In Poland excess weight is more common in men than in women: according to a 2019 survey by the Polish statistical office GUS, 65 percent of men and 49 percent of women are overweight or obese, while in drug trials, for example STEP 1, women made up three quarters of the participants. Men often come forward for a reason other than the weight itself: with a blood glucose result from an occupational health check, with high blood pressure picked up by chance, after a heart attack or because of erectile dysfunction.
What lowers testosterone when there is excess body fat?
Obesity can lower testosterone levels. Contributing factors include changes in SHBG levels and in hormonal regulation. Adipose tissue contains aromatase, an enzyme that converts testosterone into oestradiol, a hormone that is also present in men. Excess insulin and chronic inflammation can weaken the signal that the hypothalamus and the pituitary send to the testes. A deficiency of this kind is called functional hypogonadism, as distinct from damage to the testes or the pituitary. A 2026 review of the literature reports that it affects 35 to 50 percent of men with obesity and type 2 diabetes; that figure does not describe all men with excess weight. Patients often put the symptoms, such as lower sex drive, poorer sleep, loss of strength and loss of muscle, down to age. In its 2020 guidelines the European Academy of Andrology recommends diagnosing hypogonadism only when the symptoms are accompanied by repeated morning fasting measurements below the cut-off, which is taken at around 12 nmol/l, and when other causes have been assessed.
Obesity treatment when testosterone is low
Under the same guidelines, the first step in men with overweight and obesity is a change of lifestyle and weight loss, and testosterone treatment is considered only later. As body fat decreases and insulin sensitivity improves, testosterone levels may rise. Weight loss can improve the results, but it does not replace investigation of other causes of the deficiency. A 2026 systematic review covering studies of GLP-1 analogues in men with obesity, diabetes or functional hypogonadism describes a moderate rise in testosterone and improved erections. The only randomised trial, carried out in men with normal hormone levels, showed no difference from placebo. These data do not allow us to promise an improvement to every man.
Testosterone treatment has contraindications of its own. Before it starts, PSA is measured, the prostate is examined and the haematocrit is checked, because thickening of the blood is a common complication of this therapy. Testosterone also suppresses sperm production, which matters for a man planning a child. Eligibility for testosterone treatment is decided by an andrologist or an endocrinologist.
What did the T4DM trial show, and what conclusions do we not draw from it?
The Australian T4DM trial enrolled men with impaired glucose tolerance or newly diagnosed type 2 diabetes who were taking part in a lifestyle programme and did not have pathological hypogonadism. The trial looked at preventing type 2 diabetes and at improving glucose control in newly diagnosed disease. Type 2 diabetes was diagnosed in 12 percent of the men receiving testosterone and in 21 percent of those receiving placebo. A haematocrit above 54 percent, meaning excessive thickening of the blood, was found in 22 percent of the men treated with testosterone against 1 percent in the placebo group. The results apply to this particular group of men and are not evidence for giving testosterone routinely in obesity. Testosterone has no indication for treating obesity, which is why we do not prescribe it at our clinic.
How do we interpret test results in men?
The table brings together the measurements and tests we assess most often. The doctor interprets them together with the symptoms and the other results.
| Measurement or test | What it shows | When |
|---|
Waist circumference | From 94 cm abdominal obesity, from 102 cm a markedly higher risk of metabolic complications, even with a BMI below 30 | At assessment |
Total testosterone | Blood in the morning, fasting; a low result is repeated on a different day, and with a borderline result and altered SHBG, free testosterone is assessed | With symptoms |
Luteinising hormone and prolactin | Help establish the cause of testosterone deficiency; the doctor interprets them together with the symptoms and the other results | With a low result |
Blood pressure, lipid profile and glucose in erectile dysfunction | Help assess cardiovascular risk | At the initial consultation |
Erectile dysfunction and the risk of heart disease
An erection depends on blood flow through the arteries of the penis, which are narrower than the coronary arteries, so changes in the blood vessels may cause symptoms there earlier. Erectile dysfunction is a reason to assess cardiovascular risk, but on its own it does not mean a diagnosis of atherosclerosis. In observational studies, men with erectile dysfunction had a 44 percent higher relative risk of cardiovascular events and a 62 percent higher relative risk of heart attack than other men. These are associations observed in studies and they do not prove cause. We ask a patient who reports this problem to measure his blood pressure, and we check the lipid profile together with glucose.
In some men, weight loss can improve erections. In an Italian randomised trial, 110 men with obesity and erectile dysfunction, without diabetes, high blood pressure or hyperlipidaemia, were divided into two groups of 55. For two years the intervention group took part in a diet and exercise programme. Normal erectile function returned in 17 men in that group against 3 in the control group. The data on GLP-1 analogues here come from small studies and we regard them as preliminary.
With men who have had a heart attack we discuss the effect of treatment on the heart separately. The SELECT trial enrolled 17,604 people aged 45 and over with established cardiovascular disease, a BMI of 27 or more and no diabetes; men made up 72 percent of the participants, and more than three quarters of the participants had previously had a heart attack. They received semaglutide 2.4 mg or placebo, and follow-up lasted an average of 39.8 months. Cardiovascular death, heart attack or stroke occurred in 6.5 percent of those taking semaglutide and in 8.0 percent of those taking placebo. That is a relative risk reduction of 20 percent and a difference of 1.5 percentage points. The result applies to semaglutide 2.4 mg in this group of patients and cannot be extended to the whole class of drugs or to all men. Because of side effects, 16.6 percent of the semaglutide group stopped treatment against 8.2 percent of the placebo group. We show a patient who has had a heart attack both of these figures, and we agree the treatment plan with his cardiologist.