Dr. Darrell Wilcox · Medical Director

Will Testosterone Make Me Infertile or Shut Down My Own Production?

Quick Answer

Permanently, almost certainly not. Testosterone therapy can suppress your own testosterone production and reduce sperm production while you are taking it, sometimes substantially, and that is worth understanding clearly. But suppressing something is not the same as damaging it. In the studies that followed men month by month after stopping, sperm production came back, though how long it took varied a good deal from man to man. And if fertility matters to you, none of this has to be left to chance. Treatment can be designed around both goals from the beginning. Enclomiphene, for example, raises testosterone by stimulating your own production rather than replacing it, and in randomized trials it maintained sperm counts where testosterone gel did not. The key is making fertility part of the conversation before treatment starts, because the right approach for a man who wants children looks different from the one for a man who does not.

Why testosterone suppresses your own production

Your testosterone is controlled by a loop running from the brain down to the testicles. The hypothalamus releases GnRH. GnRH tells the pituitary to release two hormones, LH and FSH. LH tells the Leydig cells in the testicles to make testosterone. FSH, along with a very high testosterone concentration inside the testicle itself, is what supports sperm production.

That loop has a thermostat. When testosterone arrives from outside the body, the brain reads the extra androgen and turns its own signal down. GnRH falls, LH and FSH fall, and the signal reaching the testicles is substantially reduced. This is not a malfunction. It is the same negative feedback that keeps the system from overshooting normally.

The size of that effect is worth seeing. In a study of 29 men given weekly testosterone injections, LH dropped to 5 percent of baseline and FSH to 3 percent within three weeks. More strikingly, testosterone concentration inside the testicle fell by 94 percent. That matters because sperm production depends on the concentration inside the testicle, which normally runs far higher than the level in your blood. In those men, serum testosterone at baseline was only about 1 percent of the intratesticular concentration. So a man can have an excellent testosterone level on a blood test while the environment his sperm actually develop in has largely gone quiet.

This is also why some men notice their testicles getting smaller on testosterone. The accurate description is not that the testicles have been damaged. It is that they are receiving much less stimulation from the brain, and tissue that is being stimulated less becomes less active and smaller. Suppression and damage are different things, and most of the fear around this subject comes from treating them as the same. It is probably the single most useful idea on this page.

Three things people mix together

Almost every conversation about this collapses three separate questions into one. They are related, but they are not interchangeable, and separating them makes the whole subject easier to think about.

The first is your own testosterone production. The second is testicular size and activity. The third is sperm production and actual fertility.

A man can have a serum testosterone of 800 on treatment while making almost none of his own and while the concentration inside his testicles is a fraction of normal. Normal testicular size does not prove a man is fertile. LH and FSH tell you something useful about whether the pituitary is still signaling, but they do not tell you whether sperm are being produced in adequate numbers. The only direct measure of that is a semen analysis, which is why it belongs in this conversation rather than being inferred from a hormone panel.

Testosterone is not birth control

This needs stating on its own, because men get it wrong in both directions.

Testosterone reduces sperm production substantially, and in some men to zero. But it does not do so reliably. In one series of hypogonadal men on testosterone replacement, about 40 percent became azoospermic, meaning no measurable sperm. The other 60 percent did not. The degree of suppression varies considerably between men and cannot be predicted from a testosterone level.

So a man on testosterone can still father a child. Testosterone should never be used or relied on as contraception, and a man who does not want a pregnancy needs actual contraception regardless of what his sperm count was the last time anyone checked.

What happens when you stop

This is where the evidence is more encouraging than the reputation suggests, and it comes from an unexpected place. For decades, researchers studied testosterone-based regimens as a potential male contraceptive, which means they deliberately suppressed sperm production in healthy men and then followed them carefully month by month after stopping. That produced exactly the dataset a man asking this question wants.

An integrated analysis pooled 30 such studies covering 1,549 men, with 1,283 man-years of treatment and 705 man-years of monitored recovery afterward. The median time for sperm concentration to return to 20 million per milliliter, a conventional fertility threshold, was 3.4 months. The probability of getting back to that threshold was 67 percent within 6 months, 90 percent within 12 months, 96 percent within 16 months, and 100 percent within 24 months. The authors' conclusion was that recovery was full, and that the variables affecting it changed the speed rather than whether it happened.

Several things predicted faster recovery: older age, shorter duration of treatment, shorter-acting testosterone preparations, a higher sperm concentration before starting, and a lower LH at baseline. That last one is a clue worth noticing, because it points at how well the axis was working to begin with.

Three honest qualifications. These were healthy men with normal testosterone who were suppressed deliberately for a study, not men with genuine testosterone deficiency treated for years, so the timeline should be read as informative rather than as a promise. A man whose testosterone was low because of a problem in the testicles themselves, rather than in the brain's signaling, starts from a different place and may not have had normal sperm production before treatment at all.

And there is a distinction inside the word recovery that matters. Those percentages describe men returning to a population threshold of 20 million per milliliter. Returning to your own starting point is a different question, and the reviewers of this literature note that while most men recover into the normal range, recovery to an individual's pre-treatment level is not universal, particularly in men whose semen quality was already marginal before they started. For a man with robust baseline fertility that distinction is academic. For a man who was already borderline, it is the whole point, and it is the strongest practical argument for getting a semen analysis before starting rather than after a question arises.

The fair summary is that suppression from testosterone is generally reversible, that recovery takes months rather than days, and that it cannot be timed precisely for any individual man.

The better question: do you need testosterone at all?

Here is the part that changes outcomes, and it is the part usually skipped. Having low testosterone does not automatically mean the answer is testosterone from outside the body. If fertility matters to you, there is a different category of treatment that raises testosterone by getting your own system to produce more of it.

The simplest way to hold the distinction: testosterone replacement supplies the hormone. The alternative approach asks your body to make more of its own. The first suppresses the signaling loop by design. The second works through it.

Enclomiphene: stimulating rather than replacing

Enclomiphene is a selective estrogen receptor modulator. Its relevant action is at the hypothalamus and pituitary, where it reduces the negative feedback that estrogen exerts on the system. With that brake partly released, the brain increases its GnRH signal, and LH and FSH rise rather than fall. The testicles are then being told to work harder, and they respond by making more testosterone, while the FSH signal that supports sperm production stays in place.

This has been tested directly against testosterone gel, which is what makes the evidence unusually satisfying. Two parallel randomized, double-blind, placebo-controlled phase III trials enrolled overweight men aged 18 to 60 with secondary hypogonadism, meaning a total testosterone at or below 300 ng/dL with a low or inappropriately normal LH. Over 16 weeks, testosterone rose in every active treatment group, including the gel. But LH and FSH rose with enclomiphene and fell with the gel, and enclomiphene maintained sperm concentration in the normal range while the gel group showed a marked reduction in sperm production. An earlier randomized phase II trial had found the same pattern.

So both approaches fixed the testosterone. Only one of them left the reproductive signaling intact.

What that evidence supports is that enclomiphene can raise testosterone while preserving the hormonal signaling sperm production depends on, and that it maintained sperm concentrations where testosterone gel did not. What it does not establish is anything about pregnancy rates, because these trials measured hormones and sperm counts over 16 weeks rather than whether couples conceived. Actual fertility depends on sperm concentration, motility and morphology, on female factors, on timing, and on age. Preserving the signaling is a meaningful thing to preserve, and it is not the same as a guarantee.

The deeper evidence review sits in the enclomiphene guide.

When stimulating your own production makes the most sense

Enclomiphene is not a universal substitute for testosterone, and the reason is mechanical. It works by turning up the brain's signal, which means it requires testicles capable of answering that signal.

The men it suits best are those with secondary hypogonadism, where the testosterone is low but the LH is low or inappropriately normal rather than high. That pattern says the testicles are not the problem, the signal to them is. This is common in younger men and in men carrying excess weight, and it is exactly the population the trials enrolled.

It suits men with primary testicular failure much less well. If the testicles cannot respond adequately, a louder signal from the pituitary accomplishes little, and LH will already be running high because the brain is shouting. For a man actively trying to conceive now, or expecting to within the next year or two, this distinction is the single most useful thing to establish before choosing a treatment, and an LH measured alongside the testosterone is what establishes it.

Combining approaches, and where the evidence thins out

Some men feel considerably better on exogenous testosterone than on anything else, and still want to protect testicular function. Several strategies get used in that situation, and they differ a great deal in how well studied they are. Being straight about which is which is more useful than presenting them all as equivalent.

The best evidence belongs to hCG, which acts on the testicle much as LH does, bypassing the suppressed pituitary signal entirely. In the same study that measured a 94 percent fall in intratesticular testosterone on testosterone alone, adding low-dose hCG restored it: at 250 IU every other day the intratesticular concentration came back to within 7 percent of baseline. A separate retrospective series followed 26 hypogonadal men taking testosterone together with 500 IU of hCG every other day and found semen parameters maintained over an average of about six months. That is 26 men looked at backward rather than a trial, so it is supportive rather than definitive, but the mechanism and the intratesticular data behind it are solid.

Enclomiphene alongside testosterone rests on a reasonable physiologic rationale that has not yet been tested at the same level. Testosterone pushes LH and FSH down, enclomiphene releases estrogen-mediated feedback at the hypothalamus and pituitary, and the intent is to hold some of that signaling in place. The strong trial evidence for enclomiphene is for enclomiphene used on its own against testosterone, not for the two given together, and that specific combination has not been studied in high-quality fertility trials. The honest way to hold it is as a biologically plausible strategy rather than a proven fertility-preservation protocol, which is a different thing from a strategy that has been tested and failed.

The same applies to intermittent enclomiphene dosing during testosterone therapy, including every-other-day schedules. Here it helps to separate two goals that often get stated as one. Maintaining some measurable LH and FSH signaling and some testicular activity is a plausible and modest aim, and the physiology supports attempting it. Demonstrating that sperm production is preserved, that testicular volume is protected, or that recovery after stopping is faster is a much larger claim, and that one has not been established in good clinical trials. The strategy is worth considering on the first goal. It should not be presented as delivering the second.

One specific version of this comes up often enough to be worth addressing on its own: a daily low-dose testosterone cream paired with daily enclomiphene, for a man who needs testosterone replacement but wants to reduce suppression of his own testicular function. The reasoning stacks two ideas. Shorter-acting, lower-dose testosterone exposure may produce less sustained suppression than a long-acting injection, because the level falls between doses rather than staying elevated around the clock. And enclomiphene pushes in the opposite direction from the testosterone, raising LH and FSH rather than letting them drift down.

Both halves of that are plausible and neither is proven, which is worth saying rather than glossing over. The general case for shorter-acting preparations has real support behind it, including the finding that shorter-acting testosterone predicted faster recovery of sperm production in the analysis of 1,549 men. What has not been established is that a compounded cream at a particular dose behaves that way, since the trials studied conventional gel products, or that adding enclomiphene to any testosterone preserves sperm production, since that combination has not been tested in fertility trials.

So the fair description is a reasonable strategy for a man who wants testosterone and would like less suppression than conventional therapy tends to produce, and not a fertility-preservation protocol. For a man whose fertility is an immediate priority, the better starting point is an approach with stronger evidence behind it, which means enclomiphene without exogenous testosterone in a man with secondary hypogonadism, or hCG, which has the strongest mechanistic data of anything discussed here.

Formulation as a question in its own right has enough behind it now to deserve its own section below.

Which leads to the practical rule that covers all of them. If fertility is the reason you are choosing one of these approaches, the way to know whether it is working is a semen analysis, not a hormone panel and not an assumption. Get one before starting, and get another on treatment.

Does the formulation matter?

This is one of the more interesting open questions in the field right now, and the honest answer is that it probably does matter, with the evidence strongest for the idea in general and much thinner for any particular product.

The reasoning starts with pharmacokinetics. A long-acting injection holds testosterone elevated continuously, so the brain's feedback sensor never gets a break and suppression is sustained. A short-acting preparation lets the level fall between doses, which more closely resembles the body's own daily rhythm and may leave room for some pulsatile LH and FSH release to continue. A 2025 review in Nature Reviews Urology stated it this way: newer short-acting formulations, including oral testosterone undecanoate and nasal testosterone gel, might incompletely suppress the axis and partially preserve sperm production. There is one hard piece of supporting evidence from the recovery side as well, which is that in the analysis of 1,549 men, shorter-acting testosterone preparations predicted faster return of sperm production after stopping.

Then the specifics, which matter a great deal because what is known differs sharply by product.

Nasal testosterone gel has the only real semen data. A single-center, open-label, single-arm trial enrolled 60 hypogonadal men aged 18 to 55 and dosed nasal testosterone three times daily for six months, with 33 men still evaluable at six months. Ninety-one percent reached a normal testosterone. FSH stayed within the normal range in about 82 percent of men and LH in about 73 percent. Total motile sperm count stayed above 5 million in 88 percent of men at three months and 94 percent at six months. Of the 60 men enrolled, one became azoospermic and three became severely oligospermic. A separate study that switched 41 men from clomiphene to nasal testosterone found semen parameters maintained, with one man becoming severely oligospermic and recovering after his dose was reduced.

Oral testosterone undecanoate, the category that includes Kyzatrex, Jatenzo and Tlando, is the most interesting of these and now has evidence on both sides of the question.

On signaling the case is reasonably good and peer reviewed. In the phase 3 trial supporting Kyzatrex, 155 hypogonadal men treated for 180 days, mean FSH and LH fell from baseline at both 90 and 180 days while the mean values stayed within the normal reference range. An earlier trial of 166 men on a different oral preparation found LH down about 75 percent and FSH about 65 percent, with FSH staying inside the range across all age groups and LH only in men aged 18 to 40. The axis is suppressed but not silenced, which is what the pharmacokinetic argument predicts. Neither trial measured sperm.

On sperm, the first prospective data have now been reported, and they are more mixed than the signaling data. A pilot study at Baylor College of Medicine enrolled testosterone-naive men aged 18 to 49 and measured semen analyses before and after three months of oral testosterone undecanoate. Testosterone roughly tripled, from a mean of 221 to 705, while FSH barely moved, 3.10 to 2.94, and LH fell modestly, 2.60 to 1.75. Semen volume rose. But total sperm count fell from a mean of 118 to 90, total motile count fell from 63 to 22, and the motile percentage fell from 49 to 37. One participant became azoospermic. The investigators describe the parameters as largely unchanged, which is a fair summary if the changes did not reach statistical significance, and this interim report does not state how many men were enrolled.

Two things are worth holding at once there. A mean total motile count of 22 million is still comfortably above the 5 million mark used as a benchmark elsewhere in this literature, so the average man in that cohort was not rendered infertile. And a fall of roughly two thirds is not nothing, particularly when the gonadotropins barely moved, which is a reminder that preserved LH and FSH do not automatically mean preserved sperm production.

The fair reading is that oral testosterone undecanoate suppresses the axis less completely than long-acting injections appear to, that the first semen data are early, small and not reassuring enough to call it sperm-sparing, and that it should not be chosen on the assumption that it protects fertility.

Conventional transdermal testosterone gel clearly suppresses gonadotropins and sperm production in clinical trials, and the clearest evidence comes from the enclomiphene trials themselves, where the gel arms showed marked reductions in sperm production over 16 weeks as LH and FSH fell. Whether every topical formulation and dosing strategy produces the same degree of suppression has not been established, since the trials used conventional gel products rather than the range of compounded creams, doses and application sites in use.

Testosterone troches have no direct fertility evidence in either direction. They are short-acting, so the same theoretical argument is available for them, but no published study has measured gonadotropins or semen parameters in men using them for this purpose. Absence of evidence is the accurate description, and it should not be read as reassurance or as alarm.

Two cautions belong with all of this. The gonadotropin findings come from short studies, mostly 90 days to six months, and the reviewers make the point that levels still drifting downward inside the reference range at three months could fall below it over longer treatment. And professional guidance has not adopted any of it: the AUA does not recommend nasal testosterone for men interested in current or future fertility, precisely because the long-term data do not exist yet.

Which lands in the same place as everything else on this page. If a formulation is being chosen partly to protect fertility, that is a reasonable bet rather than a proven strategy, and a semen analysis is what turns a bet into information.

The other options worth knowing about

Enclomiphene is not the only tool. hCG, described above, directly stimulates the Leydig cells and can be used on its own or alongside testosterone. FSH-containing therapy is used in selected fertility cases where the FSH signal specifically needs support. Clomiphene, an older SERM of which enclomiphene is one of the two isomers, has been used for the same purpose for far longer. And sperm cryopreservation, banking a sample before starting treatment, is the one option that does not depend on any drug working as hoped. For a man who is certain he wants children later and does not want to rely on recovery timelines, it is the most direct form of insurance available.

Which of these fits depends on what you are actually trying to accomplish, and those goals are not the same: raising testosterone, maintaining testicular size and activity, keeping current fertility intact, conceiving now, or restoring fertility after testosterone has already been used for some time. Each points somewhere slightly different.

What if I want children?

Three situations cover most men, and they lead to genuinely different answers.

If you are trying to conceive now or expect to soon, testosterone on its own is generally the wrong choice, because suppressing sperm production is working against the thing you are trying to do. A strategy that stimulates your own production, such as enclomiphene in a man with secondary hypogonadism, is the more sensible starting point. A semen analysis before treatment and again during it tells you where you actually stand, and other fertility-directed treatment may be appropriate depending on what that shows and on your partner's evaluation.

If you want children someday but not right now, the conversation belongs before the first prescription rather than after. Depending on the specifics, that might mean an enclomiphene-based approach, or testosterone with an adjunct intended to maintain testicular signaling, or a baseline semen analysis with periodic rechecks, or banking sperm, or some combination. This is the scenario where planning pays off most, and also the one most often skipped.

If your family is complete, fertility preservation carries much less weight, and treatment can focus on symptoms and on getting the testosterone right. Some men still care about maintaining testicular size and their own testicular activity for reasons that have nothing to do with having more children, and that is a legitimate and separate thing to discuss.

And if you are already on testosterone and reading this with a sinking feeling, that is worth addressing directly, because it is probably the most common way men arrive at this question. Being on treatment is not a door that has closed. Suppression is not damage, the recovery data above describe men who had been suppressed and then were not, and fertility-directed strategies exist specifically for restoring sperm production in men who have been on testosterone. The useful next step is not worry, it is a semen analysis, which turns an open question into a number. Bring that number to a conversation about what you want to do next, and if conception is the near-term goal, a reproductive urologist is the right person to involve.

What the guidelines say, and why

Professional guidance on this point is cautious, and the caution deserves to be understood rather than either hidden or overread.

The 2018 Endocrine Society clinical practice guideline recommends against starting testosterone therapy in men who are planning fertility in the near term. The AUA and ASRM guideline on male infertility likewise addresses exogenous testosterone in men pursuing fertility, and recognizes medical therapies including SERMs, hCG and aromatase inhibitors as approaches for infertile men with low testosterone in appropriate situations.

Read that for what it is. It reflects the well-documented suppressive effect of exogenous testosterone on gonadotropins and sperm production, which is the same physiology described at the top of this page. It is not a statement that testosterone causes permanent infertility, and it is not a reason for a man with low testosterone and future fertility plans to go untreated. It is a reason for the treatment to be chosen with those plans in view, which is the entire argument of this page.

A good testosterone level does not mean you are fertile

Worth repeating on its own because it is the most common error in this area. A testosterone of 800 ng/dL tells you about testosterone. It tells you nothing about sperm. An LH and FSH in range tell you the pituitary is signaling, not that sperm are being made in adequate numbers. Normal testicular size does not establish fertility either.

If fertility is the thing you care about, it has to be measured directly. That means a semen analysis, ideally before treatment starts so there is something to compare against later.

Testosterone replacement can suppress your own testosterone and sperm production, and suppression is not the same thing as permanent damage. In the men who have been followed after stopping, sperm production returned, though it took months rather than weeks and the timing varied. More importantly, fertility does not have to be an afterthought. A man who wants to protect it can often use a different strategy altogether, and enclomiphene has been shown in randomized trials to raise testosterone while maintaining LH, FSH and sperm concentrations where testosterone gel did not. Other approaches exist, including hCG and simply banking sperm before starting. If having children now or later matters to you, say so before you start testosterone. The treatment can then be designed around both goals instead of one.

If fertility is part of the picture, that is a conversation to have before the first prescription rather than after. Bring your testosterone, your LH and FSH if you have them, and your plans for children to your next visit.

Find My Clinic

Or email drwilcox@precisionhormoneconsulting.com · DM @wellnessdoc_4everyoung on Instagram

Dr. Darrell Wilcox · @wellnessdoc_4everyoung on Instagram

References

Coviello AD, Matsumoto AM, Bremner WJ, et al. Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression. J Clin Endocrinol Metab. 2005;90(5):2595-2602. PMID 15713727.
Liu PY, Swerdloff RS, Christenson PD, Handelsman DJ, Wang C. Rate, extent, and modifiers of spermatogenic recovery after hormonal male contraception: an integrated analysis. Lancet. 2006;367(9520):1412-1420. PMID 16650651.
Wiehle RD, Fontenot GK, Wike J, et al. Enclomiphene citrate stimulates testosterone production while preventing oligospermia: a randomized phase II clinical trial comparing topical testosterone. Fertil Steril. 2014;102(3):720-727. PMID 25044085.
Kim ED, McCullough A, Kaminetsky J. Oral enclomiphene citrate raises testosterone and preserves sperm counts in obese hypogonadal men, unlike topical testosterone: restoration instead of replacement. BJU Int. 2016;117(4):677-685. PMID 26496621.
Hsieh TC, Pastuszak AW, Hwang K, Lipshultz LI. Concomitant intramuscular human chorionic gonadotropin preserves spermatogenesis in men undergoing testosterone replacement therapy. J Urol. 2013;189(2):647-650. PMID 23260550.
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. PMID 29562364.
Schlegel PN, Sigman M, Collura B, et al. Diagnosis and treatment of infertility in men: AUA/ASRM guideline part II. J Urol. 2021;205(1):44-51. PMID 33295258.
Bernstein JS, Dhingra OP. A phase III, single-arm, 6-month trial of a wide-dose range oral testosterone undecanoate product. Ther Adv Urol. 2024;16:17562872241241864. PMID 38606384.
Saffati G, Orozco Rendon D, Kronstedt S, Hinojosa-Gonzalez DE, Khera M. Effects of oral testosterone undecanoate on semen parameters in hypogonadal men: an interim analysis of a prospective pilot study. Baylor College of Medicine. Conference poster, interim analysis.
Naelitz BD, Momtazi-Mar L, Vallabhaneni S, et al. Testosterone replacement therapy and spermatogenesis in reproductive age men. Nat Rev Urol. 2025;22(10):703-719. PMID 40346275.
Hochu G, Geyer-Kim I, Kim E. Preserving spermatogenesis in testosterone deficiency: innovations in replacement and stimulatory therapies. Transl Androl Urol. 2025;14(12):3975-3987. PMID 41522318.
Ramasamy R, Masterson TA, Best JC, et al. Effect of Natesto on reproductive hormones, semen parameters and hypogonadal symptoms: a single center, open label, single arm trial. J Urol. 2020;204(3):557-563. PMID 32294396.
Kavoussi PK, Machen GL, Gilkey MS, et al. Converting men from clomiphene citrate to Natesto for hypogonadism improves libido, maintains semen parameters, and reduces estradiol. Urology. 2021;148:141-144. PMID 33301741.
Swerdloff RS, Wang C, White WB, et al. A new oral testosterone undecanoate formulation restores testosterone to normal concentrations in hypogonadal men. J Clin Endocrinol Metab. 2020;105(8):dgaa238. PMID 32382745.

This content is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Testosterone, enclomiphene, and hCG are prescription treatments with their own indications, contraindications, and monitoring requirements, and fertility evaluation involves both partners. Decisions about treating low testosterone, preserving or restoring fertility, and which approach fits your situation should be made with your own physician and, where appropriate, a reproductive urologist who has your hormone levels, semen analysis, and history in front of them. Individual results differ from trial averages, and the studies described here were conducted in specific populations that may not match your own situation. Dr. Wilcox is licensed to practice in multiple states. See About for current licensure.