Why Is Testosterone Low?

Low testosterone is a finding, not a diagnosis. The clinical question is always why, and the answer determines everything that follows: whether the cause is reversible, whether fertility can be preserved, whether imaging is needed, whether testosterone is even the right drug.

Skipping this question is the defining failure of commercial testosterone prescribing. Research presented at ENDO 2026 reviewing 200 men started on testosterone found only 12% had a guideline-concordant workup — which includes measuring the two hormones that answer this question.

The one test that sorts it out

Luteinizing hormone and follicle-stimulating hormone come from the pituitary and tell the testes what to do. Measuring them tells you where the problem is.

Low testosterone with HIGH LH and FSH → the testes are failing. The pituitary noticed and is shouting louder. This is primary hypogonadism.

Low testosterone with LOW or inappropriately NORMAL LH and FSH → the testes may be fine but nobody is telling them to work. The problem is in the pituitary, the hypothalamus, or something suppressing them. This is secondary hypogonadism.

“Inappropriately normal” matters. If testosterone is genuinely low, LH should be elevated. An LH sitting in the middle of the range alongside a testosterone of 200 ng/dL is not reassuring — it is a failure of the feedback loop, and it points upstream.

One blood test, drawn at the same time as the confirmatory testosterone, splits the entire differential. It costs very little. It is routinely omitted.

Primary: the testes

The pituitary is working. The testes cannot respond.

Klinefelter syndrome. The most common cause of primary hypogonadism, affecting roughly 1 in 500 to 1 in 1,000 males — and up to two-thirds are never diagnosed. Only around 26 to 37% are ever identified, fewer than 10% before puberty, with a mean age at diagnosis around 30. Typical features are small firm testes, tall stature, gynecomastia, azoospermia and reduced facial and body hair, though presentation varies widely and many men have none of the classic features.

A man with genuinely low testosterone, elevated LH and FSH, small testes and infertility has an indication for a karyotype, not for a prescription. The diagnosis matters beyond the testosterone: Klinefelter syndrome carries increased risks that need managing, and median lifespan is reduced by around five to six years.

Testicular injury or torsion. Trauma, or torsion that wasn’t corrected in time.

Mumps orchitis. Post-pubertal mumps infection can damage the testes permanently.

Chemotherapy and radiation. Both damage Leydig cells and the germinal epithelium, dose-dependently. Alkylating agents carry the highest risk.

Undescended testes. Even after correction, testicular function may be impaired.

Hemochromatosis. Iron deposition can damage both the testes and the pituitary — a cause worth remembering because it is treatable and has consequences well beyond testosterone.

Age-associated testicular change. Some decline in testicular function occurs with age, though as covered in What Low Testosterone Actually Means, the age-related fall in testosterone is driven substantially by accumulating comorbidity rather than by aging alone.

Secondary: the pituitary and hypothalamus

The testes are capable. The signal is inadequate. This category matters enormously because it contains most of the reversible causes.

Structural

Pituitary adenoma. A tumour can compress normal pituitary tissue and reduce gonadotropin output, or — if it secretes prolactin — suppress the axis hormonally. Warning features are headache, visual field loss, and abnormalities in other pituitary hormones.

Hyperprolactinemia. Prolactin suppresses GnRH, which suppresses LH and FSH, which lowers testosterone. It can come from a prolactinoma, from medications, from hypothyroidism, or from chronic kidney disease.

Two assay traps cause real harm here. Macroprolactin — biologically inert aggregated prolactin — is present in around 20% of samples with an elevated prolactin, is usually asymptomatic, and is detected by polyethylene glycol precipitation. Men get treated for it unnecessarily. In the other direction, the hook effect: in very large prolactinomas with true prolactin above 1,000 ng/mL, antibody saturation causes a falsely low reading, often 30 to 120 ng/mL, and a macroadenoma gets misclassified as a non-functioning tumour. Serum dilution corrects it.

Treating hyperprolactinemia with a dopamine agonist reverses hypogonadotropic hypogonadism in roughly 50 to 65% of cases — meaning the testosterone often normalizes without any replacement at all.

Congenital hypogonadotropic hypogonadism, including Kallmann syndrome, where GnRH neurons fail to develop or migrate — often with absent sense of smell, and usually presenting as delayed or absent puberty.

Infiltrative and inflammatory disease — hemochromatosis, sarcoidosis, hypophysitis. Traumatic brain injury and cranial irradiation can also damage the axis.

Drug-induced

Opioids. One of the most common and most missed. Reported prevalence in men on chronic opioids ranges from 19% to 86%, with most studies above 50%. Intrathecal morphine is associated with rates of 86 to 100%; high-dose methadone maintenance with around 75% in men. Risk rises above roughly 100 mg oral morphine equivalents daily, and long-acting preparations carry more risk than short-acting at equivalent doses. Fentanyl, methadone and oxycodone carry the highest risk. Buprenorphine has only limited endocrine effects and can be used for extended periods without inducing hypogonadism; tapentadol appears minimal.

Glucocorticoids. In a case-control study of 152 men, a cumulative dose of 240 mg prednisone-equivalent or more produced detectable biochemical hypogonadism, and dexamethasone was disproportionately potent — a cumulative dose of only 18.9 mg conferred a 7.5-fold increased risk relative to other steroids.

Anabolic steroids. Exogenous androgens suppress the axis directly, and recovery after stopping can take many months to over a year. See Performance Enhancement.

Others — antipsychotics through prolactin elevation, anticonvulsants through raised SHBG, spironolactone, ketoconazole, chemotherapy, and GnRH agonists used in prostate cancer.

Systemic suppression

Obesity. The largest single category. Aromatase in adipose tissue converts testosterone to estradiol, which feeds back to suppress the pituitary; insulin resistance separately suppresses SHBG, lowering total testosterone. Around 40% of non-diabetic obese men in one large primary-care sample had low testosterone.

Crucially: low SHBG means the total testosterone can look deficient while free testosterone is preserved. In an obese man, checking SHBG before concluding anything is not optional.

Severe systemic illness. The axis is suppressed by acute and chronic illness. The Endocrine Society’s guidance is explicit that men who are acutely ill or recovering should not be tested at all — the result will be low and it will not mean what it appears to mean.

Chronic disease — kidney disease, cirrhosis, HIV, COPD, heart failure, active malignancy.

Chronic sleep restriction. One week of five-hour nights lowered daytime testosterone by 10 to 15% in one small experimental study.

Energy deficit from severe caloric restriction or very high training volume without adequate fuelling.

Alcohol, in chronic heavy use.

Thyroid disease, which alters SHBG in both directions and distorts the whole panel.

The terminology argument

You will encounter the terms “functional hypogonadism,” “late-onset hypogonadism” and “age-related hypogonadism,” typically applied to obesity- or comorbidity-associated low testosterone. Whether they describe a real diagnostic category is contested between major societies.

The Endocrine Society’s July 2026 statement rejects them, saying such terms “are hard to define operationally and blur the line between treatable disease and normal aging.”

The European Academy of Andrology built a guideline around functional hypogonadism as a distinct, treatable entity.

This is not semantics. If obesity-associated low testosterone is a disease, it warrants treatment. If it is a physiological consequence of obesity, it warrants treating the obesity. The Endocrine Society’s position is that where obesity with a BMI above 27 is the only identified cause, weight loss is typically first-line therapy.

We cover the disagreement at Why Experts Don’t Always Agree.

The practical approach this site takes: describe the cause anatomically and mechanistically — testis, pituitary, or systemic suppression — rather than reaching for a contested label. It works regardless of which society is right.

What weight loss actually does

Because obesity is the commonest contributor, this deserves numbers.

A meta-analysis of 24 studies found weight loss through dieting raised total testosterone by an average of 2.87 nmol/L (95% CI 1.68–4.07) — around 83 ng/dL — and bariatric surgery by 8.73 nmol/L (95% CI 6.51–10.95), around 251 ng/dL. A 2025 study of 69 hypogonadal men after bariatric surgery found mean testosterone rising from 208 to 371 ng/dL, with 45% reaching eugonadal status.

Which also means 55% did not. Weight loss first does not mean weight loss only.

When to image the pituitary

Not every man with secondary hypogonadism needs an MRI. Features that raise the threshold for imaging include a markedly low testosterone, elevated prolactin, headache or visual field disturbance, other pituitary hormone abnormalities, and a young man without an obvious systemic explanation.

A middle-aged man with obesity, sleep apnea and a testosterone of 280 with normal prolactin is a different situation from a 30-year-old with a testosterone of 90 and a headache.

Questions patients ask

Where to go next

Getting the diagnosis right: How Testosterone Should Actually Be Tested When the cause has its own treatment: When Testosterone Isn’t the Answer What a specific lab value means: The Lab Library The society disagreement: Why Experts Don’t Always Agree