attractive to us because for people that might want to take these things for improving their healthspan or aging, that might be a more attractive therapeutic avenue, right? So we're looking at all types of analogs and to see which could work the best and to try to find other things that are not hallucinogenic that act on the same pathways that could have the same impact for healthy

aging. So, so exciting, Louise. If you're looking ahead in, let's say, 2, 5 years' time, what does that landscape look like? Assuming maybe that the regulatory environment finally opens up, what do you see as the potential here for the research that you're working

on? Yeah. So one of the things that we're really closely looking at now is just all of the organ systems and how they're impacted. I mean, we have this really dramatic improvement in survival. And so why is that? You know, what's happening? And so we're studying all the organ systems individually, and we're finding that it's incredibly protective in most organ systems. We're finding like some organs it's not as pro— it's not detrimental, at least the data so far, but not as protective as other organs. Like, so for example, the lung, we find you would think the brain has the most kind of rescue, but actually we're finding the dramatic impact in the lung in terms of rescuing pathways. Wow. That making the lung have signaling that looks more similar to young than old. So that was kind of

surprising. I'm thinking like, you know, for COPD patient, things like that as well, potentially, right? Especially ones that are really struggling. Why would the lung be so particularly sensitive more than say the

brain? Yeah. So one thought is that, well, we're seeing a dramatic impact on inflammatory responses. That's one thing that it doesn't matter what organ we look at, blood, organ, proteomic profiling, transcriptomics, everything points to decreased inflammation for sure. But one thought is that, you know, the lung has probably perhaps more cells cell types than most organs in the body, including a lot of inflammatory cells. So that could be one reason. Um, also your lung is the one organ that's like exposed to the environment constantly. And so maybe there's a need for greater protection in the lung than some of the other organs. So trying to tease out which, which organs have more protection, what is it doing? One of my grants that I've submitted gets funded is is, you know, can you use this as, you know, and where I see the holy grail of all of this is not, not that we can take psilocybin and live forever. That's, I don't want to live forever, but I'd like to live healthier, longer, you know? And, and so some of our data, our newer data indicates that taking this as a geroprotective agent can potentially reduce your incidence of age-associated diseases and also improve the outcomes if you were to get one of those diseases. And so that's what I think the holy grail is with psilocybin. Can you take it and not maybe have, maybe not get some of these diseases that we, you might get in your 60s and 70s and that those things would be delayed. And so they might, you know, have onset of that disease until you're 80 versus 60. That's what I'm hoping. And we have some really exciting data that suggests that that is the case. And so we are really working hard to kind of see. You know, what could it be used for? And is it better for, like I said, things like, certainly has a major impact in the brain, the lungs, and a lot of other organs where more than, more than half of the pathways seem to be rescued. And so, yeah, understanding which organs could potentially have the most benefit and thinking about disease indications and, and how that could work. So yeah, it's exciting. Just a lot more research needs, I need some funding to get to answer those

questions. So any funders out there, where should they come to Louise? Do you have a website that you would send people to for anyone looking to

donate? You can always find kind of updates on my research on my LinkedIn and my, my X account. So post updates to our research, but sure, I'm, I'm an associate professor at Baylor College of Medicine in Houston. So certainly anyone can look me up and contact

me. And fund the research as well. And just so people understand also, I mean, I know from speaking with other scientists as well, this whole getting funding and grants is like you could spend your whole day every day doing that. And obviously you want to be at the bench doing the research, right? What type of numbers would be like the ideal if you had a magic

wand?

Yeah. What would be ideal in order to fund studies that, you know, make sense? You're not just doing the 1-year study and then you have to pivot because, you know, some things have come up that weren't expected, etc. Just walk people maybe through that a little bit. What would be the magic wand scenario? Because what you're doing is really so

impactful. For humanity? Yeah, well, thanks. You know, I, there's no magic number. I mean, the reality is like the more funds we have, the faster this research happens. That's just reality, right? And we can build teams around that. So the way that I'm kind of thinking about it is like I've applied for grants that would specifically fund ancillary studies to evaluate, you know, ongoing clinical trials in human elderly, healthy patients, things like that. Right? So we can get answers to, does psilocybin impact human aging? And then I can take samples from those patients and do all the biological characterization and give you that answer. I have other projects that are more focused on things like taking a step back and saying, let's use really unique model systems like Drosophila and C. elegans where they have a rapid life cycle, but you can test dozens of protocols, right? So rapidly. So we could get a better idea of what is the best protocols for geroprotection by kind of stepping back and using kind of more rapid models of, of lifespan that, you know, those types of studies. Two studies we just had before I got on with you was talking to one of our collaborators who is working with us on, you know, identifying the receptors and the pathways it's working through. We have so many projects focused on different angles. My colleague Kosuke, he's really focused on the wound healing aspects. We're finding a lot of interesting properties with psilocybin and wound

healing.

Really?

Yes.

Wow.

Right. How is that working? I'm trying to understand the correlation. Is it because of mitochondrial health and that's expediting it,

or— I mean, mechanistically is tough to say. I mean, one thing, and the reason we started thinking about this is because of the really, um, you know, striking impacts on the skin that we just noticed. And so that was visible, right? We're seeing this visible skin. And we have done some studies in the paper. We've done some studies with skin fibroblasts too. And so we saw that, hey, it extends cellular lifespan and delays the onset of cellular senescence. So, um, wound healing, you know, in the context of aging is less efficient. And that's probably because you have more oxidative stress, more senescent cells, less proliferation. And since silicin treatment of cells can rescue all of those things, we thought, well, let's see how this impacts wound healing. It just kind of makes sense. And, you know, dermal applications. And so, uh, and as it turns out, it seems to be really potent, a modulator of more efficient wound healing.. And so we're following up on different angles of that. But yeah, there's, so we have so many different projects going on and it really depends on, you know, what gets funded. So some, some grants are more focused on this project or this project. And, you know, we had a private donor come in. He had a very specific interest in wanting us to test something and we tested what he wanted to test, you know? So we're, we're open to, the bottom line is there's so much to be tested that it's, It's sort of hard to, and we have this talk all the time about prioritizing, you know, and when funding comes in, it'll be easier because then we'll have projects that, you know, are already mapped out. This funding will fund this piece and this funding will fund this piece. So it's, it is, it is a full-time job trying to get big funding. And keep in mind that all of this work came out from these very small pilot grants that I was fortunate enough to get from Emory when the work started when I was at Emory. And that's why pilot like funding is so important for these projects like this, because I had submitted a number of grants that just got completely trashed. I was just too early, you know, and no one wanted to believe this. Understandably, right? It's pretty off the wall idea. And now that the paper is out and it's been peer reviewed and people can see that we've done a rigorous study, the interest has changed, you know? So I think, so I'm, I am, I've submitted like a huge round of grants in the last, you know, 6 months and I'm just sitting with my fingers crossed that, you know, that it'll all get funded. I mean, that would be my

worry. Let's put, put that out to the universe, right? So they'll all get funded. And, uh, one thing I'm curious about is for women's health, obviously ovarian aging. I don't know if you know Dr. Jennifer Garrison of the Buck Institute, um, and she's involved in different initiatives around it too, but I'm, I'm sure you might know that the ovaries tend to age 2.5 to up to 5 times faster than any other organ in the body. So I'd be very curious, and I don't know, is there any of your studies and grant applications around

that? It's really funny that you asked that because when I was presenting my data, it's kind of like, you know, to smaller audiences, you know, here at the university and people in the audience kept picking up— the study happened to be done in female mice and people in the audience kept picking up when I'm showing the data, like, have you noticed there are a lot of like hormonal rescue in, you know, your data? And I said, no, I haven't actually noticed that, but that's Interesting. And so we actually did, we had the bioinformatics team do some analyses and actually showed that there was a significant amount of rescue specifically of women's health pathways. So there's a lot of potential, I think, for all kinds of things related to that. Again, we haven't tested it in male mice, so we don't know, but certainly in the female mice, it seems to be really beneficial in terms of specifically women's health pathways that are rescued. And there are a lot of, with that, a lot of cancer pathways that popped up as being rescued. So we don't know. I think, so taking steps back, like doing studies like in Drosophila, for example, which we have studies ongoing now, that will help to start answering those questions because in those studies we can actually measure reproduction and if there are changes in like egg laying and things like that, which we're monitoring now. So hopefully we'll have more information, but it, it does look really promising for women's health

actually. That's so exciting. So I'd love to connect you with Jennifer Garrison cuz she spends a lot of her time organizing research grants for people working on women's health initiatives. So I'm thinking for you and then out of Columbia University, there's the rapamycin and ovarian aging study happening. I wonder, is there some sort of collaboration that you could potentially do with them with the studies that they're

doing? I'm just thinking outside of the box a bit. Yeah. Neat. Yeah, for sure. This is the greatest part about having this paper come out is like, like people like you connecting me and people reaching out and connecting. And like, I've been able to develop all these amazing collaborations with people where I can say, hey, can you look at your organ of interest in these mice and tell me what's going on? You know, that's been

fantastic. Yeah. I'll be very happy to, to do that and advance women's health research, which is so, so lacking. As we know, we've been ignored for far too many years. Louise, it's been such a pleasure. Thank you so much for taking the time. I know how busy you are and being pulled in all directions and doing such important research. Is there anywhere that you would like— you mentioned your LinkedIn profile and your X profile— where you'd like to send people or to learn more? And we'll obviously link the study as well in the show

notes. Yeah, no, that's, that's great. Um, keep following us, and we're gonna have some more really exciting data coming out very

soon. So we'll follow that. And any parting thoughts or message or piece of advice or ask from my audience

today? Yeah, just keep your eyes out for, you know, the new stuff coming out. I think it's super exciting, and I'm really excited to see what comes out of this from other people's science and labs, right? Because that's the true mark of a, a good discovery is when other people are independently validating that. So I'm excited and I hope your audience is excited to watch for psychedelics and their impacts on aging. Cause I think we're, we're gonna see a lot more coming

up. Really, really exciting. Thank you so much, Louise, for taking the time to come on. I really appreciate it. Thank you to your audience for tuning

in. Thanks for having me. Hi everyone, it's Claudia again. Before you take off, would you like to get a short email from me to you several times a month with top tips, insights, and strategies to help optimize your life, health, and business? This could be interesting posts or articles I've read on life and longevity optimization, cool biohacking or lifestyle products that I've discovered, and other fun things to help you be at your best. It's a very short piece of inspiration for you, so if you To receive it, check it out by going to llinsider.com. That's llinsider.com. And leave your email to get the next