WHAT EVERY PARENT SHOULD KNOW BEFORE THEIR son STARTS TESTOSTERONE THERAPY
By: Joy Stephenson-Laws, Holistic Coach, J.D., Founder
He is twenty-one. His testosterone came back low, the prescription was written the same day, and no one asked him whether he wants children.
That last part is not an oversight in his case alone. A 2019 review in the World Journal of Men's Health reports that fewer than two percent of men on testosterone therapy had a baseline semen analysis before starting. More than twenty percent of men aged eighteen to forty-five never had a baseline testosterone level drawn either. So a young man walks in tired, walks out with a prescription, and nobody has established what is wrong with him or what the drug will cost him.
Here is what it costs him.
The drug is a contraceptive
Start with how the system is supposed to work.
The testes do two jobs, and they run on the same signal. The hypothalamus releases GnRH in pulses. The pituitary answers with two hormones: LH, which tells the Leydig cells to make testosterone, and FSH, which supports the Sertoli cells that nurse developing sperm. The testosterone that matters for sperm production is not the testosterone in his bloodstream. It is the testosterone inside the testis, which sits at a concentration roughly a hundred times higher than serum. Sperm cannot mature without it.
Now introduce testosterone from outside the body. The hypothalamus reads the high circulating level and concludes the system is oversupplied. GnRH pulses slow. LH and FSH fall. The Leydig cells stop being told to work, so intratesticular testosterone collapses, and the Sertoli cells lose the FSH signal they need. Serum testosterone looks excellent on the lab report. Inside the testis, production has stopped.
This is not a side effect anyone stumbled onto. It is the mechanism that made testosterone a serious candidate for a male contraceptive, and those trials worked. In the World Health Organization's multicentre study, 271 healthy fertile men were given weekly testosterone injections. Within six months, 65 percent had reached azoospermia, meaning no measurable sperm at all in the ejaculate. Most of the men who did not reach zero were suppressed far enough that the researchers counted them as contracepted anyway.
Read that with a twenty-one-year-old in mind. The drug he was handed for fatigue is the drug researchers tested because it reliably makes men infertile.
Medicine already knows this
This is the part that should make you angry rather than resigned, because the guidance is not missing. It exists, it is unambiguous, and it was written by the people who train his doctor.
The Endocrine Society's 2018 clinical practice guideline recommends against testosterone therapy in men planning fertility in the near term. That is Recommendation 2.2, a strong recommendation.
The American Urological Association and the American Society for Reproductive Medicine go further in their male infertility guideline. For the male interested in current or future fertility, clinicians should not prescribe exogenous testosterone therapy. They label it a Clinical Principle, which in guideline language means the evidence is so settled that no one is arguing about it.
The conversation is not absent from medicine. It was absent from his appointment.
Nobody asked why the number was low
A low testosterone level in a twenty-one-year-old is not a diagnosis. It is a finding. Finding out why is the entire job, and it is the job that got skipped.
Some causes are structural, and no amount of sleep or diet will touch them. Klinefelter syndrome is a chromosomal condition, one of the most common causes of primary testicular failure, and it goes undiagnosed into adulthood far more often than it should. A pituitary adenoma is a benign tumor that can suppress the signals from above. A varicocele is an enlarged vein in the scrotum, common and treatable, and a recognized cause of both low testosterone and impaired sperm production.
There is a blood test that begins to sort this out, and it is neither exotic nor expensive. Draw LH and FSH alongside testosterone. If LH is high and testosterone is low, the pituitary is shouting and the testes are not answering, which points to the testes. If LH is low or inappropriately normal while testosterone is low, the problem is upstream, in the pituitary or hypothalamus. The Endocrine Society makes this Recommendation 1.3. It is the first fork in the road, and everything downstream depends on taking it.
A pituitary tumor does not stop growing because a young man started testosterone and felt better for a while.
Let me be clear about something, because this article is not an argument against testosterone. If the workup shows a young man has permanent hypogonadism, testosterone is the right treatment and he should have it. Androgens are not optional for a body that cannot make its own. They build bone, they build muscle, they drive the sexual development an adolescent is entitled to, and withholding them causes real harm. The argument here is not that he should refuse the drug. It is that nobody established he needed it.
Then there are the causes that are reversible, and these are the ones that make the prescription so hard to defend.
Obesity is the single largest risk factor for testosterone deficiency in men. The condition even has a name, male obesity secondary hypogonadism, and it is described in the literature as the most common form of functional hypogonadism. In men with a BMI above forty, prevalence runs as high as seventy-five percent. The mechanism is understood: excess adipose tissue raises leptin, insulin, and inflammatory cytokines, and aromatizes testosterone into estrogen, and those signals converge on the hypothalamus to suppress GnRH. It is central suppression, and it reverses with weight loss.
Opioids do it. Anabolic steroid use does it, which matters for a young man who has been in a gym culture. Chronic sleep loss does it. So does low energy availability, the state a young man reaches when he is training hard and eating too little.
Sit with what that means. A twenty-one-year-old with obesity-related low testosterone can be made permanently infertile by a drug prescribed to treat something that weight loss would have corrected.
What the low number might actually be
There is a further possibility, and it reframes the whole encounter.
A paper published in the Journal of Clinical Endocrinology and Metabolism in April 2026 by researchers at the US Army Research Institute of Environmental Medicine asks the question directly in its title: is stress-associated testosterone suppression central adaptation, or is it hypogonadism?
Their answer, drawn from decades of military field studies and work with endurance athletes, is that testosterone suppression under sustained stress is commonly a centrally mediated, reversible adaptation rather than intrinsic testicular failure. Severe energy deficit, sleep disruption, and uncontrollable psychological stress slow GnRH and LH pulsatility, reduce androgen production, and raise sex hormone binding globulin, which disproportionately lowers free testosterone.
In extreme conditions the drop is dramatic. Norwegian military cadets lost roughly seventy-seven percent of their testosterone over five days. It is worth being precise about what those five days contained: near-starvation, relentless physical exertion, and almost no sleep, all at once. That is not stress in the way most people use the word. That is a body pushed to the edge of what it can sustain.
And then it comes back. With food and rest, it recovers. When researchers give these men hCG, the testes respond normally, which proves the Leydig cells were never broken. The signal from above had been turned down, deliberately, by a body deciding this was not the moment to reproduce.
That is not a disease. That is a body doing its job under load.
There are cases where the suppression persists and needs treatment. In a prospective study of seventy-eight men with severe traumatic brain injury, median age twenty-eight, forty-four percent had persistent hypogonadotropic hypogonadism through the first year, and it predicted worse recovery. That is real, and it is a reason to test rather than assume.
I want to be careful about how far this goes, because the honest limits are part of the argument. The strongest human evidence for stress-driven suppression comes from military and athletic models where psychological strain, energy deficit, and sleep loss all arrive together, and no one has pulled them apart. Direct evidence in young men with PTSD is thin and inconsistent.
One prospective study followed 918 Dutch soldiers, average age twenty-eight, through a combat deployment. Testosterone rose afterward rather than falling. Men who went on to develop symptoms showed no different hormonal trajectory from men who did not. Lower testosterone before deployment was associated with symptoms later, though an association is not a test and does not establish cause in either direction. What it does not do is support the story that trauma pulls testosterone down.
Nor is trauma a simple high-cortisol state. A commonly reported pattern in PTSD is elevated CRH alongside low or normal cortisol and stronger negative feedback, which is close to the reverse of what most people assume. The findings are not consistent enough to call that pattern settled. The point is only that the tidy version, in which stress raises cortisol and cortisol lowers testosterone, is not a version the evidence supports.
So here is the narrow claim worth making, and the wide one that is not. Severe, combined stress can transiently suppress the male reproductive axis, and a man's hormonal state may turn out to be associated with the trauma symptoms he later develops. That much holds. What does not hold is that PTSD generally causes hypogonadism, that low testosterone is the main biological engine of trauma, or that testosterone therapy treats what happened to him.
What none of the major guidelines do, from the Endocrine Society or the AUA or the European Association of Urology, is prompt a clinician to ask about trauma, chronic stress, or adverse childhood experiences when a young man turns up with a low number. They name obesity, opioids, sleep disorders, eating disorders, and excessive exercise as functional causes. They do not name this. That is a gap in the text. Whether it is a gap in practice, nobody has audited.
If he is already taking it
The suppression is usually reversible. The numbers are encouraging, and they are also narrower than they look.
An integrated analysis of thirty male contraceptive trials, published in the Lancet in 2006, found that sperm concentration returned to a normal threshold in sixty-seven percent of men within six months of stopping, ninety percent within twelve months, and essentially all within twenty-four. Two caveats belong with that sentence. Those men were healthy, had normal fertility to begin with, and had been on testosterone for under a year on average, so a young man on TRT for a decade sits outside the data entirely. And the study counted sperm. It did not count pregnancies or babies. A sperm concentration crossing a threshold on a lab report is not the same thing as a man becoming a father, and no one should read those percentages as a promise of one.
For men who cannot wait, there is medical treatment that works, and the honest picture comes from two studies rather than one. In a series of forty-nine men with testosterone-related azoospermia or severe oligospermia, hCG-based combination therapy restored sperm production in ninety-six percent, with an average time to return of four and a half months. A second study, of sixty-six men who came to a fertility clinic already infertile after testosterone use, is more sobering. Seventy percent reached a workable sperm count within a year on hCG and a selective estrogen receptor modulator. Thirty percent did not.
That second study found something else worth knowing. The two things that predicted slower recovery were age and how long he had been on testosterone. Every year on the drug makes the way back harder.
Both are retrospective case series rather than randomized trials, and both belong in the hands of a reproductive urologist.
Notice what is not on that list. No light panel, no cold plunge, no supplement. The intervention with the strongest evidence behind it is the one nobody is selling.
And if he has not started yet, the cheapest insurance available is a semen analysis and sperm banking, before the first injection rather than after.
Four questions
If your son has been offered testosterone, or is already on it, these are the questions that should have been asked in the room.
Were LH and FSH drawn? Without them, no one knows whether the problem is in his testes or his pituitary, and no one has a diagnosis.
What is the cause? Not the number. The cause. Obesity, opioids, sleep, overtraining, a varicocele, a pituitary lesion, a chromosomal condition. If nobody named one, nobody looked.
Was a semen analysis done before starting? If not, there is no baseline, and no way to know later what was lost.
Does he want children? Somebody should have asked him. If nobody did, ask him yourself.
A low testosterone level is a question. He was given an answer instead.
References
Patel AS, Leong JY, Ramos L, Ramasamy R. Testosterone is a contraceptive and should not be used in men who desire fertility. World J Mens Health. 2019;37(1):45-54. doi:10.5534/wjmh.180036
World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia in normal men. Lancet. 1990;336(8721):955-959. doi:10.1016/0140-6736(90)92416-F
World Health Organization Task Force on Methods for the Regulation of Male Fertility. Contraceptive efficacy of testosterone-induced azoospermia and oligozoospermia in normal men. Fertil Steril. 1996;65(4):821-829.
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. doi:10.1210/jc.2018-00229
American Urological Association, American Society for Reproductive Medicine. Diagnosis and Treatment of Infertility in Men: AUA/ASRM Guideline. Published 2020; amended 2024.
Bojesen A, Gravholt CH. Klinefelter syndrome: the commonest form of hypogonadism, but often overlooked or untreated. Dtsch Arztebl Int. 2013;110(20):347-353.
Clinical features, diagnosis, and management of Klinefelter syndrome. UpToDate. Accessed July 2026.
Varicocele: an endocrinological perspective. Front Reprod Health. 2022. PMCID: PMC9580708.
Whelan P, Najari BB. Effects of varicocelectomy on serum testosterone. Transl Androl Urol. PMCID: PMC5182225.
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New perspectives in functional hypogonadotropic hypogonadism: beyond late onset hypogonadism. Front Endocrinol. 2023. PMCID: PMC10344362.
Friedl KE, Nindl BC, Potter AW. Stress-associated testosterone suppression: central adaptation or hypogonadism? J Clin Endocrinol Metab. Published online April 27, 2026. doi:10.1210/clinem/dgag181
Barton DJ, Kumar RG, McCullough EH, et al. Persistent hypogonadotropic hypogonadism in men after severe traumatic brain injury: temporal hormone profiles and outcome prediction. J Head Trauma Rehabil. 2016;31(4):277-287.
Reijnen A, Geuze E, Vermetten E. The effect of deployment to a combat zone on testosterone levels and the association with the development of posttraumatic stress symptoms. Psychoneuroendocrinology. 2015.
Lawrence S, Scofield RH. Post-traumatic stress disorder and the hypothalamic-pituitary-adrenal axis. Brain Behav Immun Health. 2024. PMCID: PMC11401111.
Liu PY, Swerdloff RS, Christenson PD, Handelsman DJ, Wang C; Hormonal Male Contraception Summit Group. Rate, extent, and modifiers of spermatogenic recovery after hormonal male contraception: an integrated analysis. Lancet. 2006;367(9520):1412-1420. doi:10.1016/S0140-6736(06)68614-5
Wenker EP, Dupree JM, Langille GM, et al. The use of HCG-based combination therapy for recovery of spermatogenesis after testosterone use. J Sex Med. 2015;12(6):1334-1337. doi:10.1111/jsm.12890
Kohn TP, Louis MR, Pickett SM, et al. Age and duration of testosterone therapy predict time to return of sperm count after human chorionic gonadotropin therapy. Fertil Steril. 2017;107(2):351-357.e1. doi:10.1016/j.fertnstert.2016.10.004
(This article is for educational purposes and does not constitute medical advice. Anyone considering starting or stopping testosterone therapy should work with qualified healthcare providers who can assess their individual situation).
Joy Stephenson-Laws is a healthcare attorney, certified holistic wellness coach, and founder of Proactive Health Labs. She is the author of "From Chains to Wings: A Poetry Revolution for Healing" and the children's book "Secrets That Sparkle (and Secrets That Sting)," which teaches children about emotional safety and the importance of trusted adults.
