Peptides: The Science, Uses & Safety | Dr. Abud Bakri | Andrew Huberman Transcript

Andrew Huberman interviews internal medicine physician Dr Abud Bakri on the science, uses, and safety of peptides

Andrew Huberman speaks with Dr Abud Bakri, an internal medicine physician with deep expertise in peptide science.

Summary

Dr. Abud Bakri, a board-certified internal medicine physician, joins Andrew Huberman for a masterclass on peptides, covering everything from FDA-approved GLP-1 agonists to lesser-studied compounds and the science of thymic aging. The conversation covers the full spectrum from FDA-approved GLP-1 agonists like semaglutide and retatrutide to lesser-studied compounds like BPC-157, pinealon (EDR), epithalon, thymosin alpha-1, TB-500, thymulin, and GHK-copper. He argues that the word "peptide" is far too broad to be scientifically useful, and proposes a key organizing distinction: peptides with known receptors (like the GLP-1s) versus those without identified receptors (like BPC-157), which may act through epigenetic or structural mechanisms. He reveals that virtually all raw peptide materials originate from China regardless of whether they end up in pharmaceutical pens, compounding pharmacies, or gray-market research-only websites — and that the quality and safety of the latter two categories varies enormously. He also presents a largely overlooked case for the thymus gland as a central driver of aging and immune decline, arguing that thymic involution after puberty underlies increased cancer, autoimmunity, and cardiovascular risk, and that a simple lymphocyte-to-monocyte ratio from a standard CBC blood panel may serve as an accessible proxy for thymic health.

Key Takeaways

FULL TRANSCRIPT

Introduction and the Two Categories of Peptides

Andrew Huberman: Dr Abud Bakri, welcome.

Dr Abud Bakri: Good to be here.

Andrew Huberman: Peptides — huge topic and huge category of biology and medicine. We should start off by breaking this into categories so that people can wrap their minds around it, because that word "peptides" has come to mean stuff people buy and take and maybe should or shouldn't buy and take. But there's a lot of important and quite simple biology to understand before anyone should even be thinking about any of that. So if I just push the word "peptides" towards you, how do you carve that up in terms of thinking about it as an MD, as a clinician, and maybe also put yourself into the mind of a peptide-curious person out there?

Dr Abud Bakri: Scientifically, I would say it's one of the languages of the human body. The body likes these different languages to communicate between cells — going from DNA to RNA to proteins, which can be broken down as polypeptides and peptides. Peptides are one of these languages. Steroid hormones are another language. And then peptides can be broken down further into subcategories: whether or not they have receptors, or they have no receptor. That kind of changes the clinical effects we'll see — like the GLP-1s, which have a very strong clinical effect, compared to these more obscure peptides like BPC-157, TB-500, and TB-4 that don't have a clear target.

Andrew Huberman: They have receptors but they just have many of them, or they don't even have receptors?

Dr Abud Bakri: We don't have a receptor identified for BPC-157 or TB-4.

Andrew Huberman: Just stopping you right there. There's a very interesting distinction. I don't think anyone else has described peptides this way. Let's take BPC-157 for the moment — we're going to talk a lot about it today. If it doesn't have a receptor, what are some ways that it could impact cells and organs? Or is it that there are receptors, we just don't know what they are?

Dr Abud Bakri: It could be the latter — that maybe the receptor is still elusive. Or it could be that it's modifying certain proteins that already exist, or linking different proteins together in a more favorable fashion for gene transcription. The Russian peptides are all epigenetic modifiers. They bind to the groove of the DNA in certain spots that either open up or close the chromatin to certain areas of genetic expression. They've modeled this out — like a steroid hormone. Steroid hormones bind — like the androgen receptor binds DHT, or testosterone goes into the nucleus and turns on all the androgenic genes.

Andrew Huberman: Yeah. Like puberty is a good example of that.

Dr Abud Bakri: Exactly. So pinealon, for example, shuttles heat shock proteins with androgen receptors.

Andrew Huberman: Got it. So if I just pause us for a second — we should think about this word "peptides" in two major categories at least. One is: has known receptors, plural, like the GLP-1s. The other category would be: does not have known receptors, might have receptors, but can definitely impact biology in interesting ways — or so say the animal data.

Dr Abud Bakri: Yep. A lot of animal data.

The Origins of BPC-157

Andrew Huberman: All right. I know a lot of people are interested in GLP-1s and I want to go there. But because I know most people are probably listening to this foremost because they want to hear about the other stuff, let's start with BPC-157. What is it? What do we know about it? We'll explore safety and what is your stance on it from the perspective of a consumer and a clinician.

Dr Abud Bakri: The best way to look at it is — as humans, we've been looking for medicines in plants for thousands of years. And in the last, let's say, 150 years, we've been looking for medicines in cells. So animal-derived versus plant-derived medicines is the way to think about it. You think about aspirin, metformin, the statins — those were all discovered in plant tissues. Statins more so in fungi, but you get the point. Now we've been looking into animal tissues to find cures, medicines, treatments. So a group in Croatia in the '90s looks for this peptide called BPC, and eventually named it BPC. It's a 40,000 dalton giant peptide called BPC. BPC-157 is 15 amino acids from that giant peptide. We don't naturally make BPC-157 — that's what you'll commonly hear online. We make BPC, the big protein.

Andrew Huberman: Did this group go looking for "body protection compound"? For those that aren't familiar, in the laboratory you can take a tissue, grind it up, and do what's called fractionation — you start separating cells and tissues and liquids according to the size of different proteins. Like different filters will let sand through, or pebbles, or boulders. That's kind of what you do. And then you figure out what the sequences are, and then you throw them on cells or put them into animals and try to figure out what they do. Why were they motivated to look for what eventually became BPC?

Dr Abud Bakri: Pavlov — the famous scientist who did the experiments on dogs with the bell, making the dogs salivate — the other work he did was on gastric juices of dogs. What he'd do is put a hole in the dogs' stomachs, feed them food, get the gastric juices, and sell that as a medicine. That was part of his business.

Andrew Huberman: He got a Nobel Prize. He was also kind of like — what, he had a promo code? It was like "enter Pavlov" for a discount at checkout.

Dr Abud Bakri: So this is BPC before BPC-157 exists. There are probably other peptides and compounds in there, but they found that gastric juices had positive effects on healing in people that had GERD and these kinds of conditions.

Andrew Huberman: Wait — so people were taking BPC in the time of Pavlov?

Dr Abud Bakri: They didn't know what BPC was. They were taking gastric juices from dogs — for GI distress, GI discomfort. Some people were trying it for wound healing. There was a big push in this era for finding animal tissues and putting them into humans. That science fizzled out. At the same time, there's a scientist, Selye, who's coming up with the stress adaptation theory. He notices that when animals are stressed out, three things happen: their adrenals get really big so they make more cortisol, their gastric lining gets destroyed, and then their thymus gland and their lymphatics shrink down. He has this published paper showing a clear adrenal from a stressed animal versus a non-stressed animal, a thymus from a stressed animal versus not. So this group is looking and thinking — hey, Pavlov had this gastric juice, Selye said there was damage during stress, there must be some kind of cytoprotective or organoprotective compound in the gut. The stomach is a very rich endocrine tissue. It makes ghrelin and all these other hormones. So they're thinking there must be something else in the gut juice that protects the gut lining from further damage.

Andrew Huberman: Were people drinking the gastric juices of dogs? Were they injecting them?

Dr Abud Bakri: Drinking was mostly what they did. And it was supposed to be a medical elixir, presumably. It had many many things in it, many peptides. Dyspepsia and upset stomach and this kind of stuff is what people were thinking.

Andrew Huberman: Do the reports point to the fact that it might have worked, independent of what was sold on Dr. Pavlov's non-existent website?

Dr Abud Bakri: This was in like the early 1900s. And then Selye was what, 1930s? So yeah, 100 years ago. And this other group in Croatia — their first paper was 1991. Their first paper talks about this — hey, there must be some kind of compound. They identified the big 40-dalton protein BPC. And then they were like, what's causing the actual biological effects? They identified BPC-157, the 15 amino acid peptide that's causing all these effects. There are actually more peptides in gastric juices that some other scientists may or may not have already identified. This field of peptides is going to be very interesting because almost every organ has a signature of peptides. If you think back — Dr. Vladimir Khavinson in the 1850s to 1880s finds carnosine and carnitine in muscle of cattle. So you can think that the first peptides that are found are carnosine and then carnitine — the amino acid that has positive effects on strength training and performance. But that was the whole idea: gut peptides might have gut effects, muscle peptides might have muscle effects.

BPC-157 Animal Studies and Mechanisms

Andrew Huberman: So this Croatian group isolates this 15 amino acid kind of mini segment of BPC. They and others start injecting it into mice, inducing injuries to nerve, to tendon. Maybe describe a few of those effects. I'm familiar with that literature, but I can tell that you are far more familiar with it. What are some of the impressive effects that they observed that led to where we are today?

Dr Abud Bakri: So they did all kinds of horrible things to these mice. They would sever tendons and then give them BPC through oral or intraperitoneal administrations and they'd have faster healing times. They would sever the ACL of the mice. They would do burn wounds. So when a patient has a burn wound in the ICU, they end up having crazy gastric ulcers — but if they were able to put BPC on topically for the mouse, they would have no gastric ulcers. They name it as this anti-stress compound. Now, when they do that Achilles paper on the mice, that's what explodes the bodybuilder interest and leads us to today where we are — like, oh, musculoskeletal injuries must be BPC, tendons and muscle injuries. But the original idea of BPC was to use it as a gastric treatment, not to use it as a musculoskeletal one.

Andrew Huberman: What is so striking to me about BPC — and by the way, that's not an endorsement for BPC — is that my lab worked for a long time on optic nerve repair and neural regeneration. Nerves don't like to regenerate in the central nervous system. Peripheral nervous system, they do it slowly, but they do it. Not in the central nervous system. Ask anyone who's had a stroke or an optic nerve injury. There are data that I've seen with my own eyes that show that you can accelerate healing of tendon, of ligament, of nerve pathways — in animals. Thank you. And that it just generally promotes repair. That's kind of weird, right? Because I could spend the next 10 hours or more telling you about all the ways that people have tried to get nerves to regenerate and couldn't. And as you point out, this thing doesn't really have one specific, at least known, receptor. So the data on the gut make a lot of sense — this is after all a gut peptide. But what is it doing mechanistically, if we know, to support regeneration or replenishment of all these different tissue types? Because a neuron is a very different cell type than a fibroblast or one of the bits of collagen that make up different connective tissues.

Dr Abud Bakri: It's modulating a lot of these growth and healing pathways. In the models of damaging the endothelial layer or the epithelial layer of different tissues, you'll get more VEGF signaling — that's the vascular endothelial growth factor. So you get more blood vessels and angiogenesis being formed, which creates a lot of the controversy around BPC safety. You'll get cell migration, especially when coupled with TB-500 and TB-4. You'll get more access of the healing factors to the area through androgenic pathways. On top of that, you'll get an anti-stress effect. The other big thing they did was give corticosteroids with BPC-157 to these mice. And usually when you have a wound and you give corticosteroids, the corticosteroids will slow or even stop the wound healing from happening. When BPC was administered, the healing was either the same or even better.

Andrew Huberman: Is BPC considered anti-inflammatory? Because based on what you just said, it almost seems like it helps maintain some of the pro-inflammatory response. Some people might be thinking, why would you want inflammation? What Dr. Bakri just said is if you block inflammation with corticosteroids, you aren't going to call in the signals to repair tissues. So lowering inflammation is a dicey thing. But is it thought that BPC is lowering inflammation, or is it somehow hitting the gas pedal on all these regenerative, restorative biological processes?

Dr Abud Bakri: It's more putting the gas pedal on these processes to bring in the immune system, the healing factors. For example, in one tendon model, they noticed that it increased the amount of growth hormone receptors on the tendon. So theoretically, this would allow more growth hormone to dock in and cause the outgrowth and regrowth of the tendon. Downstream, it'll modulate nitric oxide synthesis. So that's a big thing when it comes to wound healing because you need to dilate the blood vessels, you need to call in different cells. So it's really changing the way cells behave at that level — but that's only for the tendon side of it. They also did weird things on the neurological side, like they would make these mice drunk, and then give them BPC and they'd get less drunk when they go through mazes.

Andrew Huberman: We did not just recommend you take BPC with alcohol. Want to be very clear. But very interesting.

Dr Abud Bakri: And then also, they would get the mice drunk and then have them withdraw from alcohol. Withdrawal is deadly — if we have a patient in the hospital that withdraws, they could die during that withdrawal if they're not given benzodiazepines. They got BPC and they didn't have the withdrawal symptoms. I think it gets all the hype for the musculoskeletal stuff, but I think the neurological, neuropsychiatric, and gastric effects are way more interesting, because it's modulating the gut-brain axis in an interesting way. We'll have people come to us and they're like, "My Adderall is not working since I've been taking oral BPC."

Andrew Huberman: Are they happy with that effect?

Dr Abud Bakri: No, they're very mad because it seems like it's blunting their Adderall. So it's doing something from dopaminergic signaling on both sides — both withdrawal when it comes to the GABAergic side, but also the peak of signaling. If you peruse Reddit — which you should never do — you'll find all these anhedonia discussions about BPC, people feeling depressed and low energy.

BPC-157 Safety, Legal Status, and the Gray Market

Andrew Huberman: Let's do something that normally I would do in a few minutes. I'm going to ask you some very direct questions about this. Are there any known adverse events from people taking BPC — known and documented, unrelated to contamination or something of that sort?

Dr Abud Bakri: In the literature, when it comes to the animal data, they've injected animals with a thousand times the dose of BPC with no real adverse effects. We don't even know the LD50 of BPC, which makes it hard for it to become FDA approved.

Andrew Huberman: Maybe define LD50.

Dr Abud Bakri: LD50 is the dose at which 50% of the animals would die if it was administered to them. We don't even know what that is. And that's actually an important number — as barbaric as it sounds — to determine for any drug. What's the LD50 for caffeine? What's the LD50 for aspirin? Every drug you take, on or off the counter, prescription or non-prescription, has gone through LD50 testing in animals. To be a clinician and prescribe this, we need to know what that is, which limits us. Now, there were two very small phase one and phase two trials on rectal BPC enemas in the early 2000s from that same Croatian group. That's the big concern with BPC — all the data comes from one group. So people can be skeptical. There are a couple of Chinese groups that have also replicated some of their work. But those groups wanted to try to treat ulcerative colitis. They used enemas of BPC up to like 80 milligrams, which is much more than people would take.

Andrew Huberman: Most people are injecting micrograms — 100 or 200 micrograms per day or something. Maybe more. But you're talking about 80 milligrams.

Dr Abud Bakri: Yeah, rectal enemas. They did a phase one and phase two trial. They did it for a few weeks and then re-measured. It was placebo-controlled. The data is not available — only the abstracts are available. So that also gives us some pause, especially when the legal discussions are happening here in the next few months on BPC. The phase one trial showed no adverse effects. And they didn't even find BPC in the systemic system. That's a key point — orally administered or rectally administered BPC doesn't seem to go systemic.

Andrew Huberman: Maybe define that a little more specifically.

Dr Abud Bakri: If you take aspirin and then you measure blood aspirin levels, you'll notice the levels go up. When they measured BPC-157 levels in these individuals, they didn't find it in the blood. So either it was broken down very quickly, or it stayed locally to the lining of the gastric tissues.

Andrew Huberman: That raises a question for me. Let's say somebody doesn't take any BPC-157 by enema or otherwise. If I were to just draw your blood right now, is there BPC-157 in there?

Dr Abud Bakri: In the bigger BPC protein, yes. But we don't have that data on whether it's circulating or restricted to the gut.

Andrew Huberman: Well, that's incredible, right? Because we're talking about these effects all over the body and we don't even know if it leaves the gut.

Dr Abud Bakri: The injectable is going to go systemic. And most people, if they decide to do this, are going to take an oral or an injectable. They're either going to inject local to the injury if they can, or intraperitoneal. There's actually a paper in 2024 that looked at this — they could figure out if somebody had BPC administered for doping reasons, because it's on the WADA list now. So they could figure out if someone had taken BPC. But we don't know the dynamics. We don't know where it goes, how it goes.

Andrew Huberman: And we don't know the results in terms of what those 80 milligram enemas of BPC did for the colitis.

Dr Abud Bakri: In the phase one trial, it was just a safety trial — there were no adverse effects. In the phase two trial, which was very small, like 40 patients, there was at least a positive signal on the ulcerative colitis.

Andrew Huberman: And this was done in Croatia. So to be quite direct — on the one hand, you have groups who I think are mostly well-intentioned saying, hey, 80 milligrams of BPC by way of enema did not cause any adverse events. On the opposite side, many people — especially in the United States and Northern Europe where the regulations tend to be similar — would say, well, yeah, but that study was in Croatia. Now I have many Croatian friends. That's not a knock on Croatia. Why would it be that clinical trials in Croatia would hold less weight?

Dr Abud Bakri: That's a good question. The groups seem to be very robust and they do really good randomized controlled, double-blind, placebo-controlled trials. I think we're very US-centric. We view ourselves as the premier science, and we are the premier science. So people kind of trust that more. And there may be perverse incentives when it comes to different government bodies — like Soviet-era research that might be pro-fabrication when it comes to certain compounds that makes people hesitant. Because there are a lot of these Soviet-era compounds — not all peptides, some are peptides — that sound fantastic, but when they get tested, maybe they're not as potent as the Soviet data would suggest.

Andrew Huberman: I always thought that the Russian stuff was like the really potent stuff that they didn't want anyone else to know about.

Dr Abud Bakri: It could go both ways. They were more interested in performance — they wanted better astronauts, better Olympians, better soldiers. We care more about a profit drug model that gets people on a monthly subscription, unfortunately.

Andrew Huberman: So nowadays, is BPC-157 legal in the United States? If I wanted to go online and buy BPC-157, I can do it, right?

Dr Abud Bakri: Legally, for research purposes only.

Andrew Huberman: I thought now under the new regulations recently passed that you can get it from a compounding pharmacy.

Dr Abud Bakri: Technically not just yet. And it depends on medical boards. BPC-157 never got FDA approved. So it gets into these compounding pharmacy lists. There's a category one, two, and three. Category one means the FDA thinks, hey, this is not an approved drug, but we're okay with you compounding this. Category two — do not compound. In late 2024, BPC-157 and about 20 other peptides got moved to this category two list. Since about 2017 to 2024, people had been prescribing BPC in these alternative medicine and anti-aging practices. It gets removed from that list. Of course, compounding pharmacies then relabel it as PDA — pentadecapeptide arginate — but it's the same thing.

Andrew Huberman: Really?

Dr Abud Bakri: Yes. One of them will be an acetate, one of them will be an arginate, but the PDA is BPC-157. Because there are many many people selling compounded pentadecapeptide. I think the acetate one is the one that's on the category two list. Now, just in April of this year, it got removed from the category two list and it's not yet on the category one list, which would allow physicians to prescribe it through compounding pharmacies. But they can prescribe the PDA version. Now, state medical boards view that very differently. I got a letter from one of the states I'm licensed in — one of these states reached out and said, you cannot prescribe non-FDA approved peptides no matter what.

Andrew Huberman: So there's controversy there. Even if the FDA says okay, we're okay with you prescribing it — is your medical board in that state going to be okay with it? So it's state by state. What about with telehealth? So somebody's on the east coast in a state that allows them to write a script for, let's just call it BPC — can they send that to California or Wisconsin or someplace else if the patient is there?

Dr Abud Bakri: The telehealth laws go into effect where the patient is. So if in California it's not allowed to have BPC according to the state board of pharmacy — even if you're a New York doctor licensed in California, that would be against the California Medical Board, and they would ask you to stand in front of them if they found out. Now, are boards cracking down on this? Not really. There are a couple of states that are cracking down on people and people know to avoid those states, but it's going to be very dicey over the next few years.

Anecdotal Reports and Clinical Observations

Andrew Huberman: Anecdata. We don't want to place too much on it, but the big kind of rumor out there that pricked up my ears a few years ago was when I heard that some athlete before the summer Olympics — this was two summer Olympics ago — from Eastern Europe, had a complete Achilles transection. Not just a tear or a pull, but a complete cut the whole way through. And the rumor was they took BPC-157, locally injected, for a few months and they podiumed in the Olympics. They still got a medal. Familiar with that story?

Dr Abud Bakri: Yes. I think that story was hearsay. I don't think they wanted to reveal what they actually did. I don't think they only did BPC-157. They'd be stupid if they did. They should have had all the best and latest greatest treatments — whether exosomes, stem cells, other peptides, anything that wasn't banned. And by the way, BPC-157 was not on the banned substances list at that time. It was so unknown. Just like there are compounds right now that athletes are using — not just in the Enhanced Games, but in preparation for the Olympics. It's a common practice that athletes will forage into things that can help them that are not yet on the banned substances list.

Andrew Huberman: And good luck proving that BPC was injected a week ago, because by the time the peptide's already gone out of your system — or at least we think, based on the pharmacokinetics we understand now. What's your favorite personal BPC story involving you and your body?

Dr Abud Bakri: I tore my tricep a few months ago. Tore it lifting with people I should not have been lifting with — they're much stronger than I was. Purple from here to here. I'm like, I'm going to have to have surgery. This sucks. I don't have time for surgery because you're in a brace for like three months. And I put BPC in locally — don't try this at home, not medical advice — locally in the tissue spot with a couple of other peptides. And within three weeks, my PT is like, "What the hell are you doing? This is healing so fast." Would I have healed that fast anyway? I don't know. But that's typically a grade two tricep tear with a purple arm from top to bottom. It wasn't grade three because I could still extend my elbow. That's usually a three-month recovery. And to be back in three to four weeks was fantastic for me, which is why I'm so excited.

Andrew Huberman: What dosage were you injecting?

Dr Abud Bakri: A larger dose than people would typically use. Not micrograms — up in the milligrams. A lot higher. I think personally, and in some of our patients, we've used bigger dosages. I think that's the problem. The low dosages, even though they translate well from the mice data, for humans I think the dose is way higher. But people just go based on the dosage that would fit in the vial through a peptide sciences website rather than what we actually know — and we don't know what the human dose is for BPC-157. So there's a lot of work to do just to figure that out.

Andrew Huberman: I can't match your story. I can just say that I had a bad trap-neck pull where I couldn't turn my head. I had some BPC — only about 200 micrograms — and just injected it right into the upper trap area. Two days later, completely gone. Of course I don't know what would have happened had I just waited, but it seemed eerily fast. And then I stopped taking it. So this is a guy that you know. And by the way, that was not gray market — it was obtained through a doctor's prescription from a compounding pharmacy, labeled BPC-157, not PDA. Those are anecdotes. I've also read, just to be fair — certainly on X, people can say anything they want — people saying they didn't feel well and stopped taking it. Could be due to what it was dissolved in, could be due to their own unique response, could be due to bad sourcing, contamination. Not everyone has a great result, and some people have no result. But many many people report what can only be described as pretty astonishing positive results that cannot be directly ascribed to the BPC because of the placebo effect.

Dr Abud Bakri: There are two possibilities. Either BPC is as amazing as we think it is and it's unfortunate that millions of people don't have access to it — or BPC is actually either ineffective or harmful to people and millions of people are injecting it right now by buying it through online sources. Both cases are very bad endpoints. One's worse than the other. You can argue which one, but that's why we need this data. We need people to push this forward to figure this out. Because if in 20 years we find out BPC is as good as the science suggests, then man, people are pissed off — all the joint replacements and injuries that didn't heal, all the athletes that maybe could have had a longer career. That would be very unfortunate. But if it's the opposite, and every 18-year-old kid in the gym is injecting BPC — where do you get it from? I'm like, dude, you're 18. You have all the peptides you need in you.

The GLP-1 Market, Compounding Pharmacies, and Supply Chain

Andrew Huberman: Let me ask about the supply chain. Standard pharma — we know it goes through the most stringent process. The stuff that you get that's non-generic from Novo Nordisk, from Eli Lilly — you can be certain based on the product packaging that it's as clean as it gets, as pure as it gets. Compounding pharmacies are a mix. Do we know that gray-market peptides had problems? Because there are people out there — Robert Breedlove, who's best known for his work in crypto but is also very open about the fact that he's taken all these peptides and anabolics — I heard him online saying he's tested the gray-market research-purposes-only peptides and compared them to the compounding pharmacy versions and they're identical. Now he's not a physician and I don't think he's lying, but many people are taking that sort of evidence and saying, oh, I'll just get it from gray-market sources. As a physician, what is your stance on this?

Dr Abud Bakri: The API — the active pharmaceutical ingredients — for all these compounds comes from China. There are no such thing as American-made peptides. It gets finished here. The synthesized semaglutide gets made in China. It would be very expensive to make it here. There are people starting to look at that because that's the next thing in the arms race — to make American peptides. But everything's Chinese peptides. China is the best at doing it. Now, the compounding pharmacies vary in grading. Some of them are really good. They do all the testing, sterility, they have very good quality control. So you get a good product. But they usually have to compound it with something else to get by the regulations — like they'll add in a B12 or a B6 to say the patient had nausea from the traditional semaglutide, and we can compound them with B12 or B6 to get around the nausea. That meets the patient rule, because there are two ways to get compounded medications: either a shortage, or there's a unique need that the patient has.

Andrew Huberman: Do we know that compounding with something else actually deals with the nausea?

Dr Abud Bakri: It might help some people. Anecdotally, people will say that they respond better to the pharma pens than to the compounded stuff. The research stuff is all over the place. Like some of it could be better than compounded stuff. It could be the wrong substance. There's a guy who went viral on Twitter a few weeks ago — he got retatrutide and started getting darker. He's like, I don't think I'm injecting retatrutide.

Andrew Huberman: He was injecting melanotan 2.

Dr Abud Bakri: Yes. So all of the raw materials are coming from the same source. Then they're getting filtered into these different stringency bins. Standard pharma being the most stringent. Some are going into compounding pharmacies — and compounding pharmacies have varying levels of stringency. Some are going to be excellent, some are good, some are going to be lousy. The gray-market peptides, the ones where it's for research purposes only — those presumably also come in anywhere from excellent to dreadful. And we don't know which are which. Batch to batch — that's the big problem.

Andrew Huberman: So it is risky to get research-purposes-only peptides. That's the majority of the way people are consuming peptides. Unfortunately, the move in 2024 to get these from the category one to the category two list and make them banned opened up this gray-market zone. The gray market existed for the last 15, 20 years. Bodybuilders would have anecdotes about BPC-157, they'd inject it post-squats for different injuries. Nobody really cared about it. It was with the GLP-1s and then the banning of the peptides, plus this anti-medicine kick that's been happening over the last five years since the pandemic, that people are like, you know what, I want to inject this because it gives them a sense of autonomy, or they feel like their bro recommended it. The best job in 2025 was to be a peptide affiliate. People made my yearly salary in a month selling peptides illegally on TikTok.

Andrew Huberman: And I will say — because for people that think it's just bro science — it's also gal science. My understanding, and not from Reddit, is that more than half of the peptide market is female.

Dr Abud Bakri: Oh, that's right. Especially when we start getting into things like GHK-copper and talking about things for collagen and skin rejuvenation. There's a big peptide market towards women. I actually think in the long run it's going to exceed, at least financially, the peptide market in men. I think it already has, because soccer moms have become affiliates — like Amway and Herbalife was the big thing 20 years ago. Now soccer moms just do peptide affiliation.

Andrew Huberman: Where are they getting their peptides?

Dr Abud Bakri: Research-grade websites. The gray market. Black market is like if you bought it directly from China — it's very cheap. A vial of BPC costs five bucks to make. Someone will sell it to you for $1.99 depending on where. But black market is either your friend in China on WhatsApp sent you a vial of BPC — do not do this — or someone claims they synthesized it in their bathtub. Just like the underground gear, all the steroids that were in the '90s and the 2000s. Who knows what that is.

The Compounding Pharmacy Financial Model

Andrew Huberman: What's so interesting to me is with steroids, it went from the bodybuilding community to eventually hormone replacement. TRT became a thing. HRT has become very popular in women. Peptides is different because the big explosion came through the GLP-1s. And I would argue — I'd love your opinion on this — why so many people are now peptide-curious is because of the GLP-1s. People are now very comfortable injecting themselves. Like five years ago, if you said you're going to inject yourself, people would go, oh my god. Then they realize it's this little tiny pin. It hurts less than a mosquito bite. And somebody's girlfriend or wife is doing it as if it's nothing.

Dr Abud Bakri: That changed everything. That destigmatized it.

Andrew Huberman: To be fair, I want to touch on the question about adverse events. The concern I've always had was the angiogenesis — the growth of vasculature. If somebody happens to have a little tumor or what will eventually become a tumor sitting on their liver or in their gut or in their pancreas, in theory, it could vascularize that tumor and cause it to grow more quickly. Is there any evidence that that's actually happened?

Dr Abud Bakri: No. For example, most compounds, if they're carcinogenic, we will see that signature in the animals. Like cardarine GW — it was a drug that was very promising because it had diabetic implications for metabolism, and now it's a bodybuilder drug that they use for cardio. It had a signal of cancer in animal data. So that whole thing was scrapped. There's no signal from the animal literature on BPC-157 for cancers. Now, all that literature comes from one group. So we have to be very careful — that one Croatian group tells you it's the safest thing in the world. Almost all of the animal data come from one group. Very few others. Like there are a couple of Chinese studies on BPC-157. Now there's starting to become more interest here. I think there's a phase two trial on hamstrings happening in the United States.

Andrew Huberman: Really? Humans. Phase two.

Dr Abud Bakri: Yes. We talked to a group, an orthopedic group somewhere on the East Coast. They wanted to do a BPC trial. So we consulted with them. It's going to happen. Especially if it moves to the category one list and people can be prescribed it — at least we can get a phase four trial where it's being prescribed and we can see what's happening to the people as they're getting it, and aggregate all this anecdata into one place ideally and report on it.

Andrew Huberman: Is that something you're personally working on — aggregating all this data together into a nested study to put it all together? Because all the anecdata exists, but put it together somewhere so at least we can see what the signals are. For example, on Reddit, you'll find signals of hematomas getting worse, which makes sense with the VEGF pathway.

Dr Abud Bakri: I've heard this. A friend and physician who is peptide-curious and positive told me that when he takes BPC-157 for a shoulder or knee or whatever, angiomas on his face — the sort of spiderweb angiomas — get worse. That's his personal observation. It makes sense if it's promoting angiogenesis based on the mechanism. Now, BPC-157 is not a uniform angiogenesis upregulator. In some models it decreases VEGF — in a melanoma model, a cell line. So it might be potentially anti-cancer, but we need to test it. We don't know, which is what's really unfortunate about this compound. It's very promising. It has all this cool literature in animals and we just don't know when it comes to humans. And we'd love to know, because if it does work, I could see a million use cases in the ICU. In the ICU, people get gastric ulcers. If we knew that it would work, I would love to give them an infusion of BPC-157 to really help people out, especially during critical illness. But we need data.

Designing Clinical Trials for BPC-157

Andrew Huberman: When is there going to be a formal randomized control trial on BPC and who holds the patent?

Dr Abud Bakri: There are multiple patents on BPC-157 depending on which salt they're in. The patent has been passed around a couple of times. Unfortunately, the company that had the patent got acquired by Teva. Teva is this generic pharmaceutical company and they make, you know, Adderall. So they're making tons of money making Adderall. They don't really care about BPC-157. The other patent expires in like 10 years. I think the Croatian group still has it. Dr. Sikiric is the guy behind BPC-157. He's in Croatia.

Andrew Huberman: Would Teva sell the patent?

Dr Abud Bakri: I'm sure they would if someone made an offer. The problem is I don't see the purpose of even having the patent because you can add on one chain to the amino acid. This is the problem with peptides. You can add on one amino acid, you can modify one thing on it, and suddenly it's a different compound.

Andrew Huberman: This is true for other pharmaceuticals. I'm familiar with some of the ketamine and ibogaine trials — there's a company that took ibogaine and basically added a magnesium component to it and you can make that a completely new drug. So this game of protecting patents is rough. Plus millions of people have already used BPC-157 through research-use-only websites. So how do you reel that back? The cat's out of the bag. There's no financial incentive to run the giant study unless we crowdfund it as peptide-curious people.

Andrew Huberman: Within the category of interesting anecdotal data — and in your role as a physician — what do you think are the most interesting potentially valid claims? If we were going to fund a clinical trial, we need to pick an endpoint or a couple of endpoints. Is it going to be recovery from injury? If so, what kinds? Is it going to be the gastric stuff? Is it mood interaction with dopamine receptors? If we had a chunk of money and we're going to design a study and have someone else do it so it's truly independent — what are the top three to five outcomes that you've heard that you have a good feeling there's something there?

Dr Abud Bakri: I would say to complete the phase one and phase two on the ulcerative colitis — do that phase three trial proving that it has benefits for ulcerative colitis. And I don't think we need to use enema. We could probably have an encapsulated version that releases deeper into the intestines. In conjunction with that, you could do a trial on GERD. That's a simple condition. A lot of people have it — randomized to BPC-157 oral capsules versus pantoprazole.

Andrew Huberman: And you're basing this on the fact that you've seen and heard that people who have GERD get better when they take it.

Dr Abud Bakri: Anecdotally, when I travel, I have a bottle of BPC orally. I don't get travelers' diarrhea or, you know, when I eat exotic foods in random places. My friends all get sick and I happen not to. Anecdote, right? But that's interesting. There seems to be some kind of gut protective effect. And that's what they noticed in the mice literature — they would have an offending agent into the gut and they'd notice that there would be protection deeper down in the gastric tract from that offending agent. Because if you think about it, the gut is the most vulnerable part of the body. It's open to the outside world. It's a tube that runs through you. You can eat something and it could completely destroy you. So you have to have some kind of mechanisms — the prostaglandins, all these different hormones that are made. Potentially BPC-157 is part of this robust armory that the gut has to protect itself from further injuries.

Andrew Huberman: What are some things outside the gut or indirect from the gut that are also compelling?

Dr Abud Bakri: I would love to see some neuropsychiatric BPC studies when it comes to addictions. There's enough anecdote about people talking about addictions and like, hey, I don't need to crave insert drug here. Not recommending that anyone tries that out. But for alcohol or whatever it may be. Do you think that is likely due to interference with the reinforcing properties — just like earlier you said people are getting less drunk, so people are getting less high, it becomes less reinforcing — or is it somehow touching the craving mechanisms themselves?

It's probably touching the craving mechanism through the gut-brain axis, because I don't think it's going systemic either. I think it's locally in the gut shutting down the neurons. If BPC is what they claim it is — and that's a big if — if you have a noxious agent going into your gut, your body has to have a mechanism to lock down and protect your vital organs. So is BPC part of this giant transduction pathway to protect your vital organs — your brain, your heart, your kidneys — from further damage? We had Dr. Diego Bohórquez, who's out at Duke, who's really the world expert on these neuropod cells in the gut that signal through the nodose ganglion up the vagus to either promote or suppress release of dopamine to make you either approach or avoid certain foods. Very, very interesting. I would be more than happy to encourage his lab to do something on this.

Andrew Huberman: What are some other categories of interesting effects that deserve careful study?

Dr Abud Bakri: We need to see what BPC does on the musculoskeletal system. That's what the hype is. As I look through what model I would look for, you want something that's not very vascularized but could be improved if the blood flow was good — like a tendon injury. So perhaps a bicep or tricep tendon type of post-surgical outcome. Like you get your bicep tendon torn, you get a repair, you get BPC either intraoperatively or postoperatively, and you see if that person heals faster. The idea is not that BPC is going to magically reattach an ACL that's torn. But can it further accelerate the healing from an ACL surgery so you come back in six months rather than twelve months? That's the big question, and that's what a lot of athletes are using BPC-157 for.

Andrew Huberman: Has anyone ever done the one-limb versus opposite-limb control experiment? I mean, I know that people take it orally or inject it systemically — if you apply it that way, it goes systemically in the bloodstream. If you can get to the injury site, sometimes people will inject locally. But it seems that the challenge is that if you have tendonitis in one elbow and tendonitis in the other elbow, you could inject into your left elbow and not your right, but there's going to be systemic transfer. So it's hard to do that internal control experiment.

Dr Abud Bakri: Yeah, I know. I've used BPC for one injury and I've had results on a different injury. Positive results. I had positive results. I'm like, oh, interesting — my shoulder feels better even though I was doing it for my elbow or whatever it may be.

Pinealon (EDR) — Origins, Mechanisms, and Effects

Andrew Huberman: Let's talk about pinealon.

Dr Abud Bakri: Pinealon is a tripeptide — EDR — discovered by Dr. Vladimir Khavinson. He's a Soviet researcher that comes out of this Soviet-era research to make soldiers, astronauts, and pilots better. There was concern that the US might be using lasers to shoot at soldiers. So the Soviet Union tasks him with identifying peptides to defend soldiers' eyes, and then their aging — because what would happen is they'd be in a submarine for a few months, a nuclear sub, and they'd come back to shore and they'd look 10, 20 years older. The same thing happens to astronauts.

So Khavinson is looking at this and thinking, there's got to be a solution. There's been literature about using extracts of other tissues — notably the pineal gland and the thymus — from the late 1800s till this 1970s point where we're starting our story. And he starts grinding up these extracts and injecting them into these people and undoing a lot of this aging effects through pineal extracts and thymus extracts. Because what did these soldiers have? They had very bad circadian rhythmicity. They couldn't sleep properly. They had terrible immunity. They'd get sick often. They'd have autoimmune problems. All these conditions that come with it. And then they were able to undo this using these organ extracts. So Khavinson takes it a step further. He looks at what's causing this effect in these tissues. He finds peptides in these extracts. He's like, I wonder if these effects are from the peptides, not from the gland itself. So then he sequences from the pineal gland epithalon, and from the thymus gland a couple of different peptides — vilon, thyogen, crystagen — that you'll be hearing about in the next few years, that on their own do a lot of the effects that the whole extract would do.

Andrew Huberman: Now you're talking about epithalon, but pinealon is not from the pineal gland — even though everyone assumes it is.

Dr Abud Bakri: No. As far as I understand, it's called that because there are animal data suggesting that pinealon can help either regenerate or enhance the general functioning of pinealocytes. So it's having an effect on the pineal when you take cultured pineal glands — you put it in a dish, dissociate the cells, give it pinealon, and it seems to improve the timing and perhaps even the amount of melatonin output from the pineal. Epithalon does that. I don't know why he named them the way he named them. But epithalon is from the pineal gland. Pinealon comes from a ground-up brain extract called cortexin — and the brain has a pineal in it, but it was the cortex specifically, not the subcortical regions.

So Khavinson identifies — he makes a drug in Russia called epitalamine, which is the pineal gland extract, and it had great effect on circadian rhythmicity. It's rich with melatonin — basically giving people melatonin, but also upregulating the enzyme that creates melatonin from serotonin to acetyl-serotonin to melatonin. So when he gave it to young monkeys, the monkeys had no effect, but he gave it to aged monkeys that have decreased melatonin — and from puberty onwards your melatonin levels dramatically decrease — he was able to restore melatonin production in these aged animals and eventually replicated it on humans.

Andrew Huberman: So pinealon comes from the cortex, not the pineal. That's annoying. Maybe we just rename it today. We'll call it EDR — that's the three amino acid sequence. What are some of the known effects? Or am I just imagining this REM increase? Because I can't change what's happening to me during sleep. That would be an amazing placebo effect. And the reason I say amazing is there are many things that one can do to improve the amount of slow-wave deep sleep. Very hard to increase REM — except by heating your sleep environment in the last third of your night, and maybe some alpha-GPC in the late day can bump it up a bit. Or you can REM-deprive yourself. Or you can smoke cannabis for 10 years, then quit, and then you'll get a lot of REM because you got no REM for 10 years. Do not recommend that protocol. But for me it was just striking. So why would EDR — a tripeptide with no receptor — have this effect on REM sleep?

Dr Abud Bakri: I actually searched through all of the literature from Khavinson. He never mentions REM sleep once in his studies. He studied pinealon quite extensively on different neuronal tissue extracts, animal studies, even in athletes, and never mentions REM sleep. They didn't have Whoop in the 1970s in the Soviet Union. They didn't have an Eight Sleep. So there were no reports on that. But what seems to be happening — EDR is a tripeptide that meets the groove of the DNA of different key regions and helps the promoter region be exposed, so that DNA transcription can happen. So you get it turning on genetic programs. It's acting a little bit like a transcription factor, or maybe assisting transcription factors in accessing the DNA in the right places. So pinealon in one sentence — it's leading to better brain metabolism through modulating all these different pathways. For example, GDF11, SOD1, SOD2, irisin, PPARα, PPARγ. What seems to be happening is he made pinealon as an anti-stress cognitive performance compound. And it was available orally in Kazakhstan.

Andrew Huberman: So if I'm taking it before sleep, I should be taking it in the morning?

Dr Abud Bakri: Yes. If you take a high enough dose there is sedation from it, but if you take it in the morning or pre-workout you get quite an interesting effect. He studied this compound on athletes — he would have them do their training session, go to exhaustion, and then do a test afterwards. There are two groups, pinealon and placebo. The pinealon group could keep their performance up despite being maximally exhausted from their training.

Andrew Huberman: I feel like such a dummy. Here I am having elaborate dreams I don't really remember or care about when I could be actually thinking better during the daytime.

Dr Abud Bakri: Yeah. A lot of people report less brain fog, better thinking. A friend that has a nine-figure company has all of his employees on pinealon. They're taking it in the morning.

Andrew Huberman: Do you know the dosages? Not that we're recommending it.

Dr Abud Bakri: Orally, people will take anywhere between half a milligram up to three milligrams is where people settle in. The Khavinson ones that come from Russia are like 200 micrograms. Some people are injecting it. It goes systemic. It's orally available through these dipeptide transporters. It most likely crosses the blood-brain barrier — it's a tripeptide, small enough.

Andrew Huberman: Have you tried it?

Dr Abud Bakri: I mean, I took some last night. So I will take larger dosages if I want to get good sleep. I'll describe it as 8K. Some people it will cause them to have a little bit of awakening at first. That may be why your deep sleep was going away.

Andrew Huberman: If I take half of what was recommended, I'm great. But I'm very sensitive to everything. If I take what was recommended, I fall very deeply asleep, I have elaborate dreams, and I wake up. I couldn't tell if that was a disruption in sleep architecture. I just found that I'm only doing this three times per month maximum. And I often forget, and then I go months and months, and then I was like, oh, maybe I'll take a little pinealon. Whoa, this is wild. And then I'd stop taking it because I don't know enough about it. Now I know it's cleanly sourced because I trust the compounding pharmacy it's coming from. But I should ask — are there any known risks of EDR?

Dr Abud Bakri: So far, nothing in the Russian literature. Big caveat — it's Russian literature. It's not gold-standard American research. Nothing has come up as a clear sign. The big theory of Khavinson is that when you're younger, you make a lot of these peptides naturally — these di-, tri-, and tetrapeptides — and as you age they go down in function and quantity. By replenishing these peptides you're restoring some aspect of youthfulness. Something similar happens in America with GHK-copper, which is another tripeptide — that's technically the collagen regulator, and EDR is the brain regulator. But so far the side effects we've noticed — we probably have the biggest anecdotal compilation of N-equals-1 data. Every day I wake up someone texts me about what pinealon did to them. Some will have a little drop in blood sugar because it activates PPARα and PPARγ. So it'll have positive metabolic effects. Some people have even had their A1C's drop. So hypoglycemics and other people with blood sugar issues should take extra caution. And then very vivid dreams for some people — that could be disheartening if they have nightmares or something like that. But very vivid dreams as a result of pinealon, especially the color and quality of the dreams is very different than you'd normally expect.

What seems to be happening is — just like psychedelics change the redox state of the brain — pinealon is doing something similar where you're getting more alertness during the day, less brain fog at least anecdotally, better performance during high-intensity interval training, and then more REM sleep at night. Because the neurons are in a better oxidative state thanks to the PPARα, PPARγ, irisin, and all these different pathways that it's modulating — with no clear single receptor that it's doing it through.

Epithalon and the Pineal Gland

Andrew Huberman: What about epithalon, which turns out comes from the pineal? I'd love your thoughts on this. I've heard — and I thought it was complete nonsense when I first heard it — that the pineal becomes calcified as people age. The reason I thought it was nonsense is I used to co-teach neuroanatomy when I was at UCSD before moving my lab to Stanford with a guy named Harvey Karten. Unfortunately, he passed away. He was in his late 80s and had this incredible career as one of the greatest neuroanatomists of the last hundred years. I asked him about this calcification thing because he had looked at the brains of so many different species including humans. He was also an MD, and he goes, "Yeah, I don't know whether or not this calcification thing is real." He kind of brushed it aside and I thought, well, Harvey doesn't take it seriously so I'm not going to take it seriously. But even though he was absolutely right about many many things, I think he might have missed that one. When I go to the literature now, it's a little bit tough because the cadavers that you looked at in medical school are not all processed on the same timeline. Does our pineal calcify and even if it does, does that somehow inhibit its ability to communicate with our other tissues?

Dr Abud Bakri: It's a big, debatable thing in pineal research. If you look at the pineal gland Wikipedia, it's very underdeveloped because it's kind of woo-woo. When you think of pineal gland, you think of someone who's going to sell you crystals or something. It's not a very sexy research area. But I think it's a key aspect of aging and longevity. The pineal gland — it seems from Khavinson's work that the decrease in pineal gland function with aging is more of a physiologic than an anatomic problem. Now I will see some calcification on MRI when we have a patient come in for a stroke or TBI. But the question is what is actually leading to the deterioration of melatonin synthesis, because it decreases quite dramatically. Some people even think that might start puberty — like if you have a pineal cyst you can have precocious puberty at eight or nine years old. The rhythmicity in melatonin — a very young baby's melatonin secretion is not very rhythmic, but they're in REM a lot. With time it becomes more rhythmic. And of course in today's day and age with all the artificial lighting and the lack of sunlight exposure, people are making themselves somewhat arrhythmic or phase-shifted.

Andrew Huberman: But epithalon is somehow restoring pinealocytes, somehow enhancing function of the pineal and other tissues.

Dr Abud Bakri: Yes. In Khavinson's work, he's found that it will increase the expression of the different clock genes. In lymphocytes that he'll measure in peripheral tissues, he'll notice that the clock genes actually change to a more rhythmic pattern. He'll notice that morning cortisol is higher — which, by the way, you want your morning cortisol super high. You want your evening and nighttime cortisol low. So it was restoring a more circadian-appropriate hormonal profile through the HPA cortisol axis.

Andrew Huberman: Taken when?

Dr Abud Bakri: Anytime. Because the idea with these bioregulators — unlike a GLP-1 drug that you take today and have the effect for the next week — the idea from the Khavinson model is that you take these and then you accrue benefits when you're off of them. You noticed with pinealon you took it for a day or two or three days a month and you had effects until you took the next dose. So the idea is: can you accrue benefits from these compounds as they upregulate or downregulate certain genetic pathways in a more favorable state, and then keep those effects later on?

So in Khavinson's seminal work was this 15-year longevity study. He got people in nursing homes — two groups. One of them got epithalon in the form of epitalamine, which is the whole pineal gland extract, and then a thymus peptide called thymalin. Not thymulin — there are two different peptides, a lot of people confuse them. Every peptide website confuses them. But he injected them for 15 years — a 10 or 20-day course per year, just beginning of the year, middle of the year, and that's it. And they had significantly lower mortality when it came to cardiovascular disease, infectious risk, and cancers. Russian study, caveat, but that would be the most interesting longevity study I've seen done if accurate, if true — because he was able to take nursing home patients, give them peptides for a very small amount of the year, and yet they accrued benefits the rest of the year.

Andrew Huberman: One of the things that really got me excited about epithalon is some interesting papers — and I can really gauge the data even though they're in mice — using epithalon to combat some of the neurodegeneration in things like retinitis pigmentosa, downstream neurodegeneration in RP, which is a very common unfortunately blinding disease, or even in glaucoma. I should mention that BPC-157, to my knowledge, hasn't been looked at extensively in terms of optic nerve repair, but it absolutely should be. So I was intrigued. There's this molecule that's somehow involved in DNA repair, and it's either maintaining or restoring some of the machinery that would otherwise definitely be lost in one of these optic nerve damage conditions that models things like glaucoma, retinitis pigmentosa, stroke, traumatic head injury. It's a big deal. Vision and movement are kind of the biggies. So the reason it's so interesting to me is that it's getting to DNA repair as opposed to these downstream, working on any number of vague receptorish — maybe no receptor — things. And this is what gene therapy is about. Do you think of epithalon as kind of a gene therapy of sorts, or do you think about it more as support for genetic machinery that has lots of downstream targets?

Dr Abud Bakri: I think it supports this genetic machinery. When it comes to the eyes, it seems to be repairing some of the photoreceptors that might get damaged in retinitis pigmentosa. Melanopsin wasn't discovered when Khavinson was working on this. But my theory is that epithalon is working on melanopsin — that it may be upregulating melanopsin levels and then making that morning sunlight more effective. Because the big problem is a lot of people will tell me, "Doc, I did morning sunlight and I didn't feel the effects." I'm like, have you had enough darkness to regenerate melanopsin levels? Because we know that in animal studies, five days of pure darkness dramatically increases the amount of melanopsin in the retina.

The Thymus Gland — Aging, Immunity, and Thymic Peptides

Andrew Huberman: I want to talk about the thymus because it's fascinating and you are truly versed in this. But before we do that — tell me about the thymus. Super interesting organ.

Dr Abud Bakri: We all have one when we're born. The thymus is grown under the influence of a lot of these youthful hormones — melatonin, growth hormone, DHEA — and then is shrunk at the moment you hit puberty. So from the day of birth until puberty, you grow this massive thymus. It's right above your heart, right behind the collarbone. In a baby, it could be quite large on the chest — as big as a baseball. Right now in our bodies, it's going to be a bunch of fat with a couple of different globules of thymic residue. Very tiny. In fact, most surgeons will just remove it when they do surgery nowadays for like open heart. But there's good data from the New England Journal of Medicine that removing the thymus tissue, residue tissue, leads to a mortality signal within the first five years after those surgeries.

Andrew Huberman: So people have died because of thymus removal.

Dr Abud Bakri: They'll have either higher rates of cancers or higher rates of autoimmune diseases if they have their thymuses removed. Now there are thymomas where people have to have their thymus removed, but we're talking about people where the surgeon is going in to do a coronary artery bypass surgery.

Andrew Huberman: Is the thymus neurally innervated?

Dr Abud Bakri: Yes. Vagus nerve. So it's getting signals from the brain — there's sympathetic and parasympathetic innervations for the thymus that dictate its hormonal output. Because the thymus — what is the thymus? It's a gland that both secretes hormones and develops the T-cells. Your lymphatic cells are found in your bone marrow — that's where they're made. The T-cells will travel up to the thymus and get trained so they don't kill you and they don't attack your own tissue, but attack a foreign invader or a cancer or whatever it may be. That process is very good in youth, and as you age you get more autoimmunity, more cancers, et cetera, because the immune system is not as robust — both because the thymus makes less of the hormones that train the immune cells, and makes less of these immune cells themselves. So when you're 15, you're making 10 to the eighth magnitude of these cells every single day. They're called naive T-cells. They will eventually become your CD4 and CD8 T-cells. As you age, this number dramatically decreases. And those cells will live somewhere between 10 and 15 years. That can kind of gauge when the mortality window kicks in for a lot of these different disorders. When your thymus reaches a minimum level of output, you get a lot of these disorders — cancers, heart disease, autoimmunity. If you put almost any disease and look at the thymus risk associated with it, it increases as thymus function decreases. There's a Nature paper from 2026 that just came out that looked at cardiovascular disease and cancer mortality and all these different metrics — they did MRIs of people and the people that had the higher thymic scores had less mortality across every single one of these conditions.

Andrew Huberman: What's surprising about that very interesting result is that you said that by the time you're in your 30s or 50s, you've got just a bit of residual tissue there. It's just a few cells, and yet it's somehow maintaining function.

Dr Abud Bakri: The rate of decrease varies dramatically from person to person. So we call this thymic involution. From the moment puberty starts till you die, your thymus is slowly shrinking. That really happens in your 20s and 30s — the majority of that under the pressure of androgens, estrogens, progestins, and corticosteroids. Those are driving a lot of the shrinkage.

Andrew Huberman: So the hormones that everyone seems to want to increase the rest of their life, and that become very active during puberty, actually cause thymic involution.

Dr Abud Bakri: Yes. So castration will undo some of the thymic involution. Pregnancy is a great time to involute your thymus, which makes sense because you don't want to be having an autoimmune attack against the baby. Women's thymuses involute and then will regrow during the breastfeeding period under the influences of growth hormone and prolactin. Hibernating animals will have a dramatic shrinkage of the thymus during hibernation and then a regrowth during the feeding window.

Andrew Huberman: Is there any benefit to doing or taking something to either maintain or regenerate thymic size?

Dr Abud Bakri: There's an interesting study — the TRIIM trial from Dr. Greg Fahy. He's doing a study where he's giving a cocktail of growth hormone, metformin, and DHEA. He gave that for 12 months and had the thymic size increase on imaging. The amount of CD4 and CD8 T-cells increased and the ratio improved. And then some of the markers that would show immune cell exhaustion — like PD-1 and all these different aspects of T-cell dynamics — also improved. So they're trying to use growth hormone to regrow the thymus.

Thymosin Alpha-1, TB-500, and Thymulin

Andrew Huberman: Getting us directly to peptides. Many people who are peptide-curious start asking about thymosin alpha-1. Is thymosin alpha-1 a peptide that comes from the thymus?

Dr Abud Bakri: Thymosin alpha-1 is part of this thymic family of hormones that gets secreted. It's at least 21 amino acids. It increases T-cell development in the thymus, increases T-cell proliferation outside the thymus, and makes the T-cells more likely to properly attack a pathogen. It's like jet fuel for the T-cells.

Andrew Huberman: So it's pro-immune. I've heard of people taking it when they feel run down, if they're traveling, they're sleeping less than usual, they're a new parent.

Dr Abud Bakri: It was FDA approved as Zadaxin for kids that were born without a thymus or a malfunctioning thymus — like DiGeorge syndrome, these different genetic abnormalities — to be used for these kids to help develop the T-cells that they had that weren't properly developed. I don't think that FDA approval still exists. So people are trying to grandfather thymosin alpha-1 into this peptide conversation. In other countries it's approved as an adjuvant therapy for hepatitis B, hepatitis C, and in different cancers. So far the sepsis literature and the infectious literature is not that promising. It might be like — if you take antibiotics with thymosin alpha-1 you might have a quicker bounce back. What I would be interested to see is if you went to nursing homes, injected everybody with thymosin alpha-1 in November and December, would you have less flu in January and February? That'd be the interesting thought experiment.

Both thymosin alpha-1 and thymosin beta-4 come out of the Goldstein lab — the very famous lab that studied the thymus in the '70s, '80s, and '90s. But thymic research kind of fell out of favor the last few decades.

Andrew Huberman: Have you taken thymosin alpha-1?

Dr Abud Bakri: Oh yeah. I've used thymosin alpha-1 when I travel to avoid the cesspool of planes and hotels. And this year on the wards — the first time — I don't get flu, cold, whatever kind of infection. I did one course throughout and I didn't get sick a single time.

Andrew Huberman: What time of day or night are you injecting?

Dr Abud Bakri: Twice a week, time agnostic. We're talking about 2.5 milligrams as a prophylactic. That's not FDA approved — this is just me doing my thing, trying to stay healthy so I can take care of patients.

Andrew Huberman: When we hear about thymosin alpha-1, we usually hear about TB-500 also. What's TB-500 and how are the two related, if at all?

Dr Abud Bakri: While Khavinson is finding thymalin and injecting that into people, the Goldstein lab finds thymosin fraction 5, which is this giant protein that has many different peptides in it — thymosin alpha-1 being one of them and thymosin beta-4 being the other one. Thymosin alpha-1 and thymosin beta-4 were discovered in the thymus but they're not exclusive to the thymus gland — they're also made in other tissues. Thymosin beta-4 seems to be this 43 amino acid peptide that helps in the actin cytoskeleton of cells. If you think about it, immune cells have to move a lot. They have to reorganize their actin cytoskeleton quite quickly. So it seems to upregulate that movement — which the horse racing community and other athletes have found a niche for thymosin beta-4 to use as a doping agent.

Andrew Huberman: For the horses?

Dr Abud Bakri: For the horses. Yes. Thymosin beta-4 is a very common doping agent in horse racing.

Andrew Huberman: There's been so much interest in NAD, NMN, and NR to upregulate NAD. NAD is a pro-longevity thing — one of these things that drops over the lifespan, although the paper last week says that it doesn't drop in blood. I will say I do augment NAD using NMN. It gives me more morning energy. I will say it does make my nails really thick and my hair grow fast — two effects I was not looking for, but I like the energy effect. I've never said it increases lifespan ever. So this was mentioned in the New York Times and elsewhere, and it's absolutely false that my name is included in that statement. Their fact checkers need fact-checking. NAD has been kind of the thing for a lot of people who want to go beyond supplements — beyond creatine, beyond magnesium — but they don't want to go all the way to blood cleansing and all this other stuff, which I certainly don't do myself. When I hear about thymosin alpha-1, TB-500, BPC, it occupies this kind of middle ground. And so I think this is why a lot of people are saying — and here we go, Pavlov and his dogs — I do think this is another category of interest for pets. They can't consent. We have to be very thoughtful there.

Dr Abud Bakri: The veterinary community has been very open. The pet peptide industry is going to be enormous.

Andrew Huberman: I injected my previous dog with testosterone later in life. And I expected the vets to come after me with pitchforks. And I got calls saying we would love to prescribe this. In fact, we wish we could just do vasectomies on male dogs — let them keep their testosterone and then you don't have to worry about the breeding problem.

Dr Abud Bakri: My sister was at a compounding pharmacy here locally that would give dogs their testosterone. And it made him so much healthier and happier.

Andrew Huberman: I'm pro-peptide for pets. Let's say I think there would be beneficial effects. We know dogs when they vomit end up licking some of the vomit. Instinctively, they might be trying to get BPC out of that. Who knows? But I think there would be less hesitation for people to use these on animals. They come from animal literature. A lot of the positive signals are going to come out of people giving them to their pets. Unfortunately, there are so many brands now popping up every day giving their pets peptides.

Dr Abud Bakri: Because BPC — is it going to be treated as a supplement when it comes to oral capsules or is it going to be treated as a medication? We haven't got that answer from the FDA. RFK himself has kind of said these are supplements, they're not medications. So the FDA said we're not going to regulate them as meds because they're not meds — which I don't know if the agency themselves is going to be too happy with that.

Thymulin, Zinc, and Immune Function

Andrew Huberman: Is taking thymulin something that generally could be a good idea under certain circumstances?

Dr Abud Bakri: Thymulin itself has a very short half-life. The goal would be to increase endogenous production of thymulin itself.

Andrew Huberman: How would you do that?

Dr Abud Bakri: Sufficient zinc status is necessary to make thymulin. The first sign of zinc depletion — before RBC zinc or serum zinc decrease — is your thymulin levels tank.

Andrew Huberman: What is thymulin and what does it do endogenously?

Dr Abud Bakri: Thymulin is a nine amino acid peptide with zinc inside it to do its effects. It will develop NK cells and T-cells, stimulate the immune response. But also in the animal models — not replicated in humans yet — when they take out the pituitary and then inject hCG, the amount of thymulin sensitizes the end organ to production of the targeted hormone. For example, if you were just to give hCG alone to the animal, they would get more testosterone produced when they got hCG with thymulin versus hCG alone.

Andrew Huberman: So thymulin specifically can augment the effects of endogenous and perhaps also exogenous hormones.

Dr Abud Bakri: Yes. And it makes sense because if you're not robust when it comes to immune status — you can think of your thymulin as high in youth, low in aged — you have no business investing in reproduction. You have no business creating a lot of corticosteroids. But if you're making a lot of corticosteroids, you're shrinking your thymus. So it creates a negative feedback loop to prevent you from overrunning your system. A lot of young guys will be like, "Oh, my immune system sucks and my testosterone is low." Is there a thymus link? That is the question.

Andrew Huberman: And I'm sure that you're the first person in the last 20 years to be talking about this publicly. I really appreciate that you are. People taking thymosin alpha-1, TB-500, and thymulin — is this something that people would cocktail, or is taking thymulin something that generally could be a good idea under certain circumstances?

Dr Abud Bakri: Thymulin itself has a very short half-life. The goal would be to increase endogenous production of thymulin itself. Sufficient zinc status is necessary to make thymulin. The first sign of zinc depletion before RBC zinc or serum zinc decrease is your thymulin levels tank.

The Lymphocyte-to-Monocyte Ratio as a Thymic Health Proxy

Andrew Huberman: Can I get some sense of my thymic size and output from a blood draw, or do I have to do whole-body imaging?

Dr Abud Bakri: On blood tests, we've been trying to work with a couple of different labs to figure out a thymic score. The most commercially available is going to be a lymphocyte count — looking at CD4 to CD8. There's an ideal CD4 to CD8 ratio that's more youthful. You don't want to have more CD8 cells than CD4 cells. You don't want to have too few of either of them. That goes more into the HIV literature. But the most simple thing that almost every single person has gotten done but no one's looked at is their lymphocyte-to-monocyte ratio on their CBC. Almost everybody's gotten a CBC with diff. It's a $3 lab test. If you type in any disorder — cardiovascular disease, cancer, diabetes — and put lymphocytes to monocyte ratio, there's a study that will talk about how low lymphocyte-to-monocyte ratio is associated with poor outcomes when it comes to that disease state. So it gives you a general gestalt of what's going on with immunity. You want a high absolute lymphocyte count — not too high, because it's associated with lymphomas — but somewhere around 1,000 total lymphocytes is where the hazard of different cancer sites starts to increase. A young healthy person will be between 1,500 and 3,000 total lymphocytes. And you want the ratio to the monocytes. Monocytes are different types of immune cells that are more inflammatory. So if you have a robust amount of lymphocytes with a low amount of monocytes, that suggests you have a more ready and robust immune state.

Andrew Huberman: So a $3 lab test that everybody gets — almost every lab testing company now checks it — and no one really reports on it. But you can stratify people into disease risk based on that score. Out of a hundred randomly pulled physicians who received their license in the United States, how many of them probably know what you just described?

Dr Abud Bakri: Zero.

Andrew Huberman: Why not?

Dr Abud Bakri: It's like rabbit holes that you kind of go down and find out. I've been lobbying everyone in the hospital to look at this. I started to care about the thymus post-pandemic because I noticed people's lymph counts were lower. I could notice that anecdotally, looking at small data sets — hey, people had lower lymphocyte counts and had worse disease. People that had cancers in their late 30s, early 40s — they all had lower lymphocyte counts. So I started to dig into the literature and I'm lobbying a lot of the hematologists and infectious disease doctors in my hospital to start looking at this. Unfortunately, they're kind of textbook. It's not part of the guidelines. It's not clear that if I check your lymphocyte-to-monocyte count right now, it's going to change my management of you in the hospital today. Not really. It's more of a long-term look. So that's where all these direct-to-consumer companies have an opportunity to modulate the way medicine is practiced in the United States. But if we have this metric that we can study, why not use it and then try different interventions and see what actually helps people? We've had people go from like a 4:1 lymph-to-monocyte ratio to an 8:1 ratio. Now is that significant? That seems to be significant. But no one's really discussing it unfortunately.

Growth Hormone Secretagogues and Somatopause

Andrew Huberman: There's a category of peptides such as growth hormone secretagogues, tesamorelin, MK-677 — these are to my understanding FDA approved for certain indications. They've gone through randomized control trials. The framework I'm teeing up is that these molecules have been explored for their known biological function in animals. It's established these molecules lead to an increase in growth hormone above what would normally be secreted. They do it indirectly — they're sort of the gas pedal on that system. Growth hormone secretagogues cause more growth hormone to be secreted, not actual growth hormone. They vary in terms of how much they stimulate hunger or don't. Most people who are taking these things, whether they get it from pharma or compounding pharmacy or gray market, are doing this because they want to lose fat, gain muscle, recover from exercise more quickly, and look more youthful. Can we assume that those effects are real given that they were FDA approved for other things?

Dr Abud Bakri: When it comes to the different types of compounds that exist in this category — there's the ghrelin side, the ghrelin agonists like MK-677, not FDA approved, orally available pill that makes you bleed out growth hormone. You make so much growth hormone in response to that, and in a non-pulsatile fashion. Growth hormone is a very circadian hormone that gets released in the first 90 minutes of slow-wave sleep. If you miss that big pulse, you're going to get small pulses throughout the day. The question is, is that big pulse better than small mini pulses throughout the day?

The secretagogues will address the broader category of something called somatopause. You've heard of menopause, you've heard of andropause. Somatopause is this event that happens somewhere in the 30s where growth hormone production dramatically decreases. So if we paint a picture — your pineal gland is aging before puberty, your thymus right after puberty in your 20s, and in your 30s you're having somatopause where your growth hormone production is decreasing. You're having what they call adrenopause where your adrenals stop making as much DHEA and the different ratio of cortisol. And then you're having menopause, andropause, and all the other chronic conditions. So it's like your first 50 years of life, that's what you have to expect.

The question has been — and it's a big debate in the medical community — is replacing growth hormone and addressing somatopause useful? Because you can measure: if we had your IGF-1 when you're 18 and your IGF-1 when you're 30 and 50, it's going to be a dramatic decrease. Should we now replenish this IGF-1? The proponents will say IGF-1 is important for skin and good quality sleep and for muscle recovery and joints, and those are true. We know growth hormone has all these beneficial effects. We also know growth hormone is thymus regenerative because it stimulates the regrowth of an aged, involuted thymus gland — based on Dr. Fahy's work. The question is, is there an oncogenic signal when it comes to growth hormone?

Andrew Huberman: Does it cause cancer?

Dr Abud Bakri: Yes, that's the big debate. And when people are like, "BPC causes cancer" — there's no mutagenic effect from BPC. Is BPC like smoking a cigarette? Smoking a cigarette, you get carcinogenic damage to the lung tissue that causes a cancer later on. There's no direct mechanism that would link any of these peptides to a carcinogenic effect. But is it a growth factor that could grow a cancer potentially? There isn't good data showing that. The debate may be — by boosting thymic function from growth hormone, are you increasing immunity and immune surveillance of different tumors, and therefore decreasing cancer risk? There's a big debate about whether growth hormone is even beneficial when it comes to aging, because growth hormone does grow certain tissues. There are models where people are growth hormone deficient and they live a lot longer. And growth hormone is not positive when it comes to a cardiometabolic perspective.

Andrew Huberman: And in species like dogs, where there's tremendous variation in the amount of IGF-1 made between a Chihuahua and a Great Dane — the breed that makes more IGF-1 lives a lot shorter life than smaller versions of the same species. Then you get into antagonistic pleiotropy. Is this something that's good in youth but detrimental for longevity? That's the big debate in the longevity field — whether or not to use growth hormone.

Dr Abud Bakri: Growth hormone has become very difficult to acquire through clinical prescriptions after the whole anabolic steroids act and Barry Bonds and all that stuff. So people have now shifted to using secretagogues in lieu of growth hormone. Also, growth hormone is very expensive. Pfizer's pens are in the thousands of dollars. So if you want growth hormone and you're rich, you can afford it. Otherwise, a secretagogue will cost you less than 100 bucks.

Andrew Huberman: I'm told that growth hormone doesn't shut down one's own production.

Dr Abud Bakri: It's not a strong shutdown like the testicular axis. I'm also told that when people take it, they feel awesome.

Andrew Huberman: That combination of looking younger, feeling great, cognitively feeling great — I have some friends who've taken like an IU a night or even two IUs a night, five nights a week for years. And you go, "Hey, are you worried about some of the tumor effects?" And they're like, you just function at a whole other level. And then you go, oh god, that's really enticing. But even with great imaging, you don't know if you've got tumors that you're accelerating. So it's kind of scary.

Dr Abud Bakri: And we don't have a data set that would show that. Like, where's the body count from growth hormone? The bodybuilder body counts are from other compounds, not growth hormone.

Andrew Huberman: When you go into a gym, you can tell who's doing growth hormone versus not based on their skin shining. You see a 45-year-old dude who's through somatopause but has perfect young skin.

Dr Abud Bakri: Growth hormone favors the conversion of T4 to T3, so it changes the thyroid dynamics. It can have pro-testicular effects as well from the IGF-1 perspective. So there are a lot of youthful effects to it. The question is, is it a good idea to replace it? Traditionally the medical field is kind of anti using these secretagogues to augment somatopause. But I think there's going to be a role for it, perhaps cyclically — because I don't think anything in nature is year-round. So what if you did a cyclical cycle of tesamorelin for a certain amount of time, got your IGF-1 to a certain level under clinician guidance, measured your thymus on an MRI before and after, and saw that the thymus grew and you had higher CD4/CD8 count? That would be pretty interesting.

Andrew Huberman: A few years back I tried sermorelin. It dramatically increased my deep sleep and like nuked my REM sleep — the opposite of pinealon. The other thing it did — and the reason I halted it almost right away because I was really just running it as an experiment on myself — was that it spiked my PSA, my prostate-specific antigen. It had always been in range and relatively low. Boom. Spiked it and I was like, whoa, that's wild. And I don't want that. Off it. It reverted to a low level. So that was pretty striking.

Dr Abud Bakri: As you age, your prostate gets bigger. The bane of every man is going to be BPH — that's going to be the reason that you hate your life when you're in your 60s and 70s, because you have to wake up at night to pee. There are some prostate peptides we're looking at. There are people — this guy named Brennan Henry who's translated thousands of these papers from Russian to English — he's translated a lot of this Russian literature and helped us. The prostate is growing with age under the control of DHT and estrogen and probably growth hormone. So the question is, do you want to be messing with that and increasing the size of that? There are concerns about cardiac growth, liver growth. And also growth hormone and the secretagogues have a negative effect on insulin sensitivity. People's A1C's will usually jump. The joke in the bodybuilding community is you have to get lean enough and healthy enough to be able to take growth hormone.

Andrew Huberman: What's happening?

Dr Abud Bakri: Growth hormone or the secretagogues can make you insulin insensitive. Especially tesamorelin, especially when combined with ipamorelin. Sermorelin is kind of a weaker GHRH. Tesamorelin especially when combined with ipamorelin — those two together can create a giant growth hormone response where your IGF-1 is in the 380s, 390s. That's quite high — puberty levels of IGF-1. And you're hungry all the time. With MK for sure. Tesamorelin has more fidelity, less ghrelin effects especially, because you can have ghrelin effects, prolactin effects, and cortisol effects from whenever you're mucking around with the pituitary because they're all in that same area. MK bleeds out the worst when it comes to having the other effects. MK is not a peptide — it's a non-peptide GHRP.

The Trinity Stack and Celebrity Protocols

Andrew Huberman: What's happened now is people are stacking their GLP-1 as their insulin sensitivity tool, their growth hormone or their GHRH, and their androgen modulation therapies as this trinity stack to get very fit, very healthy quickly. So a lot of these transformations you see in CEOs and celebrities is using a combination of those three things — your TRT plus maybe Anavar with tirzepatide or retatrutide, and then using a growth hormone modulation with ipamorelin, and you're seeing people lose a lot of fat, gain a lot of muscle in short amounts of time. Is that healthy?

Dr Abud Bakri: We'll find out. But that is like the celebrity protocol.

Andrew Huberman: Very interesting. And I'm guessing that for women, it's the combination of growth hormone secretagogue plus something like retatrutide or one of the other GLP-1s. I'm going to acknowledge — because people are going to start throwing darts at me about this — yes, retatrutide is hitting things other than the GLP pathway. It's also the GIP and glucagon pathway. But most people put it under the category of GLP. You are encyclopedic, my friend. I really appreciate the clarity and thoughtfulness of your answers on these. We could spend 50 hours talking about selanank, about cerebrolysin. We will have to have you back to explore those other ones.

GHK-Copper — Collagen, Skin, and Aesthetic Uses

Andrew Huberman: We should close the hatch on GHK-copper. Most of the questions I get about it are from women. I sent out a little informal poll to the women in my life including siblings and things like that, and almost all of them said, "What about GHK-copper? I hear it can be good for my skin. Should I use it topically, take it orally, or inject it?" A lot of interest in this. What is it? Why has it made it into this aesthetic category?

Dr Abud Bakri: GHK-copper is a tripeptide with a copper ion in the middle. It's glycine, histidine, and lysine. It's actually found in type one collagen fibers — so it's all over your skin and hair and connective tissue. Just like Khavinson discovers these 40 different peptides from different organs, there's an American researcher, Dr. Loren Pickart — who has passed now — who discovers GHK-copper in the collagen tissue. He's like, hey, this might be the factor that controls collagen synthesis and also collagen breakdown. So he does a bunch of studies. Almost all the literature comes from this one lab — a common theme in peptides, unfortunately. He discovers it in maybe the mid-'70s. It's found to be very high in youth in serum levels — up to like 200 nanograms or whatever the unit was — and then gets down to the levels of the 60s by the age of 65. So it dramatically decreases with age. It's thought to be maybe what leads to the youthful appearance of young skin, and with age you lose that effect.

He did a bunch of trials both topically for skin and for hair. There's now injectable work being done. Similar to BPC, they would cut rats open, inject GHK-copper in a different site, and they'd get faster wound repair of the skin tissue. So it's become synonymous with BPC-157 and TB-500 — the Wolverine stack, which is someone online just made up.

Andrew Huberman: That's the Wolverine stack — TB-500 and BPC-157. Now people will add on GHK-copper and call it the glow stack.

Dr Abud Bakri: The glow stack. Someone made it up in a research chemical context. There's a big debate about whether or not mixing those together causes denaturing of different peptides. That's beyond this discussion. The point is GHK-copper — it both upregulates the synthesis side of collagen and the breakdown side of collagen. Because when you're remodeling tissue, if you're just rebuilding it, you're going to get very pathogenic structures. And if you're just breaking down, you're getting bad structures. So you're doing both. The idea is — does it have a skin effect? It seems to. Pickart compared it to retinol and vitamin C creams with positive effects, and people anecdotally talk about their crow's feet going away. There was a study on hair that didn't seem too promising. So it's not going to — the peptide sites try to tell you this is better than minoxidil. Not really. Maybe it could be an adjunct. And now there's a Chinese group studying it for lung regeneration because there's a lot of connective tissue in the lungs between the different alveoli.

Andrew Huberman: Maybe long COVID lung damage. I know some people debate it, but it seems like there are enough people walking around who were vaccinated and non-vaccinated who claim that they have symptoms post-COVID that have lasted a long time.

Dr Abud Bakri: And thymic atrophy is a big part of post-COVID, I suspect. Because any infection actually leads to thymic atrophy — the thymus kind of shrinks down and then the idea is that you recover, you convalesce, and then you regenerate your thymus in the state of health. I think the problem in modern day is people are stressed out, they're at work, they get sick, and they keep getting sick. So they never get this chance for thymus rejuvenation. So then they're constantly getting hit down and they're ending up with these diseases of aging that could have maybe been ameliorated, maybe pushed down, had their thymus function been better in youth.

Andrew Huberman: If you look back at the literature on convalescing — how long were people recommended to take some time off after a cold or a flu? Because I think this would tell us something important. Our biology hasn't changed that much in the last couple thousand years. After one has a cold, typically people go back as soon as they deem themselves non-infectious. Do you think people are getting back to work too quickly?

Dr Abud Bakri: Well, if you think about it, nothing that they do once they come back is additive to healing. Their circadian rhythms are thrown off. They're under malilluminative lights all day. They're not getting sunlight. Their vitamin D levels are atrocious. Their blue light exposure at night is high. Their stress levels are very high. Their guts are inflamed from eating processed, hyperpalatable foods. They have obesity or they're pre-diabetic. So all these things now lead to this inflammatory state, and they just got sick and their thymus didn't bounce back. So then they get sick the next time in two or three weeks. Post-pandemic, a lot of my colleagues were like, "Dude, I get sick three or four times a winter now. Before I'd get sick once a winter." So this is where the interest in thymic peptides is very elusive. We have to figure out if the synthetic thymic peptides or the purified thymic extracts are the more interesting ones. There are two different research committees that exist when it comes to the thymus. Khavinson came up with the thymalin injectable and oral versions, and he had positive immune markers — CD4 cells come up, CD8 cells improve, all his immune markers become a more youthful state.

But unfortunately what's happening here is we don't have thymologists. We don't have a branch of medicine dedicated to this aspect of immunity. There are allergy and immunologists, but they focus more on allergies to different agents or very severe immune diseases. They're not really addressing the immunity of the general public and how you can boost that. Post-pandemic, a lot of people started to ask, hey, how can I have better immunity for myself? And now finally people are starting to talk about the thymus. Unfortunately it's been too little too late. That would have been great during the pandemic — because we could have used these thymic-focused interventions, whether it be zinc or thymic peptides or purified thymic extracts, to augment immunity of the population as a whole. Especially because Khavinson was doing this in the '70s in Russia. Even in Russia, they don't really look kindly to this research. The Soviet-era research has been kind of pushed aside and it's more big pharma style because it's more profitable. How many thymuses are you going to inject into people, and how many thymuses exist on the planet to make these different peptides from?

Andrew Huberman: But you could inject a lot of synthetic thymosin alpha-1, TB-500, and maybe BPC. So it'd be very interesting if we can get that — because now that everyone's getting these Prenuvo scans and different full-body MRIs, we can see the thymus size. I was going to ask — can I get some sense of my thymic size and output from a blood draw, or do I have to do whole-body imaging?

Dr Abud Bakri: I've been trying to lobby them to give the thymic score to everybody who gets one of these scans. Because someone might come in for five different scans over five years — they did a TRT protocol or a GH protocol or whatever it may be — and we could see, did that improve thymic status or make it worse? Different infections, different interventions. That'd be very interesting to tease out.

GLP-1 Agonists — History, Effects, and Risks

Andrew Huberman: There's a category of peptides such as growth hormone secretagogues, tesamorelin, MK-677, and things like melanotans. These are to my understanding FDA approved for certain indications. The sort of framework I'm teeing up is that these molecules have been explored for their known biological function. Let's talk about GLP-1s. Now we can comfortably exhale into this. The GLP-1s are the reason why people are comfortable injecting themselves. It's why this whole thing of peptides has really taken off. BPC kind of rode in on the GLP-1s in my opinion, even though it's been around for a long time.

Dr Abud Bakri: These medications are really transforming medicine, especially where I practice. If we kind of zoom out — our medical system, if we didn't have these interventions, was going to collapse on itself thanks to the obesity, pre-diabetes, and diabetes epidemics. Because we don't have enough clinicians or finances to get everybody who was pre-diabetic in the last 20 years and they all transitioned to diabetes and ended up with diabetic medications and dialysis and eventually cardiovascular disease. We don't have the resources to take care of all these people. Our medical system was going to collapse. Now these GLP-1s are coming in and kind of transforming that phase of medicine because now we have a chance to dramatically change the rate of obesity, diabetes, pre-diabetes, and all these cardiometabolic disorders.

We needed something to happen. Ideally, everybody would get morning sunlight and eat only healthy, unprocessed foods, and have low stress and sleep great at night, and maybe no one would develop obesity. But the reality is people become overweight and obese. They get stuck in that hole. And if you just try to step out of the hole the way you came in, sometimes that doesn't work. You need a different path out of that problem. And that's been the diet and exercise literature for the last 40 years. Millions of books have been sold on how to get people leaner. We now have interventions medically that can dramatically change people's weights for the first time. We've had drugs in the past that gave 5 to 10% of body weight loss. Now with the GLP-1s we're getting 10, 20, even 30% of body weight being shaved off of people, especially with the new retatrutide data. Is there a free lunch? That's the big question. So far the data is very promising when it comes to GLP-1s and reversing this rate of chronic disease. Is it going to stay that way? I'm cautiously optimistic when it comes to these medications. I've been prescribing them since I was a resident. In my VA clinic, I was putting all these vets that are 300 pounds on GLP-1s, they were losing 50, 100 pounds — before it was FDA approved for weight loss. We knew that if you put diabetics on this drug, they would lose weight, thanks to a lot of the bodybuilders that kind of pioneered that.

Andrew Huberman: When did the bodybuilders first start using GLP-1s?

Dr Abud Bakri: Late 2010s. And then the signal — I don't think Novo Nordisk or Lily wanted to make these for obesity. They were focused on making diabetes drugs. Because if we zoom out even further, this is another animal-derived compound, right? It's found in the saliva of the Gila monster. GLP-1 was discovered. It's too short-acting to have worked on its own. Then pharmaceutical companies — and this is where you've got to give pharma their credit — they developed these drugs into more functioning versions that had longer half-lives and could stick around in the serum longer to have the clinical effect. So then we started noticing that diabetics — like my grandma got Byetta, which was one of these first GLP-1 drugs, like 25 years ago. It was, out of all the drugs she was on, the drug that changed her whole trajectory because she had less insulin needs and she was losing weight and more energetic. So we had seen the effects on diabetics, and then it gets translated into obese people and overweight patients.

The question is, what is the long-term effect of this? Do you have to stay on this drug forever? Can you titrate it off? The pharmaceutical companies have not given us good guidelines on that. They've shown us what happens if you stop the drug — you can max out on maximum dose, pull the brakes on, and people tend to sometimes gain the weight back. Some people don't, but some people will regain back to baseline. Because if you think about it, the better way to think about weight loss — it's a calculation your brain does every single day with all the different hormones and peptides that are made from the gut, the GIP, GLP, glucagon, insulin, testosterone, estrogen — all these things kind of modulate whether you should eat or not eat. The GLP-1 is a giant signal to the brain of "don't eat." So we're modulating this pathway. What happens to all these young kids that are 18, 19 years old on 5 milligrams of retatrutide that have lost 30, 40 pounds? Are they going to have to be on that for life now to maintain that weight?

Andrew Huberman: When people say perhaps you have to be on a drug for the rest of your life, I think — okay, what's the availability? What's the cost? What's the real-world cost of taking six months off because you can't access it? There's a shortage and maybe better drugs will come along. I kind of feel like eventually there'll be some slow-release polymer that will just kind of give you a micro dose of it. But what about these brain effects? I do worry about a brain that's developing in the context of a thousandfold or more increase in these GLP-1s. Because when we had Zach Knight on the podcast — he's not a clinician, he's a scientist up at UCSF, Howard Hughes investigator — he described that the diabetic drugs would increase GLP by like double, quadruple, but the weight loss effects weren't really there. But the drugs that you rattled off a few minutes ago — Mounjaro, Ozempic, etc., and certainly retatrutide — we're talking about thousandfold increases in GLP-1. We don't know what the long-term effects of those are on neuroplasticity and learning. Could be great.

Dr Abud Bakri: Could be positive. We shouldn't always assume those effects are bad. Like the effects for a 60-year-old pre-diabetic or diabetic on Alzheimer's disease seem to be potentially positive. We know diabetes and cardiometabolic disease speeds up that transition. So controlling insulin dynamics might be beneficial there. The question is, what about these cognitive effects? Is the effect happening from the drug itself? Is it from misuse of the drug — too high of a dose? You're not getting enough electrolytes, not getting enough micronutrients, macronutrients. Your blood sugar is low. Because a lot of these patients — the way we approach it is a training wheel effect when it comes to GLP-1s. Hey, you come to us, you're a patient, you want to use GLP-1s, we'll give you the lowest dose possible that has an effect for you, in conjunction with lifestyle modification, dietary advice, exercise programs, et cetera. And then hopefully peel away those training wheels or keep them on if you need them until we get to the endpoint that we want. When people do it that way, I don't hear a lot of these effects anecdotally from our patients that we hear about online where people are like, "Oh, I'm depressed, I hate my life from these drugs." The question is, are they just having low blood pressure because they're not consuming enough electrolytes or enough food period?

Because some people will take a mega dose of these drugs and end up not eating — a day goes by, they've eaten one meal. That's not conducive to feeling good. Everyone — the reason people are eating in the first place is because eating is such a pleasurable experience for humans and a social experience. The other thing is if you're not eating with people at the same table, are you having less of that socialization aspect? A lot of times you meet up to eat or drink or whatever it may be. So I'm very curious when it comes to the cognitive effects — is it from the drug directly interacting with receptors in the brain, where we've seen that the right amount of dose decreases inflammation in the brain? Or is it because of the social aspects of the drug changing the way you behave and therefore leading to negative outcomes?

We know the literature shows that people now are having less alcohol cravings from this. It might be changing the way the dopaminergic signaling is happening in the brain, which is concerning, right? Because a lot of people will be stacking this with ADHD medications. They might be using some of these peptide stimulants. So the question is — what happens when people go to these websites, they buy one more peptide, they got a great result, and they'll be like, let me add three more peptides on top of peptides.

Andrew Huberman: Yes, it's an increasing average order value problem from these research sites.

Dr Abud Bakri: We'll see where GLP-1s go. The reality is it's here. There is no pre-GLP-1 world for us as clinicians, as health enthusiasts. We're in a post-GLP world and everything kind of dictates downstream from that. The people I know who've taken these — and I don't know exactly which ones — are taking much lower dosages than were prescribed to them. Several of those people say they feel like they can think better. But I told them, well yeah, if your insulin sensitivity is improved, if you're carrying less body fat — body fat is an endocrine organ — there could be a number of reasons for that. I don't know if these are direct effects on the brain.

Andrew Huberman: Yeah. Well, leptin sensitivity increases as you decrease the body fat mass. There are GLP-1 receptors on the POMC neurons in the brain and no one's really examined what that means downstream for the leptin-melanocortin pathway and what that means for energy status, thyroid hormone production, reproductive status. We know a lot of people are having what I'd call Ozempic babies — a lady will be subfertile or infertile, start a weight loss drug, and then find out by accident she's pregnant.

Dr Abud Bakri: These are overweight and obese women that are having their fertility improve as a result of losing the weight. Because we know your leptin status is a key driver of fertility. If you're having low leptin levels, you're starving — you shouldn't be fertile. If you have too much leptin and you're leptin resistant, you shouldn't be having kids either. So both of those things kind of get modulated by these drugs as well.

Andrew Huberman: There was a science paper some years ago that leptin hitting a certain threshold is actually what signals the onset of puberty in females. Is that still considered true?

Dr Abud Bakri: I think that's part of it. Makes sense — like enough body fat to signal that there are enough resources, and then animals or females become reproductively competent at the point where there's enough energetic resources.

Andrew Huberman: Have you ever taken one of these?

Dr Abud Bakri: Oh wow. Yes. I had a family member with a GLP-1 pen from four years ago that said it wasn't working. So I'm like, okay, let's see what's going on here. I got a pen — don't do this at home. And I was like, yeah, it's not working. They got it from overseas. It was a brand name Ozempic pen, but gotten from overseas. I was like, you know what, if it's bunk, let's see what it is. Biohacker in me came out and tried it. I injected what I think was a milligram of Ozempic.

Andrew Huberman: What's a standard dose?

Dr Abud Bakri: You start at 0.25 and escalate to 0.5.

Andrew Huberman: You went straight to a milligram.

Dr Abud Bakri: Yeah. They're like, "It doesn't work. I'm eating so much." I'm like, okay, whatever. I go to do a shift — I was on a night shift that day — and I've never had Charizard-like projectile vomiting. I would go admit a patient, go upstairs, vomit in the call room, then go back to the ER, admit a patient. It was the most miserable night of my life. So be very careful how you use these drugs. That's why you titrate very slowly. Luckily with the newer ones the effects are much less — people who report retatrutide even have less of these gastrointestinal effects.

Retatrutide and the Future of GLP-1 Drugs

Andrew Huberman: I put out a post on X. I thought — and I do still think — that retatrutide is going to be a trillion-dollar industry. Not because so many people are necessarily going to use it for weight loss, but because many people will use it for weight loss, and many people will use it for other things. Because you can be sure that Lily is going to find other ways to market it. And you can protect a patent by finding additional uses for things. So I'm guessing that retatrutide is going to be discovered to be useful for a number of things, and from the clinical trials there's a reason to believe that's going to be the case.

Dr Abud Bakri: And the big thing they're trying to do now is classify it as a biologic. So retatrutide has 39 amino acids. To be a biologic you have to be above 40 amino acids. And once you get to above 40 amino acids, if you are a biologic, then the patent lasts way longer.

Andrew Huberman: How much longer?

Dr Abud Bakri: It's like 15 years. Much much longer. If it's 40 or below amino acids, then it's something like five to seven years. So we're talking hundreds of millions of dollars, maybe billions of dollars. And you can tinker with this — you can add amino acids. And more importantly, no one can compound it if it's a biologic, or it's very difficult to compound. Something similar happened with hCG where it was taken out of the compounders recently. This is a very important thing because if Lily gets retatrutide classified as a biologic, the compounders are out of luck. The compounders all have the formula for retatrutide — they're ready to make it. They can get the API from China and start compounding it as soon as it's available. It will make them all billions of dollars. But if Lily is able to do this, they'll be able to protect themselves from what was going to happen. You see the Trump administration now is trying to get Lily and Novo Nordisk to drop their prices to make it more available, which has happened — now I think you can get a $300 monthly dose of tirzepatide available through these websites. Used to be $1,500. Without insurance, some insurance will cover it, some wouldn't. But cash pay — between you know even some of the pills, I think you can pay $150 a month for the oral semaglutide pill, which is not a peptide but still a GLP-1 agonist — which kind of gets to the point. It doesn't matter if it's a peptide or not. What matters is where it touches, what receptor it touches. Because oral semaglutide is more similar to injectable semaglutide. Both of them are GLP-1 drugs. One's a peptide, one's not. Then BPC is to semaglutide. So everyone online talking about peptides are good or peptides are bad — there's no actual scientific category of peptides that gives you a functional definition that's discussable between two people. Because what do you mean by peptide? Do you mean carnosine or do you mean retatrutide?

Andrew Huberman: Excellent point. Speaks to a lot of the confusion. I actually am going to put in a vote publicly right here and now — I think you should be in charge of a nomenclature committee. In the world of genetics for a long time, people would just name genes Sonic Hedgehog or whatever, and it was a mess. So what ends up happening is you find similarity between genes across different laboratories and eventually you have a meeting and you come up with a nomenclature committee. The general public are diving right into this — they are the experiment. So what I think would be very very useful would be a clear and accessible nomenclature to divide up what we've talked about today. The word "peptides" is just too general. I'm putting my vote in for you — not that you don't already have enough to do — to come up with some nomenclature that maybe I can help propagate, and some of the other people in the podcast community. We'll even contact our close friends in legacy media and explain to them how this works and maybe they can help propagate it, just for sake of clarity. We're not taking the stance these are good or bad, but just for sake of clarity, given that there are so many people that are peptide-curious.

Questions from the Audience

Andrew Huberman: So before we wrap — I solicited X and Instagram for questions about peptides. I did not reveal exactly who you are, but I gave some of your credentials and got back many, many excellent questions. Most of which, thanks to you, were answered during the course of our conversation up until now. But there are a couple that many people asked that we didn't touch on, at least not directly. One thing that's come up several times is the question about women who have endometriosis or fibroids or other things related to reproductive health and potential. Can things like BPC-157 help and or hurt those circumstances given their potential role in angiogenesis and the other things you described?

Dr Abud Bakri: No literature exists on either animal or human data that relates to those peptides in that context. I'd say those are more hormonal and metabolic issues that a good OB-GYN should take care of. They're very difficult to treat conditions and very miserable to have, and they have fertility implications. But those are more on the hormonal side. I think the hormonal lever is way stronger than a peptide lever like BPC or any of those. And as far as I'm concerned, there are no case reports or studies that would suggest positive or negative.

Andrew Huberman: CNS effects — central nervous system — of BPC-157 or other peptides that we've talked about that don't fall under the typical umbrella that people go to when they think about BPC-157. You talked about some of the stuff related to alcohol and perhaps other things like Adderall, but anything known about people feeling better or worse on different peptides just psychologically, neurologically? TBI — I'll throw TBI in there. I don't have TBI fortunately, but I know many people that do. They reach out to me. Could it be beneficial in those cases?

Dr Abud Bakri: There were studies in Russia on TBI when it comes to cortexin and cerebrolysin, which would probably never be available in the United States. There's no good data on BPC and TBI. They theoretically could be useful from an anti-stress perspective. That would be interesting to explore. BPC's neurological effects are very homeostatic in nature. They don't let you get too high in the mice data at least. The mice can't get too drunk and they can't withdraw from alcohol. They can't get too high on methamphetamines and they don't withdraw either. So there's a homeostatic mechanism that might explain some of these anhedonia side effects that people are reporting — where BPC modulates the gut-brain axis in a way which we do not understand. It's kind of putting you into a rest-and-digest state to heal whatever problem you have. If that's why BPC exists as a big parent compound — that might be part of the fact that if you secrete BPC, your body goes into a convalescent mode. It will take away stimulants, it will take away sedatives. There seems to be a homeostatic mechanism in BPC that needs to be explored further with good data.

How to Safely Obtain Peptides

Andrew Huberman: The major question was: what should people do if they are actually interested in obtaining peptides — let's just set the GLP-1s aside because it's kind of a separate category — and they want to explore their use and they want to be as safe as possible? Where shouldn't they look? And where should they look? Who should they talk to? At what point can they be confident that what they're taking is what the bottle claims and that it's free of contaminants?

Dr Abud Bakri: It's the most difficult question to answer because the majority of people are getting their peptides from research-only websites. Unfortunately, those are not reliable. We don't know what's in them. They could be good, could be bad, could be as good as a compounding pharmacy, could be much worse, could be the wrong peptide in the vial. So we don't know what's in there.

What should happen over the next 6, 12, 24 months is there will be a lot of physician-led options for patients to get peptides. Number one, you should encourage your physician — if you don't have one, get one, and get a good relationship with one, because having a good relationship with your physician is a key aspect of driving good health. But having a physician that's educated on peptides — to my doctor friends, all of you are now living in a peptide era. You have no choice but to get educated. So get educated. We should create resources for that. There will be a lot of telehealth options opening up soon through various companies that will offer these peptides, and it will be good for the consumer because it'll be a race down in price. And then we'll know which compounding pharmacies are better, which ones are worse, so you can get a better source for peptides. But you should get them from clinicians.

The question that's going to happen is there are going to be a lot of these orally available peptides and they're going to be all over supplement websites — you'll find them with your magnesium and your creatine and then your pinealon or your BPC-157. The question is, what is that going to look like? We'd like our FDA overlords to give us some guidance there on what can and cannot be sold and bought. But it should be physician-led. You should be doing this under the guidance of a physician that's monitoring you. You shouldn't be taking tesamorelin without checking IGF-1 levels. A GLP-1 even should be monitored with physicians that can counsel you on too much weight loss. Some of these celebrities should have had better clinicians monitoring their GLP-1 journeys because they lost way too much weight. That doesn't look healthy at all.

Unless someone has the basics in place, there's no point in putting all these peptides in. Morning sunlight, sleep, darkness at night, good diet, minimally processed food. The next phase of peptide-curious and peptide-driven discussions is going to be how do you incorporate it into a giant health system — like you do morning sunlight, blue light blockers, and epithalon, you do BPC and you work out in the gym, whatever it may be. There are going to be protocols that develop. But I think within six months there'll be very good physician options for everybody.

Andrew Huberman: Abud, amazing. Thank you so much for coming here today and again shedding so much light on what all of these things are. You have clearly a virtuoso-level understanding and ability to communicate about the history of these things, what they are, what they aren't, what we know, what we still don't know, the potential upsides, the potential hazards, the regulation, and on and on. There are 50 other topics that you and I must talk about at some point — your knowledge of hormones in men and women, pregnancy and women's hormones affecting the fetus, how progesterone impacts DHT and male offspring. Incredible. Absolutely want to have you back to have that discussion. But we'll let people digest this in the meantime. And I just want to say thank you for doing what you do. And if you don't mind me sharing — you're 33 years old. I love that you're a clinician and you're practicing medicine, but please please please keep up your efforts as a public educator wherever you can. Come back and talk to us again. You're a gift to us all.

Dr Abud Bakri: Thank you. It's a pleasure to be here and thank you for the kind words.