Episode #380: The Peptide Market Audit: Injury Healing or Biohacking Hype?

23:44Yeah. So CJC and ipamoralin are the injectable options, but the industry knew that if they wanted to reach the mass market, they're going to need a pill. That brings us to MK677. This was the first drug designed to successfully bypass the needle while still hitting the growth hormone axis. This is billed as the ultimate oral mass builder. It's marketed as a pill that gives you the recovery of human growth hormone, plus a primal hunger that allows hard gainers to finally eat enough to get massive. So you can kind of think about this as a sustained hunger mimetic because it does bind to the ghrelin receptor.

24:18Now, if you remember, ghrelin tends to increase hunger, but when you stimulate this receptor, it also tends to increase growth hormone. So when you fast, for example, or you're between meals, your human growth hormone levels go up. That's just a kind of an energy balance related signal. And so by stimulating this receptor, you also get an increase in growth hormone. So on the one side, this signal hits the hypothalamus to increase hunger. That's ghrelin's sort of one of its functions. On the other side, it also tells the pituitary gland to release large, frequent pulses of human growth hormone.

24:50They basically balance each other out, though, so there's apparently no significant increase in fat mass. So you have more hunger going on, and people may consume more calories, but the increase in growth hormone does seem to prevent any additional weight gain. As far as the evidence on this, that's kind of what was found. There was a landmark one-year study in healthy seniors. 25 milligrams of this peptide, MK677, increased IGF-1 levels by 60 % and lean body mass by about one kilo. Concerns about whether or not this was actually skeletal muscle mass, again, that's the problem. Lean body mass is not just muscle tissue.

25:29It's everything that's not fat. so that includes things like water bone visceral organ tissue glycogen etc so not sure if this is really um skeletal muscle tissue and again there was no increase in fat mass like we said despite the increase in appetite and the reason why there was this concern that the lean mass increase wasn't actually muscle tissues because there was zero improvement in strength power or physical function in these seniors. So the active muscle tissue to me was likely water and glycogen or like bloat rather than quote functional muscle. We see that in other studies on actual like human growth hormone and other agents in this class.

26:09So yeah, to me, I think this, you know, agent, while it does avoid fat gain, which we would, we would be against generally speaking, it comes with a high metabolic tax by constantly mimicking hunger and raising growth hormone. It forces the body into a state of physiological insulin resistance. In trials, participants saw a significant rise in fasting blood sugar and hemoglobin A1c. That's a measurement of what your blood sugar has been like over the past few months. It essentially trades the aesthetic problem of body fat for the clinical problem of prediabetes. Other common issues include severe, quote, moon face, which is like edema of the face, and again, joint pain, arthralgia.

26:48So Austin, we're seeing these young adults and others taking this peptide for months at a time. If a patient shows up to your clinic, or you have an online sort of consultation with them, and they've got a rising hemoglobin A1c, they've got a puffy face with edema from this peptide, how would you explain the long-term risk to someone who's only focused on scale weight? Yeah, I think while it might be tempting to just right off the bat tell the person to stop, we know that that doesn't tend to work very well, and you might immediately ruin your rapport with the person, and they might never come back and see you again.

27:21And so I would just, as I have talked about before with respect to behavior change and belief change, ask like, why are you taking this? Tell me your thought process, tell me your reasoning, tell me your goals, tell me how you got there. And then kind of what are they experiencing while they've been on it? And are there any downsides that they have experienced? And then from there, I might be able to tie in my concern specifically that they're developing insulin resistance, which despite what nearly whatever aesthetic effects that they might be enjoying, maybe, maybe not. That insulin resistance is something that is at the root of so many different diseases that are very common these days can lead to potentially devastating long-term complications ranging from stroke and heart attack to many other things as well.

28:00So I would just, yeah, elicit the person's beliefs and goals and then see if I could tie in my concerns and see if I can get them on board with the idea of, hey, maybe not the move here. Yeah, you're trying to basically build this therapeutic alliance with the person so you can't right out of the gate and say, Yeah, not only does this thing not work, I have concerns about its safety. More so trying to figure out why do they believe what they believe, and then seeing if they're, like you've mentioned so many times, are there any threads to pull on here? All right, the last compound in this anabolic mirage category, again, these are drugs that increase growth hormone, it's tesamorelin.

28:35Now, this is the only FDA-approved drug in this list. It's for lipodystrophy or abnormal fat distribution in individuals with HIV. It's marketed as a targeted visceral fat assassin that specifically strips away the hard, dangerous fat around your organs and maybe reveal your six-pack while improving your memory. So a lot of interesting stuff that are claimed on Reddit. That's where I scrubbed for what claims are being made about these agents. As far as the history of this drug, it was developed by Thera Technologies, and it was FDA-approved in 2010. It was created, again, to treat HIV-associated lipodystrophy.

29:11patients on early antiretroviral therapies, those are medications used to treat HIV, they were developing accumulations of visceral fat, and it's belly fat, that couldn't be solved by diet and exercise alone. So visceral fat cells, again, belly fat, they're incredibly sensitive to growth hormone. Tessamorelin stimulates a powerful pulsatile release of growth hormone that appears to go straight to these belly fat reservoirs to burn them off. And there's good human data on this. It successfully reduces visceral fat by 18 % in HIV patients on average, but there was no weight loss. There was also a phase two clinical trial for executive function in seniors, although these results were not conclusive, showing really no significant effects compared to placebo, but potentially something there.

30:00And again, there's no data on performance in other individuals. Like if you're a healthy young person taking this, does it increase your lean body mass? Does it decrease fat mass? We don't know. As far as the toxicity goes or side effect profile, it's well characterized. Joint pain is a potential sort of side effect and a relatively mild increase in blood sugar. So there's some concern there, but less than the other agents. So to summarize, this is an FDA-approved drug for reducing visceral fat. The problem that is most reported on Reddit for this particular agent is that it's very expensive. It's thousands of dollars a month for pharmaceutical options.

30:40However, many wellness clinics and specialized providers offer research chemicals or compounded versions that are around$200 to$600 a month. Interestingly, we have new medications that are actually better than this drug for reducing visceral fat like terzepatide, Zepbound, Manjaro, even Ozempic and Wegovi. They not only cause more weight loss, and because they cause more weight loss, you get more reductions in belly fat on top of that. They're also cheaper, appear to be safer, and have more additional benefits than this particular agent. Yeah. I mean, there's the cardiovascular benefits, the renal kidney-related benefits, the liver health-related benefits, and many others that are being characterized on an ongoing basis.

31:26So I'm kind of with you. This is not a drug, while I'm aware of it. It's not one that I've ever had to use. And I think the main reason why is that that original indication that it has for HIV-associated lipodystrophy is fortunately something that we see less and less of these days. Those original HIV drugs, mainly in the class of what are called protease inhibitors, they call this, cause this horrific metabolic dysfunction, insulin resistance, and visceral fat accumulation. Those drugs we use less and less of these days because we have newer and much better, you know, agents to treat HIV that don't come with that negative side effect.

31:57There are still other drugs that can cause that type of dysfunction. Some of the drugs in the quote-unquote anti-psychotic class that are often used for various mood-related disorders and things like that can contribute to weight gain and visceral fat accumulation. So there's still kind of, to some extent, a need for being able to manage these things. But now we're, as you alluded to, studying the situation of, hey, this patient really needs a medicine like olanzapine in this antipsychotic class that can contribute to this. Okay, well, if we treat them at the same time with a combination, say, of metformin and trizapatide or something like that, then we can, how much of that insulin resistance and visceral fat accumulation can we ameliorate while maybe even getting the benefits in other ways related to their mental health issues, to substance use, to heart, to kidneys, to liver, et cetera.

32:39So that would be my move if I was in this kind of situation. If I had a medical condition that was contributing to a ton of visceral fat accumulation, I'd be looking in those territories before I came to something like this. Yeah. Yeah. I agree. All right. Well, we're going to move on to the next category of peptides. This category I call the healers. We're going to start off with everyone's favorite, BPC-157. So the claims are that BPC-157 is the holy grail for injury rehab. The claims are that it can physically knit together torn tendons and ligaments in a fraction of the time, allowing athletes to bypass surgery and return to the platform or the competitive arena within weeks.

33:20This was isolated from human gastric juices. That's basically the stuff in your stomach by Croatian researchers in the 90s. It was named BPC as an acronym for body protective compound. As far as its mechanism of action, to the extent it's been characterized, you can think of BPC-157 as a fertilizer for blood vessels. One of the reasons that tendons heal slowly is because they have little blood flow, poor blood flow. And it's thought that BPC-157 forces the body to sprout new blood vessels, that's angiogenesis, into the injury site to bring in repair cells. There may be some modulation of the nitric oxide system as well, which can cause vasodilation to further increase blood flow to the area.

34:04Now, as far as the evidence on this, we covered this on a previous podcast. I think it was episode 298. I'll link that in the show notes below. There is zero published human randomized control trial data for BPC-157, period. period. Zero published human randomized controlled trial data for BPC-157, period. And that includes sports injuries, that includes gut health, anything you want to say, there's no human data on this. Most of this miracle healing evidence comes from rats and from a single research group, the ones that discovered the peptide. There has been a small human pilot study on knee pain where basically this clinic that prescribed the drug called about a dozen individuals and said, hey, is your knee pain better?

34:48And then got an answer, yes or no. That's the only human study on this period. There were phase one and phase two clinical trials conducted for ulcerative colitis in the early 2000s, but the results were never published and development subsequently stalled. As far as like the, you know, does this make sense, you know, test? Yeah, sure. Tendons need more blood flow in order to repair and remodel. And BPC-157 brings blood. However, the sheer breadth of the claims around this agent, it heals the brain, the gut, the bone, muscles, tendons, corneas. That's biologically suspicious to me. A drug that heals everything usually does so by overriding safety checkpoints like apoptosis, which raises long-term safety questions.

35:32So, and on top of that, when I see something that does everything, I kind of initially think maybe it does nothing, to be honest. What do you think about that? Yeah, that's, I have a similar take when I I see something touted for everything. Although the caveat is that is when we do not have clear evidence indicating that it does those things because somebody might hear you and then say, well, if I rewind like two minutes, I just heard you talk about GLP-1 receptor agonists helping with heart and liver and kidneys and neurologic stuff. And I think part of the difference is that there is a shared underlying mechanism of all of the conditions there that are being addressed, oftentimes related to excess body fat and insulin resistance and some inflammation and things like that.

36:10And so by targeting that systemically, we're seeing benefits in multiple different organ systems. But most importantly, aside from all that mechanistic stuff, is we have human randomized trial data showing that people die less. They have fewer heart attacks. They have less kidney failure. They have better outcomes with respect to fatty liver disease and things like that. So we have that at least that we can point to. Here, if there's a lot of claims about it having significant health benefits across all of these different systems, I'm open to the possibility that there is something there. But you kind of have to show me.

36:39You have to convince me. And it requires more than just mechanistic kind of hand-waving or speculation or saying it should do this or it should do that because the history of medicine is littered with things that we thought should do something beneficial and then either turned out to do nothing or in some cases actually did quite a lot of harm to people instead. And the other aspect of this that you mentioned, you know, some of the stuff that came to mind is like, oh, if it helps by increasing blood flow to tendons, there's a lot of ways to do that, right? It doesn't have to be this particular peptide.

37:07So if that's the only mechanism that you're promoting, I have some questions and I'd want to see like, okay, is it better than activity? Because that can increase blood flow. There are even people who use topical nitrates on tendinopathy. I have my skepticism about the use of topical nitrates for tendinopathy, but that's another way. It causes vasodilation, increases blood flow, things like that as well. So we've come at this problem a bunch of different ways. And so it's one where, again, it's like, okay, well, if we can at least feel confident that there is safety here, then I'm open to the possibility of further exploration.

37:37But before I make confident claims or certainly before I recommend it and definitely before I prescribe it from a source of unclear quality, then I just want to feel better about that instead of hawking it overconfidently with underdeveloped backing. Yeah. Yeah. So overall, the safety in humans is unverified, and that's even before we get into efficacy. But the FDA recently banned it from compounding, citing significant safety risks like immunogenicity. This effectively banned legitimate U.S. compounding pharmacies from creating it, pushing users to the black market, so like research chemical sites.

38:13So, Austin, quickly, what is immunogenicity and why is that a concern? Immunogenicity is something we've talked about a couple times before. I think if people want to go back to our episode on exercise as it affects the immune system, this is probably from a couple of years ago now, but immunogenicity refers to the ability of a substance, an antigen, a drug, an exposure, whatever the thing is that it's stimulating, to actually provoke an immune response in the human body. And so when the body recognizes something as foreign, again, it could be a drug, it could be a pathogen, it could be not a pathogen, but something you're allergic to, it could be even your own body if you have an autoimmune disease, then it produces antibodies and other kind of immune effectors against that thing.

38:56And so the more it kind of revs up your immune system, the more immunogenic we would describe it as being. And so, you know, in this situation, if you're injecting a peptide or a drug, and that drug itself is immunogenic to itself, then you can generate antibodies to that very substance. And those can be binding, meaning that they bind the drug and can accelerate its clearance because the body says, look, this drug is now tagged with all these antibodies indicating that I need to get rid of this, or it could be neutralizing, where it doesn't necessarily bind it and accelerate its clearance, but rather prevents it from having the effect that it wants to have.

39:28And so if a drug or a substance that we're giving somebody itself is immunogenic, then we have concerns that it is going to be ineffective altogether, or it might progressively lose its efficacy as the immune system learns to either prevent it from doing its thing or accelerating its clearance by way of antibodies or other immune-mediated responses. To put a finer point on that, the FDA didn't just move BPC-157 to category two because they're being cautious. They specifically cited that the risk of these synthetic versions is that it could trigger the body to create antibodies that cross react with our own endogenous proteins.

39:59Now in plain English, you aren't just risking the drug not working. You're risking a scenario where the immune system starts attacking your own body. We're talking about a potential autoimmune response for a drug with no human evidence of efficacy to date. I can already hear or envision the people who love this compound. They think it healed the rotator cuff. It healed their knee tendinopathy very quickly. They say, well, look, man, it works, and I don't care what you guys say. And it's like a lot of things improve pain. Time improves pain. A lot of different placebo-mediated things improve pain.

40:31And so just because it, quote, worked for you, we should not attribute that to the actual compound itself, especially if we're trying to make broad recommendations to individuals. I have serious concerns about that. Yeah, this has also been a recurring topic for us. I'm not here to argue with people's experience if they say it worked for them and they're willing to spend the money, take whatever risks there are. I've had patients who decided, hey, for one guy who I remember years ago, decided, hey, he has bad enough shoulder osteoarthritis and he was willing to do pretty much anything except get a shoulder arthroplasty or a shoulder replacement.

41:04So he flew down to Central America and got stem cell harvests done and then flew back a few months later and then got him injected back in his shoulder. And I'm like, okay, like there's going to be, I would expect a pretty significant placebo type response because of all the cost and expense and time and effort that went into that. But I also know of a lot of tropical and exotic infections that I see coming from patients in South and Central America as well, just because that's, you know, something that happens in those parts of the world. Of course, we have our own too in North America and everywhere else has its own type of distribution of these things and complications.

41:34and indeed, you know, spinal epidural steroid injections, various other types of joint injections over the years, stem cell injections have led to documented infectious complications and things like that as well from contamination or improper technique and things like that as well. If somebody says, hey, I'm fine with all those risks, those things are treatable on the back end, I'll survive it, whatever. It's like, okay, then you are entitled to make those decisions. You know, once somebody is adequately informed on these things, I actually don't take like personal affront if somebody decides to pursue something of their own volition.

42:05That's fine. I'm just here to be an advisor. Yep. Yeah, I like that. So to me, overall, BPC-157, it's the wolverine that hasn't crossed the species barrier yet. The rodent data is spectacular, perhaps too spectacular, and it's heavily concentrated from a single research group. The lack of human trials after 30 years of research to me is a massive red flag, in addition to sourcing it from a trusted place rather than research chemicals off a shady website. Yeah, I'm with you. This podcast is brought to you by Biggs. At Barbell Medicine, we spend a lot of time talking about what it takes to build a body that can handle high level performance, but the recovery and health side is just as critical.

42:44Now, over the last six years, an incredible team of healthcare professionals did something that most people thought was impossible. They helped rebuild the body of legendary Olympian, Lindsey Vonn, after a series of devastating injuries. And now she's actually headed back to the 2026 Winter Games in Milan, and she's ready to break records once again. This February, Lindsey's team and the entire USA medical team will be wearing figs, and you can rock their official uniform too. The new Team USA collection from Figs is engineered with Fiber X. It's their most durable fabric yet. It really is setting a new gold standard for high-level performance scrub wear because it's lightweight, it's breathable, and it's ultra-resilient for those long shifts.

43:20And of course, the style comes in red, white, and blue. Now, if you want the gear that the medical team behind the world's best athletes are wearing, check out the limited edition Team USA collection. You get 15 % off your first order at wearfigs.com with code FIGSRX. That's wearfigs.com, code FIGSRX. I think that if you're dealing with a nagging injury and realizing that BPC-157 is not the miracle cure the internet promised, you're going to need a real management plan. You can head over to barbellmedicine.com and check out our rehab templates. These are evidence-based programs designed by our clinical team to help you get back training without the risks of unproven research chemicals.

43:53Also, our pain and rehab team, they're the best in the game. And if you need one-on-one help, they're happy to do so. Next in the healing group, we're going to talk about TB500. And the leap here is that this is an eye drop drug that individuals have decided to inject into a quad tear thinking it could work to repair their muscle fibers. But there's really no data to support this. It was isolated in 1981 and it is essential for how to repair wounds. So there's human data for surface wounds, so venous stasis and pressure ulcers. There's two phase two randomized controlled trials that found that topical gel accelerated healing by nearly a month in patients who received TB500 compared to placebo.

44:37However, it did not always show a statistically significant difference in the total percentage of patients who achieved wound closure. It also failed phase two clinical trials to help cardiac regeneration after a heart attack in humans, despite miraculous results in mice. There's zero human data for muscle tears at all. As far as toxicity concerns, chronic use may carry a theoretical cancer risk as cancer cells hijack the same slippery mechanism to spread to other organs. We call that metastasis. So some theoretical risk there, but again, no data on it overall. To me, the data isn't awesome for humans outside of some eye conditions and maybe some surface wounds.

45:19Otherwise, it's unproven. It does share the same tragic fate as stem cell injections for joints. Spectacular mechanistic hype in animal data, but generally not so impressive results in high-quality human trials. And then there's another problem. TB500 is a synthetic fragment of the full peptide, which is thymocin beta-4. That's what's been used in the clinical trials above, but the gray market primarily sells the fragment, TB500. So we're seeing people take this fragment of a protein and assuming that it does the thing that the whole protein does. Austin, have we seen other instances in medicine where a small peptide fragment failed to live up to the parent molecule's reputation?

46:00I mean, biology is just really complicated. Proteins can get sliced and diced in all sorts of different ways, and that can lead to differences in the downstream function, again, depending on how these proteins get cut up. So in clinical practice, the things that I kind of see and use on a regular basis that have some variation, despite kind of a shared origin, are things, peptides in the body like BNP or brain type natriuretic peptide and the NT-proBNP, which is kind of a cleaved variant of that. And then similar, another one has to do with the idea of pro-insulin getting secreted and getting cleaved into insulin and then C-peptide as well, which are different things that do not share the identical effect, even if you might assume that they both indicate the same thing.

46:44They're going to have different levels, different interpretations, different clinical uses. And so, yeah, not a safe assumption to say that, hey, this tiny piece of the fuller protein is going to deliver the same clinical effects just because it's part of the bigger daddy molecule. Yeah. Can you imagine if these research chemical sites, instead of selling insulin, they sold C-peptide and they're like, look, this will lower your blood sugar way to optimize your nutrient partitioning. And it's like, if you gave an individual diabetes a ton of C-peptide, it does nothing because it's just not an active fragment.

47:15Yeah, I agree. All right. Moving on to the next one is GHKCU, this copper peptide. Now the claims here are that this is the ultimate biological reset for aging. Proponents argue that it restores the skin's youthful snap. It rescues hair follicles from dormant states like balding and acts as a software update for your genes, instructing cells to prioritize repair and collagen production over scarring and decay. Man, Reddit's wild if they're making all these claims. I've never heard of this thing, so this is education for me. All right. So this was isolated in 1973 by Dr. Lauren Pickard, who noticed that plasma from young donors made liver tissue from older donors behave as if it were decades younger.

47:57So you can think of this peptide GHKCU as a copper courier. Now your body needs copper to build the structural scaffolding of your skin and hair, but free copper is toxic and hard to transport around the body. So this peptide acts like a specialized armored truck that picks up copper and delivers it directly to the cellular construction crews. As far as the data on this, human data for wound healing is pretty significant. A 2 % topical gel significantly increased ulcer closure in 120 individuals with diabetes. For cosmetic skin quality, the data for wrinkles and skin rejuvenation is not quite as good.

48:37There was a trial of 71 women that showed that there was increased skin density and thickness with use of this agent. But these studies, again, are small. They're short-term, less than 12 weeks, and rely on surrogate markers like ultrasound density or subjective grading scales rather than long-term dermatological outcomes, things that we can measure reliably. This is the same problem we saw with collagen supplementation. It's like skin elasticity, and then you look at the actual test, and you're like, well, this test actually doesn't seem very good. even though it improves the outcome of that test, does it actually improve how people look in some sort of way that we can reliably measure?

49:14As far as toxicity goes, it appears to be pretty safe when applied topically. When injected, it's notorious for a burning sensation at the site. Toxicity at typical doses is unverified, but theoretically could carry a risk of like copper toxicity, I suppose. So to summarize, I think this is probably fine for as a topical agent for wound healing. The skin data I am not convinced on. Um, and there's no human data, uh, for like any sort of systemic performance improvement or recovery from like injury. Um, to me, it's kind of like vitamin C. We know that we need it for collagen production. And like, if you're deficient in it, that can hold things up, but mega dosing, it doesn't seem to make it work any better and can in fact cause some, uh, harms.

49:58Yeah. Uh, interesting, uh, you know, presentation that you put together on this one here so far, I would have certainly less concerns about somebody who wanted to use this compared with some of the other ones we've talked about so far, especially if it was isolated to topical use. I think anything, you know, systemic that you're injecting with essentially no or very limited human data, typically in most situations is going to carry a little bit greater potential risk. But yeah, this one seems more benign, I suppose. Yeah. Yeah. Especially if someone was doing it topically, I'd be limited amount of pushback, but injecting it i'm like are we sure that that's a good idea right but again important not to uh break the therapeutic alliance yeah i agree uh moving on to the next category these are the metabolic modulators starting off with one of the hottest new drugs it's likely to be approved uh soon this is retatratide uh this may be the godzilla of weight loss it's presented as metabolic bariatric surgery in a vial claiming to melt away nearly 30 of your body weight not just by stopping your hunger, but by actively revving your metabolism like a furnace.

50:58So this is a triple agonist from Eli Lilly, currently in a phase three trials. They just wrapped up, I think, the Triumph study. The mechanism of action, it's similar to Manjaro, Zepbound, in that those are the two sort of agonists, the GLP-1 and the GIP agonist, but retatratide adds a third signal, which is glucagon. And this tells the liver to actively dump fat and burn calories for energy, really mostly heat in this case. So it addresses both sides of the calories in versus calories out equation. As far as the human data on this, it's pretty good. They just wrapped up Triumph 4. This showed an unprecedented 28.7 % weight loss at 68 weeks.

51:43And this was for individuals with obesity and knee osteoarthritis. So in these individuals, yeah, the average weight loss was 28.7 % up to 71 pounds at 68 weeks. And beyond just weight loss, it reduced knee pain as measured by the Womack scale by 76%, demonstrating that the weight loss and potentially other effects of the medication improved pain experience. By comparison, the placebo group only lost 2.1 % of their body weight. Also has some interesting effects on metabolic associated steatic liver disease, also known as non-alcoholic fatty liver disease. They had a phase two trial on this and it showed a pretty impressive clearance of liver fat that had been accumulated.

52:27Over 85 % of patients achieved complete resolution of the fat that was in their liver. That's defined as having less than 5 % liver fat at 48 weeks, which we think is due to the glucagon receptor agonism that this drug adds. As far as the toxicity and side effect profile, unfortunately, there does seem to be a higher side effect profile, particularly at max doses. There was an 18 % dropout rate in this latest trial, and it does seem to increase resting heart rate by about five beats per minute, which does require some monitoring. So there's some concerns there, particularly at max doses. Now, to me, retatratide represents a massive shift in how we approach fat loss.

53:10Now, what makes retatratide so different from the previous generations of anti-obesity drugs is that third signal, the glucagon receptor. While older drugs mostly focused on slowing down the gut and telling the brain that you're full, this is actively increasing energy expenditure through thermogenesis. It's essentially turning up the heat in the fat cells and the liver. In the past, the only way we knew how to like rev the engine was through stimulants like ephedra, which essentially dumped adrenaline to the system to force a higher heart rate and a higher metabolic rate, ultimately the person would burn more calories.

53:39But retatutide achieves a similar metabolic increase, but it does so through hormone signaling, specifically the glucagon receptor, rather than a catecholamine dump. Now, Austin, when you see a drug that is revving the engine this hard to clear liver fat and drop weight, what are your primary concerns regarding cardiovascular stress, if any? Yeah, I would say a few things. I share your enthusiasm for this medication. I think it is, if we're calling it a peptide as part of this podcast, it is likely to be super effective and super beneficial for the population once it finishes up its trials and very likely ends up getting approved.

54:12I do not claim to be an expert on the mechanistic implications of glucagon receptor agonism outside of kind of the more general descriptions that we've laid out here. I am more reluctant to characterize it as in any way meaningfully similar to ephedra. I think that that probably would spook more people off because any time in recent years with respect to GLP-1 conversations, these meds have come up, people say, oh, well, they remember what happened in the 90s, right? And it's like, look, we're in a different time now. We're not seeing the same signals in the data for these medications. And so when it comes to accelerating this or cardiovascular stress, quote unquote, I have a few thoughts.

54:53You're right that a lot of these tend to raise resting heart rate by a little bit. They tend to actually lower, quote unquote, heart rate variability by a little bit of, again, unclear real consequences. But those are things that we've noted. Now, if somebody is going to experience harm from that cardiovascular implication, I would expect that the people who are at highest cardiovascular risk at baseline who are exposed to these medicines are going to be the first to show that sort of harm, right? And the worst would be situations where people, for example, have significant heart failure, especially heart failure with reduced ejection fraction, where their heart is not functioning well, not pumping well.

55:28They don't really tend to tolerate, you know, cranking up their heart rate and various other sorts of things. And so in those populations, if we start to see signals of, oh, this is like they're dying more or getting hospitalized more, things like that, okay, then that is a signal that is worth paying attention to. Now, it might lead to, for example, saying that these meds shouldn't be used in that population. And we can study it a bit more in people who don't have heart failure or those who have heart failure but have preserved ejection fraction or those who just have coronary disease in whom many of these drugs have already been studied and they actually show benefit, right?

55:59And so I'm reluctant at this time to summarize, to make any assumptions about cardiovascular implications outside of what the evidence shows us, because these are going to be studied on a very large scale in a lot of populations, many of whom either have diagnosed or underlying undiagnosed cardiovascular disease. And so it's going to be a situation where, well, we're just going to see what the outcomes are. It may end up being that the loss in body fat, improvement in insulin sensitivity, resolving diabetes, resolving fatty liver disease, maybe that outweighs any potential negative effects of a few beats per minute higher resting heart rate.

56:28You know, I wouldn't be actually surprised at all if that ends up being the case. So it's a TBD in my mind. I don't have the same types of concerns, you know, at the start here as I would have, you know, about the drugs that were being used in the 90s or like somebody saying I'm going to use dinitrophenol to try to accelerate my metabolism. Like that's a totally different category of like accelerant. So I'm reluctant to kind of describe this in that way, just to not, you know, muddy the waters about how these drugs really work and the potential implications safety or efficacy wise uh how familiar are you with the fen fen saga we've talked about it we've talked about it before that was actually identified relatively quickly uh at the time in terms of the negative side effects in valvular heart disease pulmonary hypertension things like that yeah it's kind of interesting because fen fen itself so fentramine and fenfluramine these were both uh agents that were approved in isolation and then subsequently paired together kind of off label so these it was not like an FDA approved sort of thing, but effectively there was a single study that was published, um, in the early nineties, uh, by, by an individual showing, Oh, look, weight loss with, with this thing.

57:32Right. And that, that was like early nineties, but it wasn't until later in 96 when a different patentable version of it called Redux got on the market. But this, there was like concerns about volvular heart disease, pulmonary hypertension, stuff like that, that were like raised prior to being approved but ultimately it got past approval and then as you mentioned yeah pretty shortly thereafter they were like no this does cause problems we can pull it from the market yeah so you know there was some some regulatory issues there but if you compare the amount of evidence that was available on fenfen the thing that wasn't really fda approved and then redux the thing that was fda approved if you compare the evidence we have on ozempic wagovi zephown manjaro and even now retatratide uh to what we had evidence-wise on that it's overwhelming not even close yeah it's not even close yeah so people like look at the cautionary tale about fen-fen i'm like yeah the cautionary tale is wasn't really good evidence on it and people were using it anyway kind of like peptides yep yep and one of the nice things about these glp1 meds including you know redda that's uh again we're anticipating is coming out is that there is a dose range right and people are different and this has been my experience so far i've worked with lots of people now on these medicines.

58:47And everybody responds kind of differently. And so to the extent that we're seeing maybe a little bit more side effects in some of the trials, that might mean that we adjust the dose range to achieve the intended effects. Some people do just fine on much lower doses and we don't tend to see those things. And some people need to max it out to get the effect that we're looking for. And that's the beauty of it. You can kind of sliding scale it based on what people need. Yep, yep. All right, moving on into the same category, these metabolic modulators. We're moving to a zombie drug, AOD 9604. AOD stands for anti-obesity drug.

59:17Austin, you ever heard of this thing? I don't think so, no. Okay, well, this was touted as the holy grail of fat loss about 30 years ago. Why are we still talking about it? Well, that's a great question. Yeah, if you look on Reddit, this is like a fat-burning blade of human growth hormone with none of the metabolic baggage like water retention, risk of diabetes, joint pain, etc. It's marketed as a fat melter that leaves the muscle untouched. And so this was developed in Australia in the late 90s as an obesity drug. And so the thought here is that this is a segment or a fraction of human growth hormone.

59:54It binds to fat cells to stimulate the breakdown of fat. We call that lipolysis while ignoring other receptors that cause unwanted growth or metabolic damage. As far as the literature on this, human data confirms this drug is a proven failure. In a large 24-week trial of over 500 subjects, this particular drug failed to show statistically significant weight loss over placebo. While safety is pretty good for it based on these human trials, it doesn't seem to work. And so safe and useless is a pretty poor value proposition. I got a lot of things I can suggest to you that have the same effect. Yeah.

1:00:30Yeah, and so I don't know why people are still using this or advocating for its use, particularly for weight loss, because there are so many better options that, again, safety profile is well-characterized, monitoring profile well-characterized, effects well-characterized, and oh, by the way, it actually works, whereas this particular drug, we know that it doesn't work. Yeah, I'll do my favorite thing. I'll just put two graphs side by side, put the 24-week weight loss data of this, just blinded, anonymized, you don't know what the drug, what the intervention is, up against, blinded anonymized you don't know what the drug is 24 week weight loss data onters appetite and you you just get to pick pick which one you'd rather take if your goal was weight loss would not be a contest yeah so unclear why this is still being sold or why people are still buying it i think it's got to be has to do something with like human growth hormone modulation people like oh human growth hormone if i i just need to affect that axis and uh i'm gonna be great i'm like if you're gonna do that like again we're uh we're very understanding of you know people's intense and their goals and things like that here.

1:01:28And if we're going to take a very harm reduction type perspective, it's like, just go on terseptide and then just take testosterone. Like, yeah, yeah. All right. Uh, we're moving on to MOTS C. Uh, have you ever heard of this? Uh, I have actually seen this acronym, but not something that I've investigated myself. Yeah. MOTS C is billed as an exercise in a syringe. The claim is that it replicates the metabolic signals of a five mile run, forcing your body to burn fat, improve insulin sensitivity, and build endurance, even if you spend the day sitting on a couch. Now, the biohacking community is obsessed with this being an exercise memetic.

1:02:03Austin, help people understand the difference between the body producing a signaling molecule naturally during a five-mile run versus injecting a massive bolus of it into an otherwise sedentary body. Does the context of the signal matter? Oh my gosh, my brain goes so many different places when I hear this question. We've talked a lot about the idea of kind of a, it matters how you got there. When we talk about blood pressure, for example, it's like, oh, did your blood pressure go up because you have hypertension or did it go up because you're actively exercising? The same with a lot of other things.

1:02:32When it comes to dietary fiber, did the fiber come in the form of an isolated fiber supplement or did it come in the form of a persistent, chronic, high-fiber, whole food dietary pattern? It does have fundamentally different effects. If the body produces a particular signal in response to exercise, especially with the demands of exercise, then if you take that same molecule and inject it in separately, does it deliver all the same benefits when it is given, when there was no demand present in the first place? Kind of reminds me of when we talk about heart rate. Does getting your heart rate up from a panic attack give you the same cardiovascular aerobic adaptations as actually doing the thing that demanded the heart rate increase?

1:03:10All of these things, the context fundamentally differentiates the downstream health impacts that we can expect. That's not to say that there can be no plausible or potential benefit from an isolated, you know, molecular signal like this. Again, I remain open to the possibility pending human data showing it to me, but I will always have a baseline degree of kind of like my prior will be a low probability of at least the same benefits as you would expect from exercise. Because again, the context, the demand, things like that are different. If there's a partial effect, maybe that partial effect is worthwhile if it can be shown, because there's some people who maybe are physically unable to meet current physical activity guidelines.

1:03:48And so if you can get them at least part of the way there, great, fantastic. It's a tool, right? We are not like moralizing around the use of these tools, just like with respect to GLP-1 receptor agonist when it comes to treating obesity. So show me, you know, the effect, and then I will kind of put it in context and judge its potential uses. Tell me what you think about this analogy. When we talk about like fiber intake, for example, or eating fruits and vegetables, we talk about this food matrix effect in that it's not just the fiber that's delivered by the fruits or vegetable, but it also co-occurs with flavonoids, you know, polyphenols, etc.

1:04:20There's more than just the fiber. The food is greater than the sum of its parts. What about an exercise matrix effect? You're getting like one thing, one aspect of it, but you don't have the entire symphony that you experience from exercise. You're just getting one instrument, one molecule instead of the whole band. Yeah, exactly. That's it. All right. So this was discovered in 2015, and at the time it was a breakthrough because it was encoded by the mitochondrial DNA, the powerhouse of the cell, rather than the cell's main nucleus. So what it does, or what it's supposed to do, is when your mitochondria are drained by stress or exercise, the MOTC tells the rest of the cell to turn on PowerSafe mode.

1:05:05In the body, this power-safe mode means activating amp kinase, which forces the cell to stop building new stuff and start burning fat and sugar for fuel. Now, as far as the evidence, we don't have any on humans. We know that humans produce this naturally during a workout, but no study has ever shown that injecting it into a human improves fitness. The bottom line on MOTC is that while the rodent data on grip strength and endurance looks incredible, we don't know if that translates to a human being. We're seeing a 12-fold increase in natural MOTC production during exercise, but injecting a synthetic version into a sedentary human is a completely different biological event.

1:05:40Until we see human trials, this is pure speculation. Having an exercise memetic that we could use for individuals who either can't exercise sufficiently or otherwise wouldn't, that would be awesome. We don't know if it works. I'm pretty skeptical on this right now. We need some human data, especially on safety and side effect profile first, and then we need efficacy data. and then afterwards if all it passes all that then i suspect this would be a blockbuster like if true yeah i think that's a helpful paradigm for people to think about when approaching the potential use of these things first is it appear to be safe second does it appear to do the thing that it's being claimed to do and then you get to weigh those things on the back end and decide if it's worthwhile for you in terms of cost and access and all sorts of other things but we're like at the very early stages of that journey it seems here and i and i'm not sensing that there's like an overwhelming amount of active research happening that we're like expecting at any time soon.

1:06:33That's what I'm saying. We would have heard about it. Yeah, exactly. There's been a lot of these kind of exercise memetics that have been hyped over the years and none of them have really panned out. Not yet, but we're hopeful. Yeah. Moving on to 5-amino-1mq. Now on social media and Reddit, this is being sold as a fix for a quote, broken metabolism. The claim is that it prevents your metabolic rate from slowing down as you age by inhibiting an enzyme called NNMT. Mechanistically, by blocking that enzyme, 5-amino-1mq indirectly raises NAD plus levels, specifically within your fat cells. The theory is that this shifts the cell from a fat storing mode to a fat burning mode.

1:07:10Now when we look at how 5-amino-1mq actually works in these mouse models, it's not just about shrinking the number on the scale, it specifically targets fat cell size. By inhibiting the NNMT enzyme, it prevents the hypertrophy or the overexpansion of individual fat cells. In these studies, the mice saw a 30 % reduction in total body fat. And here's the kicker. They did this while staying on a high-fat diet and without exercise. I think this is why the biohacking community is likely so obsessed with it. They see it as another exercise in a pill. But we have to be realistic. A mouse in a controlled lab environment is not a human being living in the real world.

1:07:46This kind of goes back to that NAD plus correlation we see with NMN and NR supplementation. Just because you can force a fat cell to behave differently in a rodent doesn't mean you'll see a meaningful change in humans, especially without addressing lifestyle factors. Now, Austin, this is exactly why the longevity space is so cluttered right now. We have these incredible mechanistic stories about NAD plus and fat cell metabolism, but the human data just isn't there to back up the hype yet. Yeah, the NRNMN supplementation space is a big one in like anti-aging circles and longevity circles and things like that.

1:08:17And my current understanding is that it has not been proven or shown effective enough at this point in order for me to actually spend the time to learn about it in great detail, right? If it does not seem to be that potent of an effect for good things that we're looking for in a safe way, then I'm at this point not going to bother. Too busy dealing with actual things that work. So that's my approach. Yeah, there you go. All right, moving on to the lifestyle drugs. We have melanotan 2 and PT-141. Now, these are often called the Barbie drugs because they affect tanning, appetite, and libido. Both molecules work on the melanocortin system in the brain, which acts like a master control panel for survival, but they have very different levels of precision.

1:09:00Melanotan-2 is a non-selective agonist. It hits the tanning receptors, the appetite suppression receptors, and the arousal receptors all at once. The problem is that it also carries significant side effects, including intense nausea and documented case reports of rhabdomyolysis and even kidney failure. By contrast, PT-141, which is also known as bromelanotide, is a much more selective sniper. It's designed to target the receptors specifically associated with libido and sexual arousal while leaving the tanning and the stress signals alone. In fact, PT-141 is actually an FDA-approved medication for hypoactive sexual desire disorder in women.

1:09:35While it is often used off-label for men who don't respond to traditional PDE5 inhibitors like Viagra or Cialis, it is a legitimate pharmaceutical with a much better characterized safety profile than the research chemicals people are buying online. As far as the toxicity side effect profile main thing here is nausea with uh pt 141 it has a 40 percent rate of nausea uh because it acts on the brain some men report spontaneous erections that occur without physical stimulation which can last several hours but are generally not classified as pre-epism which uh don't google how to treat pre-epism yeah spare yourself spare yourself as far as melanotan 2 this appears to have a more significant side effect profile uh case reports of muscle breakdown like rhabdomyolysis and kidney failure.

1:10:20Um, so to summarize, I think melanotan too may be effective for tanning, um, but lack safety data and has more red flags than DNP that, uh, infamous often fatal fat burner. We did a mystery case on a PT 141 seems to be pretty proven, uh, for sexual health, but the nausea side effect is probably what's limited for being like a blockbuster, uh, Barbie drug or lifestyle drug. Austin, in clinical practice, when a drug has that high of a side effect burden, like with the nausea, for a quality of life issue like libido, how do you approach the informed consent conversation with the patient? Yeah, tons of this involves a conversation with the person about what their goals are and how far they're willing to go to achieve those goals.

1:11:03And so if they are at their wits end and looking for something to help with this particular issue, then that may be a risk that they're willing to accept. I would say a couple things, though, even as part of that conversation, because it's difficult for me to imagine that, oh, I'm taking a drug to really crank up my libido. And then if it's going to make me throw up, that that's going to be the thing that, you know, keeps me in the mood, you know. And so that conversation would involve a couple things. One has to do with dosing, right, because many medicines might have a high incidence of GI-related side effects.

1:11:33It could be a dose response type effect. It could be something that requires a little bit of adaptation to kind of get over that hump. That's actually something that we're seeing with, you know, many patients who take GLP-1 receptor agonist, nausea is the most common upfront side effect that they take, whether at the starter dose or with dose escalations. Sometimes that takes a little bit of time to get used to. Sometimes we use some anti-nausea medicines at the same time as the medicine or the dose escalation to try to mitigate that. And then in this context, where it's probably, I would imagine something that has like a time component to it, you take it in a particular context, maybe trying it not when you're, you know, getting ready so that you don't learn for the first time, whether you're in the 40 % or not.

1:12:09So starting a low dose separately as a tester might be a way to go. But that would be how I would approach this in practice is like, how far are you willing to go? What are you willing to risk if you're willing to experience some nausea and then testing it out at a low dose separately? And then you can kind of introduce it in the right context to see if it helps you. Yeah, no, that's a good clinical pearl there. All right, so let's summarize this as a little if-then sort of discussion. So with respect to peptides. If you want more muscle mass, more muscle hypertrophy, think that peptides right now are a bad trade.

1:12:43Um, we have not seen a good, an agent with good evidence for improving actual muscle tissue and subsequent, uh, performance like strength, power, et cetera. So I don't think that that would be a good option to use to gain muscle mass. Um, you mentioned it earlier. You're like, look, if you want to get some of these benefits, just take trisepatide and testosterone it's like look we have way more data on anabolic steroids as far as like not only on their efficacy but also safety and monitoring and so i think the the thought is that oh peptides are way safer one and then two people can get them without having to go through uh as backdoor of channels like vinnie at the you know gold's gym down the street doesn't have to like give you vials and like a dark corner or dark alley so but you know i'm not telling anybody to take anabolic steroids.

1:13:29I'm just saying that when I, when I look at the sort of evidence on this, I'm like, well, I know those things work and I know what to monitor. And I, I kind of, I just more well characterized. I'm like, it seems like a better option to be honest. Yeah, I agree. That's it. I have the same take. I'm not going around recommending it, but if I have somebody in front of me, who's like, look, I'm going to take something. I'm going to take something. What's it going to be? I'm going to take the thing we know more about and that I know how to monitor than the thing we don't. Yeah. Uh, for injury, uh, again, And with respect to peptides, there seems to be some non-zero risk, whether it's high risk, moderate risk, low risk.

1:14:04We just don't know because the data is kind of absent. But the reward is even more unknown. So I don't think I can recommend using BPC-157 or TB-500. I have concerns about their mechanisms and just, again, lack of human data for safety, efficacy, monitoring. Everything's anecdotal, right? So that's a problem. and then without any real efficacy data just seems like a bad trade-off. I would try to optimize load management instead. That seems like a much more successful and less risky proposition. Yeah, to an extent. I mean, both of us have had our share of injuries participating in all sorts of different sports.

1:14:40And, you know, we've been fortunate to be able to rehab essentially all of them to this point. That is not to say that that is going to be the case for everyone in all circumstances of musculoskeletal injury. And so, you know, I totally understand where your mind can go when you're in the depth, especially of severe pain or persistent pain that is difficult to rehab. You're willing to try a whole lot of things. This would not be very high on my list of things to try, especially early on, be way far down that list. And even then, I have my concerns about it at this point. I wish, you know, somebody would.

1:15:11I just see so many people on these podcasts, people who claim that they run clinics and they're seeing all these people that are having miraculous results. And it's like, would it be so difficult, so, so difficult to, you know, even a small pilot, you know, placebo controlled trial, like it would set it would you would be the leader of the field automatically if you just ran one of these things. Right. But instead, you know, they're obviously quite lucrative practices that are doling this stuff out. Well, I would say this stuff, but whatever it is, because, again, the purity aspect and things like that remains in question when it's being formulated in the way that it is.

1:15:46But, you know, you would be immediately at the forefront of this field if you were able to just document these data, show these results, right? We see this in a lot of, again, I don't want to like lump these in with like all folks in the quack space. But even, you know, during pandemic times, there was all sorts of claims about cures for, you know, infections. And now there's still people on the internet talking about the use of some of these drugs to cure cancer. And it's like, look, if you're curing all these cancers, if you're curing Parkinson's disease with Fibendazole and stuff like that that I see on it, I'm like, just document it.

1:16:18You would, again, revolutionize all of medicine because of how common these conditions are. It would not be that difficult if the effects are as large as you say. You actually don't need a very large sample size. You don't even need a very long study duration. Like, it would be trivially easy to show with the sizes of effects that you're claiming. Big if true. Big if, very, very big if true. And so that's what we would prefer to see, but we don't yet. All right. So we talked about building muscle and strength. We talked about what happens if you're injured. And then now if you want fat loss and you're in the market for peptides, don't buy the zombie.

1:16:51Like AOD 9604 failed clinical trials. And so I think we would both agree. And we've talked about this so many times on the podcast. But if you're an individual who would benefit from one of these anti-obesity medications, whether it's semaglutide, trisepatide, and potentially a retatutide when it's approved, there are many avenues for you to obtain this in a way that is not only safe, you know what you're getting, somebody's monitoring you appropriately, but also these things actually work. So like, we would recommend that. Probably not a DIY situation, although this is an interesting question maybe.

1:17:27We know that fortunately the prices on these medications are coming down, And so while there's some controversy around compounding pharmacies who continue to make these, even though against the FDA's sort of ruling on this, what do you think about there's like pharmaceutical grade versus compounding pharmacy versus research chemical? Do you think there's more risk than benefit for individuals using a research chemical like semaglutide compared to like getting the Ozempic or the Wegovi? Yes, I think the spectrum follows exactly what you described. If I had my druthers to use one of your sayings, that would be my order of preference if I had to choose.

1:18:09And I see no scenario where I am personally willing to take any sort of research chemical. It's going to be pharmaceutical grade. And then in very rare situations, would I be pursuing compounding? And there'd have to be a good reason or justification for it. And there are very legitimate, valid reasons to use compounding pharmacies for all sorts of things, whether due to dose adjustments or due to certain medicines, the way they're formulated might contain something that somebody is intolerant of or allergic to. There's all sorts of reasons to do that kind of thing. But research grade, yeah, I can't get behind that for GenPop.

1:18:40Yeah, I think that just highlighted a very important takeaway here. We would both recommend pharmaceutical grade stuff. You know what you're getting. The manufacturing standards are much higher. the amount of financial resources to make sure that you have, you know, pure and materials to start with and end with and testing along the way, all of that is like well-established procedurally. You don't have that in research chemicals. And interestingly, I don't know if you pulled the study a while ago or if I did, but I remembered it and I instantly went to the right one. So there was some third-party testing done of research chemicals in the selective androgen receptor modulator space, so SARMs.

1:19:25And of the 44 tested products, no active compound was detected in four of the substances. Substances not listed on the label were contained in 11 of the compounds tested, and only 18 of the 44 products actually had what they said that was on the label in the thing. That's kind of terrifying. I mean, And to somebody who is not in this space or thinking about these kind of things regularly, like I'm imagining, hey, I have a patient with uncontrolled diabetes in front of me, or like they're in diabetic ketoacidosis, and I want to prescribe them some insulin to save their life, as I do very frequently.

1:20:05If less than half of the patients to whom I prescribe that actually ended up getting any degree of the actual drug in their prescription, that would be bad. That would be quite concerning. And so obviously we're not, you know, in this context dealing with such acute potential risks like the person's likely to die on the matter of hours if they don't get the thing that I want them to get. But on a longer time span, you could end up with a similar type of thing, whether due to contamination, impurity, or if you think you're treating something that you're actually not treating, you know. So it's kind of a scary stat to see the percentages of like, hey, almost 10 % had none of the compound at all.

1:20:47And then a bunch, you know, a quarter had a bunch of stuff that wasn't on the label. That's super concerning. And then, you know, only a tiny fraction had any degree of what it said it had. That's not acceptable, in my opinion, and not a risk I'd be willing to take personally. Yeah, and that's just the, like, active compound, right? I mean, like, bring up heavy metal testing, for example, lead, arsenic, cadmium, mercury. You know, imagine the cost for like, you know, high performance liquid chromatography to, you know, make sure that it's not in there and scrub the product of any residual agents, you know, for research chemical manufacturer.

1:21:21Yeah. Yeah. Where's the FDA? We don't know. All right. So, Austin, to bring this home, if you had to give a clinical pearl to the person who's currently staring at a vial of a research chemical they bought with Bitcoin, what is the one question they aren't asking themselves that they should be? there are a lot of questions they should be asking but i think if you had to ask one up front is like what else could this thing be doing to me besides what i hope it is doing to me and how many of those potential uh kind of what we'll call off target effects am i willing to accept in this kind of really gray area of not even medicine whatever this is yeah there are no biological free lunches so that does wrap up our deep dive into the world of peptides as we have discussed today, the gap between the marketing hype and the actual clinical evidence is currently a canyon.

1:22:10While the biochemistry of these molecules is fascinating, the reality is that the gray market carries significant risks from impure manufacturing to unknown long-term effects on your endocrine and immune systems. We're not trying to be anti-technology, but instead we want to be pro-evidence. And right now, the evidence suggests that most of these agents remain unproven for how they're being used. If you found this episode helpful, please leave us a five-star review. It really helps drive traffic to our podcast so we can keep bringing you all the latest nuance in health and fitness. From everyone here at Barbell Medicine, I'm Dr.

1:22:42Jordan Weigenbaum. Special shout out to Dr. Austin Baraki for joining us. We'll catch you next week and every week right here on the Barbell Medicine Podcast.