FSH and LH in Men: How to Read Your Result

They tell a doctor where in the system the problem sits. They do not tell anyone how many sperm you are producing -- only a semen analysis does that. Three patterns cover most reports.

• FSH high, sperm count low. The pituitary is pushing harder and the testis is not answering. The problem is in the testis.
• FSH low, LH low, testosterone low. The instruction is not arriving. The problem is above the testis, and this is the one pattern with a treatment that has been shown to start sperm production.
• FSH and LH normal, count low. Common, and not a contradiction: the panel reports on the signals and the count reports on the output.

A fourth pattern is worth naming because it is often missed: LH and FSH both suppressed while testosterone is normal or high. That is what taking androgens from outside the body looks like, prescribed or not. What FSH, LH and testosterone actually do explains the mechanism behind all four.

Possibly not, and knowing that is useful before you pay for a repeat.

The AUA Male Infertility Guideline states that an endocrine evaluation of the infertile male is not recommended as a primary first-line test. It asks for FSH and testosterone in men with impaired libido, erectile dysfunction, a low or absent sperm count, small or soft testes, or a sign of hormonal abnormality found on examination, and adds that endocrine testing is also suggested for men with sperm concentrations below 10 million per mL. The AUA Testosterone Deficiency Guideline is blunter still: clinicians should refrain from measuring testosterone in men who are asymptomatic, show no signs, and have no comorbid condition associated with low testosterone.

The first test in a male fertility workup is a semen analysis, and the guideline treats it that way: one or more semen analyses during the initial evaluation is a Strong Recommendation on Grade B evidence, while the hormonal evaluation is Expert Opinion and conditional on findings.

The guideline's first statement is also worth knowing before you book anything: for an initial infertility evaluation, clinicians should initiate concurrent assessment of both partners. Running the two evaluations one after the other costs months. See who gets tested first.

That the seminiferous tubules are not responding, and that the number does not have to look abnormal to say so.

The AUA guideline makes both halves of that explicit. A normal serum FSH, it says, does not establish that spermatogenesis is intact. And an FSH above approximately 7.6 mIU/mL indicates an abnormality in spermatogenesis even when it still sits inside the reported normal range -- which the guideline notes varies by testing platform, generally running somewhere between 1.0 and 20 mIU/mL. So the range printed beside your result is not a decision threshold.

The 7.6 figure comes from a single study, and it is worth knowing what that study actually measured. Schoor and colleagues retrospectively reviewed 153 azoospermic men treated at one centre between 1995 and 2000. Within that cohort, 89% of the men who turned out to have non-obstructive azoospermia had either an FSH above 7.6 mIU/mL or a testicular long axis of 4.6 cm or less. Within the same cohort, 96% of the men with obstructive azoospermia had either an FSH of 7.6 mIU/mL or less or a long axis greater than 4.6 cm.

Read the direction of that carefully, because it is easy to invert. Those are the proportions of men inside each diagnosis who crossed the threshold. They are not the probability that you have one diagnosis rather than the other given your own FSH.

Two things follow. The hormone is read alongside testicular size, not on its own -- which is why the examination matters as much as the blood test. And this particular evidence is about telling a blockage apart from a production failure in men with no sperm in the ejaculate, which is the decision set out in whether azoospermia is obstructive or not.

Where the count is very low rather than absent, a high FSH also changes which genetic tests the guideline asks for: karyotype where the concentration is under 5 million per mL with a raised FSH, testicular atrophy or a diagnosis of impaired sperm production, and Y-chromosome microdeletion analysis at 1 million per mL or below in the same circumstances.

That the signal is missing rather than the factory being broken, and this is the one result on the panel that is genuinely good news.

The AUA guideline calls hypogonadotropic hypogonadism an identifiable and reversible cause of male infertility, and asks clinicians to establish why it is happening and treat according to the diagnosis rather than reaching for a hormone. Its list of secondary causes includes pituitary and suprasellar tumours, infiltrative disorders such as tuberculosis and sarcoidosis, raised prolactin, prior head trauma, chronic narcotic exposure, severe chronic illness -- and androgens taken from outside the body.

What gonadotropin treatment achieves in that group has been quantified, and the honest figure is mixed. Muir and colleagues pooled 41 studies and 1,673 men with pathologic gonadotropin deficiency treated for a median of 18 months. Sperm appeared at all in 78% of 1,673, but only 36% of 1,673 got above 5 million per mL and 24% of 1,673 above 10 million per mL. The drugs, and who is offered which, are set out in hormonal therapy for male infertility and what hypogonadism is.

This is the commonest version of the result, and it is not a laboratory error.

The AUA guideline states that the cause of an abnormal semen analysis cannot be identified in roughly three men in ten, in which case it is called idiopathic male infertility. A normal panel in that setting is doing its job: it has ruled out the two hormonal patterns above.

What is worth doing next is mostly not a hormone test: a repeat semen analysis, because the guideline notes results carry most weight when multiple abnormalities are present; an examination looking for a palpable varicocele or small testes; and, where the count is very low, the genetic tests at the thresholds above.

What is not worth doing is a sperm DNA fragmentation test as part of a first workup. The guideline recommends against it in the initial evaluation of the infertile couple, on Grade C evidence, and reserves it for recurrent pregnancy loss. That test, and when it is defensible, is covered in whether a DNA fragmentation test is worth paying for.

The rules differ for the three hormones, which is why so many repeat panels are wasted.

• Testosterone: morning, and twice. The AUA Male Infertility Guideline specifies a sample drawn between 8 and 10 a.m. because levels drop through the day. The AUA Testosterone Deficiency Guideline, Statement 2, requires two total testosterone measurements on separate occasions with both taken early morning before low testosterone is diagnosed, as a Strong Recommendation on Grade A evidence, and asks for them at the same laboratory on the same assay.
• FSH and LH: usually once. The guideline notes that gonadotropins are secreted in pulses, so the figure wobbles, but that a single measurement is usually sufficient to establish a man's endocrine status.
• The semen analysis: not for about three months. Misell and colleagues labelled 11 men with normal sperm concentrations using deuterated water and first detected the newly made sperm in the ejaculate at a mean of 64 days give or take 8, range 42 to 76.

That last figure is the one that saves money. Hormone levels move much faster than sperm do, which is why a better testosterone number at six weeks is not evidence that sperm production improved. And if androgens are involved the clock is longer again: across 33 studies and 1,766 steroid users, gonadotropins returned to baseline within 13 to 24 weeks after stopping, while the men's own testosterone was still below baseline at 16 weeks.

Indian laboratories sell male hormone panels as bundles, and the bundle is usually larger than the guidelines ask for.

• LH: yes, if testosterone is low. The AUA Testosterone Deficiency Guideline, Statement 6, makes measuring serum LH in men with low testosterone a Strong Recommendation on Grade A evidence. It is what separates a testicular problem from one above the testis.
• Prolactin: only in one situation. Statement 7 asks for it where a low testosterone is combined with a low or low-normal LH, again Strong on Grade A. Ordered indiscriminately it mostly generates repeat tests -- the guideline itself warns about spurious elevations, macroprolactinaemia and the assay hook effect.
• Estradiol: the AUA Male Infertility Guideline includes it in the second round of tests where a fasting morning total testosterone comes back below 300 ng/dL. Read it with caution: the Endocrine Society's position statement on estradiol measurement concludes that imprecision and method-to-method differences remain problematic even on modern assays.
• Inhibin B or AMH: not on this evidence. Toulis and colleagues meta-analysed 9 studies of serum inhibin B as a predictor of finding sperm at testicular extraction in non-obstructive azoospermia and reported a sensitivity of 0.65 (95% CI 0.56 to 0.74) and a specificity of 0.83 (0.64 to 0.93), concluding that it cannot serve as a stand-alone marker. They found the evidence on AMH did not support its diagnostic value either.

Estradiol in men has its own page, because a raised result prompts a treatment conversation that the evidence does not support as well as it is usually presented: what raising or treating estradiol in men achieves.

Do not stop a prescribed drug on your own. Stopping abruptly can leave you with neither your own production nor the replacement, and the person who prescribed it should manage the change. Book the appointment, and take the semen analysis as well as the hormone report.

There is one drug where the guidance is not hedged. The AUA Male Infertility Guideline, Statement 42, states that for the male interested in current or future fertility, clinicians should not prescribe exogenous testosterone therapy. Two things are commonly confused here, and the confusion is what causes the harm: hCG and FSH are gonadotropins, which raise your own signal, while testosterone replacement removes it. They are not interchangeable. What a low testosterone result means goes through why.

One more thing worth asking about before a prescription. The AUA notes that men with an elevated LH, consistent with a primary testicular problem, may have a limited testosterone response to hCG or a selective oestrogen receptor modulator because of the testicular dysfunction itself. If your LH is high, that is a reasonable question to put to the prescriber.

Being handed a page of numbers that turns out to answer a narrower question than you hoped is a genuinely disappointing experience, and it happens to most men who get this panel. The result is still worth having. It is just worth having for what it can do.

• That there is a universal normal range for male FSH or LH. The AUA notes that adult male FSH reference ranges vary by testing platform and generally fall between 1.0 and 20 mIU/mL, and no Indian population reference interval was retrievable for this article. The earlier version of this page printed specific ranges with no source; they have been removed.
• That any FSH or LH figure predicts a sperm count. The AUA states that a normal FSH does not establish that spermatogenesis is intact, and no retrieved source provides a usable predictive relationship in the other direction.
• That the 7.6 mIU/mL threshold gives the probability of a diagnosis. Schoor 2002 reports the proportion of men within each diagnosis who crossed it, in 153 azoospermic men at one centre, retrospectively. That is not the same quantity, and it has not been reproduced in an Indian cohort in any source retrieved here.
• That inhibin B or AMH settles whether sperm will be found at retrieval. Toulis 2010 concluded serum inhibin B cannot serve as a stand-alone marker and that the evidence on AMH did not support its diagnostic value.
• That a hormone result on its own justifies a drug. For men whose LH and FSH are already normal, a 2026 systematic review in the Journal of Clinical Endocrinology and Metabolism, searching to February 2025, found no eligible studies of clomiphene or of aromatase inhibitors, and no benefit for tamoxifen or for combined hCG with hMG.
• That supplements change the panel or the outcome. FAZST randomised 2,370 couples planning infertility treatment to folic acid with zinc or placebo for six months: live birth occurred in 404 of 1,185 couples on supplement and 416 of 1,185 on placebo, a risk difference of -0.9% (95% CI -4.7 to 2.8), with no difference in sperm concentration, motility, morphology, volume or total motile count.