In 2026 JAMA published a review of adult male hypogonadism.[1] It is the most current summary of where mainstream endocrinology stands, and two things in it are worth the attention of anyone considering testosterone: how narrow the diagnosis actually is, and what the review recommends first for the most common cause of it.
How rare the diagnosis is
Hypogonadism caused by disease of the hypothalamus, pituitary or testes affects fewer than 1% of men.[1] Hypogonadism caused by obesity — a body mass index of 30 or above — affects 2% to 8%.[1]
Those two numbers do most of the work in this review. The condition that gets treated with testosterone for life is uncommon. The condition that produces most low readings is a consequence of something else, and that something else has its own treatment.
What the diagnosis requires
Testing is reserved for men who have signs and symptoms of androgen deficiency.[1] The review names the most common ones as decreased libido, decreased spontaneous erections, and small testes — a narrower list than the fatigue-and-brain-fog cluster the category is usually marketed on. Each of those symptoms has other, more likely explanations, which is why one low result on its own is not a diagnosis.
Confirmation requires a serum testosterone below 264 to 300 ng/dL in at least two fasting samples, drawn between 7 and 10 am, on an assay with external quality control.[1]
Every clause there is load-bearing. Two samples, not one. Fasting. A two-hour morning window. An assay that is checked against an external standard rather than trusted on its own. A result collected outside those conditions is not measuring the same thing.
For men with obesity, diabetes, or other conditions that lower sex hormone-binding globulin, the review says calculated free testosterone is necessary rather than optional.[1] Total testosterone in a man with low SHBG understates what is biologically available, which is the mechanism explained in free versus total testosterone.
Once hypogonadism is confirmed, FSH and LH distinguish primary from secondary.[1] Primary means the testes are failing despite the pituitary asking loudly — elevated LH, low testosterone. Secondary means the signal itself is weak, with low or inappropriately normal LH and FSH.
The causes worth knowing
The review's most common cause of primary hypogonadism is Klinefelter syndrome, which affects 2 in 1000 men and is frequently undiagnosed.[1] That is a striking number for a genetic condition most men have never heard named.
For secondary hypogonadism the review separates permanent causes from reversible ones:
- Permanent — head and neck radiation, severe head trauma.[1]
- Potentially reversible — obesity, severe illness, and medication use, specifically opioids, corticosteroids, checkpoint inhibitors, and drugs that raise prolactin.[1]
The reversible list matters more than it looks. A man on long-term opioids with a low testosterone reading may not have a testosterone problem in any durable sense.
The recommendation that cuts against the market
For obesity-induced hypogonadism, the review's first-line management is weight loss.[1] Not testosterone.
The supporting figure is specific: in men with obesity, weight loss of at least 5% typically raises total testosterone significantly, and is associated with improved physical function, libido and erectile function.[1]
This is the same direction the trial evidence points. T4DM tested testosterone against a lifestyle programme and found real metabolic benefit, but the relationship between weight and testosterone runs both ways, which is the subject of does TRT fix obesity.
For a company that sells testosterone, this is the least convenient sentence in the review, and it is also the one most worth repeating. If low testosterone is being driven by weight, the review's answer is to address the weight.
Who the review says should be treated
Testosterone is for men with permanent hypogonadism, or men who cannot discontinue the medication causing it.[1] Formulation — injection, gel or pill — and dose are individualised, with monitoring of testosterone, hematocrit, and in some cases PSA.[1]
That monitoring list is not new. Hematocrit is on it because a rise in red cell mass is the most common adverse effect of therapy, covered in polycythemia and hematocrit.
Where it sits against the guideline
The review is consistent with the Endocrine Society guideline on the substance: confirm before treating, individualise the formulation, monitor. What it adds is eight years of intervening evidence and a sharper account of obesity as a cause rather than a coincidence.
On cardiovascular safety the picture had already moved by the time this review appeared, through TRAVERSE and the FDA labelling changes that followed.
Bottom line
The 2026 review describes a diagnosis narrower than the marketing around it, confirmed by two morning draws rather than one, and, in the most common presentation, treated first by losing weight.
Testosterone therapy has a real place. This review describes where that place begins, and it begins later than most advertising implies.
References
1 source
- Anawalt BD, O'Connor KM, Grossmann M. Adult Male Hypogonadism: A Review. JAMA. 2026;335(24):2146–2159. doi:10.1001/jama.2026.8526 · PMID 42207626
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