GLP-1 Drugs and Men's Health: Testosterone, Sex, Muscle and Results

Most consumer coverage of GLP-1 drugs is written with women in mind. That is not unreasonable, because women make up the majority of trial participants and the majority of prescriptions. But the research that has landed since late 2024 answers several questions that men actually search for, and the answers are more interesting than the marketing on either side suggests.

Here is what the published evidence says about testosterone, erections, sperm, muscle, and why the scale moves differently. None of it is medical advice, and where it describes how these drugs are used it is summarizing the FDA-approved prescribing information, not giving instructions; follow your own prescription and your own provider.

Why do men lose less weight than women on the same dose?

They generally do, in percentage terms. Post hoc analyses of semaglutide trials show women achieve roughly 40 percent greater percentage weight reduction than men [1].

A 2026 analysis of STEP 1 and SELECT presented at the American Diabetes Association went looking for the reason. Drug exposure alone did not explain the gap. Weight loss in men was consistent across ages 45 to 90, while weight loss in women declined with age, and FSH and LH levels tracking menopausal status predicted how much weight women lost [1].

There is a simpler piece of the explanation too. Men carry more lean mass, and lean mass does not come off the way fat does. The same absolute pound loss is a smaller percentage of a heavier starting body composition.

Practically, this matters for expectation setting. If you are a man reading that trial participants lost 15 or 20 percent, the average man’s number in those same trials was lower. No US label recommends a different dose by sex [1].

Does losing weight on a GLP-1 drug raise testosterone?

For men whose testosterone is low because of obesity, the evidence says yes, and says clearly why.

A PRISMA systematic review published in Pharmaceuticals in August 2026 screened 326 records and included 29 studies. Its literature search closed on December 31, 2024, so it does not capture anything published in 2025 or 2026. It found that semaglutide, liraglutide and tirzepatide significantly increased total testosterone in men with obesity-related functional hypogonadism, with a mean increase of 2.5 to 5.2 nmol/L, and concluded the effect is largely mediated by weight loss and improved insulin sensitivity rather than any direct androgenic action [2].

A systematic review in the Journal of Sexual Medicine covering 10 studies and 639 men found the same direction with an important nuance: total testosterone consistently rose, but free testosterone results were inconsistent because sex hormone-binding globulin rises at the same time [3]. LH and FSH were preserved or increased, in contrast with what happens on testosterone replacement therapy, which suppresses them [3].

That last detail is the clinically meaningful one. Testosterone replacement raises testosterone by supplying it from outside and shutting down your own production. Weight loss raises it by removing the thing suppressing your own production. Those are different situations, especially if fertility matters to you.

The underlying trials are small, with sample sizes from 12 to 42 and follow-up of 12 to 24 weeks, and moderate to high risk of bias [2]. No adequately powered trial has been stratified by baseline testosterone. And no GLP-1 or dual incretin drug is approved for hypogonadism.

Is GLP-1 therapy better than testosterone therapy?

A network meta-analysis published in the Journal of Sexual Medicine in August 2026 is the best comparison available. Searching through April 2026, it pooled 23 randomized controlled trials and 1,899 men with obesity-related functional hypogonadism, comparing structured lifestyle therapy, testosterone replacement therapy, endogenous testosterone restoration therapy, GLP-1-based therapy, and testosterone replacement plus lifestyle therapy [4].

Against usual care or placebo, the largest estimated increase in total testosterone came from testosterone replacement plus structured lifestyle therapy (mean difference 7.19, 95 percent CI 1.18-13.21), followed by endogenous testosterone restoration (4.14, 0.74-7.54) and testosterone replacement alone (2.53, 0.26-4.81) [4].

Only testosterone replacement plus lifestyle therapy significantly improved International Index of Erectile Function scores (mean difference 1.29, 0.07-2.50). No intervention significantly reduced HbA1c versus usual care. Testosterone replacement reduced waist circumference and increased lean mass, but also raised hematocrit [4].

GLP-1-based therapy did not come out on top in that network, which is a useful corrective to the single-arm studies. Confidence in the comparative evidence was rated limited [4].

One small pilot has tested the combination directly: a June 2026 study in Minerva Endocrinology added testosterone undecanoate in men with obesity and hypogonadism who were late responders to tirzepatide, reporting further fat-mass loss with apparent preservation of lean mass [5]. One pilot is not a protocol, and stacking hormone therapy onto a weight-loss drug is a clinical decision with its own monitoring requirements.

Do these drugs cause or prevent erectile dysfunction?

Here the evidence genuinely conflicts, and anyone telling you it is settled is overselling.

Pointing toward harm: A study in the International Journal of Impotence Research assessed the risk of developing erectile dysfunction after semaglutide was prescribed for weight loss in men with obesity and without diabetes, and reported a higher risk of both erectile dysfunction and hypogonadism compared with controls, while noting that absolute risk was low [6].

Pointing toward benefit: A retrospective cohort in the TriNetX network covering May 2022 to May 2025 ran three separate 1:1 propensity-matched comparisons in men aged 18 to 70 with type 2 diabetes and no prior erectile dysfunction. Compared with sitagliptin, tirzepatide was associated with lower risk of a new erectile dysfunction diagnosis or PDE-5 inhibitor prescription (risk ratio 0.70, 95 percent CI 0.64-0.76). Versus injectable semaglutide the risk ratio was 0.67 (0.62-0.72), and versus dulaglutide 0.55 (0.51-0.59) [7].

Pointing toward noise: A Stanford-led cross-sectional analysis of FDA Adverse Event Reporting System reports from late 2003 through early 2024 identified 182 male cases of orgasmic dysfunction, erectile dysfunction or decreased libido linked to GLP-1 drugs. Patients were mostly aged 40 to 60. The reporting odds ratio was 0.41 (95 percent CI 0.36-0.48) — below 1, which the authors read as a weak association and low overall patient risk [8].

A 2026 narrative review in Sexual Medicine Reviews pulled these strands together. In rodents, the GLP-1 agonist exendin-4 suppressed sexual behaviors in specific brain regions. In humans, the FAERS disproportionality signals were statistically insignificant, social media reports run both ways, and a randomized double-blind crossover trial in healthy lean men found dulaglutide had no effect on sexual desire, hypothalamic-pituitary-gonadal hormones or semen parameters [9].

What you can take from this: sexual dysfunction is not a labeled adverse reaction for Wegovy, Ozempic, Mounjaro or Zepbound. The cleanest randomized signal, in healthy men, showed nothing. The observational data disagree with each other, and detection bias is a real problem — men who start a new weight-loss drug are men who are newly engaged with a doctor, and things get diagnosed that were always there.

If something changes for you, that is worth raising with a provider rather than researching alone.

What about sperm and fertility?

The Journal of Sexual Medicine review of 10 studies and 639 men reported improvements in semen parameters in men with obesity or hypogonadism, and no significant changes in healthy men [3].

The specific numbers are small. A 2025 randomized trial of 25 men with obesity, type 2 diabetes and functional hypogonadism found that 24 weeks of semaglutide 1 mg increased the share of normally shaped sperm from 2 percent to 4 percent [10]. Researchers presenting at ENDO 2026 framed the overall picture as evidence of no harm to the male reproductive axis, with a possible benefit where low testosterone is obesity-driven [10].

These are not fertility treatments and are not approved for fertility. The reviews call for long-term controlled studies with standardized fertility endpoints.

How much muscle is at stake?

This is the question men ask most and the one with the most usable answer.

A narrative review in Diabetes Care laid out the arithmetic that became the standard framing: incretin drugs producing roughly 15 to 24 percent weight loss also cause lean mass loss on the order of 10 percent, or about 6 kg, which the authors compared to a decade or more of aging [11].

The counterweight in the same review: supervised resistance training programs lasting more than 10 weeks have produced lean mass increases of about 3 kg and strength increases of about 25 percent in both men and women, and after a low-calorie diet, combining aerobic exercise with liraglutide improved weight loss maintenance better than either alone [11]. The authors proposed tailored resistance training as an adjunct to incretin therapy.

A 2026 meta-analysis of 60 studies covering 1,250,717 people found consistent lean body mass reductions with GLP-1 drugs (standardized mean difference -0.52) but rated the certainty low, noted the change appeared largely related to weight loss itself, and found no effect on bone mineral density or fractures [12]. Its most honest conclusion: almost nobody measured strength or physical performance, so whether the lean mass change causes meaningful functional impairment remains unknown [12].

A 2026 review in the British Journal of Pharmacology sharpens the point. Lean soft tissue loss is not a reliable predictor of strength change. Short- to mid-term trials in adults with obesity showed handgrip strength statistically preserved despite lean mass reductions. But in older adults with type 2 diabetes, longitudinal and retrospective research has reported reduced handgrip strength and accelerated sarcopenia with prolonged semaglutide use [13].

Notably, that same review found tirzepatide combined with resistance and aerobic training in young men did not add strength benefits beyond exercise alone [13]. The training does the work.

Every US obesity label already requires these drugs be used alongside a reduced-calorie diet and increased physical activity. The research just tells you which kind of activity is doing the protecting.

Are men getting these drugs?

A study in Annals of Epidemiology analyzed December 2023 self-reported data from a nationwide US cohort run by researchers at the CUNY Graduate School of Public Health. Awareness of GLP-1 drugs was 81.6 percent; use was 8.3 percent overall, 13.4 percent among adults meeting FDA clinical eligibility criteria (BMI of 30 or higher, or 27 or higher with at least one comorbidity; n=1,883), and 4.0 percent among those who were not eligible [14].

Among clinically eligible adults, use was lower among men (adjusted prevalence ratio 0.76, 95 percent CI 0.60-0.96) and among people reporting healthcare access barriers (0.47, 0.35-0.63), and higher among those with household income of 100,000 dollars or more versus under 49,000 (1.49, 1.12-1.98). Nearly half of people who attempted to get treatment — 49.9 percent — were unsuccessful [14].

The picture is not uniform. A scoping review of US initiation patterns for GLP-1 drugs and SGLT2 inhibitors found that in diabetes populations, patients who were younger, male, better educated, higher income, or seen by a specialist were more likely to use these therapies [15]. The direction of the sex gap appears to depend on whether the indication is diabetes or obesity.

Two caveats. The data are self-reported from December 2023, before the 2025-2026 price changes and the Medicare GLP-1 Bridge demonstration, so treat the percentages as a baseline rather than a current figure. And this is a longitudinal volunteer cohort, not a probability-sampled national survey, so the absolute rates are less reliable than the comparisons between groups within it [14].

One indication worth knowing about

Zepbound (tirzepatide) is indicated, in combination with a reduced-calorie diet and increased physical activity, both to reduce excess body weight and maintain weight reduction long term in adults with obesity or overweight with at least one weight-related comorbid condition, and to treat moderate to severe obstructive sleep apnea in adults with obesity [16].

Obstructive sleep apnea is diagnosed more often in men, so this indication is disproportionately relevant here. Whether it applies to you is a question for a provider who can order the sleep study.

Sources

1. Sex differences in weight loss with semaglutide: post hoc analysis of STEP 1 and SELECT. American Diabetes Association 2026. https://doi.org/10.2337/db26-1711-p
2. GLP-1 receptor agonists and male functional hypogonadism: a PRISMA systematic review. Pharmaceuticals. 2026;19(8):1321. https://doi.org/10.3390/ph19081321
3. GLP-1 receptor agonists and male reproductive and sexual health: a systematic review. Journal of Sexual Medicine. 2026. https://doi.org/10.1093/jsxmed/qdaf381
4. Yang L, He X, Wang S, Li T, Huang W, Feng Q. Treatment strategies for functional hypogonadism in obese men: a systematic review and network meta-analysis. Journal of Sexual Medicine. 2026 Aug 5;23(9):qdag272. https://doi.org/10.1093/jsxmed/qdag272
5. Seminara S, et al. Testosterone undecanoate as add-on therapy in late responders to tirzepatide. Minerva Endocrinology. 2026. https://doi.org/10.23736/S2724-6507.26.04541-0
6. Semaglutide for weight loss and risk of erectile dysfunction and hypogonadism in non-diabetic men with obesity. International Journal of Impotence Research. 2024. https://doi.org/10.1038/s41443-024-00895-6
7. Cowart K, Murphy C, Carris N. Association of tirzepatide with erectile dysfunction in people with type 2 diabetes. Journal of Diabetes and Its Complications. 2025 Oct;39(10):109116. https://doi.org/10.1016/j.jdiacomp.2025.109116
8. Pourabhari Langroudi A, Chen AL, Basran S, et al. Male sexual dysfunction associated with GLP-1 receptor agonists: a cross-sectional analysis of FAERS data. International Journal of Impotence Research. 2025 Aug;37(8):661-667. https://doi.org/10.1038/s41443-025-01061-2
9. GLP-1 receptor agonists and sexual function in women and men: a narrative review. Sexual Medicine Reviews. 2026. https://doi.org/10.1093/sxmrev/qeag015
10. Endocrine Society ENDO 2026 press release on GLP-1 drugs and male reproductive health. https://www.endocrine.org/news-and-advocacy/news-room/2026/natesh-press-release-endo-2026
11. Incretin-Based Weight Loss Pharmacotherapy: Can Resistance Exercise Optimize Changes in Body Composition? Diabetes Care. 2024. https://doi.org/10.2337/dci23-0100
12. Beaudart C, Malréchauffé Y, van Heden S, et al. GLP-1 Receptor Agonists and Musculoskeletal Outcomes: A Systematic Literature Review and Meta-Analysis. Drugs. 2026 Sep 12. https://doi.org/10.1007/s40265-026-02365-3
13. GLP-1 receptor agonists and muscle strength changes in older adults. British Journal of Pharmacology. 2026. https://doi.org/10.1111/bph.70355
14. Sanborn J, Fleary SA, Nash D, et al. GLP-1 receptor agonist medications for weight loss: Sociodemographic patterns of awareness, use, and access in a U.S. national cohort. Annals of Epidemiology. 2026 Jun 25;122:110151. https://doi.org/10.1016/j.annepidem.2026.110151
15. Factors and disparities influencing SGLT2 inhibitor and GLP-1 receptor agonist initiation in the United States: a scoping review. Pharmacy. 2025. https://doi.org/10.3390/pharmacy13020046
16. Zepbound (tirzepatide) US prescribing information, revised 8/2026. Eli Lilly and Company. https://uspl.lilly.com/zepbound/zepbound.html