Most of the questions people ask about Ozempic and fertility concern women: whether the medicines affect contraception, how long to stop before pregnancy, and what happens if someone conceives while taking them.
Men have received considerably less attention. Yet obesity, diabetes and reproductive health are closely connected, and growing numbers of men of reproductive age now use GLP-1 receptor agonists for metabolic treatment.
A study from Romania, published on November 5, 2026, in Biomedicines, brings that question into focus. Over 12 months of treatment with semaglutide or liraglutide, men with obesity or type 2 diabetes showed improvements in several semen measurements and reproductive hormones.
The reported changes are substantial. Average sperm concentration, progressive motility and total testosterone all increased. But the study has a limitation that prevents a straightforward conclusion: there was no untreated comparison group.
That means researchers observed improvements while men were receiving GLP-1 therapy. They did not establish whether the medicines themselves caused those improvements, whether weight loss and better metabolic health were responsible, or how much ordinary biological variation contributed.
The distinction matters because better semen measurements are not the same as proven improvement in fertility.
What the Ozempic and Fertility Study Actually Measured
Researchers associated with Carol Davila University of Medicine and Pharmacy and the Royal Hospital in Bucharest enrolled 161 men between September 2021 and September 2023.
Participants had obesity, type 2 diabetes, or both, and were beginning treatment with a GLP-1 receptor agonist. The medicines investigated were semaglutide, the active ingredient in Ozempic and Wegovy, and liraglutide, an older GLP-1 medicine administered daily.
Men using tirzepatide, the dual GIP and GLP-1 receptor agonist sold as Mounjaro and Zepbound, were excluded. The findings therefore should not automatically be applied to that medicine.
The researchers performed semen analyses and measured reproductive hormones at baseline and again after 12 months of treatment.
This was a prospective observational cohort. Participants were followed forward in time, but they were not randomly assigned to medication or placebo. There was no comparison group of similar men who remained untreated or lost weight through another intervention.
Of the 161 men initially enrolled, 108 completed the follow-up. The reported final cohort contained 54 men receiving semaglutide and 54 receiving liraglutide.
Over the year, their mean body mass index decreased from 37.5 to 31.3. Average HbA1c, a measure reflecting blood-glucose exposure over approximately the previous two to three months, declined from 6.49% to 5.64%.
In other words, the participants who completed the study experienced substantial improvements in body weight and metabolic health alongside the observed reproductive changes.
That is central to interpreting the results. Obesity and metabolic dysfunction can affect reproductive hormones and semen parameters. If a treatment improves metabolic health, reproductive measurements may change without the medicine necessarily acting directly on sperm-producing tissues.
The Sperm and Testosterone Numbers That Improved
The semen measurements are the most immediately striking part of the report.
Average sperm concentration rose from 62.9 million to 86.7 million sperm per milliliter. Progressive motility, the percentage of sperm moving forward rather than remaining stationary or moving without effective forward progression, increased from 22.8% to 38.4%.
That change in progressive motility amounts to 15.6 percentage points, a substantial shift in the group average.
The proportion of sperm with normal morphology increased from 3.14% to 4.46%, a difference of 1.32 percentage points.
These measurements have different clinical meanings. Sperm concentration measures how many sperm are present in a given volume of semen. Progressive motility describes their ability to move forward. Morphology evaluates the percentage with normal structural characteristics under established laboratory criteria.
The World Health Organization’s sixth-edition lower reference values include approximately 16 million sperm per milliliter for concentration, 30% for progressive motility and 4% for normal morphology. Those figures are derived from semen characteristics among men who contributed to pregnancies. They are not rigid boundaries separating fertile from infertile men.
That distinction is particularly relevant here. The reported average baseline sperm concentration of 62.9 million per milliliter was already well above the reference threshold. Meanwhile, group-average motility and morphology began below their respective reference values and subsequently moved above them.
Averages can conceal considerable variation between individuals. The fact that a group mean crosses a reference threshold does not establish that every participant’s semen quality normalized or that the group achieved greater fertility.
Another reported semen endpoint was less conclusive. Total sperm count per ejaculate increased from approximately 170 million to 196 million, but its adjusted p-value of 0.062 did not satisfy the study’s statistical significance threshold after correction for multiple comparisons.
The hormone results moved in a direction that researchers might expect alongside improved metabolic health. Mean total testosterone rose from 5.91 to 7.74 nanomoles per liter, while estradiol declined from 36.5 to 28.4 picograms per milliliter.
Sex hormone-binding globulin also increased modestly, according to the reported findings. Luteinizing hormone and follicle-stimulating hormone, the pituitary signals involved in regulating testicular function, did not show similarly clear changes.
Obesity can influence reproductive hormone concentrations through several pathways, including insulin resistance, inflammatory signaling and aromatase activity in adipose tissue, which converts androgens into estrogens.
The combination of rising testosterone, falling estradiol and substantial weight reduction is compatible with improvement in obesity-associated hormonal dysfunction. It does not prove that changes in aromatase activity caused the hormone results.
Free testosterone was not directly measured, limiting how completely the hormone findings can be interpreted.
The semen and hormone measurements moved in a favorable direction. The study cannot establish whether the drugs, the weight loss or other changes produced that pattern.
Why the Study Cannot Prove the Drugs Caused the Changes
The largest limitation is the absence of a control group.
All participants in the final analysis were receiving one of the two GLP-1 medicines. There was no comparable group of men with obesity or diabetes who did not receive a GLP-1 drug, and no randomized group assigned to lose weight through an alternative approach.
Without such comparisons, changes observed over time cannot be attributed confidently to a medicine’s specific pharmacological action.
Weight loss itself may be important. Participants experienced a considerable reduction in average BMI, alongside improved blood-glucose measurements. Those changes could plausibly influence reproductive hormones and some semen characteristics.
Diet, physical activity, sleep, other medicines, changes in health status and ordinary biological variation could also contribute. The described study did not monitor every potential influence closely enough to separate their individual effects.
Repeated semen analysis poses another challenge. Sperm concentration, motility and morphology can vary between samples from the same person, sometimes substantially.
Professional infertility guidelines therefore emphasize the importance of repeat semen testing, particularly when an initial result is abnormal. A single specimen at baseline and another a year later may describe a change, but it does not establish a stable trajectory for every participant.
The researchers also did not independently verify every participant’s abstinence interval before semen collection, a factor that can influence measurements.
Attrition raises a separate concern. Fifty-three of the original 161 participants did not complete the study, approximately 32.9% of those enrolled.
The draft reports that those who did not finish tended to be older and were more likely to have type 2 diabetes. If the men remaining in the study differed systematically in health, treatment response or other reproductive characteristics, their results might not represent what happened across the full enrolled population.
This form of selection bias cannot be corrected simply by reporting statistically significant changes among completers.
Nor can the two medicines be compared reliably against each other. Although the final cohort included equal numbers receiving semaglutide and liraglutide, treatment assignment was not randomized. Differences between the groups could reflect who received each medicine rather than genuine differences in reproductive effects.
The study therefore supports an association: among the men who completed follow-up, GLP-1 treatment coincided with improved average semen and hormonal measurements.
It does not establish a causal treatment effect.
A statistically significant before-and-after change is not the same as a statistically demonstrated drug benefit over a control group.
How the Findings Fit Earlier GLP-1 Research
This study does not arrive in an evidence vacuum.
Researchers have already investigated whether obesity treatment, weight loss and GLP-1 receptor agonists influence male reproductive function. The findings are encouraging in some populations, but they are neither uniform nor sufficient to establish a fertility treatment.
One important randomized study, published in Human Reproduction in 2022, investigated sperm production in men with obesity who first underwent an intensive low-calorie diet and then entered a weight-maintenance program involving liraglutide, exercise, both interventions or placebo.
After the initial diet, participants lost an average of approximately 16.5 kilograms. Sperm concentration and total sperm count increased, and the improvements were maintained among men who sustained substantial weight loss.
That finding supports an important alternative explanation for the Romanian cohort: improvements in reproductive measurements may be linked to better metabolic health and sustained weight reduction, rather than requiring a unique direct action of GLP-1 medicine on the testes.
A separate randomized, open-label study published in Diabetes, Obesity and Metabolism examined 25 men with obesity, type 2 diabetes and functional hypogonadism.
Researchers compared 24 weeks of semaglutide with testosterone replacement therapy. In the semaglutide group, the proportion of morphologically normal sperm increased, while testosterone treatment was associated with reductions in sperm concentration and total sperm number.
That is relevant because testosterone replacement can suppress sperm production, while treatment directed at obesity and metabolic dysfunction may affect reproductive hormones through a different pathway.
However, the randomized trial was small and used testosterone therapy rather than an untreated or weight-loss-matched comparator. It cannot establish whether semaglutide directly improves fertility or produces better reproductive outcomes than equivalent weight loss achieved without the drug.
A 2026 systematic review in The Journal of Sexual Medicine examined ten studies involving 639 men. It found that GLP-1 receptor agonists were often associated with higher total testosterone in men with obesity, diabetes or functional hypogonadism. Changes in free testosterone were less consistent, and the evidence on semen quality remained limited.
The existing research therefore supports a cautious interpretation. Improvements in metabolic health may accompany improvements in certain reproductive measurements, and GLP-1 medicines may play a role in that process.
What remains unproven is whether those medicines produce an independent benefit beyond weight loss, or improve outcomes that matter most to couples trying to conceive.
Grey Pepper has previously discussed the limitations of observational evidence in its analysis of real-world cardiovascular comparisons involving Ozempic and Mounjaro.
The same scientific principle applies here. Observational results can identify patterns worth investigating, but they cannot automatically substitute for randomized comparisons.
What the Study Does and Doesn’t Say About Male Fertility
Perhaps the most easily misunderstood detail is the report that partners of 38 of the 108 men described pregnancies during the study period.
Those reports are interesting, but they were not collected as a rigorously controlled fertility endpoint.
The analysis did not establish a comparable pregnancy rate among untreated couples, document complete baseline fertility histories or provide the information necessary to attribute conceptions to GLP-1 treatment.
Pregnancy depends on the reproductive health of both partners, timing, intercourse frequency, duration of attempts and numerous other factors. A report of pregnancies among participants’ partners cannot establish that a medicine improved the probability of conception.
The same distinction applies to sperm measurements.
Sperm concentration, progressive motility and morphology are valuable components of a reproductive evaluation. But fertility depends on more than those measurements, including sperm function, the female partner’s reproductive health and other clinical circumstances.
A man can have semen parameters within reference ranges and still experience infertility. Another man can have measurements outside those ranges and successfully contribute to a pregnancy.
For men taking semaglutide or liraglutide for established medical reasons, the Romanian results offer a limited encouraging signal: among completers, average semen measurements did not deteriorate and several improved over the year.
That does not prove that the medicines are free from reproductive risks, and it does not justify prescribing them specifically to treat male infertility.
The findings also cannot answer whether a man planning conception should stop semaglutide, continue treatment or change medicines. Evidence concerning paternal preconception exposure remains limited, and pregnancy-related precautions intended for women should not automatically be applied to men.
Those decisions require individualized discussion with a clinician, particularly when treatment is needed for diabetes or obesity and stopping it could affect metabolic control.
It is also important not to extend the results to tirzepatide. The cohort specifically excluded that medicine, and evidence involving single-pathway GLP-1 receptor agonists does not automatically establish the reproductive effects of a dual GIP and GLP-1 receptor agonist.
The same caution applies to men without obesity or metabolic dysfunction. This study did not evaluate whether men outside the investigated population would experience comparable changes.
Improved semen measurements are encouraging. They are not proof of improved conception rates, successful pregnancies or live births.
What a Better Trial Would Need to Show
The next study needs to answer a different question from the Romanian cohort.
Rather than simply measuring whether reproductive parameters improve after treatment begins, researchers need to determine whether those changes are greater than what would occur without the medicine or with comparable weight loss through another intervention.
A randomized trial could compare men receiving a GLP-1 receptor agonist with a carefully selected control group, while measuring weight loss, blood-glucose changes, reproductive hormones and semen quality using standardized methods.
Repeated semen samples would be particularly important because measurements can vary between ejaculates. Tracking treatment adherence, dose changes, other medications and lifestyle factors would also help researchers interpret the results.
Free testosterone, sex hormone-binding globulin and pituitary hormones should be measured consistently, allowing researchers to examine whether reproductive changes reflect broader metabolic recovery or a more specific hormonal effect.
Where feasible, studies should also record sperm DNA fragmentation and other validated reproductive measures, while acknowledging that laboratory markers still cannot replace clinical fertility outcomes.
Ultimately, the strongest evidence would involve outcomes such as time to pregnancy, clinically confirmed conception and live birth, with appropriate information about both partners.
The available evidence has not yet established those benefits for GLP-1 treatment in men.
That leaves the Romanian study in an important but limited position. Its prospective design and one-year follow-up offer useful human observations. Its semen and hormone findings are worth investigating alongside earlier randomized research.
But the absence of a control group, the substantial attrition and the lack of verified fertility endpoints prevent causal conclusions.
For now, the broader lesson may be less about a new fertility benefit of Ozempic and more about the relationship between metabolic health and male reproductive function.
Men who lose substantial weight and improve their metabolic health may also experience favorable changes in hormones and semen measurements. GLP-1 medicines are one established way to treat the underlying metabolic conditions, but their specific contribution to reproductive improvement remains uncertain.
That is a worthwhile research question. It is not a reason to market obesity medicine as a fertility treatment.
The study observed better sperm measurements after a year of GLP-1 treatment. It did not establish that the drugs caused them, or that more couples could conceive because of them.
Related on Grey Pepper: Why Semaglutide Lasts a Week and How to Interpret Real-World GLP-1 Research.
Sources and Further Reading
- Persu C, et al. Twelve Months of GLP-1 Receptor Agonist Therapy Is Associated with Improved Sperm Quality and Hormonal Profile in Men with Obesity and/or Type 2 Diabetes: A Prospective Cohort Study. Biomedicines, November 5, 2026. DOI: 10.3390/biomedicines14112546.
- Human Reproduction, 2022: Sperm Count Is Increased by Diet-Induced Weight Loss and Maintained by Exercise or GLP-1 Analogue Treatment — A Randomized Controlled Trial.
- Gregorič N, et al. Semaglutide Improved Sperm Morphology in Obese Men With Type 2 Diabetes Mellitus and Functional Hypogonadism. Diabetes, Obesity and Metabolism, 2025.
- The Journal of Sexual Medicine, 2026: Effects of GLP-1 Receptor Agonists on Male Reproductive Hormones, Semen Parameters, and Metabolic Outcomes — A Systematic Review.
- European Association of Urology: Male Infertility Guidelines, Semen Analysis and WHO Reference Values.
- American Urological Association and American Society for Reproductive Medicine: Diagnosis and Treatment of Infertility in Men, Guideline Part I.
- Journal of Clinical Medicine, 2026: GLP-1 Receptor Agonists and Tirzepatide in Men Seeking Fertility — A Structured Narrative Review and Proposed Clinical Framework.
- Endocrine Society, June 13, 2026: Clinical Trials Suggest GLP-1 Medicines May Improve Reproductive Markers in Men With Obesity.
