What's driving it low

Low testosterone is a symptom, not a diagnosis in itself. Finding the cause changes everything — many are reversible without ever touching a hormone, and a few point to a problem that needs attention in its own right.

Primary vs. secondary

The fork LH/FSH reveals: Primary (testicular) failure shows high LH and FSH — the brain is shouting but the testes can't respond (causes: Klinefelter syndrome, mumps orchitis, injury, chemotherapy or radiation, undescended testes, and to a degree ageing). Secondary failure shows low or inappropriately normal LH/FSH — the signal from above is turned down (causes: obesity, sleep apnoea, opioids, prior anabolic-steroid use, a prolactin-secreting pituitary tumour, chronic illness, severe stress). The gonadotropins tell you which you're dealing with. Evidence ●●●●●

The reversible ones

Fix the cause first: Most secondary hypogonadism in otherwise-well men is driven by excess body fat, poor sleep or sleep apnoea, heavy alcohol, opioids, and prior steroid use. These are the common, addressable causes — and fixing them often restores testosterone with no prescription at all. That's why the cause work-up comes before any talk of treatment.

Red flags

When to look harder: Very low testosterone with low LH/FSH warrants a prolactin check; a total T below ~150 ng/dL, or headaches or visual changes, warrants a pituitary MRI to rule out a tumour. High iron saturation points to haemochromatosis. These are the cases where 'just give testosterone' would paper over something that needs treating directly.

Secondary hypogonadism is often self-inflicted — and reversible

The most common low-T pattern in the clinic is a heavier, under-slept, stressed man with low-normal LH — a suppressed axis, not a broken one. That axis usually recovers when the suppressors are removed, which is the whole premise of the next four sections.

The Testosterone Guide