Do GLP-1 Drugs Raise Testosterone? 2026 Evidence

The evidence on GLP-1 and testosterone levels reversed direction in 2026. Two years ago the worry in my clinic was that semaglutide might be flattening men’s hormones. At the American Urological Association’s 2026 meeting, a Mayo Clinic team reported the opposite in more than 1,600 men: median total testosterone climbed from 320 to 419 ng/dL (11.1 to 14.5 nmol/L) after starting a GLP-1 receptor agonist [1]. That is a rise of 99 ng/dL (3.4 nmol/L) — roughly the gap between a number your doctor flags and a number nobody mentions. The headlines then made a second claim: that the rise had nothing to do with weight loss. That part is shakier than it sounds, and the distinction changes what you should do about it. Here is what the 2026 data actually support, who sees the effect, and who sees nothing at all.

What GLP-1 drugs do to testosterone levels: the 2026 numbers

The AUA 2026 dataset is the largest yet. Paired total testosterone measurements were available for 1,629 men and free testosterone for 1,216. Median total testosterone rose from 320 to 419 ng/dL, and median free testosterone from 9 to 10.4 ng/dL. After statistical adjustment for age and starting BMI, the total testosterone gain held at 97.6 ng/dL [1]. For context, most US laboratories set the lower limit of normal near 300 ng/dL (10.4 nmol/L), so a median starting value of 320 describes a group sitting on the edge of deficiency.

An 18-month cohort study of 110 men on semaglutide, dulaglutide, or tirzepatide, presented at ENDO 2025, gives a more useful patient-facing figure. Alongside 10% body weight loss, the proportion of men with normal total and free testosterone rose from 53% to 77% [7]. That is the number I quote in clinic, because it answers the question men actually ask — not “how many points” but “will I end up in the normal range”.

The peer-reviewed literature agrees on direction. A 2025 meta-analysis in Andrology pooled seven studies covering 680 men and found significant increases in total testosterone, free testosterone, SHBG, LH, and FSH, with falls in weight, BMI, waist circumference, and HbA1c [2]. A 2026 systematic review in the Journal of Sexual Medicine covering 639 men reached the same conclusion [3], and a further systematic review presented at ENDO 2026 found no evidence that these drugs harm male hormones, sexual function, or sperm quality with long-term use [8]. Testosterone is one part of a wider picture — our Sexual Health Hub maps how these threads connect.

Why the rise is not only about weight loss

Visceral fat is not inert storage. It is metabolically busy tissue packed with aromatase, the enzyme that converts testosterone into estradiol. The estradiol then travels back to the hypothalamus and pituitary and tells them to ease off — less GnRH, less LH, and therefore less testosterone from the testis. Insulin resistance compounds it by suppressing SHBG and blunting Leydig cell output directly. The result is a self-sustaining loop: fat lowers testosterone, low testosterone makes fat easier to gain. I go through this mechanism in more depth in the hormonal link between obesity, testosterone, and erectile problems.

Strip out the visceral fat and you take the brake off. That is the simplest reading, and it is almost certainly most of the story. The argument is over what is left after weight loss is accounted for.

Here is where I part company with the coverage. The AUA cohort reported that testosterone changes were not directly correlated with BMI change, which the authors read as evidence of a weight-independent mechanism [1]. But the 2025 Andrology meta-regression found precisely the opposite pattern — the men with the largest reductions in weight and BMI showed the largest testosterone gains, and the authors concluded that the current literature does not demonstrate a direct action on testicular function at all [2]. An observational cohort adjusting for BMI and a meta-regression across trials are answering slightly different questions, and only one of them is peer-reviewed.

My position: assume the testosterone rise is earned through metabolic improvement until a trial proves otherwise. GLP-1 receptors do exist in testicular tissue and animal work suggests direct effects on spermatogenesis, but that has not been shown in men. Practically, this means your testosterone follows your metabolic health — which you can quantify with our BMI and metabolic syndrome risk screen before and during treatment.

GLP-1 versus testosterone therapy: what happens to your own production

This is the difference that matters clinically, and almost nobody explains it to patients before they start. Testosterone therapy raises your blood level by supplying testosterone from outside. Your pituitary detects the surplus and stops sending LH and FSH, so your own testicular production shuts down for as long as you stay on treatment. A GLP-1 does the reverse: the 2026 systematic review found LH and FSH were preserved or increased on GLP-1 therapy, against clear suppression in the testosterone-treated comparison groups [3].

That table is not an argument against testosterone therapy. Testosterone works, it works faster, and for a man with structural hypogonadism it is the correct treatment — I set out who it suits and what it costs in my full guide to testosterone replacement therapy. The point is that these two treatments produce a similar number on a blood test by opposite biological routes, and the route determines what you keep.

One honest complication. A 24-week randomized trial comparing semaglutide against intramuscular testosterone in men with type 2 diabetes and functional hypogonadism found that both raised total testosterone and both improved symptom scores — but erectile function scores improved significantly only in the testosterone arm [5]. Raising the number is not the same as fixing the symptom. The erectile side of GLP-1 therapy has its own evidence base, including a genuine split between agents, which I cover separately in GLP-1 drugs and erectile dysfunction.

Who actually gets a testosterone rise, and who gets nothing

A 2026 systematic review in Cells, covering studies published between January 2021 and January 2026, separated responders from non-responders cleanly. In men with obesity, type 2 diabetes, or functional hypogonadism, GLP-1 therapy was associated with testosterone increases. In a placebo-controlled trial of healthy men with normal testosterone, there was no significant endocrine or reproductive effect whatsoever [4]. Response depends on baseline metabolic status, not on the drug.

Read that as a filter. If your testosterone is low because visceral fat and insulin resistance are suppressing the axis, expect movement as your metabolic markers improve. If your testosterone is low for a structural reason — pituitary disease, primary testicular failure, long-term opioid use, or a history of anabolic steroid use — a GLP-1 will do nothing for it, and waiting six months to find that out costs you six months.

Sorting one from the other before you start

The pattern that separates them is your LH. In metabolic hypogonadism, testosterone is low and LH is low or inappropriately normal, with a large waist and often a raised HbA1c. In primary testicular failure, testosterone is low and LH is high — the pituitary is shouting and the testis is not answering. That single result reframes the whole plan, so ask for LH on the same draw rather than testosterone alone. If you are unsure whether your symptoms fit testosterone deficiency in the first place, our low testosterone symptom quiz is a reasonable place to start, and low testosterone in men over 40 covers what the symptoms mean mechanically.

The muscle-loss caveat, and what to ask for

Weight lost through a pharmacological calorie deficit is not all fat. A proportion of it is lean muscle, and testosterone is the main hormonal defense against that. Men who start with low testosterone therefore have the least anabolic reserve at exactly the moment they need it most [9]. This is not a reason to avoid GLP-1 therapy — the cardiometabolic gains are substantial — but it is a reason to measure something other than the scale. A man who has lost 15 kg (about 33 lb) and cannot carry his shopping has not had a good outcome.

The AUA guideline on testosterone deficiency is specific about diagnosis: low total testosterone on two separate early-morning measurements, combined with symptoms or signs [6]. Nothing about starting a weight-loss drug changes that standard, and rapid weight loss makes a single reading even less reliable than usual.

What to request, and when

• Before your first injection: ask for a baseline panel drawn fasting, before 10am — total testosterone, SHBG, LH, FSH, and prolactin. Without a baseline you will never know whether the drug moved anything.
• Ask for SHBG explicitly. Most primary care panels report total testosterone alone. Since GLP-1 therapy raises SHBG, a rising total can sit on top of an unchanged free level, and you will feel the free level, not the total.
• Repeat at six months, on two separate mornings. Earlier than that and you are measuring the middle of a metabolic transition rather than a new steady state.
• Protect muscle while you lose weight: ask your doctor to confirm a protein target for your body weight and add resistance training twice a week from the first month, not after the weight has gone.
• If your testosterone has not moved by six months despite meaningful weight and HbA1c improvement, that is the point to ask for a full hypogonadism workup rather than assuming more time will fix it.

One caution on combining treatments. Small pilot work has looked at adding testosterone to a GLP-1 in men who lose little weight and remain hypogonadal, and the early signals on lean mass are interesting. But these are pilot studies of ten men, and no randomized trial has yet tested combined therapy properly [9]. If a clinic offers you both at once as a package, ask them which trial they are relying on.

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Dr. Muhammad Khalid

MBBS · FCPS (Urology) · MCPS (Gen. Surgery) · CHPE · CRSM · IMC #539472

Specialist urologist with 11+ years of clinical experience across tertiary teaching hospitals. Trained at Lady Reading Hospital and Khyber Teaching Hospital, Peshawar. Author of 5 peer-reviewed international publications in Cureus, WJSA, and AJBS. Procedural expertise: URS, PCNL, RIRS, TURP, TURBT, and major open urological surgery. Full profile →

This article is for educational purposes only and does not constitute medical advice. Always consult your physician or urologist for diagnosis and treatment decisions specific to your condition.