Review finds GLP-1 drugs raise testosterone mainly in men with metabolic conditions
A new review suggests GLP-1 medications may affect testosterone and sexual function only in men whose metabolic health is already impaired, not in healthy men.
A systematic review published July 23 in the journal Cells reports that GLP-1 receptor agonists were associated with modest increases in testosterone and improvements in erectile function or selected semen parameters in men with obesity, type 2 diabetes or functional hypogonadism. In healthy men with normal testosterone — described in the review as eugonadal — the drugs showed no significant endocrine or reproductive effects [1].
The review was written by Zakhi Zafrani, an independent researcher in Manchester, UK, with Sarah Suleman Khan and Michael Zitzmann of the Department of Clinical and Surgical Andrology at Münster University Hospital in Germany [1]. The authors followed PRISMA 2020 guidelines and searched PubMed/MEDLINE, Cochrane and Google Scholar for studies published between January 2021 and January 2026 that evaluated GLP-1 receptor agonist therapy in adult men and reported hormone or reproductive outcomes [1]. The paper was submitted May 3, 2026, accepted July 16, 2026, and published July 23, 2026 [1].
Eight studies met the inclusion criteria, including one randomized placebo-controlled crossover trial and six observational or interventional studies [1]. That single randomized trial was the one conducted in healthy men with normal testosterone, and it found no significant changes in reproductive hormones or semen parameters [1]. The testosterone increases and the improvements in erectile function or semen measures appeared in the metabolically compromised groups, where the authors describe the hormone deficiency as functional suppression of the hypothalamic–pituitary–gonadal axis rather than permanent failure [1].
The review's stated conclusion is that endocrine responses to these drugs appear to depend on the patient's starting point, and that the changes are largely mediated by improvements in metabolic health rather than by the drugs acting on the reproductive system directly [1]. The authors suggest GLP-1 receptor agonists could represent a fertility-preserving metabolic strategy in selected men with functional hypogonadism, but they frame that as a possible implication of the findings rather than a proven outcome [1].
Several details are not reported. The abstract does not give the number of men in each study, the doses or specific GLP-1 medications used, how long patients were treated, or the size of the testosterone changes in units such as nanograms per deciliter [1]. It also does not report whether the hormone changes persisted after treatment stopped, or whether they translated into symptoms men would notice.
Why it matters for patients
The practical takeaway is that a man's metabolic starting point may shape what these drugs do to his hormones. For men who are carrying excess weight, have type 2 diabetes, or have been told their low testosterone is tied to those conditions, this review points to a pattern of modest hormone improvement alongside better erectile function or semen measures in some studies [1]. For men with normal testosterone who take a GLP-1 medication for another reason, the one randomized trial in the review found no measurable effect on hormones or semen [1].
The evidence base is thin — eight studies, only one of them randomized and placebo-controlled — so the findings describe associations, not proof that the drugs cause the changes [1]. A rise in a lab value is also not the same as a change in how a man feels or in his fertility. Nothing in the review supports changing a prescription, adding testosterone therapy, or stopping a GLP-1 medication, and decisions about hormone testing or fertility treatment remain individual questions for a clinician who knows the patient's history.
What is not known
The review does not identify which specific GLP-1 medications were studied, at what doses, or for how long [1]. It is not established whether the testosterone increases are large enough to matter clinically, whether they last, or whether the drugs help, harm or leave unchanged a man's chances of fathering a child. The authors call for the response to be understood as phenotype-dependent, and note that male reproductive endocrinology remains incompletely defined for this drug class [1]. No follow-up study, registry or trial is described in the review's abstract.
Sources
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