Low testosterone: the diagnosis people rush
It has become a fashionable diagnosis and a frequently wrong one. Real testosterone deficiency needs symptoms and two morning measurements — and the single decision that changes the whole plan is whether the man still wants to father children.
The one-liner
Diagnose testosterone deficiency only with symptoms PLUS two low morning levels; LH/FSH separate primary from secondary. If fertility matters, do NOT give exogenous testosterone — it shuts down sperm production; use clomiphene or hCG instead. On therapy, monitor PSA and hematocrit, and hold for an Hct over 54%.
Testosterone deficiency is a real condition wrapped in a lot of bad medicine. It is over-diagnosed on single random levels, over-treated in men who have a reversible cause, and dangerously mistreated in men who still want children. Done properly, the diagnosis is strict and the decisions are clean — and one of them, fertility, quietly governs everything else.
The diagnosis is two numbers and a symptom set
You need both: symptoms (low libido, erectile dysfunction, fatigue, low mood, loss of muscle and bone) and two low morning total testosterone measurements (testosterone is pulsatile and peaks early, so timing matters; the common threshold is around < 264 ng/dL / 9.2 nmol/L). Borderline values get free testosterone and SHBG. One random afternoon level is not a diagnosis.
What everyone gets wrong
Giving testosterone to a man who wants to be a father. Exogenous testosterone suppresses the HPG axis and shuts down spermatogenesis— it is a contraceptive as much as a treatment, and it can cause prolonged or even permanent infertility. When fertility is on the table, you keep the man’s own production running with a SERM like clomiphene, or hCG, instead of replacing the hormone from outside.
Localize it: primary vs secondary
LH and FSHsort the cause and shouldn’t be skipped:
- Primary (testicular) — high LH/FSH with low T. Think Klinefelter, prior mumps, post-orchiectomy, chemo or radiation.
- Secondary (central) — low or inappropriately normal LH/FSH. Think pituitary disease, hyperprolactinemia, obesity, or opioids — and a young man with low T and a high prolactin earns a pituitary MRI.
A large share of low testosterone is simply reversible — driven by obesity, opioids, or acute illness. Fix the cause before reaching for replacement.
If you treat: the options and the monitoring
Replacement comes as daily gels, IM injections (short or long-acting), or subcutaneous pellets. Whatever the route, the safety monitoring is the same and is where residents slip:
- PSA and DREat baseline, then 3, 6, and 12 months, then annually — testosterone won’t cause prostate cancer, but you don’t want to feed an occult one undetected.
- Hematocrit — testosterone drives erythrocytosis; hold or reduce the dose for an Hct > 54%.
- Caution with severe untreated sleep apnea and decompensated heart failure.
Before you write for testosterone, ask one question that reorganizes the whole plan: does this man still want children? If yes, the answer is never a testosterone prescription.
On the long-running cardiovascular question, the TRAVERSE trial offered reassurance about cardiovascular safety in appropriately selected men — which has made the conversation calmer than it was a decade ago.
If you remember one thing
Earn the diagnosis (symptoms plus two morning levels), localize it with LH/FSH, and let fertility decide the route — clomiphene or hCG for the man who wants kids, replacement for the man who doesn’t. Then watch the PSA and the hematocrit like they matter, because they do.