In short
Low testosterone in adult men is usually “secondary” and driven by modifiable factors upstream of the testes—primarily excess body fat (MOSH: Male Obesity Related Secondary Hypogonadism), plus poor sleep. The episode argues against blaming aging or microplastics and against treating based only on a single low lab value.
Guest backgrounds
Dr. Jordan Feigenbaum (host, Barbell Medicine Podcast) interviews Dr. Austin Brockway (endocrinology/clinical practice; focuses on comprehensive evaluation and appropriate localization of testosterone deficiency).
Key claims
Obesity increases testosterone deficiency risk ~9x. Average testosterone is ~66 ng/dL lower in overweight (BMI 25–30) and ~147 ng/dL lower in obesity (BMI >30). A 10% body-weight loss raises testosterone ~84 ng/dL; bariatric weight loss (20–30%) raises ~250 ng/dL. Mechanisms include aromatase converting testosterone to estradiol, estradiol suppressing GnRH/LH/FSH, inflammatory cytokines, and leptin’s hypothalamic “low fuel” signaling. Sleep restriction can drop testosterone ~15% after one week; obstructive sleep apnea is underdiagnosed and can worsen symptoms even if testosterone labs don’t rise much with CPAP.
Notable examples
“Mark” (45, sedentary, waist ~40 in, total T 240) was prescribed TRT without addressing MOSH, leptin/aromatase effects, or suspected sleep apnea; the episode highlights that CPAP and weight loss may improve symptoms even when testosterone numbers change modestly.
Written by AI. May contain mistakes. Listen to the episode to check what was said.
Chapters
Tap a time to open that second in VOUnderstanding Low Testosterone Causes
1:31 to 3:26
Explore the major factors contributing to low testosterone in men, particularly obesity.
“So I wanted to start this episode with a discussion of what actually causes low testosterone in men.”
The Mechanism of Male Obesity Related Secondary Hypogonadism
3:26 to 4:28
Delve into the research behind male obesity related secondary hypogonadism and its effects on testosterone levels.
“but it's been in the literature for a decade.”
Primary vs. Secondary Testosterone Deficiency
4:28 to 7:27
Differentiate between primary testicular failure and secondary testosterone deficiency due to obesity.
“Yeah, the two things that that means to me, like one, I do feel a little worse if it's from like the 80s or 90s and I'm like, oh boy, not bad about that.”
The Role of Leptin in Testosterone Production
7:27 to 11:28
Investigate how leptin levels influence testosterone production and the concept of leptin resistance.
“But there are also many others, relating to pituitary issues, chronic opioid use, various other things that can lead to that secondary cause as well.”
Case Study: Mark's Testosterone Journey
11:28 to 14:00
Follow the case study of Mark to better understand practical applications of testosterone management.
“this obesity sort of cause of testosterone deficiency that almost nobody talks about.”
Understanding Leptin and Testosterone
14:00 to 16:10
Learn about how low leptin levels can impact testosterone production.
“When leptin levels drop due to low levels of body fat, the brain signals scarcity pretty loudly, right?”
The Patient Case of Mark
16:10 to 18:52
Explore the case of Mark and the implications of testosterone levels and fat.
“But before we do, Austin, this is a patient you probably see very commonly.”
Patient Conversations and Considerations
19:00 to 23:01
Discover how to approach patient discussions about testosterone prescriptions.
“high pretest probability of testosterone deficiency, right?”
Weight Loss and Testosterone Levels
23:01 to 26:47
Analyze the relationship between weight loss and testosterone levels and discuss medications.
“So less of the prescribed testosterone is going to get converted to estradiol, that type of estrogen.”
Second Drivers of Low Testosterone
26:47 to 28:01
Investigate how sleep and sleep apnea relate to testosterone levels in men.
“So that's typically what I would aim to negotiate is like, hey, remain open to it.”
Show all 21 chapters
Impact of Body Composition on Testosterone Levels
28:01 to 28:34
Learn about how excess body fat affects testosterone deficiency.
“Well, that handles the largest single driver of testosterone deficiency, which would be excess adiposity, body composition.”
The Role of Sleep in Testosterone Levels
32:50 to 39:39
Understand how sleep quality and duration impact testosterone production.
“We were talking about the effects of body composition on testosterone, and we said a second driver was sleep.”
Managing Testosterone Deficiency: A Case Study
39:40 to 42:00
Explore a patient's journey in managing low testosterone symptoms.
“He's there because he wants the testosterone fixed.”
Understanding Testosterone Therapy and Sleep Apnea
42:00 to 43:46
Learn how sleep apnea affects testosterone therapy and overall health.
“you know, low levels of activity, can worsen, you know, people's cognition, their depression, their energy levels, all sorts of things that can then be experienced as a loss of libido, as fatigue, things like that.”
Impact of Training on Testosterone Levels
43:46 to 46:28
Explore how excessive training can lead to lower testosterone levels.
“The other things to think about are, again, that this blood number is just a snapshot in that circadian rhythm.”
Low Energy Availability and its Effects
46:28 to 49:17
Understand the concept of low energy availability and its implications on testosterone.
“Some people listening to this podcast right now almost certainly have done it.”
Exercise Hypogonadal Male Condition Explained
49:17 to 51:52
Learn about the exercise hypogonadal male condition and its effects on testosterone.
“It is predominantly fat earlier on, which is why this signal is recovered.”
Discussing TRT with Asymptomatic Patients
51:52 to 54:45
Find out how to approach patients wanting TRT despite low testosterone without symptoms.
“He lifts five days a week, he runs 30 miles a week on top of that, his body fat is less than 12%.”
Navigating the Complications of TRT
54:45 to 56:00
Explore the complexities of testosterone replacement therapy in athletic populations.
Understanding Testosterone Levels and Their Impact
56:00 to 59:59
Explore how varying training loads and testosterone doses influence individual hormone levels and health outcomes.
“Yeah, I would expect that to have more of an impact.”
Key Factors Influencing Testosterone Levels
1:00:00 to 1:02:28
Learn about the five main drivers affecting testosterone levels in men and implications for treatment.
“Okay, five things to take away from this episode about why a man's testosterone level ends up where it does.”
Transcript
Automatic transcript. May contain errors.0:00Jordan Feigenbaum:A man with obesity is roughly nine times more likely to be testosterone deficient than a man at a healthy weight. It's not aging and it's not generational. It certainly isn't whatever your Instagram influencer is blaming on microplastics this week. It's a body composition story and it's had its name in the medical literature for years. It's called Male Obesity Related Secondary Hypogonadism or MOSH. A man who's overweight on average has a testosterone level that's about 66 nanograms per deciliter lower than a man at a healthy weight. A man with obesity, on average, it's about 147 nanograms per deciliter lower, large enough on its own to drop a previously normal man below the diagnostic threshold without anything else going on.
0:38Jordan Feigenbaum:The reverse also holds. A 10 % reduction in body weight produces an average testosterone increase of 84 nanograms per deciliter. Metabolic bariatric surgery, where the weight loss is around 20-30%, produces increases on the order of 250 nanograms per deciliter on average. This week's episode, what is actually driving men's testosterone levels down, the modifiable levers that we have to bring it back up, body composition, sleep, and the opposite extreme that men in this audience will certainly recognize, training too hard on too little fuel. And we come back to Mark, because the thing that produced his testosterone level of 240 is finally on the table.
1:13Jordan Feigenbaum:Episode 3 of our Signal Book Launch series. I'm Dr. Jordan Feigenbaum. This is the Barbell Medicine Podcast.
1:31Jordan Feigenbaum:here to walk through what is actually driving men's testosterone levels down and the modifiable lovers we have to bring them back up it's the second most handsome doctor in north america dr austin brocky what's going on man doing great uh recovered from my recent back tweak and had some good training this morning so ready to get at get after it today okay yeah i have uh nothing of note to add, I am persisting and recycling oxygen as planned. So I wanted to start this episode with a discussion of what actually causes low testosterone in men. And we've been building towards this in the previous two episodes.
2:05Jordan Feigenbaum:So regular listeners may already know that most of the time, the answer is body fat. Most cases of low testosterone in adults in the United States are not due to a problem located within the testes because they sit downstream of the metabolic disease and respond predictably to the signal they're being given. Now, a man with obesity is roughly nine times more likely to be testosterone deficient than a man at a healthy body weight. The dose response is consistent here too. An overweight man with a BMI somewhere between 25 and 30 has a testosterone level that is on average 66 nanograms per deciliter lower than a man at a healthy weight.
2:41Jordan Feigenbaum:A man with obesity or a BMI over 30 is 147 nanograms per deciliter on average lower than a man with a healthy body weight. Now, those figures are large enough on their own to drop a previously normal man below the diagnostic threshold for testosterone deficiency without anything else going wrong. But there's also a kind of loop here where reduced testosterone levels also drive even more body fat accumulation, which subsequently lowers testosterone further, which is part of the story that most men have never been told. Now, the mechanism has a name and it's been in the research literature for years.
3:15Jordan Feigenbaum:We tend to discover these things decades after the original researchers have something. I don't know. What do you think about this? Like whenever you come across something that you're like, man, this is new to me, but it's been in the literature for a decade. Do you feel bad about that? Is it more like, I'm glad we have smarter people than us doing this stuff. Yeah, no, I mean, I think that everyone's operating within their niche and I'm glad that people have these different niches. We know, you know, we've heard all sorts of figures over the years of like, on average, it takes, you know, research findings 17 years to make it into, you know, clinical practice and things like that.
3:46And it's like, well, I like to think of myself as being at least somewhat a little bit more up to date on things through various means that we have available to us now that were not as accessible in the past. So me staying up to date with thought leaders in my practice niche on Twitter and things like that is actually helpful to me compared with 20 years ago, people would have had to stay subscribed to various journals and actively seek out all this stuff. I've kind of curated my attention so that this stuff comes to me and I'm able to stay a little bit more up to date. but it's never surprising to us when we talk about something or have an idea and then we look it up and it's like, oh, this paper from 1995, you know, first hypothesized this thing and people have been at it for a while.
4:23But, you know, those people are solidly within their niche and we have a much broader scope.
4:28Jordan Feigenbaum:Yeah, the two things that that means to me, like one, I do feel a little worse if it's from like the 80s or 90s and I'm like, oh boy, not bad about that. But also just the time course it takes. So you have an idea, a testable hypothesis, and then enough data has been accumulated where like, yeah, this is generally accepted as the consensus right now. Meaning that I probably shouldn't jump to, yeah, this is probably right if there's no evidence there yet. Right. So kind of interesting. But yeah, this mechanism has been around in the research literature for years. And it's called male obesity related secondary hypogonadism or MOSH.
5:04Jordan Feigenbaum:So let's walk through it. Now, if you recall from the previous episode, we talked about the hypothalamic pituitary gonadal axis or HPG axis. So the hypothalamus sends GnRH to the pituitary gland. The pituitary gland picks it up and then generates LH and FSH, which goes through the testicles, which produce testosterone in response. Now, excess body fat suppresses that pathway at two different points. Centrally, which just refers to the brain, the hypothalamus stops producing as much GnRH with its normal pulse amplitude. And then peripherally, outside of the brain, it's the fat tissue itself. Visceral fat, so that's the fat that surrounds your internal organs, is rich in an enzyme called aromatase, which converts testosterone into estradiol.
5:53Jordan Feigenbaum:It's a type of estrogen before the testosterone can do its job. and this aromatase sort of loop is self-reinforcing. More visceral fat means more aromatase, which means more testosterone to estradiol conversion. And estradiol itself is a more potent inhibitor of the HPG axis than testosterone is. At the level of the brain, the hypothalamus senses higher estradiol levels and reduces GnRH release further. This is the same response the hypothalamus would normally have to elevated levels of testosterone, but it's even stronger in response to estradiol. So the conversion does a sort of double duty.
6:29Jordan Feigenbaum:It depletes the testosterone and the resulting estrogen feedback on the brain quiets this sort of broadcast of GnRH even further. Also, low testosterone promotes more visceral fat storage on its own. It makes the visceral fat cells more efficient at taking up fat and storing it. And then the expanded visceral fat generates more aromatase activity, which suppresses testosterone even further. If that wasn't enough, on top of that, adipose tissue puts out inflammatory cytokines like TNF-alpha, IL-6, and more, which add their own inhibitory signal at the level of the brain. So multiple different pathways to dial the system down without anyone touching a needle.
7:11Jordan Feigenbaum:Now, Austin, when a guy in his 40s or 50s shows up to see you with the complaint that ends up being testosterone deficiency or just a low testosterone level, how often is the actual driver body fat versus something happening at the testes themselves? What's your sort of calculus on how often this happens at the bedside? Yeah, I think what you're really getting at here is how often are we dealing with situations of primary testicular failure, meaning scenarios where the testes themselves are not doing their job versus how often is the kind of the lesion so to speak the problem higher up in the system uh being secondary kind of testosterone deficiency from something going on in the brain or or even higher um in the in the hypothalamus and the breakdown is overwhelmingly in the secondary category way way way more often than primary testicular failure there are there's a long list of possible causes and diagnoses that can contribute to primary testicular failure but fortunately, at least in, you know, adults in kind of typical modern outpatient practice, the likelihood of that being what's going on is much less common compared with secondary causes.
8:20Now, among the secondary causes, you're right that body fat, obesity, metabolic disease, insulin resistance is a predominant cause or a large fraction of those secondary hypogonadism or secondary testosterone deficiency situations. But there are also many others, relating to pituitary issues, chronic opioid use, various other things that can lead to that secondary cause as well. With that said, I think that there has been some under-recognition of scenarios where there are testicular failures, situations that are kind of under-recognized. And so I think that because it is so much more common for us to see secondary in practice, a lot of these, I'll call them shadier clinics or places that don't do comprehensive workups, they might check the testosterone level and see it's low and then put the person on testosterone therapy without doing the additional evaluation that's needed to include checking those gonadotropins like FSH and LH because if you check those and they are high, then that localizes the problem, as we talked about in our last episode, to the testes themselves.
9:24And that requires a very different strategy for management and has a different prognosis and has different considerations depending on, for example, the person's desire for fertility and lots of other things that need to be considered and so that's why the you know adequate evaluation is important here because even though most of the cases that we see in adults who have symptoms like this who present and have confirmed testosterone deficiency end up being secondary and of those most of those end up being related to body fat obesity insulin resistance sleep apnea etc there is a significant enough fraction of primary disease still that needs to be detected and identified because it can have a variety of additional implications and consequences for the person that might impact their decision making over the course
10:06Jordan Feigenbaum:of their life yeah and if you get it wrong uh there's something else that you're missing which can be problematic for sure 100 yeah but i yeah i think it's fair to say that the majority of the cause of testosterone deficiency particularly in modern times has to do with obesity metabolic disease this aromatase loop and these inflammatory cytokines uh if you were thinking about a sort of population level decline in testosterone if it were to be there it's not due to this sort of you know increase in primary primary testicular failure it's it's usually due to um an increase in obesity but there's just point out one other thing before you move on because of the the one of the common causes of primary testicular failure that is historically been very under recognized um that i've seen increasing calls for more aggressive kind of awareness screening diagnosis is actually a genetic condition called klinefelter syndrome it's something that we all learn about in med school and then we're like i'm probably never going to see a case of that and it's like turns out to be a lot more frequent than people recognize and so this is that that's the kind of the one that i was thinking about the most when i talk about under diagnosis of primary testicular failure it's that one as well as a few others that are that are less common but that's the one that's like not to be missed from a primary failure standpoint but most of the rest totally up in the brain secondary is the source.
11:25Jordan Feigenbaum:Yeah, absolutely. There's a third piece here to this obesity sort of cause of testosterone deficiency that almost nobody talks about. And it has to do with my favorite hormone, leptin. This is my pet hormone, mainly because there's a lot of misinformation around it. Now, if you don't know what leptin is, it's a hormone that's made by the adipose tissue or body fat tissue itself. The more body fat that you carry, the more leptin you produce, the less body fat that you carry, the less leptin you produce. Now, you may have heard about this hormone and its connection to appetite and hunger and eating related behaviors.
12:04Jordan Feigenbaum:It's been thought for a long time that it is a satiety hormone, meaning it promotes fullness. And so if you have low levels of body fat, you also have low levels of leptin. And so you're supposed to eat more. And if you have high levels of body fat and subsequently high levels of leptin, you should eat less. This is sort of framed as the body's natural solution to prevent obesity. As body fat goes up, leptin levels would go up too. So people should eat less and body fat should go back down. Voila, nature has its own solution to make sure that we don't gain too much body fat. However, this does not happen.
12:39Jordan Feigenbaum:Hunger, appetite, feelings of fullness, etc. They do not correlate to leptin levels very well, especially when they're high. Giving people high doses of leptin exogenously by injecting them with metroleptin also doesn't work. I've tried this. So this term leptin resistance has been coined, meaning that the brain can't, quote, see higher levels of leptin, which is why obesity persists despite this hormone that should make you full being elevated. One problem with this theory, the brain does respond to high leptin levels, meaning that leptin resistance isn't really happening. It just has nothing to do with appetite when it's elevated.
13:19Jordan Feigenbaum:So how does the brain respond to high levels of leptin? Well, in the hypothalamus, chronically high leptin levels downregulate what are known as kispeptin neurons. Now, these are a specialized group of neurons that are upstream of what drives GNRH production in the hypothalamus. So if you have less KISPEPTIN signaling, you get less GNRH and subsequently less LH and FSH from the pituitary and then subsequently less testosterone production by the testes. Now, leptin resistance as a concept has very little supporting evidence despite decades of research. As of now, we think leptin's strongest evolutionarily preserved role is a sort of low fuel alarm.
14:01Jordan Feigenbaum:When leptin levels drop due to low levels of body fat, the brain signals scarcity pretty loudly, right? And it suppresses non-essential systems and prioritizes survival. So people get ravenously hungry. They start to eat a lot. And also, as we'll talk about, low levels of leptin can also signal decreased testosterone production, particularly in adolescence. We cover that pretty thoroughly in the book. Either way, the man with chronically elevated leptin has a hypothalamus that is not producing GnRH the way it should. And as a result, the signal to the testes is less than it should be. So let's go back to a man we've already met.
14:41Jordan Feigenbaum:In the previous two episodes, we've discussed Mark. He's this 45-year-old guy. He's a partner at an architectural firm. He's sedentary by the nature of his work. And he's got an enlarging waist that's been creeping up for years, a textbook profile that the wellness clinic markets to. He had a total testosterone of 240 on a single afternoon draw, and that's what triggered the prescription for TRT. Now, this guy has some element of mosh. The visceral fat in his abdomen has been generating chronically high aromatase levels, which converts testosterone into estradiol before it can reach its targets.
15:17Jordan Feigenbaum:And that same fat has also been raising leptin, which tells the hypothalamus to stand down and produce less GnRH, which ultimately lowers testosterone production. Now, on its own, that is enough to drop a man like Mark with a previously normal HPG axis, normal testosterone level below the threshold that his clinic was looking for when they ran their little algorithm. There are documented cases in the published literature of men who walked into a clinic or to a doctor's office with a testosterone level below 150 nanograms per deciliter and got back above 450 on weight loss alone. No exogenous testosterone, no TRT prescription needed.
15:55Jordan Feigenbaum:the mechanism is reversible. But Mark's clinic didn't ask for any of that. They saw a lab number below a cutoff and they treated it to buff the chart. Body composition is one driver in the story, but there's a second driver that's clinic also did not look for. And we'll talk about that after the break. But before we do, Austin, this is a patient you probably see very commonly. Mid-40s, BMI is above 30s, waist is, you know, about 40 inches, total testosterone is 280 nanograms per deciliter. He's got fatigue, low libido, and he's read enough to know that he's below the sort of cutoff and he wants the prescription for testosterone.
16:31Jordan Feigenbaum:What does that conversation actually sound like when you see a patient like this? Yeah, it's going to first involve a lot of listening and then some more expansive history taking on this person's journey to this point and what's kind of motivating them to seek out a prescription this immediately. And then the other thing is kind of taking an inventory of the other what we'll call adiposity related kind of chronic diseases. In other words, he has the waist measurement of 40 inches, the BMI, you know, well over 30 and some of these symptoms, which I agree raises concern for a likely secondary testosterone deficiency.
17:05But he may well have lots of other things that need my attention as well as a generalist, not somebody who is, you know, a script monkey for testosterone alone. I'm going assess his blood pressure, assess his blood lipids, assess his, you know, glycemia, his blood sugar, his insulin sensitivity, things like that. Assess his sleep, do a sleep apnea screening, get a sense of his exercise habits, his dietary habits, things like that that need to be considered. And then thinking about what, when we move forward, what is this person's, what are this person's primary goals and why, what are they willing to do?
17:35What are they not willing to do? And then trying to negotiate through that plan together. It may end up being the case that, you know, somebody might not have a complete understanding of what's involved in going on testosterone therapy. If he may have enough other kind of complications of his body fat, that it may actually be a wiser choice to use a different treatment compared with testosterone alone. He may benefit from either using, for example, a GLP-1 receptor agonist. He may benefit from using both a GLP-1 receptor agonist and testosterone. He may benefit from something else entirely. He may end up deciding that he doesn't want to immediately jump on any of these medicines, but once he learns how much of all of these things that he may have are likely to be related to his, you know, body fat accumulation, visceral adiposity, and its complications.
18:20Maybe, you know, he might not have ever tried anything before from a lifestyle standpoint, even though it is not easy to do. I have seen patients who, you know, when they learn about this stuff for the first time, they do find themselves able to like, kind of we'll call it buckle down and make a pretty substantial amount of lifestyle changes. Not the most common thing, but it's also possible. So I basically see this conversation going a lot of potential different directions, but I need to spend a lot of time listening, inventorying the other kind of complications that he may have, rather than being like ultra myopically focused on just the testosterone number alone.
18:51And then even when it comes to the testosterone, I need to make sure that the evaluation has been proper and complete, right? Now you're telling me somebody in whom I have a, we'll call a very high pretest probability of testosterone deficiency, right? I'm very suspicious. So the fact that his level was drawn in the afternoon compared with the morning it's like i could be an ultra stickler for it being in the morning but at the same time i'm like this fits right but as far as that being enough on its own to drive my prescription not quite yet because i do i'm i am going to be a stickler for making sure that my evaluation is complete and then not only the testosterone and subsequent for example fsh and lh and things like that for completeness sake there but also again checking for his you know insulin resistance diabetes screening lipid screening blood pressure screening depending on his age range you know will oftentimes especially in this situation do like a baseline PSA various other sorts of things to be considered before we commit to that course of treatment or some combination therapy that he might benefit from
19:49Jordan Feigenbaum:yeah yeah I mean obviously preferences are look I can't really change a lot of these lifestyle things, then, you know, perhaps medication might be the answer. There may be additional things going on that also need to be treated on top of that. But if he's open to it, yeah, lifestyle could be the first move. And then the natural question there is, well, how much does the testosterone number actually move when a man does these sort of lifestyle changes? We see that a 10 % reduction in body weight produces an average testosterone increase of about 84 nanograms per deciliter. So for a man who walked in at 280, that's the difference between being maybe deficient in the normal range and then definitively above that sort of cutoff with lifestyle alone.
20:35Jordan Feigenbaum:Metabolic bariatric surgery, which we've covered in detail on this podcast before, which can produce an average weight loss of somewhere between 20 % to 30%, produces an increase on the order of 250 nanograms per deciliter on average. Obviously, individuals vary. We think, though, that this sort of 7 % to 10 % weight loss threshold is roughly where leptin drops enough to produce a large increase in testosterone levels from that mechanism itself. In one study, 11 % weight loss produced a 44 % drop in circulating leptin in six months, which is actually pretty impressive. Which leads to the next question.
21:13Jordan Feigenbaum:Does Ozempic raise testosterone? Do GLP-1s raise testosterone levels? And this is pretty well established here. GLP-1 receptor agonists like semaglutide and terzepatide raise testosterone by roughly 20 % to 30 % in men with obesity on top of other additional benefits to the cardiometabolic system, sexual function, etc. And this is directly proportional to weight loss mostly. Plus the parallel improvements in things like glycemic control and the metabolic milieu, as Claude Bernard would appreciate me saying. the HPG axis just responds better. There's also some preclinical work. I don't know if you've seen this on GLP-1 and their direct effects on the penile tissue itself.
21:58Jordan Feigenbaum:So yeah, pretty interesting stuff. There might be some, again, independent benefits of GLP-1 agonists on those tissues so we can watch this space. But practically speaking, for the guy who walks in who's already on a GLP-1 agonist and he's six months into the sort of weight loss management. He's probably watching his testosterone level climb on its own. And so I think it's reasonable to recheck their labs if they were concerned about testosterone deficiency. Once they're kind of maybe past this point of like, you've lost a significant amount of weight already, like I wouldn't check it one month after, but maybe three months, six months, and certainly 12 months if that was a concern.
22:39Jordan Feigenbaum:Maybe a different scenario, I want to get your take on this. What about a guy who's already on TRT? And then he starts a GLP-1. So his endogenous production of testosterone was already shut down by being on TRT. That's the nature of that medication. But what does change is how his body is sort of handling the dose. As he loses weight, he's going to have less visceral fat, which means less aromatase. So less of the prescribed testosterone is going to get converted to estradiol, that type of estrogen. His SHBG is likely going to go up as his metabolic health improves. So they may have an even higher testosterone level in addition to maybe some altered estrogen levels.
23:19Jordan Feigenbaum:So Austin, are you seeing this in practice? Is something you've come across? Yes. And seeing it not just in the realm of testosterone, but in other endocrine related conditions as well, a much more common one that we see and manages, you know, hypothyroidism. And so it's actually very common for people's dose of thyroid hormone replacement to need to be adjusted while they are losing substantial amounts of weight on these medications. And the same would go for something like testosterone. It would not be at all surprising to me if somebody, you know, who's on a particular dose at one weight after they have lost a substantial amount of that, their blood levels end up becoming high.
23:54And as a result, they end up essentially having too much in their system, which can be evidenced by a variety of downstream consequences. And so it would be, you know, pretty common or typical to need to adjust that dose to stay in the target range for that person, especially as they lose substantial amounts of weight.
24:11Jordan Feigenbaum:Yeah, pretty interesting stuff here. One question that comes up then is, well, look, does adding testosterone, even if you don't maybe need it, make this better? Okay. So there was an interesting study called the Testosterone for Diabetes Mealitis Trial. Over 1 ,000 men with prediabetes or type 2 diabetes all overweight or with obesity. They were all enrolled in the same sort of structured lifestyle program. Half got testosterone alongside the program. Half got placebo alongside the program. Now, both groups improved significantly. They both lost weight. They both reported better quality of life, better sexual function, better mental health, better psychosocial measures, et cetera, et cetera, et cetera.
24:52Jordan Feigenbaum:Now, adding testosterone produced almost no additional improvement on top of the lifestyle program for any of those sort of quality of life outcomes. The lab numbers for testosterone were higher in the group that got testosterone, but the men didn't really feel any different. This is kind of the same finding from the Chaslin trial we talked about last week. Different population, different stage of the disease, same answer. When the lifestyle intervention is doing most of the work, adding testosterone, particularly like a replacement dose, doesn't seem to move the patient any further. So Austin, I think there's probably a pattern you're seeing more often now than maybe what you were seeing five years ago.
25:29Jordan Feigenbaum:A patient comes in who's already on a GLP-1 and their weight is dropping, and then they ask to also get on testosterone. What's your sort of play if that happens? Yeah, more history, asking why, what's driving their thinking, their reasoning, what are they seeking to gain from this? And then oftentimes, if somebody is already making excellent progress, then we can oftentimes negotiate a kind of monitoring plan. I am, as I've alluded to in previous episodes, like not super rigid about this. And I think mainly this is based on the fact that testosterone therapy, when it is used reasonably, and it is at least monitored, it's actually quite safe.
Read the full transcript
26:05And so I'm not necessarily just like shutting the person down right off the bat, because that's, of course, a way to lose your rapport. And then they're just not going to be interested in, you know, you're probably never going to see them again. So I will remain open to the possibility, but rather do a little bit of education, understanding of their goals, maybe a monitoring plan and suggest that we kind of maybe manipulate fewer variables at once. And then maybe we see, hey, let's get to a place of weight stability. Let's see how you feel. Because then you're looking at the possibility of, for example, taking a second injection every week or twice a week or whatever the case long term.
26:39And if there's not too many more benefits to be gained by doing that, then maybe it's not worth it to you. Because there's time and expense and effort and all sorts of things that you need to be thinking about in that context as well. So that's typically what I would aim to negotiate is like, hey, remain open to it. If there's a clear reason to expect that it might help you, then totally we can go down that path. but maybe we see what things look like, see how you feel once you've achieved a kind of more of a weight stable place, weight maintenance level territory. Now, if they push back on that, then again, I'm just gonna ask why and get a sense of where they're coming from on that and potentially negotiate a plan from there.
27:16Jordan Feigenbaum:Yeah, it seems like the most likely person fitting this criteria would be trying to, quote, optimize like a number. They're like, look, my testosterone right now is 350. It should be 700. I read online, it should be 700. And you're like, that requires some unpacking. But yet to your point, if this person was dead set, I want to use testosterone. I'm going to find a way to do it. Then at that point, you know, you're basically then assessing risk benefits. And the person, while not terribly likely to benefit from the testosterone therapy, it's also not incredibly risky. It would be more risky if they went through another channel, perhaps obtaining these from an inappropriate source, no monitoring, so on and so forth.
27:57Jordan Feigenbaum:but that would be the more risky sort of option there. Yeah, I agree. Yeah, all right. Well, that handles the largest single driver of testosterone deficiency, which would be excess adiposity, body composition. The second one nobody asks about in the one Mark's clinic walked past is sleep. Now, when we come back from the break, how a week of bad sleep moves a man's testosterone level and why obstructive sleep apnea is the most underdiagnosed contributor to symptomatic low testosterone in middle-aged men and what the data actually says about treating it.
28:33Jordan Feigenbaum:Here's something I realized about myself. I eat well when the setup is there. When there's something healthy and ready to go in my fridge, I'll eat it. When there's not, I end up staring at a cast iron skillet at about 8 p.m. and just, yeah, I'm not doing that. Well, Factor solved that for me. These are fully prepared meals designed by dieticians and crafted by chefs delivered right to your door. I've been using the Muscle Pro Collection because the macros tend to line up with my energy targets, but they have meals built around whatever your goals are. Weight loss, overall nutrition, more protein, GLP-1 support.
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32:00Jordan Feigenbaum:This isn't just a powerlifting focused event. The modifications content has been expanded to cover athletes across different sports. So wherever you're meeting your current patients or clients, there's gonna be something you can put directly into practice. For example, the lower extremity post-op lecture and the subsequent breakout walks through the full rehab spectrum after surgery, with a strong emphasis on the middle phase of training. This is the phase that gets the least attention and causes the most problems. We spend real time on the return to sport criteria and how to structure progressions that actually get somebody there.
32:28Jordan Feigenbaum:The pain lecture also has new cases this year and is built around helping folks make sense of what they're experiencing, not just here's what the research says, but how to use that information in a real conversation with the real person who's frustrated and confused and wants to know what to do next. Spots are limited, so if you want to learn more and register today, head over to barbellmedicine.com and look for the Bozeman Pain and Rehab Seminar. We also have a link in the show notes below.
32:54Jordan Feigenbaum:All right, welcome back. We were talking about the effects of body composition on testosterone, and we said a second driver was sleep. Can poor sleep lower testosterone? Yes, absolutely, and faster than most men realize. Now in 2011, Rachel Lepreau and Eve Van Cotter took 10 healthy young men, average age was in their 20s, and their average testosterone, where you would expect it to be for healthy young men, normal, they restricted them to five hours of sleep per night for one week. While they were healthy at baseline, after one week, their testosterone levels dropped by about 15 % on average.
33:30Jordan Feigenbaum:Now a 15 % drop in testosterone is big and the relationship runs the other way too. Older men, morning testosterone levels is independently predicted by measured sleep duration. The men sleeping less had lower morning testosterone, controlling for age, body mass, and the rest of the standard adjustments. Testosterone production depends on sleep, though this is not strictly circadian. So the hormone itself, testosterone, is released during sleep itself. Impulse is tied to REM cycles. The morning peak that everyone references, this is just a post-sleep peak, which can vary depending on when somebody's actually sleeping.
34:04Jordan Feigenbaum:So for a man who has a standard overnight sleep schedule, that means a 7 a.m. to 10 a.m. draw catches the peak. But for a night shift worker who sleeps from 8 a.m. to 4 p.m., the peak lands in the late afternoon when they wake up. If you drew that person's labs at 8 a.m. before they've slept, that's going to catch the low point or the trough. Now, the mechanism on chronic sleep restriction also goes through the hypothalamus, the same place that obesity hits. The specific mechanisms are still an active area of research. Is it Kispeptin or is it the hypothalamus more broadly? Is this mediated by cortisol to a significant degree where that could have direct effects on the hypothalamic pituitary gonadal axis or Kispeptin itself?
34:45Jordan Feigenbaum:We don't really know yet, so it's still an active area of research. But reduced sleep, you get a reduced GnRH pulse amplitude either way, which means reduced LH, which is a reduced signal to the testes to produce testosterone. So a few things that translate in the real world here. There are confounding effects. Now, a 15 % decrease in testosterone is big. There's another study on military recruits where they also are sleep restricted, and it's even bigger drop, 50%. But the longer-term effects of chronic sleep restriction, which might apply to people listening to this podcast, they're harder to measure cleanly because the same lifestyle that results in sleep restriction also tends to drive the body composition that suppresses testosterone on its own.
35:28Jordan Feigenbaum:It's two drivers kind of stack here. Also, the laboratory assessment. Now, night shift workers, rotating shift workers, and men with severely disrupted sleep schedules, thinking back to my intern year in medicine, they're going to need their testosterone drawn within the first hour or two of waking, whatever time of day that is. The phrase sort of morning fasted lab draw is shorthand, but the actual instruction is, hey, look, the first hour or two after waking, also fasted. Now, Austin, how do you approach the guy who works nights and is concerned about low testosterone? I imagine there's some scheduling issues here, trying to get the lab at the right time, like before the lab closes and before the person has to go to work.
36:04Jordan Feigenbaum:How do you navigate that? Yeah, on an individual basis as best we can. Really, it's a matter of kind of seeing what's feasible for the person, trying to get it done within the first couple hours after they wake up. Sometimes if they have a day off or a night off during the week, that might be the time to get it done. So you just try to thread that needle with working with the person's schedule and when their days or nights off are and trying to get it done at that preferable time whenever possible. The system does seem to be built around these nine to five patients. Yeah. I mean, so is our biology is built around, you know, circadian daylight cycles.
36:41We're not kind of evolutionarily, you know, set up for nocturnal work on a long-term basis.
36:47Jordan Feigenbaum:Yeah. Yeah, that sort of covers sleep duration, how long people are sleeping. But there's one more category related to, quote, bad sleep that doesn't show up as fewer hours on a clock. More has to do with sleep quality. You know, the man who sleeps eight hours and wakes up tired because the sleep itself is messed up. And this is one of the most underdiagnosed contributors to symptomatic low testosterone. Certainly the features that people associate with low testosterone also happens to be what Mark has. His airway was closing while he was sleeping. He stops breathing, his oxygen level drops, and as a result, his brain pulls him back towards consciousness enough to clear the airway.
37:27Jordan Feigenbaum:He gasps, his airway reopens, and he goes back to sleep 30, 50, 100 times an hour. He has no memory of any of it. He sleeps eight hours, but he still wakes up tired. It's also extremely common, especially with obesity, with increasing age, and in people with thicker necks. Both of your hosts included in this. and really anyone who snores. By some estimates, around a quarter of middle-aged men have it, and I think that's an under-diagnosis. Most of them have never even talked about it with their doctor. Now, Mark's wife has been complaining about it every night for years. Snoring was loud enough that she slept in the other room, and the pauses in his breathing were long enough that she would lie there waiting for the next breath.
38:06Jordan Feigenbaum:Unfortunately for Mark and his wife, his clinic never asked either one of them about it. And again, to clarify, this is not unusual. Obstructive sleep apnea is both very common and massively underdiagnosed, but there is some nuance here. In many, the causation runs through obesity more than the apnea itself. Most men with obstructive sleep apnea also have the metabolic and visceral fat profile that drives testosterone down on its own. And also using a CPAP, which is one of the treatments for obstructive sleep apnea, does not reliably raise testosterone on its own in many. It does improve fatigue, these symptoms of daytime tiredness, daytime function, and even sexual function, but the number on the lab report doesn't always move as much as the man might want it to.
38:52Jordan Feigenbaum:So what does this really mean? For a man with sleep apnea, treating the apnea is the right call regardless of what it does to his testosterone levels. Because the symptoms it improves are the symptoms that probably drove him to the clinic in the first place, daytime sleepiness, sexual dysfunction, etc. The testosterone may then come back as the body composition improves alongside a lifestyle program he can actually tolerate because he's actually sleeping now. So for Mark, his testosterone was being attacked from multiple different angles. He's got this mosh, right, excess adiposity. He's got sleep apnea.
39:22Jordan Feigenbaum:And all of this was being ignored by the clinic, did an inappropriate and incomplete workup, which is also unfortunately very common. Importantly, we know that this is not primary testosterone deficiency, a problem with the testes themselves. So the fix is upstream. and episode four is where we get into that and what the fix actually looks like for him. All right, so Austin, two questions. We'll start with the first. Patient walks in just like Mark. He's in his 40s. His BMI is 31. His waist is 40 inches. His total testosterone is 240. He's got fatigue, low libido. His wife says that he snores.
39:56Jordan Feigenbaum:Never had a sleep study. He's there because he wants the testosterone fixed. What is your immediate next step besides asking him why the lab was drawn in the first place. Well, I mean, it's apparent to me why the lab might have been drawn based on his symptomatic presentation, but definitely, you know, completing the comprehensiveness of the evaluation, making sure we've done our due diligence with the testosterone related things, but also these other, you know, complications of his excess body fat. So again, checking his blood pressure, blood lipids, and then doing more of a sleep assessment.
40:27And so he, this guy just needs a sleep study. He is ultra high risk for obstructive sleep apnea. You know, This is a situation where earlier in my practice, I might have formally gone through each of the stop bang questions and been checking off and assessing this risk. And after a certain number of hundreds or thousands of patients that you've done this with, you're just like, no, you just need a sleep test. I'm not, now if you need to do the scoring to justify it to insurance, then so be it. But after a certain point, you just know what the person needs. And so this person does need a sleep study.
40:58There are different ways to go about that. These days, more than ever, it's super convenient because especially when you have a at least moderate, definitely here I have a high pre-test probability that this person has obstructive sleep apnea, we can usually catch it on a convenient home sleep test. The person gets a kit, they just wear it at home for a night, maybe two, send it back. We get a study result. And then it's even more convenient. If we're gonna pursue something like positive airway pressure therapy, I could just prescribe an autopap to the person with some baseline settings to get started with and then kind of troubleshoot from there.
41:28There are other ways to go about this process. there are in lab sleep studies, there are other non-positive airway pressure related treatments for sleep apnea and of course managing his body weight and his obesity will go a long way to improving it. In fact, you know, you had mentioned the GLP-1 agonist earlier, so trisepatide itself has a specific indication for treating obstructive sleep apnea in patients and that might be also a consideration here. And so a lot of the symptoms he has are these kind of non-specific symptoms that can emerge from a variety of different causes. Poor sleep, poor mood can perpetuate, you know, low levels of activity, can worsen, you know, people's cognition, their depression, their energy levels, all sorts of things that can then be experienced as a loss of libido, as fatigue, things like that.
42:14And so I'm just trying to take a comprehensive of an approach as I can to give this guy the best shot at improving all of the symptoms, improving his overall health, his longevity, while minimizing potential harms and so maybe testosterone has a role in his therapy but i think that again completing all of this work up front is the smarter strategy compared with saying you know here's the situation you feel bad and then we'll go ahead and start therapy kind of
42:38Jordan Feigenbaum:right up front yeah and uh i don't know how closely you've read the testosterone some of the testosterone guidelines or whatever but you're well aware for sure that exogenous testosterone TRT prescription in a person who has untreated sleep apnea is a contraindication to therapy. And there's some thought based on some studies that exogenous testosterone actually relaxes some of the soft tissue of the airway on its own, which would complicate and make the sleep apnea even worse despite the number going up. So yeah, effectively, if you have sleep apnea, you're going to treat it, should treat it regardless.
43:18Jordan Feigenbaum:The point is that the person may still also benefit from TRT or additional interventions if they have something that's causing their testosterone to be lower otherwise. So look, let's say Mark comes back from the sleep study, severe obstructive sleep apnea. He gets started on CPAP. Six months later, he feels dramatically better. Repeat testosterone comes back. It's 320. A little bit better than where he started, but not setting the world on fire. He wants to know why he feels great if the number didn't really move. What do you say to that? Yeah. So I'm curious about a few things, including did we do a more expansive evaluation, you know, after that initial low testosterone value, but it may be the case that more of his symptoms were coming from really poor sleep than it was specifically from the low blood number.
44:02The other things to think about are, again, that this blood number is just a snapshot in that circadian rhythm. We talked about this last time when I joked around about, for example, having your, you know, continuous testosterone level monitoring, and it goes up and down all the time throughout the day, and so we might just be catching it at a different period of the day when really his testes are able to produce, you know, maybe physiologically sufficient testosterone for him and more of his symptoms were coming from having essentially no restful sleep because his brain was, you know, waking him up upwards of, you know, 50 plus times an hour as you alluded to, which I've seen that and much worse in these situations.
44:36And so this is a situation where if he feels great, he's performing well, he's doing well, then this is something that I would say, let's like enjoy that, lean into it and kind of move forward with the rest of our healthy lifestyle interventions that we're wanting to focus on and work on. And there may not actually be a ongoing clinical need to measure his blood testosterone levels. I would say that a fair amount of the time patients in this situation are going to want to recheck it. And so kind of like when you talked about the patient on a GLP-1 agonist earlier, and I said, why don't we plan to like recheck once we've, you know, given this a little bit more time, we've achieved a state of kind of weight stability, then this might be another situation where it's like, okay, let's, you know, we, if, if you're really wanting to keep an eye on this over time, then we can recheck, you know, once we have really settled into a steady rhythm of your like healthy lifestyle behaviors and you're consistent with the CPAP use and all sorts of things like that.
45:28Of course, in the back of my mind, I'm like, even then, if you come in and you tell me you're feeling phenomenal and let's say your testosterone level at that time is like 340, you know, are, are, are we still going to be having a serious conversation about putting on testosterone, it's like, again, the potential gains in that situation are slim to more likely none for your quality of life. If you're already telling me it's quite good. And it's not to say that the risks are like sky high off the charts, but rather it's like, what are we trying to accomplish here in terms of potential benefits?
45:56And then what are we most worried about in terms of potential risks and balancing those out? When you lay it out like that, a lot of people will kind of, I wouldn't say come around in the sense that I'm trying to coerce them, but they kind of understand the clinical thought process here. Yeah.
46:08Jordan Feigenbaum:Yeah. So these are the patients that the wellness clinic sees most often, but there's a different reason. The patient might come in and it's kind of the opposite. Some of these folks might be sitting in the audience right now. The question is, can you lower your testosterone by training too much? The answer is yes. Some people listening to this podcast right now almost certainly have done it. Now, most of this episode has been about excess. Excess body fat, excess sleep deprivation, excess load on the metabolic system through a variety of mechanisms. The opposite extreme produces the same decrease in testosterone through the opposite mechanism.
46:46Jordan Feigenbaum:The body cannot distinguish between not eating enough and starving. The hypothalamus reads both as scarcity and shuts down reproduction in the same way. This is low energy availability or LEA. Now in the athletic world, there's a sort of more serious type of this called relative energy deficiency in sport or REDS. And it has been historically described in female athletes, but it's been increasingly recognized in men. And the men in our audience would probably be some of the highest risk folks for this condition. So what is LEA? Energy availability just refers to the number of calories in minus the calories that your training and lifestyle burns.
47:26Jordan Feigenbaum:This is divided by lean body mass. What's left over after exercise is what you have to run the rest of the body to keep the lights on. Now, operationally, LEA is defined as eating less than about 30 calories per kilogram of lean body mass per day. Below this point, the system starts shutting down non-essential functions to protect what is essential. Reproduction is one of the first things on the chopping block. The mechanism here, low intake, low body fat, low circulating leptin, and the sort of low leptin level signals scarcity to the hypothalamus the same way that elevated leptin signals abundance.
48:01Jordan Feigenbaum:You get reduced KIS-peptin signaling, reduced GnRH signaling, reduced LH and FSH signaling, and subsequently reduced testosterone production. It's the shutdown with the sort of opposite trigger here. So some interesting data has emerged here, some from natural bodybuilders. This particular study from Metsu took seven natural male bodybuilders. They went through 11 weeks of contest prep. These were trained athletes who knew what they were doing, presumably. And they were measured against a matched group of bodybuilders who were training also, but not prepping for a show. By contest day, those who were prepping for the show had dropped from 9.6 % body fat to 6.5%.
48:40Jordan Feigenbaum:During this period, their average testosterone fell about 90 nanograms per deciliter, with most of that drop happening in the first half of the cut and then remaining at that lower level. Now, in trained healthy men And cutting to contest level leanness produces a measurable suppression of the same HPG axis we've been talking about for the last two episodes. It is unclear, though, do these people have symptoms of testosterone deficiency? And we know, based on other data, that it tends to recover when people regain the weight. Some people do this. They just cut because they've been told, now, look, if you reduce your body fat and you get real, real lean, then when you regain body weight, it's going to be mostly muscle.
49:22Jordan Feigenbaum:This is almost certainly not true. It is predominantly fat earlier on, which is why this signal is recovered. Chasing leanness can have a real cost. There's a sort of additional related sort of condition that probably is even more common in some of our listeners has to do with what we call EHMC. So exercise hypogonadal male condition. This is basically from folks who are not necessarily cutting, right, or getting too lean per se, but they're exercising too much. So you imagine a person who's lifting six days a week, doing conditioning on top of that, eating around maintenance because they're trying to stay lean, and they're sleeping poorly because life is busy and sleep is challenging.
50:05Jordan Feigenbaum:The testosterone levels can often come back low, normal, or even, frankly, below the sort of cut points that we've talked about so far. so far. And this person might think that they need testosterone replacement therapy. And the reality is they probably need more food and or a revised training program. So this condition, EHMC, is best documented in endurance athletes, but the same adaptive suppression shows up in resistance trained men that are running high volume programs with not enough food on board. This low normal reading that in that type of person is a sort of down regulation of the system doing what it should do under those conditions.
50:41Jordan Feigenbaum:It's adaptive in a way, not necessarily a deficit or deficiency in testosterone that needs replacement. Mostly the reasons why you know they don't need replacement is because people tend to be asymptomatic. Performance is often preserved. And so deciding to treat or intervene with training or nutrition changes, that's also on a case-by-case basis. Effectively, if nothing's broke, are we just searching for a problem to fix here? So this gets kind of interesting and we talked about this a little bit in episode two, theoretically, a standard prescription dose of testosterone in a man whose own production is suppressed by their training load functions, could function as a performance enhancing drug riding on top of an artificially suppressed baseline, even at the sort of textbook replacement dose.
51:27Jordan Feigenbaum:The number is gonna go up perhaps to an even higher level than their adaptive sort of floor right now. Whether that is a sort of real deficiency being corrected or in normal adaptation, being papered over is a different conversation. And it's a conversation that pretty much never happens at any of these wellness clinic visits, you know, how much you exercise and what are you eating? Is this EHMC? And do you need to treat that? That's a controversial section here. So Austin, let's let's think about this. You got a guy, he's in his mid 30s. He lifts five days a week, he runs 30 miles a week on top of that, his body fat is less than 12%.
51:59Jordan Feigenbaum:He's got a low normal testosterone level at around 320 nanograms per deciliter, but no other symptoms outside of the number. He is convinced that he is testosterone deficient and wants to start TRT. How do you talk him through this besides asking him again, why was his testosterone level? It's an interesting case. And I don't know if it's weird that I heard those stats and I'm like, yeah, that's not that much. That's why I say our listenership is probably like, Kind of like me. I don't run quite as far as 30 a week at the moment, but I'm in this ballpark of training load with definitely a different level on the last time I had labs checked.
52:36But yeah, the fact that this person has no symptoms whatsoever, again, I try to bring it back to like, what are we trying to accomplish with this? And when you frame it that way of like, you're interested in going on therapy to make this number that you didn't know was at this level look better, for what potential gain? And at some potential downside, not in terms of like catastrophic risks, but you know, again, it's not a negligible thing to commit to a potentially long-term therapy like this. And so I'm gonna have a little bit more of a conversation around his training, maybe do a little bit of education around it.
53:09And then maybe just if he's willing to, just get it like rechecked and recheck it maybe after a bit of a, try to figure out like, when is his next planned, you know, back off or deload or something like that? Is that in the plan at all? Being at a body fat, you know, you said under 12%, if we wanted to characterize this more, because 12 % is not, in my mind, like, you know, insanely low for this kind of thing. If he was much, much leaner, if he was, you know, stage ready, then we'd be having yet another type of conversation. But really, it's a matter of, I would say, rechecking this under slightly different circumstances, because if we observe, for example, he backs off a little bit, he has, you know, maybe a little bit more energy intake in the short term, and things like pop up well into the, say, 400s, 500s, 600s, something like that, then you have your answer as far as what could have been contributing to it.
53:56Not to mention that these things should generally be rechecked once anyway in most of these situations. But continuing to come back to getting an understanding of what are the person's primary goals and figuring out what are we trying to achieve by doing this aside from the number. The number is what it is on that initial lab. We can recheck that. But what are we trying to achieve for you, your health, how you feel? And then pointing out that, to your point, this is essentially going on PEDs. If you don't have a clear medical indication and are you a competitor, that might have some considerations depending on the sport that you're in.
54:28Are you going to need to pursue a TUE for like asymptomatic testosterone level at 320? I wouldn't do that if it were me and I felt fine. So there's a lot of different ways this conversation can go and it's going to be guided a bit by the back and forth there. But yeah, not being terribly excited by this result in terms of wanting to jump into action right away. more so recommending some temporary if they're willing to uh you know modify a bit of training rest recovery calories and recheck this before committing to anything else i think would be wise
54:58Jordan Feigenbaum:yeah i do i just i do wonder about that ped sort of like thought you know uh dr carl nadolski years ago now we did a podcast with him and kind of broached this topic um and you know i've been just kind of wrestling with this ever since it's like look if your testosterone level is suppressed appropriately through just a high training load um and maintenance level fuel so we're not we're not have like a low body fat type situation right it's just training load it's very very high so we kind of kind of expect that you get a low testosterone level low normal maybe and then you go on a trt replacement dose 100 100 you know milligrams a week 150 something like that and now your new testosterone level is 700 800 whatever yes right yeah yeah how could you tell if it actually was like ped level because we think that within the yuganatal or normal range there's not really a dose response relationship between testosterone levels and training outcomes whether that strength whether it's hypertrophy cardiovascular fitness so on and so forth but if you weren't doing that training load and you were taking that dose would that actually put you into super physiological levels because it's just a trt you know a replacement dose and so it's shutting down your own production so it's not like they're stacking so then you're back in them still this ungonadal range so i'm trying to like wrap my head around that and how do you how do you think about that am i just making this too complicated or maybe uh yeah i'm not entirely sure either i think that you know that plateau range that you're talking about a lot of that has to do with like what people's natural kind of baseline levels might tend to be that having slightly higher versus slightly lower at baseline physiologic situations is not a reliable predictor of having much higher strength or muscle mass or performance.
56:44I think that if your natural levels though at, you know, you would equilibrate otherwise very naturally in a healthy state to like, let's say around, you know, 360 or 400 or something, and then you go on a dose that pushes you up to 900. Yeah, I would expect that to have more of an impact. It's not because it's not so much comparing your baseline, you know, equilibrium physiology with somebody else's at that level, but rather like your own pre and post is now you've doubled it. And I actually probably would expect a more substantial impact there. And that's kind of what I've seen in practice, not only in terms of some of the impacts, say, on their adaptation, but also somebody who like is clinically eugonatal, right, but goes on testosterone maybe because the number was lower than they wanted it to be.
57:25I've seen a higher incidence of like side effects, intolerance, and the people quitting in those situations. I can think of many cases that I've consulted with over the years of people who were on and then they're worried about it and they wanna chat with me and I found out, oh, I went on and then I suddenly had, started having tons of acne and I started having anxiety and panic attacks and all these other things. I'm like, yeah, you probably never needed it in the first place. And the more sensitive you are to adverse effects up front, I'm, to be clear, this is made up. But my hypothesis here is that the more sensitive you seem to be to those types of adverse effects from initiation, it feels to me that it's more likely that you didn't need it in the first place compared with people who are, you know, truly clinically deficient, they much more often will tend to feel way better when they get restored to physiologic levels compared with pushing from your, you know, yugonatal baseline to super physiologic levels for you, even if it's not well outside the physiologic range on the lab test.
58:17Jordan Feigenbaum:Yeah. I just think like if there are rate limiting steps in response to training and outcomes that are related to testosterone, right, taking more testosterone is going to help. I just think that that rate, the level where it becomes rate limiting is far lower than what you see in EHMC. And so by adding just more testosterone to it, you're not really going to see a benefit until now you're in the super physiological range. At that point, this sort of calculus changes. That's kind of my thought. That's how I'm rationalizing all of this. I don't know if this is true. I would love a study on, you know, a thousand people with the HMC, you put half of them on TRT and just see what happens.
59:05Jordan Feigenbaum:Do they like suddenly become world beaters or does nothing happen? My prediction, most people would see nothing happen. And then the people who actually wasn't EHMC was actually testosterone deficiency. And it was, you know, then they're going to see a response. Yeah. Yeah. That'd be one of the challenges is having more of a heterogeneous mix than you'd like at the outset because there's not like a single test that can prove to you that that's in fact that it was in fact the HMC versus something else but anyway yeah maybe someday somebody will do that for us there you go all right so a real diagnosis takes the workup that we covered last week and the drivers we just walked you through tells you what you're actually treating once that workup is done most of the time the answer is not necessarily just more testosterone Austin anything you want to add before we wrap this up I feel like I have repeated, you know, a lot of my key messages so far in our episodes of like, you know, talk to the person, listen, get a sense of what their concerns are, their motivations are, and then make sure your evaluation is sufficiently broad and thorough before committing to one particular treatment path.
1:00:05That's kind of my approach to this.
1:00:08Jordan Feigenbaum:Okay, five things to take away from this episode about why a man's testosterone level ends up where it does. One, body composition is the single biggest driver and it runs in both directions. A man with obesity is nine times more likely to be testosterone deficient than a man at a healthy weight. And if you lose weight, testosterone level goes up to a 10 % reduction in body weight produces an average testosterone increase of 84 nanograms per deciliter. With GLP ones that can push the number up by 20 to 30 % and metabolic bariatric surgery is usually even higher. It's proportional with the weight loss to adding testosterone on top of a working lifestyle program doesn't really add any benefit to how the man feels.
1:00:46Jordan Feigenbaum:In the T4DM trial, they put more than a thousand men through it, half on testosterone, half on placebo, and the quality of life improvements tracked with weight loss, not the hormone levels. The man who's doing the work does not need the prescription on top. Three, sleep is another big driver, mainly because testosterone is sleep dependent. One week of restricted sleep dropped testosterone by 15 % in healthy young men. Obstructive sleep apnea is the structured chronic version of the same insult and the wellness clinic almost never asks about it. Four, treatment for sleep apnea, CPAP or autopap, fixes the symptoms that most men come in for.
1:01:22Jordan Feigenbaum:It doesn't reliably move the testosterone number on its own because that number tracks body composition more than it tracks sleep apnea. Both get treated in the right order by the same kind of program. Five, the opposite extreme produces the same shutdown. Men running aggressive cuts, men in a chronic energy deficit, lifters running high volumes of training on insufficient food all can suppress the same signal that obesity does. A low normal number in a chronically under-fueled or perhaps even overreached man is a set point. It's adaptive. It's not really a testosterone deficiency. The fix there is more food or adjusting the training program, perhaps both, not really exogenous testosterone.
1:02:00Jordan Feigenbaum:If most cases of low testosterone are downstream of something else, then the obvious question is, when is TRT the right answer at all? Now look, there's a real population of men for whom TRT is the right call and they're currently undertreated. On the other side, there's a much larger population of men who are currently on TRT when it's not the right call at all. In the next episode, we close the series. What's the actual evidence on TRT? Who needs it? Who doesn't? And what the cardiovascular safety data actually says now that we have some evidence on it. Also, what are the fertility consequences?
1:02:30Jordan Feigenbaum:What do those look like? And why do most men who start TRT discontinue it within a year? and the framework that we use at Barbell Medicine to put all of this together. We also come back to Mark because the question of what happens to his number and to him is the question this whole series has been building towards. Episode 404 in our Signal book series, that'll be in the next episode. Everything we covered today, whether it's MOSH, the leptin aromatase loop, the dose response on weight loss and their effects on testosterone levels, T4DM trial, obstructive sleep apnea pathway, low energy availability, REDS, it all comes from our upcoming book, Signal.
1:03:04Jordan Feigenbaum:Podcast gives you the conclusions and the key evidence. The book is where the complete approach, the case studies, the decision trees, and the practical protocols live. Got a man in your life whose numbers don't match the stories being told about him. The book is a thing that we wrote for him, possibly you. Coming soon. Link in the show notes and at barbellmedicine.com. Before you guys go anywhere, please leave us a five-star rating and a review. It's the best thing that you can do so we can bring in you all the latest nuance in health and fitness. I'm Dr. Jordan Feigenbaum. That's Dr. Austin Baraki.
1:03:32Jordan Feigenbaum:We'll catch you next week and every week right here on the Barbell Medicine Podcast.
From the publisher
Most cases of low testosterone in modern men are not a problem with the testes. The number is downstream of body composition, sleep, and energy availability. The wellness-clinic algorithm walks past every one of them.
Jordan and Austin walk through what actually drives men’s testosterone down, the mechanisms behind it, and the modifiable levers that bring it back up. MOSH, the leptin and Kisspeptin pathway, the aromatase loop, the sleep apnea picture most clinics never ask about, the GLP-1 and weight-loss data on testosterone recovery, the low energy availability case that hits high-volume lifters harder than they realize, and the closing question of when a standard-dose TRT prescription actually functions as a PED.
This is Episode 3 of our four-part Signal book launch series. Mark, the patient we have been threading from Episode 1, finally gets his diagnosis revealed.
Timestamps
- 00:00 The 9x stat and Mark's diagnosis revealed
- 02:10 How body fat suppresses testosterone (MOSH)
- 07:26 Primary vs secondary causes, and Klinefelter
- 11:35 Leptin and the Kisspeptin pathway
- 14:38 Mark: the body-composition picture
- 16:10 The 40-inch-waist case
- 20:01 Weight loss, GLP-1s, and does Ozempic raise testosterone?
- 24:21 T4DM: adding testosterone to lifestyle
- 28:35 Sleep, OSA, and Mark's diagnosis
- 38:39 TRT in untreated sleep apnea
- 41:47 Can you train your testosterone down? (LEA / EHMC)
- 50:12 Replacement dose vs PED
- 55:47 Four takeaways
- 57:46 Episode 4 preview and book pre-order
What we cover:
• How body fat suppresses testosterone at two different points in the HPG axis, and why the loop is self-reinforcing
• The leptin and Kisspeptin pathway most clinics never address
• Mark’s case: a 45-year-old with a 240 ng/dL afternoon draw, no workup, and an immediate prescription
• Primary versus secondary causes, and why Klinefelter syndrome is the under-recognized one to not miss
• Weight loss dose-response: how much testosterone climbs on lifestyle alone, with GLP-1 agonists, and after bariatric surgery
• T4DM: why adding testosterone to a structured weight-loss program produced no extra quality-of-life benefit over placebo
• One week of sleep restriction drops testosterone by about 15 percent in healthy young men; eight days of military field exercises drop it by 50 percent
• Why CPAP for obstructive sleep apnea reliably improves symptoms but does not always move the lab number
• The opposite extreme: low energy availability, relative energy deficiency in sport, and the exercise-hypogonadal male condition
• The lifter calculus: when a textbook replacement dose is functionally a PED in a chronically underfueled trainee
Resources mentioned:
- Signal book pre-order: https://barbellmedicine.com/signal
- Training Plateau Action Plan (free): https://www.barbellmedicine.com/training-plateau-action-plan/
- Barbell Medicine programs and coaching: https://www.barbellmedicine.com/
- Episode 1 (Is the Testosterone Crisis Real?)
- Episode 2 (Is Your Testosterone Actually Low?
Referenced studies:
Wu F.C.W. et al. 2010. Identification of late-onset hypogonadism in middle-aged and elderly men (EMAS). N Engl J Med 363(2):123-135.
https://pubmed.ncbi.nlm.nih.gov/20554979/
Travison T.G. et al. 2011. The natural history of symptomatic androgen deficiency in men. J Am Geriatr Soc.
https://pubmed.ncbi.nlm.nih.gov/18454751/
Corona G. et al. 2013. Body weight loss reverts obesity-associated hypogonadotropic hypogonadism: systematic review and meta-analysis. Eur J Endocrinol 168(6):829-843.
https://pubmed.ncbi.nlm.nih.gov/23482592/
Kounatidis D. et al. 2025. The impact of GLP-1 receptor agonists on erectile function. Biomolecules 15(9):1284.
https://doi.org/10.3390/biom15091284
Grossmann M. et al. 2024. Testosterone treatment, weight loss, and health-related quality of life and psychosocial function in men: 2-year RCT (T4DM QoL arm). J Clin Endocrinol Metab 109(8):2019-2028.
https://pubmed.ncbi.nlm.nih.gov/38311835/
Leproult R., Van Cauter E. 2011. Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA 305(21):2173-2174.
https://pubmed.ncbi.nlm.nih.gov/21632481/
Penev P.D. 2007. Association between sleep and morning testosterone levels in older men. Sleep 30(4):427-432.
https://pubmed.ncbi.nlm.nih.gov/17520785/
Wittert G. 2014. The relationship between sleep disorders and testosterone in men. Asian J Androl 16(2):262-265.
https://pubmed.ncbi.nlm.nih.gov/24435056/
Alemany J.A. et al. 2008. Effects of dietary protein content on IGF-I, testosterone, and body composition during 8 days of severe energy deficit and arduous physical activity. J Appl Physiol 105(1):58-64.
https://pubmed.ncbi.nlm.nih.gov/18450989/
Mountjoy M., Sundgot-Borgen J.K., Burke L.M. et al. 2018. IOC consensus statement on relative energy deficiency in sport (RED-S): 2018 update. Br J Sports Med 52:687-697.
https://pubmed.ncbi.nlm.nih.gov/29773536/
Areta J.L. et al. 2021. Low energy availability: history, definition and evidence of its endocrine, metabolic and physiological effects in prospective studies in females and males. Eur J Appl Physiol 121(1):1-21.
https://pubmed.ncbi.nlm.nih.gov/33095376/
Mäestu J. et al. 2010. Anabolic and catabolic hormones and energy balance of the male bodybuilders during the preparation for the competition. J Strength Cond Res 24(4):1074-1081.
https://pubmed.ncbi.nlm.nih.gov/20300023/
Hooper D.R. et al. 2018. Treating exercise-associated low testosterone (EHMC). Phys Sportsmed 46(4):427-434.
https://pubmed.ncbi.nlm.nih.gov/30074435/
Hackney A.C. 2020. Hypogonadism in exercising males: dysfunction or adaptive-regulatory adjustment? Front Endocrinol 11:11.
https://pubmed.ncbi.nlm.nih.gov/32082252/
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