What Causes Low Sperm Count?

Often nothing that can be named. That is the least-told fact about this result, and it is worth hearing before the list of causes rather than after it.

In a 9-year prospective study at the Andrology Centre of Tartu University Hospital, 8,518 men were assessed and 1,737 of them (20.4%) were diagnosed with severe male factor infertility. A primary cause was defined for 695 of those 1,737 patients — about 40%. The rest had no identifiable cause (Punab 2017, Human Reproduction).

The pattern inside that 40% is the useful part. The worse the finding on the report, the more likely a cause is found. Where there was no ejaculate at all, a cause was assigned in 46 of 46 cases. Where there was no sperm in the ejaculate, 321 of 388 (82.7%). But where the count was merely low, about 75% of those 1,737 cases stayed unexplained.

So the question to ask a doctor is not only what caused this, but which of the causes that can be found have actually been looked for. Those are a short, specific list, and they are below.

Two things are commonly wrong in how this number gets read to men, and both matter before anyone starts hunting for a cause.

The first is the number itself. The WHO laboratory manual moved to its sixth edition in 2021, and the fifth-centile concentration became 16 million per mL. The 15 million per mL still quoted on most pages, and in the previous version of this one, is the 2010 fifth-edition value.

The second is what kind of number it is. These are not pass marks. They are the fifth centile of a group of about 3,500 men whose partners conceived naturally within 12 months, which means that 1 in 20 of those 3,500 fathers sat below each figure. Björndahl (Andrology 2023) puts it directly: the limits 'are often misinterpreted as strict boundaries between fertility and infertility', and a valid diagnosis 'cannot rely solely on semen examination results'.

Being under one line is not a diagnosis, and being over all of them is not a clearance. If you want the parameters read one by one, see how to read a semen analysis report, and for the specific term on many Indian reports, what oligospermia means.

This is the group worth spending diagnostic effort on, because finding one changes what happens next.

• Secondary hypogonadism — the pituitary signal driving sperm production is absent or low. Of Punab's 1,737 patients, azoospermic men accounted for 86.4% of every secondary hypogonadism case. It is found on hormone tests, and it is the most treatable cause on this list.
• Obstruction of the seminal tract — the sperm are being made but cannot get out. Of those same 1,737 patients, men with no sperm in the ejaculate accounted for 97.1% of the seminal tract obstruction cases.
• Exogenous testosterone and anabolic steroids — these suppress the hypothalamic-pituitary-gonadal axis and can drive the count to zero. Recovery may be spontaneous after stopping, particularly with shorter duration of use, and may be temporary or permanent depending on the agent and the individual (Hashimi 2025, Asian Journal of Andrology). Say so if this applies to you; it is frequently not asked about.
• Varicocele — dilated scrotal veins. Its role is genuinely contested and the honest position is in the next paragraph.
• Medication and cancer treatment — chemotherapy and radiotherapy in particular. Where treatment is planned, freezing a sample beforehand is the decision that cannot be made later.

On varicocele, two good sources disagree in a way worth stating plainly rather than smoothing over. Punab's group explicitly excluded varicocele as a primary cause of male infertility, while still recording it more than twice as often in the idiopathic group as in fertile controls (31.0% of the idiopathic group versus 13.5% of controls, P < 0.001). Meanwhile the Cochrane review of 48 studies and 5,384 participants found that treatment may improve pregnancy rates compared with delayed or no treatment (RR 1.55, 95% CI 1.06 to 2.26; 13 RCTs, N = 1,193) — but rated that low-certainty evidence, and was uncertain about live birth (RR 2.27, 95% CI 0.19 to 26.93; 2 RCTs, N = 204, very low certainty).

Read together: varicocele repair is a reasonable conversation to have, not a procedure with a promised outcome, and the live-birth evidence that would settle it does not yet exist.

Genetic causes are not fixable, and knowing about one still changes the plan — it redirects effort away from treatments that will not work and towards retrieval, donor sperm or genetic counselling.

• Klinefelter syndrome and other chromosomal abnormalities — found on a karyotype.
• Y-chromosome microdeletions — found on a specific genetic test, not on a karyotype.

Punab's group screened for these in men with concentrations at or below 5 million/mL. Among those 1,737 patients, the ones found to have a genetic factor had the most extreme findings in 87.4% of cases — no ejaculate, no sperm in the ejaculate, or barely any. That is the practical rule: genetic testing earns its place at the severe end, and is much less likely to explain a mildly low count.

Where no sperm are found at all, the workup and the retrieval options are a separate subject, covered in azoospermia: symptoms and treatment.

About 75% of the oligozoospermia cases among Punab's 1,737 patients remained unexplained after a standardised workup that included hormone tests, examination, a structured interview and genetic screening at the severe end. In that same cohort of 1,737, oligozoospermic men made up 86.3% of all the idiopathic infertility patients, and the authors call the gap an urgent one.

That is not a failure of your particular doctor and it is not a reason to keep buying tests. It means the honest answer to 'why?' is frequently 'not known', and a clinic that produces a confident single cause for a mildly low count is going beyond what the evidence supports.

Two things in that group are worth noting without being overstated. Punab recorded overweight or obese patients and patients with a chronic disease significantly more often in almost all patient subgroups than in controls, and leukocytospermia in 16.1% of the idiopathic group versus 7.4% of the 325 fertile controls (P < 0.001). Those are associations from a cross-sectional comparison, not demonstrated causes, and the authors excluded leukocytospermia as a primary cause.

• No supplement has been shown to improve live birth. The largest trial, in 2,370 couples, randomised the male partner to 5 mg folic acid plus 30 mg elemental zinc or placebo for 6 months. Live birth was 404 of 1,185 in the supplement group and 416 of 1,185 on placebo (risk difference -0.9%, 95% CI -4.7 to 2.8). Most semen parameters did not differ. DNA fragmentation was significantly HIGHER on the supplement (29.7% versus 27.2%; mean difference 2.4%, 95% CI 0.5 to 4.4). The previous version of this page recommended zinc, selenium and vitamin C, and cited nothing for it.
• No causal role for diet, exercise, stress or pollution in your particular count is established by anything cited here. Those sections of the previous version of this page asserted mechanisms without a single study attached.
• Punab's figures are from one Estonian andrology centre and only from men who already had reduced total sperm counts. The authors state the findings cannot be automatically applied to all male factor infertility. No comparable Indian series was located for this rewrite.
• Varicocele's effect on live birth is not established. The Cochrane authors rated that outcome very low certainty from two small trials pointing in different directions.
• That a cause is 'idiopathic' is a statement about current knowledge, not a verdict that nothing is wrong and not a prediction that nothing will work.

A single low result is not a conclusion. Before anything else, two ordinary explanations should be excluded, because they are common and they are not about your body at all.

• An incomplete collection, or too short a gap before the sample. For a low-volume sample specifically, these are described as the most common cause — ahead of every pathological explanation (Gray 2018, Translational Andrology and Urology).
• A gap outside the window the reference values assume. The laboratory needs a standardised interval for the result to be readable against the centiles at all.

Both are covered in how to prepare for a semen analysis, and if volume rather than count was the flagged line, in what low semen volume actually means. How often to ejaculate otherwise is a separate question, answered in does frequent ejaculation affect sperm count.

Then the timing. When 11 men with normal concentrations drank deuterated water so that new sperm could be labelled and tracked, the labelled sperm reached the ejaculate after a mean of 64 plus or minus 8 days, with a range of 42 to 76 (Misell 2006, Journal of Urology). Some pages in this corpus have said 74 days; 64 plus or minus 8 is the measured figure, from a sample of 11 men.

The practical consequence is that a repeat test a fortnight after any change tells you about normal sample-to-sample variation rather than about the change. Roughly three months is the interval at which a difference means something.

And the answer is often not IVF. If the cause turns out to be secondary hypogonadism, obstruction, a medication or exogenous testosterone, the treatment is aimed at that. Testing both partners, correcting the timing, or a simpler treatment resolves a great many cases before anyone reaches assisted reproduction.