Do GLP-1 Drugs Affect Sperm, Testosterone or Male Fertility? What Has Actually Been Measured

What has actually been measured in men taking GLP-1 drugs?

The whole evidence base fits in a paragraph. Most of it measured hormones, not sperm.

Deameh and colleagues, writing in The Journal of Sexual Medicine on January 7, 2026, searched four databases up to April 2025 and included randomized trials and cohort studies in adult men. It found 10 studies covering 639 men between them, assessed their risk of bias with the standard tools, and reported what each one found.¹ A second systematic review, by Zafrani and colleagues in Cells, covered much the same ground and reached a different count.² Both are reviews of the older GLP-1 receptor agonists, meaning drugs that mimic a gut hormone released after eating: liraglutide, sold as Saxenda and Victoza, semaglutide, sold as Ozempic and Wegovy, plus dulaglutide and exenatide.

A third paper approaches the question from the other side. Peel and colleagues asked what any obesity treatment does to male fertility, pooling 32 studies across bariatric surgery, drug treatment and lifestyle change in Human Reproduction Update in 2025.³ It is the only one of the three that combined results statistically, and the only one whose stated conclusion names a downside: "limited benefit and potential harm" from the medical routes, meaning surgery and drugs.³

Every paper this page rests on is in the table below, with what it was and what it counted.

Study	Type	Size	What it measured	Key result
Deameh et al. 2026, J Sex Med	Systematic review, no pooling	10 studies, 639 men	Hormones, semen, metabolic	Testosterone up in metabolically unwell men; LH and FSH preserved
Zafrani et al. 2026, Cells	Systematic review, no pooling	7 or 8 studies, about 1,200 men	Hormones, semen	Same direction; semen evidence rated very low certainty
Peel et al. 2025, Hum Reprod Update	Meta-analysis, pooled	32 studies; 119 men on drug treatment	Semen, by route to weight loss	Liraglutide and sperm concentration 0.58 million per mL (minus 24.76 to 25.91)
Gregorič et al., Diabetes Obes Metab	Randomized trial, open label	25 men, 24 weeks	Semen, hormones, symptoms	Morphology 2% to 4% on semaglutide (p = 0.012); concentration unchanged (p = 0.58)
Lengsfeld et al., via the Cells review	Randomized, placebo-controlled	26 randomized, 24 completed	LH, FSH in healthy men	No significant change
Kaltsas et al. 2026, J Clin Med	Narrative review, no new data	Not applicable	Evidence for men seeking fertility	No study powered for conception, pregnancy or live birth
Couldwell et al. 2025, JCEM	Review, no new data	Not applicable	Reproduction across both sexes	GLP-1 receptors found in human testicular Leydig cells
Pourabhari Langroudi et al. 2025, Int J Impot Res	FAERS cross-sectional	182 male case reports	Sexual dysfunction reports	Reporting odds ratio 0.41 (0.36 to 0.48)
Case report, Reprod Biomed Online	Single case	1 man	Semen on liraglutide	Count collapsed; partly recovered after stopping

What those studies mostly measured was blood. They tracked total testosterone and free testosterone, along with LH and FSH, the two pituitary hormones that tell the testicle to make testosterone and sperm. Semen was measured in a handful of them, in very small groups, and the Cells authors rate the semen evidence as very low certainty and say the inconsistent reporting "precludes robust conclusions about fertility outcomes."²

I want to be fair to the field here, because nothing about that is a scandal: these are early studies in a question nobody was funding five years ago, done by people who had to argue for the money. Where they point depends on which paper you pick up: the two 2026 reviews read as mildly encouraging, and the meta-analysis reads as a warning. The gap all three share is between what they measured and what a man reading about this actually wants to know.

Does a GLP-1 raise testosterone, and does that mean more sperm?

Testosterone rises in the men who were low to begin with.

Both reviews agree on the hormone finding. Total testosterone went up consistently in men with obesity, type 2 diabetes, or functional hypogonadism, meaning low testosterone caused by something else in the body and not by damage to the testicles.¹² Free testosterone, the fraction not bound to carrier proteins and generally considered the active part, moved less reliably, partly because sex hormone binding globulin rises at the same time and binds more of the total.¹

The gonadotropin result, meaning what happened to LH and FSH, matters more than the testosterone one. LH and FSH were preserved or increased on a GLP-1, where testosterone therapy suppresses them.¹ Cut the LH and FSH signal and a testicle stops making sperm. So a drug that raises testosterone while leaving those signals intact is doing something different from one that raises it by supplying it from outside.

Whether that translates into better sperm is a separate question, and the trial that looked at it is in the next section but one.

GLP-1 or testosterone therapy: which one leaves sperm alone?

A man with obesity and low testosterone is usually offered testosterone replacement therapy, or TRT as most men call it. The evidence supports that comparison better than any other.

One term in the table below does the heavy lifting. Sperm morphology is the share of sperm cells with a normal shape, counted under a microscope against a strict standard, and it is one of the three numbers a semen analysis reports alongside concentration and motility.

	What the randomized trial measured over 24 weeks	What the FDA label says about fertility
Semaglutide, 1 mg weekly	Normal sperm morphology rose from a median of 2% to 4% (p = 0.012). Concentration and total count did not change significantly (p = 0.58, p = 0.79). LH and FSH unchanged.4	"No effects were observed on male fertility" in rats, at doses up to 0.1 times human exposure6
Testosterone undecanoate, intramuscular	Sperm concentration fell from a median of 25 to 10 million per mL (p = 0.028). Total count fell (p = 0.018). LH and FSH suppressed (p = 0.003, p = 0.002).4	"may cause azoospermia"; "Reduced fertility is observed in some men taking testosterone replacement therapy"; "The impact on fertility may be irreversible"7

Azoospermia in that label quote means no sperm at all in the ejaculate. Read the left column as the measured difference and the right column as the regulatory one. They point the same way. That agreement is unusual, and it makes the comparison sturdier than either source alone.

In fairness to the other side, the testosterone arm did better on erectile function. A man whose main complaint is sexual rather than reproductive may reasonably weigh that differently.⁴ The label warning also describes high-dose and abuse contexts alongside ordinary replacement, so it covers a wider range of use than a clinic prescription.⁷

What did the one randomized semen trial actually find?

The improvement was in sperm shape only. The headline comparison is driven by the other arm getting worse.

Gregorič and colleagues ran the trial at a university hospital in Slovenia between November 2020 and May 2023. It randomized 25 men with type 2 diabetes, obesity and functional hypogonadism to semaglutide or to intramuscular testosterone, for 24 weeks. Median age was 50 and median BMI was 35.9.⁴

In the 13 men on semaglutide, the share of sperm with normal shape rose from a median of 2% to 4%, and that result was statistically significant.⁴ The WHO lower reference limit for normal morphology is 4%, so the median moved from clearly below the threshold to sitting on it.⁸ Sperm concentration went from 25 to 37 million per mL and total count from 34.5 to 41 million, and neither of those changes reached significance.⁴ Both figures were already above the WHO limits of 16 million per mL and 39 million total at the start, so concentration was never the problem in this group.⁸

Set against that, the testosterone arm fell from 25 to 10 million per mL, taking it below the reference limit.⁴⁸ When the paper reports that semaglutide was superior to testosterone on concentration and total count, that superiority comes from the comparator declining, not from semaglutide raising anything.

One more finding deserves attention, because it complicates the obvious explanation.

The changes in sperm parameters did not correlate with weight, BMI, body fat, HbA1c, insulin resistance, LH or FSH.⁴ Those men lost 6 kg and dropped 1.2 percentage points of HbA1c, a three-month average of blood sugar, so the metabolic improvement was real and the sperm changes did not track it. In 13 men, an absent correlation is weak evidence of anything. It does mean the tidy story, that weight loss fixes the metabolic problem and the metabolic problem was suppressing sperm, is not what this trial measured.

Its authors flag two limits themselves. One semen sample does not capture how much samples from the same man vary, and 24 weeks may be too short.⁴

Is losing the weight without the drug better for sperm?

The pooled numbers favor diet and exercise over both surgery and drugs. One catch undercuts that finding.

The Human Reproduction Update meta-analysis is the only paper that lines these up against each other. It covered 352 men who had bariatric surgery, 119 on drug treatment and 319 on lifestyle programs, and pooled each separately.³

Route to weight loss	Sperm concentration, mean difference	Normal morphology, mean difference
Lifestyle, diet and exercise, before-and-after studies	1.29 million per mL (minus 1.03 to 3.61), not significant	0.59% (0.23 to 0.94), p = 0.001
Lifestyle, randomized trials against a control group	6.66 million per mL (minus 7.21 to 20.53), not significant	4.77% (minus 4.67 to 14.20), not significant
Bariatric surgery	minus 4.84 million per mL (minus 18.23 to 8.54), not significant	0.10% (minus 1.75 to 1.95), not significant
Liraglutide	0.58 million per mL (minus 24.76 to 25.91), not significant	not pooled
Metformin	1.28 million per mL (minus 5.07 to 7.62), not significant	4.40% (1.94 to 6.86), p = 0.001

Progressive motility is where the lifestyle result looks strongest and where the catch sits. In before-and-after studies it improved by 10.56 percentage points, with a tight interval of 8.97 to 12.15.³ In the randomized trials, pooled against actual control groups, the same measure came out at 9.24 points with an interval of minus 1.94 to 20.41. That interval does not clear zero.³ Emphatic without a control group, gone with one. That pattern is what you see when men who volunteer for a fitness program also change other things, and when semen samples vary on their own.

Two other rows in that table deserve a second look. Bariatric surgery, the most drastic weight loss available, has a central estimate for sperm concentration that points down. Metformin, an old and cheap drug nobody markets for this, has the only significant morphology improvement in the whole comparison.

Their own summary of the medical routes is "limited benefit and potential harm," against lifestyle interventions "associated with measurable improvements in sperm quality."³ Certainty across all of it is rated very low to low. Follow-up in the lifestyle studies ran about two to four months, too short to see a full cycle of sperm production.³

Has anyone's sperm count fallen on a GLP-1 drug?

One published case says yes. The field has not settled what it means.

A case report in Reproductive BioMedicine Online describes a man in his thirties with obesity whose semen analysis fell apart on liraglutide.⁹ Two reviews summarize it and they do not agree on the detail. The Human Reproduction Update meta-analysis reports azoospermia roughly five months after he started the drug. Sperm concentration came partly back after he stopped. Morphology did not.³

The Journal of Clinical Endocrinology and Metabolism review reports a fall to 0.2 million sperm per mL with no motility, normalizing two months after stopping.⁵ Those descriptions differ on whether any sperm were present and on whether recovery was complete.

The Human Reproduction Update account is the more cautious of the two and the one to prefer until the primary paper is read, because it is the version that does not claim a full recovery.

One case is one case. It cannot establish cause, and a man with obesity and diabetes has plenty of other reasons for a bad semen analysis. It is also the only report of its kind that turned up, against a background of millions of prescriptions.

What makes it hard to dismiss outright is that a direct route exists. GLP-1 receptors have been found in human testicular tissue, so the drug reaching the testicle is not speculative.⁵¹⁰ That point anchors a 2024 commentary. It argues the reproductive effects of these drugs are underexplored, and that "the temporary benefits of any treatment should not obscure the understanding of potential long-term harm."¹⁰ The Human Reproduction Update authors put it as an "urgent need to establish the impact of weight loss pharmacotherapy, particularly more potent GLP-1 receptor agonists" on sperm.³

So the position to hold is narrower than either headline. Nothing establishes harm. Nothing rules it out. The people who look at this closely are asking for studies, not offering reassurance.

Has anyone measured whether men on a GLP-1 actually conceive?

No study has been designed to find out. One case report describes a pregnancy. The circumstances make it the opposite of encouraging.

Kaltsas and colleagues, writing a 2026 review specifically about men seeking fertility, went looking for exactly this and found nothing. Its words are that among the available studies "none was designed or powered for natural conception, clinical pregnancy, or live birth," and that the endpoints that matter most, pregnancy and live birth, are "essentially absent."¹¹

Our preconception and PCOS guide covers the companion question for women.

The large literature on GLP-1 drugs and pregnancy outcomes covers women taking them. It answers a different question and does not carry over to men. For men, the review states plainly that evidence on exposure before conception is insufficient, and that pregnancy-related cautions on the label do not by themselves establish a risk from the father's exposure.¹¹

Semen markers and fertility are related. They are not the same measurement. Morphology, count and motility are statistical correlates of how likely conception is across a population. Plenty of men with poor numbers father children and plenty with good numbers do not. A 2% to 4% shift in the shape of sperm cells in 13 men tells you something moved. It does not tell you anyone's chance of becoming a father changed.

The one pregnancy in this literature is in the liraglutide case report covered above. It came through ICSI, a laboratory procedure in which a single sperm is injected directly into an egg, after the man had stopped the drug.³ That is evidence about a fertility clinic. It is not evidence about a drug.

That same review ends on the point this page would make anyway: these drugs "should be used for established metabolic indications, not as male infertility treatments."¹¹

Why do the 2026 reviews disagree about how much GLP-1 fertility evidence exists?

They set different boundaries. One of them also did not keep its own count straight.

The Journal of Sexual Medicine review states 10 studies and 639 men as an exact total.¹ Its Cells counterpart says eight studies in the abstract and seven in the body text. It gives no exact number of men, describing the total as "approximately 1200" and noting that the figure depends on how overlapping cohorts are counted.²

Of the two, the 639 figure is the one to quote. It is a stated exact total from a review that followed a registered reporting standard and applied formal risk-of-bias tools, and it does not contradict itself. Call the Cells count the weaker number. Not because the review is bad work. A paper that says seven in one place and eight in another has not pinned down its own denominator, and an approximate total cannot be checked.

Neither one ran a meta-analysis. The Cells authors say so directly: "No formal meta-analysis was possible due to outcome heterogeneity."² The Human Reproduction Update paper did pool. Only one GLP-1 estimate came out of it, for liraglutide and sperm concentration. The mean difference was 0.58 million per mL, with a confidence interval running from minus 24.76 to plus 25.91.³ An interval that wide, straddling zero by a mile in both directions, is a formal way of saying the data cannot tell. No pooled figure exists at all for semaglutide, for testosterone, or for any semen measure other than concentration.

Does any of this apply if your weight and testosterone are normal?

The evidence says no. That answer rests on measurements in healthy men and not on a gap in the data.

Both reviews separate men by starting condition and find the same split. In men with obesity, type 2 diabetes or functional hypogonadism, testosterone rises and some semen parameters move. In healthy eugonadal men, meaning men whose testosterone was normal to begin with, the drugs look hormonally neutral.¹² The only placebo-controlled trial in the whole set was done in healthy men, and it found no significant change in LH or FSH.²

Finding nothing in a placebo-controlled trial is more informative than most of what sits in this literature. It is the design least able to manufacture a change out of expectation and regression to the mean.

Two things keep that from being a clean all-clear. GLP-1 receptors are not confined to the gut and pancreas: they have been found in rodent and human testes, and specifically in Leydig cells, the cells that make testosterone.⁵¹⁰ A receptor in the tissue is a route by which a drug could act directly, independent of weight.

One infusion study in healthy men reported that GLP-1 reduced the pulsatile component of testosterone secretion, meaning the rhythm of its release and not the daily total.⁵ A second infusion study found no difference in LH, FSH or testosterone against vehicle.⁵ For a man taking a GLP-1 who is not metabolically unwell, the evidence points to no reproductive effect in either direction, and it is thinner than the word "evidence" suggests.

What about tirzepatide, and the newer compounds?

Tirzepatide has almost nothing behind it.

The reviews above cover liraglutide, semaglutide, dulaglutide and exenatide, so Ozempic, Wegovy, Saxenda and Victoza are all inside the evidence described here.¹ Tirzepatide, sold as Mounjaro and Zepbound, acts on a second gut hormone receptor, GIP, as well as the GLP-1 one. The narrative review found two small human studies of it. Neither "evaluated semen parameters, sperm function, conception, pregnancy, or live birth," so the review concludes that tirzepatide "should not be presented as having reproductive evidence equivalent to classic GLP-1 receptor agonists."¹¹

For retatrutide, orforglipron and the amylin compounds, nothing turned up at all. Any claim that one of them is better or worse for fertility rests on no measurement whatsoever, in either direction, because nobody has run the study that would produce one. Our guide on GLP-1 side effects covers what has been recorded for these drugs generally.

Do GLP-1 drugs cause erectile dysfunction or lower libido?

The reporting data point slightly away from a problem.

A cross-sectional analysis of the FDA's adverse event reporting database covered six GLP-1 drugs and reports filed from late 2003 to early 2024. It looked at orgasmic dysfunction, erectile dysfunction and decreased libido in men. It found 182 male cases and a reporting odds ratio of 0.41, with a confidence interval of 0.36 to 0.48.¹²

A reporting odds ratio below 1 means these events showed up less often in reports about GLP-1 drugs than in reports about everything else in the database. A safety signal would run in the opposite direction. It is also not proof of protection, because the database collects voluntary reports, has no denominator of how many people took each drug, and reflects what gets reported as much as what happens. A disproportionality analysis can flag something to look at. It cannot establish risk in either direction.

The randomized trial found erectile function scores improved only in the testosterone arm, at p = 0.013, with semaglutide not reaching significance at p = 0.17. Sexual desire did improve on semaglutide, at p = 0.009.⁴ The narrative review's summary of the whole area is that findings are mixed and do not establish causality.¹¹

What would it take to prove a GLP-1 helps men trying to conceive?

It would have to recruit men who are actually trying to conceive.

A study that settled this would need:

• men actively trying to conceive, recruited on that basis, not men recruited for diabetes who happen to be male
• pregnancy or live birth as a stated endpoint, not semen parameters standing in for one
• at least two semen samples per timepoint, since the trial above flags that one sample misses the variation between samples from the same man⁴
• a comparison group on something other than testosterone, so that any difference comes from the drug under test
• longer than the existing trial ran, since its own authors say 24 weeks may be too short⁴
• enough men to tell a rare harm from a coincidence, since one case report cannot do that³

Nothing like that exists. The meta-analysis above calls the need for it urgent.³ If you are a man on a GLP-1 who wants children, what the evidence currently supports is that the drug is not doing to your sperm what testosterone therapy would. Everything past that point is unmeasured, including the one case where a man's sperm count fell. Our guide on talking to your doctor about peptides covers raising this without the conversation stalling, and our guide on life after significant weight loss covers what else changes on the way down.

Common questions

Do GLP-1 drugs improve male fertility?

Does semaglutide raise testosterone in men?

Does semaglutide increase sperm count?

Is a GLP-1 better than TRT if I want children?

How much did sperm morphology actually improve?

Does the Wegovy label say anything about male fertility?

Will a GLP-1 fix low testosterone without testosterone therapy?

Do I need to stop Ozempic or Wegovy before trying to conceive?

Does tirzepatide affect sperm?

Do GLP-1 drugs cause erectile dysfunction?

How many men have actually been studied?

Is there a pooled result I can quote?

Has anyone's sperm count dropped on a GLP-1?

Is diet and exercise better for sperm than the drug?

Can GLP-1 drugs reach the testicle directly?

Does weight loss explain the sperm changes?

Are these drugs prescribed for male infertility?

Sources

1. Deameh MG, Ramez M, Rowaiee R, Bani Irshid BA, Mohamed H, Abdelshafi A, Al-osoufi MA, Mohamed T, Hegazin SB, Raheem O. Effects of glucagon-like peptide-1 receptor agonists on male reproductive hormones, semen parameters, and metabolic outcomes: a systematic review. The Journal of Sexual Medicine. 2026;23(2):qdaf381. Published January 7, 2026. DOI 10.1093/jsxmed/qdaf381. PMID 41498523. Tier: abstract and record page read via the publisher's listing at academic.oup.com; the full text is behind a subscription and was not retrieved. The listing gives: a PRISMA-guided search of PubMed, Embase, Scopus and Web of Science up to April 2025; randomized and cohort studies in adult men; risk of bias by RoB 2 and ROBINS-I; "Ten studies involving a total of 639 men were included"; total testosterone rose consistently in men with obesity, type 2 diabetes or functional hypogonadism; free testosterone inconsistent and partly offset by rising sex hormone binding globulin; LH and FSH preserved or increased unlike testosterone comparators; semen improvements in obese or hypogonadal men but not healthy men. No effect sizes, confidence intervals or p values appear on the listing, and none are quoted here. PubMed itself returned a browser verification page on every attempt, so the PMID above is taken from the search result that led to the publisher page. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8
2. Zafrani Z, Khan SS, Zitzmann M. Metabolic Reversal of Functional Hypogonadism? GLP-1 Receptor Agonists and Male Reproductive Endocrinology: A Systematic Review. Cells. 2026;15(15):1319. DOI 10.3390/cells15151319. mdpi.com. Tier: read at source, open access, though the final 3,197 characters of the page were not read. The paper is internally inconsistent on its own count: the abstract says eight included studies and the body text repeatedly says seven, and its stated limitation reads "The number of included studies is small (n = 7)." It gives no exact total of men, describing it as "approximately 1200" and noting the figure depends on how overlapping cohorts are counted. Named sample sizes visible in the text: Lengsfeld 26 randomized and 24 completed, Lisco 108, Eid 53, Graybill 51, Seminara 10. Other quoted lines: "Semen parameter data were reported inconsistently and in very small samples", which it says precludes robust conclusions about fertility outcomes, and "No formal meta-analysis was possible due to outcome heterogeneity." The Lengsfeld placebo-controlled trial in healthy men is cited here via this review; the primary paper was not retrieved. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9
3. Peel A, Lyons H, Tully CA, Vincent AD, Jesudason D, Wittert G, McPherson NO. The effect of obesity interventions on male fertility: a systematic review and meta-analysis. Human Reproduction Update. 2025. DOI 10.1093/humupd/dmaf025. Tier: full text read via an open copy of the published PDF at sochob.cl; the publisher page at academic.oup.com was not opened. 32 studies. Participants by route: bariatric surgery 352, pharmacotherapy 119, lifestyle 319, with one study (Andersen et al. 2022) counted in two sections so the totals must not be summed. Pooled mean differences quoted on this page: bariatric surgery concentration minus 4.84 million per mL (minus 18.23 to 8.54), progressive motility 2.0% (minus 4.54 to 8.54), morphology 0.10% (minus 1.75 to 1.95); liraglutide concentration 0.58 million per mL (minus 24.76 to 25.91), motility not pooled for pharmacotherapy; metformin concentration 1.28 million per mL (minus 5.07 to 7.62) and morphology 4.40% (1.94 to 6.86, p = 0.001); lifestyle before-and-after concentration 1.29 million per mL (minus 1.03 to 3.61), progressive motility 10.56% (8.97 to 12.15, p < 0.001), morphology 0.59% (0.23 to 0.94, p = 0.001); lifestyle randomized concentration 6.66 (minus 7.21 to 20.53), progressive motility 9.24 (minus 1.94 to 20.41), morphology 4.77 (minus 4.67 to 14.20), none significant. Total sperm count was not pooled as a separate outcome. GRADE certainty very low to low. Stated conclusion: lifestyle interventions "are associated with measurable improvements in sperm quality" while the medical routes show "limited benefit and potential harm"; the paper names an "urgent need to establish the impact of weight loss pharmacotherapy, particularly more potent GLP-1 receptor agonists". It also reports the liraglutide case as azoospermia about five months after starting, partial concentration recovery after stopping, morphology not recovering, and a twin pregnancy by ICSI, and reports no live birth outcomes anywhere in the 32 studies. Stated limitations include "lack of or inappropriate control arms", short follow-up of about two to four months in lifestyle studies, BMI as the only adiposity measure, and no dose-dependent relationship between BMI change and sperm outcomes. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11 ↩12 ↩13 ↩14 ↩15
4. Gregorič N, Šikonja J, Janež A, Jensterle M. Semaglutide improved sperm morphology in obese men with type 2 diabetes mellitus and functional hypogonadism. Diabetes, Obesity and Metabolism. DOI 10.1111/dom.16042. Trial registration NCT06489457. Tier: full text read via a reproduction of the published PDF hosted at med.mui.ac.ir; the publisher's own page at Wiley refused retrieval. The reproduction's citation line reads 2024 and the publisher's listing places it in a 2025 issue, so the year is given as the DOI only here. Randomized open-label trial, University Medical Centre Ljubljana, November 2020 to May 2023, 25 men, 24 weeks, 13 to semaglutide 1 mg weekly and 12 to intramuscular testosterone undecanoate. Median age 50 (46 to 60), median BMI 35.9 (32.8 to 38.7). Eligibility required total testosterone below 11 nmol/L on two morning tests plus at least two symptoms. Semen analysis by WHO methods with Tygerberg strict morphology criteria. Semaglutide arm: normal morphology 2% (2; 3.5) to 4% (2; 5.5), p = 0.012; concentration 25 (15; 125.5) to 37 (16.5; 60.5) million per mL, p = 0.58; total number 34.5 to 41 million, p = 0.79; total motility 30% to 30%, p = 0.09. Testosterone arm: concentration 25 (9; 76) to 10 (5.6; 18.5) million per mL, p = 0.028; total number 31.5 to 19 million, p = 0.018; morphology 2% to 1%, p = 0.157; LH and FSH suppressed, p = 0.003 and p = 0.002. Between-group p values: morphology 0.001, concentration 0.002, total number 0.026. Total testosterone rose in both arms, semaglutide 6.1 to 7.8 nmol/L (p = 0.023) and testosterone 6.7 to 12.3 nmol/L (p = 0.002). Semaglutide arm lost 6 kg (p = 0.004) and 1.2% HbA1c (p = 0.009). IIEF-15 total improved only on testosterone (p = 0.013; semaglutide p = 0.17), while sexual desire improved on semaglutide (p = 0.009). Sperm changes did not correlate with weight, BMI, body fat, HbA1c, HOMA-IR, LH or FSH. Authors' stated limitations: a single semen sample may not reflect sperm quality given natural variation, and 24 weeks may be too short. The registry record for NCT06489457 could not be opened from here, so nothing is claimed about which outcomes were pre-specified. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11 ↩12 ↩13
5. Couldwell M, Tidwell AJ, Taylor AE. Effect of GLP1 Agonists on Reproduction. Journal of Clinical Endocrinology and Metabolism. 2025;110(11):3009-3024. DOI 10.1210/clinem/dgaf401. Published July 14, 2025. academic.oup.com. Tier: read at source, though the Discussion and Clinical Recommendations section listed in the contents was not in the text retrieved, so no clinical recommendation is quoted here. Quoted lines: "GLP1R expression has been described in rodent and human testes"; in normal human testicular tissue "GLP1R expression has been detected in Leydig cells"; one infusion study in healthy men found GLP-1 "reduced pulsatile component of T secretion" while another found no significant difference in LH, FSH or testosterone against vehicle; a 16-week liraglutide trial in obesity-associated hypogonadism reported "significant increases in LH and FSH"; a trial in men who had already lost weight on a calorie-restricted diet found "No additional effects of liraglutide on sperm parameters"; "Although preclinical toxicology studies did not demonstrate male fertility issues, there is at least 1 case report", described as a 35-year-old man with obesity whose count declined to 0.2 million sperm per mL on liraglutide with no sperm motility, normalizing two months after stopping. The abstract states that "consideration of GLP1 agonists for the treatment for obesity-associated reproductive dysfunction requires caution". The review also mentions isolated reports of reduced sperm counts sourced only to a consumer side-effect website, which are not used on this page. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6
6. WEGOVY (semaglutide) injection and tablets, US prescribing information, revised 05/2026. accessdata.fda.gov. Tier: read at source. Section 13.1 states "No effects were observed on male fertility" in the rat fertility study, in which males were dosed for four weeks before mating, at doses up to 0.1-fold the maximum recommended human dose by AUC. The same section reports an increase in estrus cycle length at all dose levels in females and a small reduction in corpora lutea, attributed to an adaptive response to the drug's effect on food consumption and body weight. No human male fertility data appear in this section. ↩1
7. Testosterone Cypionate Injection USP, 200 mg/mL, US prescribing information, revised 6/2022, application 216318. accessdata.fda.gov. Tier: read at source. Highlights: "Potential for Adverse Effects on Spermatogenesis: Testosterone Cypionate Injection may cause azoospermia." Section 5.7: "With large doses of exogenous androgens, including Testosterone Cypionate Injection, spermatogenesis may be suppressed," possibly leading to adverse effects on semen parameters including sperm count. Section 8.3: "Reduced fertility is observed in some men taking testosterone replacement therapy" and "The impact on fertility may be irreversible." Section 13.1 notes that exogenous testosterone suppresses spermatogenesis in rat, dog and nonhuman primates, reversibly on stopping. This is one manufacturer's label for one testosterone ester and not the same product used in the trial above, which was testosterone undecanoate. ↩1 ↩2
8. WHO lower reference limits for semen parameters, as reproduced in a clinical reference summary at gpnotebook.com, citing NICE. Tier: read via a reproduction. Figures given: volume 1.4 mL or more, concentration 16 million per mL or more, total sperm number 39 million per ejaculate or more, total motility 42% or more, progressive motility 30% or more, normal morphology 4% or more, vitality 54% or more. The reproduction does not state which edition of the WHO laboratory manual these come from, and the WHO manual itself was not retrieved, so the edition is not claimed here. The figures match the values in general clinical use at the time of writing. ↩1 ↩2 ↩3
9. The effects of liraglutide on male fertility: a case report. Reproductive BioMedicine Online. sciencedirect.com. Tier: unverified at source. The publisher page refused retrieval, so this case report is known on this page only through the two reviews that summarize it, at notes 3 and 5, and those two summaries disagree on whether the man reached azoospermia and on whether recovery was complete. The title, journal and link above come from a search result and not from the article itself. No figure on this page is taken from this entry directly; it is listed so the primary source can be found and read. ↩1
10. Du Plessis SS, Omolaoye TS, Cardona Maya WD. Potential impact of GLP-1 receptor agonists on male fertility: a fable of caution. Frontiers in Physiology. 2024;15:1496416. DOI 10.3389/fphys.2024.1496416. frontiersin.org. Tier: read at source. A commentary, not new data, and cited here as a stated position and not as evidence. States that "GLP-1 receptors are also present in male reproductive tissues, such as the testes", that direct effects on sperm function and hormones "remain largely unexplored in clinical studies", that animal findings are mixed with one mouse study showing improved motility, mitochondrial activity and DNA fragmentation without testosterone recovery, and concludes that "the temporary benefits of any treatment should not obscure the understanding of potential long-term harm". ↩1 ↩2 ↩3
11. Kaltsas A, Gkioxaris V, Giannakas T, Zachariou A, Dimitriadis F, Sofikitis N, Chrisofos M. GLP-1 Receptor Agonists and Tirzepatide in Men Seeking Fertility: A Structured Narrative Review and Proposed Clinical Framework. Journal of Clinical Medicine. 2026;15(18):7313. DOI 10.3390/jcm15187313. mdpi.com. Tier: read at source, open access, though the page was cut off before its dedicated limitations section. Quoted lines: "none was designed or powered for natural conception, clinical pregnancy, or live birth"; the endpoints that matter most, pregnancy and live birth, are "essentially absent"; "Evidence on paternal preconception exposure is insufficient, and pregnancy-related label precautions do not by themselves establish risk from paternal exposure"; "These therapies should be used for established metabolic indications, not as male infertility treatments"; "Sexual-function findings are mixed and do not establish causality." On tirzepatide: two small human studies, of which "Neither evaluated semen parameters, sperm function, conception, pregnancy, or live birth", so tirzepatide "should not be presented as having reproductive evidence equivalent to classic GLP-1 receptor agonists." The author order here follows the article byline; the page metadata lists the authors in a different order. ↩1 ↩2 ↩3 ↩4 ↩5
12. Pourabhari Langroudi AP, Chen AL, Basran S, Sommer ER, Stinson J, Cheng YS, Del Giudice F, Scott M, Eisenberg ML. Male sexual dysfunction associated with GLP-1 receptor agonists: a cross-sectional analysis of FAERS data. International Journal of Impotence Research. 2025 Apr 16, epub ahead of print. Tier: abstract read via a reproduction at urotoday.com; the journal page was not retrieved. FAERS reports from Q4 2003 to Q1 2024 analyzed with OpenVigil 2.1, covering tirzepatide, semaglutide, dulaglutide, exenatide, lixisenatide and liraglutide, for orgasmic dysfunction, erectile dysfunction and decreased libido in men. 182 cases, most aged 40 to 60; exenatide 24.2% of reports and semaglutide 21.4%; diabetes the indication in 43.9%. Reporting odds ratio 0.41 (95% CI 0.36 to 0.48), proportional reporting ratio 0.41 (0.36 to 0.48), relative reporting ratio 0.42 (0.36 to 0.48), chi-squared p < 0.0001. The authors describe this as a weak association and say overall patient risk remains low. The reproduction carries no limitations section, so the authors' own account of what FAERS cannot show is not quoted here. Note that all three reported ratios sit below 1, which is the direction of under-reporting, not of a safety signal. The reproduction spells the seventh author "Del Giuduce"; it is given above in the conventional spelling. ↩1

Citing this page. Peptide Decoding. Do GLP-1 Drugs Affect Sperm, Testosterone or Male Fertility? What Has Actually Been Measured. Study and participant counts from Deameh et al., J Sex Med 2026, and Zafrani et al., Cells 2026; semen trial figures from Gregorič et al., Diabetes Obes Metab, DOI 10.1111/dom.16042; label language from the Wegovy and testosterone cypionate US prescribing information. Reviewed October 17, 2026. https://peptidedecoding.com/guides/glp1-male-fertility