FSH, LH and Testosterone: What They Do for Sperm

Less than the report looks like it should. FSH and LH are instructions the pituitary gland sends to the testis, and testosterone is what the testis makes in response. None of the three is a measurement of how many sperm you are producing. That is what a semen analysis measures, and nothing on a hormone panel substitutes for it.

The American Urological Association's Male Infertility Guideline is explicit about the order: an endocrine evaluation of the infertile male, it says, is not recommended as a primary first-line test. It asks for FSH and testosterone in specific situations -- 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.

What the panel is good at is telling a doctor which floor of the building the problem is on. What it cannot do is count anything. If you are trying to read a semen result, how to read a semen analysis report line by line is the page for that.

Two different cell types inside the testis take two different instructions.

• LH reaches the Leydig cells, which sit in the tissue between the coiled tubes where sperm are made. Their job is to produce testosterone, and almost all of it stays where it was made.
• FSH reaches the Sertoli cells, which line the inside of those tubes and physically support every sperm cell through its development.
• Testosterone then works locally, at a concentration inside the testis that the rest of the body never experiences.

Take the two signals away and the sequence stops. The AUA guideline puts it in one sentence in its discussion of hypogonadotropic hypogonadism: in the absence of LH and FSH stimulation, the Leydig cells in the testes do not secrete testosterone, and spermatogenesis is disrupted.

There is a feedback loop on top of this. When testosterone in the blood rises, the hypothalamus and pituitary read that as a reason to send less LH and less FSH. The loop is what keeps the system steady, and it is also the reason the next section is true.

Because blood and the inside of the testis are two different compartments, and the numbers in them are not close.

Coviello and colleagues measured both in the same men in 2005. Twenty-nine men with normal reproductive physiology were randomised, and testicular fluid was drawn by fine needle aspiration so the concentration inside the testis could be measured directly rather than inferred. Serum testosterone averaged 14.1 nmol/L. Inside the testis it averaged 1,174 nmol/L. Across those 29 randomised men, the blood figure was 1.2% of the testicular one.

Two things follow, and it is worth being plain about both. A normal blood testosterone does not establish that the concentration inside your testis is adequate. A low one does not establish that it is not. The authors of that study said so themselves: the quantitative relationship between the testicular concentration and sperm production, they wrote, is not known.

The same study also showed what happens when testosterone is given from outside, and that is a decision rather than a piece of physiology, so it is set out separately in what a low testosterone result means and what testosterone therapy costs fertility.

It can usually separate two situations that need completely different answers.

• A high FSH means the pituitary is pushing harder and the testis is not answering. The problem is in the testis.
• A low FSH and a low LH alongside a low testosterone means the instruction itself is not arriving. The problem is above the testis, and this is the one hormonal picture with a treatment that has been shown to induce sperm production.

What it cannot do is tell you whether sperm are being made. The AUA guideline states that a normal serum FSH does not establish that spermatogenesis is intact -- and, in the other direction, that an FSH above approximately 7.6 mIU/mL indicates an abnormality in spermatogenesis even when that figure still sits inside the range printed on the report.

Which raises the obvious problem with the range printed on the report. The AUA notes that normal adult male FSH ranges vary by the testing platform used, generally falling somewhere between 1.0 and 20 mIU/mL. Comparing your number against a range you found online, from a different laboratory on a different analyser, tells you very little.

Reading an actual pattern -- this FSH with that LH and that testosterone -- is a separate job, and it is done in what FSH and LH results mean in men.

In practice, a small number of things account for most of it, and one of them is far commoner than men expect.

• Androgens taken from outside the body, prescribed or not. Christou and colleagues pooled 33 studies and 3,879 participants, of whom 1,766 were anabolic androgenic steroid users. During use, LH fell by a weighted mean of 3.37 IU/L, FSH by 1.73 IU/L and the men's own testosterone by 10.75 nmol/L.
• A missing signal from above, which doctors call hypogonadotropic hypogonadism. It can be present from birth or acquired later.
• Things that press on or damage the pituitary. The AUA guideline lists pituitary and suprasellar tumours, infiltrative disorders including tuberculosis and sarcoidosis, raised prolactin, prior head trauma, chronic narcotic exposure and severe chronic illness.
• Weight. The AUA Testosterone Deficiency Guideline's evidence review reports that obese men are almost five times more likely to have a low testosterone than men who are not, at an odds ratio of 4.89 (95% CI 2.35 to 10.17), and recommends checking testosterone in men with a BMI of 30 or above.

And often, nothing identifiable. The AUA guideline states that the cause of an abnormal semen analysis cannot be identified in roughly three men in ten, in which case the condition is called idiopathic male infertility. That is an uncomfortable answer and it is an honest one. If your hormones are normal and your count is low, see what causes a low sperm count and what hypogonadism is.

About three months, and this is the single most useful thing on this page for anyone who has just been told to change something.

Misell and colleagues measured it directly rather than estimating it. Eleven men with normal sperm concentrations drank deuterated water daily for three weeks, and semen was collected every two weeks so the labelled cells could be tracked into the ejaculate. Labelled sperm first appeared at a mean of 64 days, give or take 8, with a range of 42 to 76 days across those 11 men.

So the sperm in the sample you give today were committed two months ago. Repeating a semen analysis three weeks after starting anything is a wasted test. Repeating it at three months is the earliest it can carry information.

Hormones move faster than sperm do, and that mismatch causes real confusion. A testosterone figure that looks better at six weeks is not evidence that sperm production improved. It is evidence that a blood level changed.

Do not stop a prescribed drug on your own. Stopping abruptly can leave you without your own production and without the replacement, and the doctor who prescribed it is the person who should manage the change. Book that conversation rather than acting on a web page, and take your semen analysis with you.

On one drug the guidance is not hedged at all. The AUA Male Infertility Guideline, Statement 42, reads: for the male interested in current or future fertility, clinicians should not prescribe exogenous testosterone therapy. The Endocrine Society guideline recommends against starting testosterone therapy in patients who are planning fertility in the near term. What to do if you are already on it is set out in testosterone therapy and fertility.

If what you are taking came from a gym or an online seller rather than a prescription, say so anyway. The panel cannot be interpreted without that information, and a suppressed LH and FSH with a high testosterone is a recognisable pattern rather than a mystery. What anabolic steroids do to sperm goes through it.

It is reasonable to be annoyed that a page of hormone numbers you paid for turns out to answer a narrower question than it appeared to. The panel is useful. It is just useful for working out where a problem sits, not for measuring how much of a problem there is.

• That a hormone result predicts a sperm count. No source retrieved for this article establishes a usable predictive relationship, and the AUA states that a normal FSH does not establish that spermatogenesis is intact.
• That raising blood testosterone raises sperm production. The opposite was measured. In Coviello's 29 randomised men, the arm given weekly testosterone with saline placebo had LH fall to 5% and FSH to 3% of baseline and the concentration inside the testis fall by 94%.
• That zinc, folic acid or a fertility supplement changes any of this. 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). Sperm concentration, motility, morphology, volume and total motile count did not differ, and DNA fragmentation was modestly higher on supplement.
• That a specific FSH or LH figure identifies why spermatogenesis is impaired. In roughly three men in ten with an abnormal semen analysis, the AUA states, no cause is identifiable at all.
• That any hormone figure can be read against a range borrowed from elsewhere. The AUA notes that adult male FSH reference ranges vary by testing platform, and the Endocrine Society has published a position statement on how method-dependent sex steroid measurement is. No Indian population reference interval was retrievable for this article, so none is quoted.
• That sleep hours, organic produce, plastic containers or stress reduction move these hormones enough to change a fertility outcome. The earlier version of this page said all four. No source retrieved here tested any of them.