By Christopher Piercecchi, MD
Physician and Wellness Manager, Founder, The Men’s Clinic for Wellness & Vitality
SITREP is an evidence-based review briefing for patients and colleagues at The Men’s Clinic for Wellness & Vitality. It is educational and does not constitute individualized medical advice.
If you’ve spent any time on TikTok or Instagram over the past year, you’ve probably run into a guy claiming he “fixed his testosterone.” He’ll walk you through his morning sunlight-on-the-testicles routine, followed by a cold plunge and wrapped up with a Zone 2 session. He throws in a sleep-optimizing routine and makes little mention of the fact that he’s also injecting testosterone he bought online, with no physician guidance, baseline labs, or routine follow-up. The whole routine gets labeled t-maxxing. Guided by “Bro science.”
Some of it is perfectly legitimate. Sleep, body composition, and resistance training all influence testosterone, and I recommend those things to my own patients. The problem starts when t-maxxing moves from improving those habits to using testosterone, anabolic steroids, peptides, and other hormones without knowing whether they are needed, what dose is appropriate, or what those drugs are doing to the rest of the body. Medically supervised testosterone therapy is generally intended to restore testosterone to a physiologic range. Self-directed hormone use can become something very different, particularly when doses increase or multiple drugs are combined.
That distinction is important. Properly dosed testosterone replacement is not the same thing as pushing androgen exposure beyond normal physiology or stacking several hormone-active drugs together. The risks change as the exposure changes, and that is where much of the social-media discussion about “optimization” begins to fall apart.
How common this actually is
This is not a fringe habit, and the broader trend predates the term t-maxxing. Testosterone use has risen substantially in the United States, particularly among younger men. National prescription data found that the number of people receiving testosterone increased 27 percent between 2018 and 2022, with a 58 percent increase among those aged 35 to 44.[1] That is prescribed testosterone, not t-maxxing, but it gives some sense of how rapidly interest in testosterone has grown.
Nonmedical androgen use is also more common than most people probably realize. A large meta-analysis of 187 studies estimated that about 6 percent of men had used anabolic-androgenic steroids at some point in their lives, with considerably higher rates reported in some bodybuilding and gym populations.[2] This is not a phenomenon invented by TikTok. What social media appears to have done is bring an older culture of steroid and hormone use into the much larger world of wellness, longevity, and self-optimization.
A recent survey of U.S. men between 18 and 40 shows how much those worlds are beginning to overlap. Roughly 40 percent said they were interested in supplementing their testosterone, and nearly 14 percent reported having used testosterone or a testosterone-boosting product.[3] Among users, the products were not limited to prescribed testosterone; some reported using SARMs and anabolic steroids as well. About 28 percent obtained treatment through a urologist, 22 percent through primary care, and another 15 percent through direct-to-consumer services, with the remainder coming through other sources. The point is not that every young man interested in testosterone is buying steroids on the internet. It is that legitimate testosterone therapy, anabolic drugs, unregulated compounds, and ordinary lifestyle habits are increasingly being packaged together under the same idea of “optimization,” even though they are very different things with very different risks.
What actually raises your testosterone
Start with the part of t-maxxing that is actually worth keeping: the basic things that support normal testosterone production. There is real evidence behind some of them, although not always for the reasons social media would have you believe.
Sleep matters, but the relationship is more complicated than saying that every bad night lowers your testosterone. Large population studies have found associations between impaired or inadequate sleep and lower testosterone, and sleep-disordered breathing appears to matter as well. A meta-analysis of 18 studies involving more than 1,800 men found that obstructive sleep apnea was associated with lower testosterone even after accounting for age and body mass index, with the strongest relationship seen in men with severe sleep apnea.[4] Experimental sleep-deprivation studies point in the same direction when sleep loss becomes substantial. In one tightly controlled sleep-lab experiment, ten healthy young men were allowed ten hours in bed for several nights and then restricted to five hours. Their daytime testosterone fell by 10 to 15 percent after only a week.[5] That small experiment should not be taken to mean that everyone who sleeps five hours will experience exactly the same decline, but it does show how quickly significant sleep restriction can affect testosterone.
Body composition has an even stronger evidence base. Across dozens of studies, weight loss in men with obesity is consistently associated with rising testosterone, and the men who lose the most weight generally experience the largest increases.[6] A meta-analysis of 44 studies involving more than 1,700 men found increases in both total and free testosterone following weight loss. In an analysis of the Diabetes Prevention Program, men assigned to a structured lifestyle intervention lost about 17 pounds over a year and increased their testosterone by roughly 15 percent on average. At the beginning of the study, about one in five had testosterone in the deficient range. A year later, that had fallen to about one in nine, without testosterone therapy.[7]
There are several reasons weight matters. Fat tissue contains aromatase, an enzyme that converts testosterone into estrogen, but that is only part of the story. Obesity and insulin resistance can also disrupt the hormonal signals from the brain that tell the testes to produce testosterone. As excess body fat comes down and metabolic health improves, several of those factors improve at the same time.
Resistance training matters too, although not because it reliably raises your resting testosterone. Its value is much broader than that. Maintaining muscle and strength becomes increasingly important as men age, and resistance training also improves insulin sensitivity, body composition, physical function, and metabolic health.
Alcohol also deserves some context. The occasional drink is not going to destroy a man’s testosterone. The concern is chronic or heavy intake. A large meta-analysis involving more than 10,000 men found that chronic alcohol exposure was associated with lower total and free testosterone and higher estradiol.[8] The effect appears to depend on how much and how often someone drinks, which is another reason claims that a single drink will “crash your testosterone” should be treated skeptically.
The part of t-maxxing that actually makes sense is pretty straightforward. If you are sleeping poorly, carrying too much body fat, dealing with untreated sleep apnea, or drinking too much, fix those things first. Resistance training still matters because maintaining muscle, strength, and metabolic health matters. These are the basic things that can improve testosterone when something reversible is contributing to the problem, and they are also the things we have the best evidence for.
I realize some of the people reading this may already have strong opinions about supplements, hormones, longevity medicine, or what gets passed around as “gym bro science.” Some may distrust physicians altogether or believe that what they hear in the gym or on social media is more useful than what comes out of medical research. I understand that. But I’m not asking anyone to take my word for it. I’m showing you the data. You can agree with the conclusions or not, but the evidence is what it is. My goal with these SITREPs is to give you the best information we actually have so you can make decisions that improve your health, performance, and longevity without unnecessarily putting yourself at risk.
The problem is that t-maxxing often does not stop with sleep, exercise, or losing body fat. Once testosterone or another hormone is added, you are doing something very different. That is where the risks, and the need for medical oversight, start to matter.
Where it stops being fitness advice
This is where t-maxxing stops being lifestyle advice and becomes hormone use.
When you introduce testosterone from outside your body, the hypothalamus and pituitary recognize that testosterone is already present and reduce the LH and FSH signals that normally tell the testes to produce their own. Your natural testosterone production becomes suppressed, and sperm production can fall dramatically or stop altogether.
Making sperm requires very high testosterone concentrations inside the testes, roughly 50 to 100 times higher than the level measured in the bloodstream. Once LH and FSH are suppressed, the testes may no longer be able to maintain those concentrations.[9]
A cohort of men evaluated at a fertility clinic after using exogenous testosterone found that 91 percent were azoospermic, meaning they had no measurable sperm at the time they were seen.[10] This was a highly selected group of 34 men who were already struggling to conceive, so that number should not be interpreted as the rate of azoospermia among all testosterone users. But it does show how profound the suppression can become. With treatment aimed at restoring sperm production, the average time to any sperm recovery was 6.8 months, and only 41 percent had returned to a normal sperm count by the end of the study. Half still had low or absent sperm counts even after their hormone levels had normalized.
If you are a man in your 30s or 40s who may want children in the future, that matters. But even if fertility is not a concern, there is another issue that becomes increasingly important in t-maxxing: dose.
Medically supervised testosterone therapy is generally intended to restore testosterone into a physiologic range. When men begin dosing themselves, increasing the dose because they want more muscle, more energy, or a higher number on a lab test, that boundary can disappear quickly. Once androgen exposure becomes supraphysiologic, the evidence looks very different from the data on properly dosed testosterone replacement.
Studies of anabolic-androgenic steroid users consistently show higher blood pressure, unfavorable changes in cholesterol, and changes in cardiac structure and function. More importantly, we now have long-term outcome data. In a 2025 Danish cohort that followed 1,189 anabolic-steroid users and more than 59,000 matched controls for an average of about 11 years, the steroid users had three times the risk of myocardial infarction, more than twice the risk of arrhythmia and venous thromboembolism, more than three times the risk of heart failure, and nearly nine times the risk of cardiomyopathy.[11]
That is not the same thing as appropriately dosed testosterone replacement under medical supervision. The problem is what happens when testosterone is pushed beyond replacement levels, other anabolic drugs are added, and nobody is really controlling the exposure.
Hematocrit is another example of why monitoring matters. Testosterone stimulates red blood cell production, and in some men hematocrit rises enough to become a clinical problem. In a large database study of men receiving prescribed testosterone, those who developed secondary polycythemia had higher odds of major cardiovascular events and venous thromboembolism during the first year of treatment.[12] That is why hematocrit is checked before treatment and periodically afterward, with intervention generally recommended when it reaches 54 percent.[13]
And t-maxxing often does not stop with testosterone. Growth-hormone peptides such as CJC-1295 are sometimes added to the same regimen. These drugs can substantially raise GH and IGF-1. In controlled human studies, CJC-1295 increased mean GH several-fold and raised IGF-1 for days after dosing.[14] We do not have good long-term outcome studies of recreational peptide users, so we should not pretend that we know exactly what those risks are. But we do know what sustained GH and IGF-1 excess does in humans. Chronic excess is associated with insulin resistance, hypertension, cardiac hypertrophy, arrhythmias, cardiomyopathy, and heart failure.[15]
At that point, you are no longer dealing with one hormone. You are changing several hormonal systems at once, often without knowing what level you are producing, how the drugs interact, or what those changes are doing to the rest of the body.
What matters is what you are taking, how much you are taking, what level it produces, and what happens to the rest of your body while you are taking it. The source matters too, because a prescribed pharmaceutical product and an unregulated product bought online are not necessarily the same thing. If you actually think your testosterone is low, the answer is not to guess at any of this. Measure it properly and figure out why it is low.
What a real workup looks like
If you’re genuinely concerned about low testosterone, start with a physician who will actually figure out whether you have testosterone deficiency and, if you do, why. The diagnosis requires both a compatible clinical picture and consistently low testosterone levels.[16] Avoid clinics that seem to put nearly everyone who walks through the door on testosterone. The goal should be to make a diagnosis, not simply find a reason to write a prescription.
That begins with a morning fasting blood draw for total testosterone, not a symptom checklist on a marketing site. If the level comes back low, repeat it on another morning before deciding what it means. Testosterone varies from day to day, and one isolated low result is not enough to establish the diagnosis.[16]
If the result is borderline or does not fit the clinical picture, free testosterone and sex hormone-binding globulin, or SHBG, can help clarify what is going on. LH and FSH help determine whether the problem is coming from the testes themselves or from the hormonal signals coming from the brain. Prolactin becomes useful in selected cases when the results raise concern for a pituitary problem.
If the low testosterone appears to be related to something reversible, such as poor sleep, untreated sleep apnea, excess body fat, or another correctable problem, address that first. Improve the sleep and treat whatever is interfering with it. If excess body fat is part of the problem, work on reducing it through exercise and a sustained calorie deficit.
A lot of men have this backward. They assume they need testosterone to give them the energy to fix their sleep and body composition, when in many cases improving the sleep and losing the excess weight is what improves the testosterone.
Not every case of low testosterone works that way. Primary testicular failure, pituitary disease, and other medical causes need their own evaluation and may warrant treatment regardless of body composition or sleep. That is exactly why the diagnosis has to come before the prescription.
If testosterone remains consistently low after reversible causes have been addressed, then testosterone therapy may be appropriate. In properly diagnosed men, testosterone can increase lean mass and sometimes reduce fat mass. What it cannot do is replace the work of correcting poor sleep, excess body fat, or another reversible cause that may be contributing to the problem in the first place. The cart still goes behind the horse.
The instinct behind t-maxxing isn’t wrong. Wanting more energy, more drive, and a body that works the way it did ten years ago is a completely reasonable thing to want. The problem is that t-maxxing takes legitimate lifestyle changes and mixes them together with hormone use as though they are all just different versions of the same thing. They are not.
You can improve your sleep, lose excess body fat, lift weights, and exercise without anyone supervising you. Once you start taking testosterone or other hormones, you are doing something different. Now the dose matters, the blood level matters, the side effects matter, and somebody needs to be checking what is happening.
If you’ve looked into this for yourself, or you’re currently using testosterone or another hormone outside of a medical relationship, I’d genuinely like to hear how you got there. Reply to this email and tell me. It helps me know what to cover next.
References
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Selinger S, Thallapureddy A. Cross-sectional analysis of national testosterone prescribing through prescription drug monitoring programs, 2018–2022. PLoS One. 2024;19(8).
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Sagoe D, Molde H, Andreassen CS, Torsheim T, Pallesen S. The global epidemiology of anabolic-androgenic steroid use: a meta-analysis and meta-regression analysis. Ann Epidemiol. 2014;24(5):383-398.
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Aguiar JA, Panken EJ, Greenberg DR, Brannigan RE, Halpern JA, Dubin JM. Testosterone use trends among young men in the era of direct-to-consumer healthcare. J Sex Med. 2026;23(4).
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Su L, Meng YH, Zhang SZ, et al. Association between obstructive sleep apnea and male serum testosterone: a systematic review and meta-analysis. Andrology. 2022;10(2):223-231.
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Leproult R, Van Cauter E. Effect of 1 week of sleep restriction on testosterone levels in young healthy men. JAMA. 2011;305(21):2173-2174.
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Ken-Dror G, Fluck D, Fry CH, Han TS. Meta-analysis and construction of simple-to-use nomograms for approximating testosterone levels gained from weight loss in obese men. Andrology. 2024;12(2):297-315.
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Hayes FJ, et al. Effects of intensive lifestyle modification and metformin on testosterone levels in men with impaired glucose tolerance. Presented at The Endocrine Society’s 94th Annual Meeting, ENDO 2012. See also: Kim C, Barrett-Connor E, Aroda VR, et al. Testosterone and depressive symptoms among men in the Diabetes Prevention Program. Psychoneuroendocrinology. 2016;72:63-71.
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Santi D, Cignarelli A, Baldi M, et al. The chronic alcohol consumption influences the gonadal axis in men: results from a meta-analysis. Andrology. 2024;12(4):768-780.
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Liberto R, Katlowitz N, Sagalovich D, Davila J. Strategies for reversing exogenous testosterone-induced infertility. Cureus. 2025;17(9).
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Miller C, Burger J, Hershlag A, Berg W, Hartman-Kenzler J. Real world cohort of exogenous testosterone users demonstrates long time to sperm recovery, poor follow-up rate, and high rates of assisted reproductive techniques. J Sex Med. 2025;22(Suppl 4).148.
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Windfeld-Mathiasen J, Heerfordt IM, Dalhoff KP, et al. Cardiovascular disease in anabolic androgenic steroid users. Circulation. 2025;151:828-834.
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Ory J, Nackeeran S, Balaji NC, Hare JM, Ramasamy R. Secondary polycythemia in men receiving testosterone therapy increases risk of major adverse cardiovascular events and venous thromboembolism in the first year of therapy. J Urol. 2022;207(6):1295-1301.
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Mulhall JP, Trost LW, Brannigan RE, et al. Evaluation and management of testosterone deficiency: AUA guideline. J Urol. 2018;200(2):423-432. Updated American Urological Association guidance accessed for current monitoring recommendations.
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Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Bhore R. Prolonged stimulation of growth hormone and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of growth hormone-releasing hormone, in healthy adults. J Clin Endocrinol Metab. 2006;91(3):799-805.
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Ramos-Leví AM, Marazuela M. Cardiovascular comorbidities in acromegaly: an update on their diagnosis and management. Endocrine. 2017;55(2):346-359.
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Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715-1744.