Testosterone Explained (Low T, Muscle Growth, Aging & TRT) | Dr. Ben House
In a Nutshell
Low T is usually caused by obesity, poor metabolic health, or energy deficits, not inevitable aging, and most people starting TRT aren't getting proper diagnostics—two morning fasting tests plus documented symptoms—before treatment. Within the normal range, total testosterone levels don't predict muscle gains from training; even at castrate levels (~30 ng/dL), people still build muscle, just less of it. Before starting TRT, exhaustively investigate root causes like sleep apnea, varicocele, extreme leanness, or weight gain, as exogenous testosterone shuts down natural production and carries real cardiovascular risks if hematocrit, estrogen, and other markers aren't properly managed.
These notes were generated by AI and may contain inaccuracies.
People are not getting informed consent and that's why the TRT discontinuation rates are also bananas because they aren't being sold the true story. This can be done really really well. Testosterone can be lifechanging if it's needed. It can be absolutely huge. But it can also be done really really poorly just like anything else. And in those cases, people are not being told the true story. And really, if testosterone is ever your first line, just from a low testosterone draw, if testosterone is the answer there, I'm walking to the door. Like, it's not as simple as low testosterone, testosterone.
There's 12 things that can cause low testosterone. You should not be you should be asking like, why is this low?
The science and practice of enhancing human performance for sport, play, and life. Welcome to perform. I'm Dr. Andy Galpin. I'm a professor and scientist of human performance. And today I'm talking with Dr. Ben House. Ben is a PhD in nutritional sciences and has spent the last 20 years or so working with highlevel performers almost especially but not exclusively in professional sports. He has been one of my absolute top and go-to resources for nutrition and physiology for the better part of two decades now. He brings an unbelievable depth and understanding of both the literature as well as the practical relevance to that. In this conversation, you're going to learn a ton about testosterone. Everything from what testosterone really is, how it's impacted by aging, how it's impacted by nutrition, and other relevant factors. You're going to also learn a ton about some misconceptions and some of the things that are being purported commonly in media and other avenues about what's really going on with testosterone and how we should be thinking about it across our culture.
Thanks for having me.
Beyond excited to have you here. A lot of areas I want to go into today. You've been in pro sports for a long time. You've been in this entire world of performance and nutrition and science for as long as anybody I know. But I want to start with testosterone. I know you've done a bunch of work lately. You got a bunch of papers that you've authored and published and a whole bunch of stuff going on. So if you wouldn't mind, can you just give us everything there ever is to know about testosterone and keep it in like 30 seconds?
Sure. Yeah. It's a male hormone. I think the internet thinks it's more important than it probably is. That's not to say that it's not important and that it doesn't change that it can't change physiology, but I think we give it inside of the normal range. We give it a lot more credit than it's probably do with an asterisk there that I think you and I both appreciate that there are some things that we don't know about it. Like how important is the peak? Does dropping from 800 to 500 is how is that bad? We know 300's really bad but like how how how what's the delta there?
So a handful of ways I want to tackle this topic because it is so big and one of the things that I appreciate about you so much and over your career is you're one of the very few people I can look to that can look at the same exact problem as everybody else and just see a little bit differently. What is the the primary thing for someone who's in like a high performance mindset and they want to be the best they possibly can? We'll go into disease and medicine. That's some of their point. That's not really what you and I do for the most part.
So, a performance mindset person just kind of off the top of your head, what are the things they should be thinking about with testosterone?
I can give you the wish list. I think that's maybe the most important part. The wish list is for most of us is probably to go back in time and to get testosterone probably in our late teens and to track it over time. Testosterone total and I'll throw free in there and then also sex hormone binding globulin. Tracking those longitudinally. I think for the individual, that's where the the money is and really looking at not just one time point, but how does it relate to to all these other time points and and the the analogy that we we sometimes use is is shoe size, right? Say you're a size 10 and that's your norm, right? But then all of a sudden at 40 you're they're trying to fit you in into a size five shoe. That's probably not going to go very well. So you have to you want to know your peak so that you can kind of maintain it through hopefully throughout the life course.
Why wouldn't I want it just redlined? Why wouldn't I want testosterone just as high as possible all the time?
Left ventricular hypertrophy is a reason not to to redline it. Combine that with some sludgy blood or ariththroytosis. If I'm speaking gobblelygy to you, like testosterone upregulates EPO, which is going to tell your body to make more red blood cells. So if you have more red blood cells, then your blood will get more viscous. So you're now you're not pumping blood, you're pumping oil. So that's like kind of a double whammy on your heart and that you're you have a bunch of back pressure. So you have a bunch of muscle that all of a sudden your your heart has to pump against and it's it's pumping ketchup. I'm fairly certain that's bad idea. You don't want to run that for for decades if you get decades.
So just starting let's assume we'll get to exogenous testosterone kind of later but let's stay within the not on it yet or come often in that sort of range maybe just start us with what is the actual normal range and if you wouldn't mind give us units one time and what a normal range means then we'll start getting into manipulation.
So the normal range for a male of testosterone is debated. Let's call the low anywhere from 264 to 300 nanogs per deciliter. High-end I've seen like outside a lab range can't measure it naturally like this is legit. I I have seen that. I think you and I have both seen enough people in this space thousands of blood labs that like those people do exist. Those people are fairly big. I'm not going to lie to you. Like when I have found those people, but I've also found people who are just as big at 400 nanogs per deciliter. The biggest people, some of the biggest people I know have very normal testosterone. Females are going to be a lot lower than that. The low for females is debated. It's it's harder to measure because we're talking about very minuscule amounts, but 20 might be 20 nanogs per deciliter. You can see it 60 somewhere somewhere in that range. A lot lower 10% gets thrown like they have 10% of the testosterone as males gets thrown a lot depends on I don't know that that's super helpful knowing the ranges is probably more helpful.
You said higher than labs will measure what what's that number?
Depend on the lab like 1,200 nanogs per deciliter we hear a lot about in your bloodstream I mean we were talking about this 5 10 years ago now it's kind of mainstream like you have what five grams of blood sugar in your entire bloodstream at any one time. Diabetes is 7 g or 9 g. This is infantessimally less than that. So what I what I always tell people is to have an idea of how much testosterone in your blood. If you take the average backyard pool, you're looking at like a male is like half a paperclip. So take half a paperclipip or a paperclip, whatever. It doesn't matter. Take the whole thing. Take the whole thing. Take a whole take a couple paper clips of salt and dissolve it in your pool and then we're going to go find that with science which is just it just boggles my mind. And then we're going to have a in general we're going to have a 6% error on that which is which is crazy. Now free test you're talking about millig like five milligrams into a pool and then we're going to go find that with science. And right now we have like a 12 to 15% error on that which is which is pretty crazy. Like that is I don't know sometimes we don't give science enough respect but that that is a crazy thing that we've been able to do. Yeah.
And inside of that same pool just to kind of bring you back to this blood glucose analogy you'd have so you have 5 g of glucose you have nanogs per deciliter nanog you're talking about 10 to the 9th in terms of testosterone. When you look at that same pool, you got 150 lbs of glucose going. Like the wheelbarrow is full of glucose. Yeah. Hematocrit like you're talking like half the pool. Half the pool is half the pool. Yeah. Is red blood cells. So that maybe helps people get a perception about not only how little of this hormone and solute is around, but also its action inside of minuscule amounts. Throw another paper clip on there and you're Ronnie Coleman. Yeah. Yeah. Yeah. Right. So crazy.
So you said a very specific number. You said 264 versus 300. Yeah. Yeah. Why? Why 264? Again, I've been after this question for 15 years, like been in the space for pushing 20 and I've been doing this a long time, but I think it's good to give I haven't been in here as long as like Basin and Kramer, like people were doing this research in the '9s when I was, you know, whatever playing video games and they're still at it. And so we had 300 nanogs per deciliter was kind of this line in the sand forever. And then Basin did some harmonized 2 point we we have this bell curve and so the 2.5% of the population would be below 264 and then 300 it's like 306 or something is where 5% of the population so a lot of these are and this is maybe something to anchor us throughout are population based norms and that's where I think for on the individual level much more important to you like where your peak is same with bone mass and That's one of the big things we don't know. Like, does peak testosterone, does that correlate with peak bone mass? Does that set your skeleton up? And now all of a sudden, you're you're riding that the rest of their life. These are the questions that that we don't have answers to.
So, I think it's fair to say that at this point we have a reasonable understanding of what testosterone is. You know what total testosterone free testosterone and maybe you could you know quickly share that and why that free thing is you kind of diminished earlier you know a lot of people like I thought free testosterone matters the most so I I'll actually just maybe just answer that question.
It's good to honor that in 2026 this debate has been running it's been running hot since the 80s like we've been trying to figure this out and this debate is still running hot like we're talking about journal like endocrine society is still having debates on this. And the reason that I think they're feeling debates is cuz free testosterone is probably where the money is, but it is inherently harder to measure because it has such a low concentration.
What percentage of testosterone is free versus non-free?
2%. And then like you're at 45% is bound to sex hormone binding globulin which we think of sex hormone binding globulin as like all right this is unavailable to tissues that is untrue and it's more of the best analogy that I've ever heard for this is like all right it's a you have this globular protein and albamin is the other carrier and these are globular proteins and they're grabbing testosterone right and it's how strong the grip is sexual globulin has a much stronger grip than albamin and but it it still can be unlocked like it can be released and then the other part that this is maybe like testosterone's cool it sounds cool there's a lot of words that sounds sound cool like you have raase you have like there's so many cool sounding words but maybe my favorite is megalin what megal does is it endo it like eats endoccytosizes the the sex hormone blog gloabbulin and testosterone complex and brings it into the cell and so megalins very probably not expressed in muscular tissues. Unfortunately, as much as that would be cool, it's probably mostly limited to the kidney and the reproductive tract. Yeah. Places that have to get it have to get it. And so that's interesting in and of itself, but the the free fraction and the album infraction are probably what's available to most tissues.
Got it. So, what you're saying is I'll put a number on it. I could use a real number, but a fake one would be easier. Let's just say we had a 100 testosterone total, right? So in our pool, we got a giant pool. We got 100 out there. Of those 100, how many of those would be free?
Two. Two. They're spread there. Like one to three. Free meaning I can go into this cell and be used immediately. Yes. And this is maybe my ultimate gripe with how this science has kind of hit the internet. I think that is true, but it's also not true because the binding and dissociation kinetics of this are so fast. That's the other thing about biology that we can't fathom is like things are operating on millisecond timelines and we're like measuring this once a day luckily at 7 a.m., right? And like testosterone is disassociating. It's moving. It's going across the membranes all all the time. So yes, I think for us to think about this 2% is available to the cells and then that albaminbound testosterone can come off quite quickly. So that that is available as well to the cells. So at any given time maybe 52% of that is available and then 48% is bound to sexual globulin not coming off from.
All right, let me let me stay on free testosterone for a quick second. This is one of those issues where I think the nomenclature does all the success and causes all the damage. I think that if I were to hear the word free testosterone and then non-free testosterone, I'd probably like I want the free stuff. You keep saying 2%. What's the normalish range? Is that always 2%? Is it one to 5%? Like what maybe a typical ballpark for people to see for free? I think absolute numbers is is the play here. And the line like this is this is very pertinent right now because it looks to be like 66 is 66 I think it's pogs per milliliter and this is going to be different if you're in Europe but that absolute number is is the low and I don't really know what to do on the high side of that. Like I'm like great that's kind of my answer. Okay, it's to me it's relative like all right where is this normally for you and then and then where does it go out to but free testosterone if you look if we look at the literature where free testosterone is used is in is in edge cases that's I think really really important so how it's been used in kind of optimizing culture is not how it's necessarily used clinically like this is an edge case it's like all right testosterone's low borderline low and there's symptomatology let's go to free testosterone that's how it's predominantly used.
Why isn't free testosterone always measured?
The concentration so low and it has a lot of air. You're talking about analytical error of 12 to 15%. And then you you and I talk about compounding air all the time. Because it's you just can't get away from it. And we look at labs I think a lot differently than normal people look at labs. Like you look at the the endocrine society how this low testosterone is even diagnosed. You had you need to have two draws, two fasting draws that are lower than whatever the threshold is. That's good because you can have all the lab error, right? Or you might have caught you in a in a in a bad state. And now the the military just put in a really a really cool asterisk which I really like is that now you can't have gone undergone like a severe deficit, severe sleep restriction for 30 days before, which I would love for all the TRT clinics to adopt the new the new guidelines. You'd be seeing a lot of bankruptcy statements come through if that happened for sure. Yeah. No, I want to go through actually all that in detail, but what I want to keep going on free testosterone because I know it took me a long time. You've said this now several times, so slight detour on top of the detour here, but really interesting. What do you mean when you say analytical variability? So, there's intraassay variability. So if I grab your blood, let's just say it's the same vial and I just throw it through the same process. This is if we just run the same lab everything, you'll get 12 to 15% error intraasset. Same person, same sample. You just take the same put it through the machine once, put it through the machine second time, and you'll get a 10 to 12% difference in that number. Yeah. Cuz you're trying to find grains of salt in a pool. In a pool. Super difficult. Why does that matter? This comes back to and we've talked some about this even before the show is just separating signal from noise is that is the job to be done from like in pro sports and data science like you do not want to be reacting and causing unneeded stress because of noise. You want to be reacting to signal and that's why we've we want to model this like I want to know if this value on the individual level is this statistically significant is this inside a lab error am I reacting to noise or is there an actual signal here and that's why it's really really important to know this and that's why I wish that labs would have to publish it'll probably always be best case scenario but you know it's not the lab tech coming a little bit hung over the next day it's like this is this is their best they're the best person at it. And this is this is their air.
Is free testosterone measured the same on on all the big labs?
That's a good point. Like for the end user here, I only want to see free testosterone through equilibrium diialysis. Like that's the gold standard. Like you start I'm not really interested in calculated free testosterone. Maybe that that might be useful at the population, but I I don't I don't care about that personally. And the same thing with testosterone. Don't these aren't Yeah, these exist like you wouldn't want an aminoassay. You want that to be LCMS or massspec liquid chromatography mass spec. You want also want ultra sensitive estradile. Estradile is in that very low range, especially in men where it's very hard to pick up. You know, I'm quite bullish on that. You fictitiously are going to get high values and then everybody freaks out about high estrogen when they should be freaking out about low estrogen.
I want to go through this spin cycle one more time on e what you said. I think that was really, really valuable. I wasn't planning to go here at all, but this is great. This is a this is guidelines. If you want to pay attention to your free testosterone, you said two things there. One, there's a difference between direct and calculated. Correct. Give me more on that. And then what was the thing that people should be looking for? Equilibrium diialysis is the gold standard measurement for free testosterone. That doesn't come on a normal blood test. No, you're you have to select it. And they're in b they're in batches now. Like you would get the gold standard testosterone is in a batch of all right I'm going to get LCMS tes total testosterone then I'm going to get equilibrium dialysis free testosterone that's not on your basic panel and if they were to not select that and they see free testosterone on the report could be like a vermilion calculation something something like that which is calculated from sex hormone bio gabbulin concentrations albamin concentrations which can fluctuate based on hydration status that's the other part about this is there's a lot of acute things that move testosterone like plasma volume being one of them. If you're doing this yourself, you want to standardize the time and the hydration status as much as you can to limit your own volatility because you you start t you start stacking errors here and you're going to be in the realm of 20 to 30% real fast. And if you got to you guys can do the back of the envelope math. If your testosterone is 600, that means your spread just from noise is 120. Like that's pretty crazy. So if you went from 600 to 700, you didn't know if it was real. You don't even know it was real. It just could be because you were more hydrated one day, less hydrated another day or the lab variability or any of those things or the time of day like when you woke up like so your testosterone peaks at slow sleep and then it stays elevated through rest the rest of the night through the REM cycles and then when you wake up it's slow burn. And so like if you got it if you woke up at 5:00 a.m. for your draw the last time and you got it drawn at 9:00 a.m. That's 4 hours awake. That's going to be you might have dropped the the average person you're gonna like you look at the literature it's like 43%. So like from their peak to their to their nater. So like you might have dropped already 20%. Whereas the last time you woke up at 7 you got it at 8. Like that's a completely different draw pattern. The reason why I find this so fascinating interesting is if you're going to make a decision especially about pharmarmacology or anything your sleep or when you're going to work out or is your new exercise routine help like anything that you're trying to figure out here if you're not taking this much care and you're testing you actually don't even know if this stuff is working or conversely you might actually be going the opposite direction.
So, if you don't mind, can you just like give me some fictitious numbers here? What's the average testosterone for 40 to 50 year old male?
550 somewhere in there. Depends on the population that sampled where they are. I think like the UK that's 300. Yeah, the UK bio bank has some again, but this is because of sampling. Like they sampled in like a 10-hour window. They didn't have to be fasting. Eating like fasting is 19%. So like that's what I'm saying. Like you just start stacking errors on this thing and you you do not have signal. That's why knowing the where the noise is can set you free on your own individual data and you want to keep it as as as standardized as you can.
So the absolute amount of difference in a given day of testosterone for you you me you personally right how much would my testosterone change in amount given it in one single day yeah this is diver at all 2003 we've known this they looked at young men fit older men and then older men and the the this is the dal rhythm of testosterone which you're after say your your peak is 650 and then and this happens as when you're sleeping yes and then It drops usually afternoon is late afternoon evening is is the lowest it gets and that is going to be 30 to 40% of that of that morning high. So you're you're talking about dropping 200 250 nearly from your peak. So you could your your low could be 400. Now let's say your peak is at 500. All of a sudden like you get your oh it's 350 like that someone's freaking out or or or let let me make it more tragic you're 450 like you're you're in a most of us would say that's probably a pretty good spot and then you get at the wrong time you wake up at 5:00 a.m. and you actually don't get your blood draw till 9ine, but you fasted, you rested, but you're still four hours into your day. You could easily be in a sub300. Yeah. I think this is why like it's some
Most organizations and health insurance companies require at least two testosterone draws before starting TRT, along with documented symptomatology. Data shows 96% of people on TRT have not followed proper protocol, with only 4% having completed two draws.
When sampling 100 random men at 7 AM with proper methodology, approximately 25% will have testosterone levels below 300 ng/dL. For men of normal weight, this drops to 11%. However, only 5-6% of these individuals will also have clinical symptoms, which is the criteria required for TRT consideration.
Free testosterone testing is often misused to justify TRT prescriptions. A common misleading scenario involves a total testosterone of 450 ng/dL being presented as acceptable, while free testosterone at 45 ng/dL is used to push treatment. This manipulation ignores the fact that only 2% of testosterone is truly free, with the remaining 98% bound to proteins.
Of the 98% bound testosterone, 45-55% is bound to sex hormone binding globulin (SHBG), while the rest is bound to albumin. Albumin-bound testosterone is weakly bound and available in capillary beds where it can dissociate. SHBG levels are significantly higher in metabolically healthy individuals (40-60 range) compared to metabolically deranged populations (20-30 range), making lab reference ranges based on unhealthy populations artificially low.
The primary mechanism by which obesity drives low testosterone is through increased SHBG production due to hepatic fat accumulation. The body appears to regulate SHBG levels intentionally, as evidenced by military studies showing this relationship.
Many people are not receiving proper informed consent before starting TRT. This leads to high discontinuation rates when patients discover the true implications. TRT can be life-changing when medically necessary, but requires understanding of 120 potential causes of low testosterone beyond simple aging.
For those self-managing TRT, hematocrit above 52 is a significant red flag requiring immediate attention. Hematocrit levels of 54 or higher present serious cardiac event risks, particularly for those with potential left ventricular hypertrophy. Regular CBC differential monitoring is essential, with costs as low as $5.50.
Key parameters to monitor during TRT include:
- Hematocrit levels
- PSA tracking
- Lipid panels, particularly HDL levels
- Estradiol using ultra-sensitive LCMS measurement
- DHT conversion symptoms (hair loss, acne)
Testosterone can significantly lower HDL cholesterol, which may be mitigated with fish oil supplementation.
Estrogen is critical for males despite common misconceptions. Low estrogen with high testosterone often produces worse symptoms than low-range testosterone alone. Estrogen supports sexual desire, bone health, and brain function. Ultra-sensitive estradiol testing (LCMS) is required, as standard assays have 20-40% error rates.
Before starting TRT, cardiac stress testing and ECG screening are recommended to rule out atrial fibrillation. The combination of high hematocrit, left ventricular hypertrophy, elevated blood pressure, and potential atrial fibrillation creates significant cardiovascular risk.
Exogenous testosterone shuts down endogenous production. The testes normally produce 6-10 mg of testosterone daily (43-70 mg weekly). TRT doses often exceed natural production, leading to testicular atrophy. This information is frequently omitted from patient education.
Abrupt TRT discontinuation without proper tapering can cause severe psychological effects including psychosis and increased suicide risk. Literature documents cases where patients were chemically castrated, with testosterone levels dropping from 400-500 ng/dL to the 30s.
The hypothalamic-pituitary-gonadal axis regulates testosterone production through GnRH from the hypothalamus, which stimulates LH and FSH release from the pituitary gland. LH signals the testes to produce testosterone, while FSH stimulates sperm production. These hormones are pulsatile and difficult to measure accurately.
Testosterone production is driven by LH spikes, with both LH and FSH functioning as the regulatory thermostat of the reproductive system. This regulatory component is more important and more likely to become disregulated than the output apparatus itself. The body often regulates hormone production in the way it intends to, even when that appears negative from an external perspective. Low energy availability causes the body to downregulate reproduction, which is an adaptive response rather than a malfunction.
Hammersland and Fredo military studies demonstrate how dramatically testosterone can be suppressed in males. These studies used GnRH agonists like goserelin or zoladex to pharmacologically knock out the pulsatile nature of hormone release at the brain level. The analogy used is a trombone: the drugs initially cause an increase before suppression occurs. These interventions dropped men to 30-60 ng/dL total testosterone, which represents postmenopausal female levels. The 2006 study maintained castrate testosterone levels throughout the entire duration, while the 2022 study used a single goserelin injection.
The 2006 study maintained participants at castrate levels for 8 weeks, while the 2022 study used a single injection. Both studies lasted approximately 20 weeks total, with the pharmacological suppression lasting 10 weeks in the first study. Despite the extreme physiological stress, no participants dropped out of either study. These drugs are legitimately used for testosterone suppression in cancer management and other medical conditions, and some are used off-label as fertility drugs.
When the HPG axis is pharmacologically suppressed for weeks, recovery typically occurs over weeks to months, though some individuals require up to nine months for full recovery. The effects of years-long suppression on testicular atrophy remain unknown. hCG serves as an LH analog that stimulates Leydig cells to maintain some testosterone secretion, preserving testicular volume and function during suppression.
The Kvorning and Gandelhar 2022 study found that participants resistance training at castrate testosterone levels (30 ng/dL) still gained lean body mass, though gains were blunted to 43-73% of placebo group gains. One individual maintained sub-50 ng/dL total testosterone for two months while resistance training and still gained muscle, achieving 43% of the muscle gains compared to the normal testosterone group.
A meta-analysis of 150 hypertrophy studies found the average untrained individual gains 1.5 kg of lean body mass over 10 weeks of training. The control groups in these studies typically had 600 ng/dL total testosterone, while the suppressed groups had approximately one-tenth of that level.
In the Longland 2016 study, overweight participants lost 11 pounds of fat while gaining 2-3 pounds of muscle in just four weeks. Measurements were taken using DEXA with total body water assessment, representing one of the most accurate body composition methods available. Participants started at 23% body fat with a BMI of 29. Their testosterone dropped from 500 to 110 ng/dL during the study, while sex hormone binding globulin increased by 30%. Energy availability was calculated at 33 kcal per kg of lean body mass.
The dramatic body composition changes occurred despite participants running 12,000 steps daily and completing six workouts per week. The combination of transitioning from sedentary behavior to high exercise volume plus caloric deficit caused the testosterone suppression in this laboratory setting.
The Vidic keto study compared moderate weight loss on keto versus non-keto diets, with both groups following very high-fat, low-carb protocols with resistance training. Participants increased testosterone from approximately 600 to 800 ng/dL over 10 weeks. However, despite the significant testosterone increase, participants showed no muscle or strength gains.
The contrast between studies shows a 700-point swing in testosterone levels: from 110 ng/dL with significant body recomposition to 800 ng/dL with no muscle or strength gains. These extremes illustrate that within the eugonadal range, total testosterone does not predict resistance training hypertrophy adaptations.
Five studies (six including free testosterone) examining the relationship between total testosterone and muscle hypertrophy within the eugonadal range have all shown null findings. These studies are typically bolt-on analyses from existing resistance training protocols. Mike Roberts has conducted two of these studies. The consistent null findings suggest publication bias may exist, as positive findings are typically favored for publication.
When exogenous testosterone is introduced above the eugonadal range, a dose-response relationship emerges where higher doses produce more muscle. The Bhasin 1996 study demonstrated this effect, with participants gaining approximately 10 kg of muscle over 20 weeks on 600 mg weekly. Even moderate exogenous use can produce significant changes, with one individual reporting gains from 180 to 190 pounds at 10% body fat.
Within the studies examining natural testosterone levels, individual variation was substantial. One participant at 1,900 ng/dL was middle of the pack for muscle gains, while another at 500 ng/dL gained 8 kg of muscle in 12 weeks. Scatter plots showed no relationship between total testosterone and hypertrophy outcomes, with flat lines across all data points.
Studies have examined DHT, androgen receptor content, androgen receptor sensitivity, androgen nuclearization, changes in androgen receptor content, and IGF-1 in relation to hypertrophy. However, delta measurements of these factors may simply reflect training intensity rather than causal relationships, as harder-training individuals show greater inflammatory cytokine responses like IL-6.
Training studies reveal significant variation in participant motivation. Some individuals participate primarily for compensation like gift cards, while others are highly motivated and optimize their diet, sleep, and training throughout the study period. This creates hyper-responders who may skew results. Study ecosystems can develop their own dynamics, where motivated participants influence others or where unmotivated participants negatively affect the overall group atmosphere.
Resistance training studies are typically underfunded and underpowered. Most lack comprehensive data on sleep patterns, dietary intake, and other variables that influence outcomes. The Longland study was exceptional in controlling physical activity variables through daily step counts and structured workouts.
A hypothetical scenario involving identical monozygotic twins with one receiving pharmacological testosterone suppression via zoladex to maintain 350 ng/dL while the other maintains 750 ng/dL would likely result in similar muscle growth over 10 weeks of identical training, suggesting total testosterone within the normal range is not the primary determinant of hypertrophy outcomes.
Total testosterone alone cannot predict which individuals will be the highest responders to resistance training. Other factors like ribosome content, skeletal structure, and overall health status may be more predictive. The highest natural testosterone levels might correlate with better overall health markers like sleep quality rather than direct causation of muscle growth.
The focus should shift from who will gain the most muscle to understanding why people stop putting on muscle mass over time. This involves exploring potential rate limiters, whether capillary issues exist, or other physiological factors that halt muscle growth. The scientific interest lies in the sex hormone body piece and what prevents continued gains beyond the 20, 30, or 40 pounds of lean mass that individuals are capable of achieving.
Obesity represents the number one driver of low testosterone in males currently, operating through an SHBG mechanism and likely through a leptin mechanism. Bariatric surgery causes an average 207 nanograms per deciliter increase in testosterone. When obese or overweight males lose weight and adipose tissue, testosterone invariably goes up along with sexual drive. These individuals are generally still obese, moving from 35 to 30 BMI or from 40% to 30% body fat.
The relationship between obesity and androgens operates in opposite directions for men and women. In females, obesity causes an increase in androgenism and PCOS (now called PMOS), creating a hyperandrogenic state. In males, obesity produces a lower androgenic state. Both effects stem from the SHBG mechanism where liver fat accumulation drives down sex hormone binding globulin.
Leptin functions as a fuel gauge hormone where body fat increases cause leptin to rise. When leptin is low, as seen in military studies with names like hammers land fedal and veros noi from Norwegian special fortune studies, the body interprets this as insufficient energy and lowers testosterone. At the hypothalamic level, kisspeptin regulation causes the brain to enter low battery mode, shutting down circuits that cost energy including reproduction and muscle growth.
When obese, the brain receives a leptin resistance signal and may not properly perceive the leptin levels. Combined with SHBG downregulation from hepatic steatosis and liver fat accumulation, this creates the physiological response where the brain provides protection against scenarios it perceives as energetically insufficient.
Animal studies, including Zapolski's field study on bonobos during famine, show testosterone levels tank and sexual activity decreases significantly. When male apes are castrated, they have less sex but not zero sex. Returning just 10% of original testosterone restores sexual activity to baseline levels. Human data from Woo et al 2010 and Finkelstein's pharmacological studies indicate a hyperbola where sexual desire, libido, and sexual thoughts decline around 200-300 nanograms per deciliter, with significant drops occurring at 100 nanograms per deciliter.
Endocrine societies typically establish floors around 300 or 265 nanograms per deciliter rather than providing guidance between 600 and 400 because no clear changes in libido or desire occur in that range. However, the delta between individual baseline levels matters significantly. Some 21-25 year old professional athletes maintain levels of 1080, 1050, or 1150 without optimization, while others perform at elite levels with 500. These athletes demonstrate fat-free mass indexes of 25, which represents the threshold for concern about drug use and indicates lifetime natural status.
Testosterone levels do appear to be declining population-wide over the past 50 years, with significant drops when comparing 40-year-olds today to 40-year-olds from 50 years ago. While obesity contributes substantially, environmental factors including microplastics and endocrine disruptors likely play a role. Some measurement error from assay differences between 1970s and 2020s technologies may contribute, but a genuine signal exists beyond these technical factors.
Mendelian randomization studies demonstrate that body composition affects testosterone far more than testosterone affects body composition within the normal range. The inverse relationship shows that higher fat-free mass indexes correlate with both higher obesity and lower testosterone levels. While genetic conditions like Klinefelter's syndrome create exceptions, the vast majority of cases show obesity as the knockdown factor for testosterone.
Using a fasting morning draw with a threshold of sub-300 or sub-264 nanograms per deciliter, approximately 25% of the United States population qualifies as having low testosterone. Among obese individuals defined as BMI greater than 30, this rises to 40%. For individuals at the lowest BMI possible, there exists nearly a 50% chance of clinically low testosterone. Conversely, normal weight individuals have a 90% chance of not having low testosterone and a 0.9% chance of having both low testosterone plus symptoms.
Metabolically healthy individuals under 50 years old with waist circumference not exceeding half their height, good blood glucose control, solid triglycerides, healthy HDL, and regulated blood pressure have less than 1% chance of testosterone below 300. Even extending this estimate fivefold suggests 95% protection. The NHS paper referenced showed sub-1% prevalence in metabolically healthy populations.
Scatter plots reveal 80-year-olds with 800 nanograms per deciliter testosterone and 75-plus year olds who have never taken peptides or vitamins, eat McDonald's regularly, and maintain levels around 750. These individuals exist in current databases as common rather than exceptional cases.
The narrative that testosterone drops 1-2% per year after age 30 represents a race to the bottom on social media, but prospective longitudinal studies of healthy aging show different patterns. Cartto et al 2023 found that when examining only individuals without comorbidities longitudinally, the annual decline dropped from 1.5% to 0.8% and lost statistical significance. Sheall 2013 demonstrated that individuals meeting zero criteria for metabolic syndrome at both entry and follow-up showed no testosterone decline.
Personal tracking reveals that an individual whose highest measured level was 650 nanograms per deciliter experienced drops to 500, 300s during cuts, and potentially the 20s at 3-6% body fat with hot flashes from extremely low estrogen. After refeeding from a leptin level of 6, testosterone remained in the 400s while sexual binding globulin rose from the 40s-50s range to the 60s over two weeks without weight gain.
Spontaneous loss of 10 pounds of muscle mass within 3 weeks, such as dropping to 165 pounds, warrants investigation for serious conditions like cancer rather than immediately checking testosterone levels. Andropause does not appear to be a normal function of aging in very healthy individuals, though sex hormone binding globulin does increase with age.
After age 70, steeper testosterone decline likely occurs due to oxidative stress susceptibility of Leydig cells. Until age 70, individuals can potentially maintain normal testosterone levels if healthy. Marriott 2023, examining what predicts testosterone decrease across large populations, found that age was not a factor until after 70, while diabetes, metabolic dysfunction, smoking, and alcohol consumption were significant predictors.
The 1-2% annual decline observed in longitudinal studies reflects the price of aging in current society, where BMI and body fat increase until later life when appetite decreases and muscle loss occurs. If waist circumference remains stable from age 30 to 70, testosterone would likely stay within 10% measurement variation. The scatter plot patterns show flat lines until age 70, when increased dots appear on the low side, driven by sampling variance and apparatus failure rather than universal decline.
Scatter plots demonstrate that on an individual level, people should disregard what the mean testosterone level is doing. There are so many data points around the mean that individuals should focus solely on their own results rather than population averages. The average person potentially maintains the same testosterone levels from their 20s through age 90, though variance increases after age 70.
Testosterone functions as a canary in the coal mine. If testosterone drops, the first response should not be exogenous testosterone. Instead, the underlying cause among the approximately 110 factors that could affect the hypothalamic-pituitary-gonadal axis should be investigated. Age is not a significant driver of testosterone decline within healthy aging when metabolic health is maintained.
Obesity is the number one factor affecting testosterone levels. When considering symptoms of low testosterone, sexual symptoms are the reliable indicators rather than generalized fatigue, which has many possible causes at age 40 including life stressors like mortgages and children. Marriage and pair bonding can lower testosterone by approximately 10%, with additional effects from co-sleeping and having children.
Before starting TRT, especially for therapeutic use exemptions in sports, sleep apnea must be ruled out. Weight gain, particularly visceral adiposity around the midsection, is the first checkpoint. Gaining 16-18 pounds of pure fat from a normal weight of 180 pounds to 205 pounds at age 40 is likely enough to significantly impact testosterone levels, though the magnitude depends on existing muscle mass. Moving from normal weight to obese category produces significant testosterone reduction.
Testosterone effects depend on an individual's personal fat threshold. Gaining adiposity while remaining under the personal fat threshold does not affect testosterone. However, once subcutaneous fat stores are filled and fat begins storing ectopically around organs, SHBG decreases and testosterone drops. DEXA scans are unreliable for tracking visceral adiposity.
The supplement research for testosterone enhancement is weak. The highest quality supplements may increase testosterone by 75-100 ng/dL at best. In contrast, losing 10 pounds when above the personal fat threshold can increase testosterone by 150-200 ng/dL. For someone at 30% body fat, weight loss produces linear testosterone increases without any supplementation needed.
Sleep apnea is highly prevalent and requires checking, particularly given its association with larger tongue size. SSRIs and opioids significantly suppress testosterone. Medical causes that need evaluation include pituitary adenomas and brain tumors.
Weight loss affects testosterone differently depending on starting point. Losing weight when already lean suppresses testosterone, while losing weight when carrying excess adiposity increases it. Multi-stressor environments reliably lower testosterone. Refeeding after caloric restriction can rapidly restore testosterone levels, with documented cases showing sexual function scores improving from 20 to 50 within one week of refeeding.
Sleep deprivation causes moderate testosterone reduction. The Leproult 2011 study found that 8 days of 5 hours sleep per night caused a 15% testosterone decrement. While this represents acute rather than chronic data, the recommendation is to avoid betting on long-term sleep restriction. Inflammation from chronic sleep issues acts as an independent driver of lower testosterone.
Zinc and magnesium deficiencies should be avoided. Copper status also matters for mitochondrial function. Stomach acid production is metabolically expensive, and digestive issues may signal mitochondrial dysfunction. Hair, nails, and skin quality can indicate systemic energy production problems. The current generation faces third-generation micronutrient deprivation despite adequate caloric intake.
GLP-1 medications show promise for increasing testosterone through weight loss effects, though more data is needed. Bariatric surgery can increase testosterone by approximately 200 ng/dL through substantial weight loss, but creates challenges for maintaining adequate micronutrient intake.
Alcohol in excess of 7+ drinks per week likely suppresses testosterone, though moderate consumption is less concerning. Marijuana effects are mixed. Overtraining studies are confounded by concurrent sleep reduction and caloric deficits. Studies examining increased training volume without significant weight loss have not shown testosterone changes.
Varicoceles represent an underrecognized cause of low testosterone in lifters. These enlarged veins off the testicle occur in 80-90% of Olympic lifters due to repeated Valsalva maneuvers increasing pelvic floor pressure. Surgical repair can increase testosterone by 150-200 ng/dL, comparable to obesity-related suppression effects. Urologists can identify these from across the room, and they create physical blocks preventing proper testosterone circulation.
Varicocele is a condition where veins come off the testicles. It's a laparoscopic procedure to fix and reliably increases testosterone. For low-grade cases, it probably isn't causing a problem, but if testosterone is 250-300, it should be addressed. The recommendation is that anyone with reasonably lean body composition, lifting weights, adequate sleep, and verified low testosterone (250-300 range confirmed two or three times) should get checked by a urologist before considering TRT, as a simple procedure might restore natural levels.
Cyclists using seats without gaps for the testicles are constricting them in a hot space for extended periods. Triathletes training 20 hours per week may be causing similar damage. Training volume should be brought down if testosterone is low. Other markers related to overtraining include DHEA (another androgen), testosterone to cortisol ratio, IGF-1, CRP, and creatine kinase. These values can indicate whether low testosterone is due to an overtraining or overreaching scenario.
Before going on lifelong prescription TRT, all possible mechanisms leading to low testosterone should be investigated, as these could also be hurting performance. When testosterone is low, it's not the only benefit being missed—addressing root causes provides additional benefits beyond just raising testosterone.
For lean males (sub 25%, sub 20% body fat), the story is different than for obese individuals. Population studies show one pattern, but individual case studies of bodybuilders are more relevant. One documented case showed an individual reaching 26 total testosterone (not free testosterone) with immeasurable thyroid hormones and unmeasurable free T3 while at extreme leanness. This represents castration-level suppression achieved through extreme dieting.
When refeeding from extreme leanness (under 5% body fat), testosterone can recover significantly. In one case, an individual went from 26 total testosterone at extreme leanness to 650 total testosterone at 12% body fat. Sex hormone binding globulin stayed relatively stable (25-35 range) during this transition, with the testosterone increase coming from total test rather than changes in binding globulin. Literature on this degree of leanness generally shows recovery over months while gaining body fat back.
Energy intake is 100% regulating testosterone in case studies of bodybuilders. The brain is the primary driver—the spectrum from 600 to 30 to 600 total testosterone demonstrates this brain-based mechanism. Energy in the brain is the largest signal because calories are converted into reproduction, which is the fundamental point of existence.
There's a U-shaped relationship between body fat and testosterone. Going from 35% to 30% body fat can increase testosterone 50-100-200 points. However, once below 20% body fat, the opposite occurs—continued caloric deficit causes testosterone to drop again. Individual dynamics matter more than absolute percentages because the brain adapts to whatever leptin level was the highest point. Some clients lost half their body weight (300 to 150 or 330 to 180 pounds) without going below 15% body fat, yet had dramatically different testosterone outcomes (850, tanked levels, or 200 total testosterone).
Relative percentages of body fat change matter more than absolute numbers. The Biggest Loser study would have been more informative with these metrics. Instagram challenges where trainers gain 40 pounds of fat demonstrate that even temporary obesity can permanently change physiology and what the brain perceives as safe.
For someone in the obese category wanting to lose weight, the goal should be reaching the drop point where testosterone increases without going too far. For someone at 20-25% body fat wanting to reach 15-12%, monitoring is needed to avoid cutting too much.
The Longland study showed participants going from 23% to 19% body fat in 4 weeks with significant results. The suggestion is that refeeding these participants and lowering training volume would likely bring testosterone back to 500. When calories are returned after being too low for extended periods, testosterone returns to middle range.
For someone at 25% body fat wanting to reach 15%, nutritional flexibility is extensive. Micronutrient repletion is essential, but macronutrient approach (high carb, low carb, vegan, non-vegan) can vary. The focus should be on reaching the other side and refeeding appropriately.
Long-term caloric restriction studies (10-20% deficit) show bodies adapt by downregulating thyroid hormone. These individuals had low IGF-1, low testosterone, and high sex hormone binding globulin. Whether extending life by 5 years in this state is worthwhile remains unknown. Long-term low-level caloric restriction in lean individuals lowers anabolic signals, with testosterone dropping to the 300-400 range.
Someone dieting for 6-9 months who feels crappy with low energy and libido may not necessarily have low testosterone—the symptoms could be from hunger itself. The solution is to get calories back up and observe what happens. For extreme cases where someone went from 350 to 150 pounds and remains at 20% body fat with 200 testosterone even after refeeding, this represents a new world problem requiring pharmacological intervention rather than more self-discipline.
Refeeding should go right back to maintenance calories. For someone who dieted at 2200 calories with an 800-calorie deficit over 20 weeks while maintaining muscle, stair-stepping calories back up is recommended. This involves increasing by 25-50 grams of carbohydrates per week. The first priority is getting fat intake above 80 grams for males (50-60 grams for females) or above 20% of calories. Carbohydrates should be ramped up using whole food sources like fruit.
During refeeding, psychological burden should be offloaded by reducing neurotic tracking. Food-first approaches are preferred—adding a sweet potato three days per week rather than precise measurements. Premortem discussions are essential: warn clients they will gain 2-3 pounds from GI tract mass and 2-3 pounds from water weight when increasing calories, explaining this is not fat gain. Glycogen depletion over 20 weeks means the math doesn't support actual fat gain from moderate calorie increases.
Professional athletes across NBA, NFL, MLB, NHL, MLS, golf, tennis, and F1 face unique constraints. They have the deepest data capture capabilities but often lack schedule control and external load management. The survival matrix of professional seasons is brutal regardless of sport. The primary advantage that can be provided is recovery enhancement through supplements, sleep optimization, and recovery protocols rather than manipulating external loads they cannot control.
Athletes can marry external load manipulation with recovery strategies to optimize adaptation. An athlete's peak generally comes from recovering more effectively so they can adapt to the high volume they will inevitably face. Mid-first round draft picks commonly complete 20 to 30 draft workouts in just three to four weeks, leaving them completely burnt before entering summer league. This makes the rookie year extremely difficult, as athletes have no control over external load and must simply survive the demands placed on them.
NFL commentators frequently note that rookies fade toward the end of their first season, attributing this to the longer professional schedule compared to college. However, the real issue is that these athletes had no offseason. Football players start training camp in June, compete through January bowl games, immediately transition to combine prep, train intensely to post their best numbers in April, get drafted, receive only a four-and-a-half week break, then return for rookie mini camp. By the following December, they are exhausted not because they failed to adapt to a long season, but because they had virtually no break for a year and a half. This pattern appears across professional sports, with athletes fading late in year one after running on three weeks of rest plus tremendous psychological stress.
Two distinct athlete profiles exist: those who need help recovering from stress, and those who have capacity to adapt to stress rather than merely survive it. Helping athletes shift from survival mode to adaptation mode provides tremendous value. NBA data shows that veterans tend to get leaner and fitter throughout the season, likely because they enter training camp in better condition than younger players, though significant variance exists across individuals and positions.
Recovery interventions can potentially raise an athlete's peak performance, especially in younger athletes who retain adaptive capacity. This applies across multiple tissue levels. Key areas include helping athletes learn and understand their sport with adequate energy for cognitive processing, optimizing body composition for the specific demands of their position, and addressing soft tissue adaptation. Soft tissue remains the hardest element to quantify, with MRI and other imaging modalities through facilities like Springbach failing to provide adequate mapping of these tissues.
The financial payoff in professional sports comes from securing third and fourth contracts, though in some cases even the second contract represents the critical milestone. The NFL differs significantly by position, with some players earning substantial money on their second contract while others require a third contract to achieve financial security.
Recovery tools matter most when paired with appropriate loading strategies. Teams hire performance specialists primarily to discuss loading protocols and determine how to increase training volume safely. The stimulus itself holds equal importance to recovery interventions. Managing that stimulus becomes challenging when schedules are fixed, such as the NBA or NHL's 82-game seasons or the NFL's 17-game schedule.
At the professional level, the stakes justify throwing every available tool at recovery. Athletes vary widely in their willingness to adopt supplements, with some embracing all available options while others remain appropriately skeptical. Building trust forms the foundation of any intervention, as athletes already carry tremendous psychological burden from managing relationships, handling game stress, and dealing with 60,000 fans yelling at them.
Sleep represents the foundational recovery element. Athletes often play under bright lights until 10 or 11 p.m., requiring rapid onramping to sleep and effective offramping from the heightened state of competition. Some athletes may need to adopt a more nocturnal schedule, sleeping until 10 a.m. after late games. GI function should be assessed and optimized, as gastrointestinal distress undermines supplement effectiveness. Data capture has become extensive, making the trusted advisor relationship essential so athletes feel comfortable sharing sleep difficulties without fear of information being reported to coaching staff.
Heat therapy ranks among the most effective recovery modalities. Compression devices and any tools that promote blood flow provide meaningful benefits. Contrast therapy can be incorporated if desired. Restorative movement that does not compromise adaptive capacity includes low-level isometrics, prehab and rehab exercises, and low-level aerobic work. Despite their high-intensity sport demands, athletes tend to be quite sedentary outside of practice and games, which impairs recovery. Targeting approximately 8,000 steps daily supports recovery, though for athletes experiencing significant impact from jumping or contact sports, non-ambulatory options like cycling may be preferable.
When athletes take exogenous testosterone, they lose their natural daily rhythm where levels might start at 650 ng/dL and drop 30-40% throughout the day. Instead, their hormone levels follow the pharmacokinetics of their delivery method, whether injections, gels, or other formulations with specific half-lives.
The TRAVERSE trial represented a significant advancement by removing cardiovascular disease risk warnings from testosterone labeling. This study used AndroGel in men diagnosed with hypogonadism, returning them to mid-normal range, and found no increase in major cardiac events compared to hypogonadal men receiving placebo. However, the trial did not examine individuals pushing testosterone to peaks of 1500 ng/dL, allowing levels to remain at 1200 ng/dL three days post-injection without managing hematocrit, hydration status, or estrogen levels. This pattern does not constitute TRT but rather represents running supraphysiological doses.
A study found a 51% increased risk of major cardiac events in individuals without hypogonadism diagnosis who began TRT. Approximately one-third of people receiving testosterone fell into this category. While confounders exist, this population demonstrates elevated risk. The military has established new guidelines targeting peak testosterone levels in the 600-700 ng/dL range, with dose reduction recommended if levels exceed this threshold.
TRT refers to exogenous hormone administration returning levels to normal physiological range. Running gear refers to using hormones to maintain levels at 1500-1800 ng/dL without allowing drops below 1100 ng/dL. When individuals choose supraphysiological dosing, informed consent becomes essential. The long-term consequences may not appear for 5-10 years, and individuals may remain unaware of accumulating risk. No definitive study exists on this practice, and such research will likely never be conducted due to ethical constraints on administering supraphysiological doses to healthy populations.
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