Untreated Sleep Apnea Matters. Fertility Is Not the Main Reason

On the current evidence, there is no study that answers that. Obstructive sleep apnoea, also written sleep apnea, is associated with lower testosterone and, in one small controlled comparison, lower semen parameters — but nobody has measured whether treating it changes the chance of a pregnancy, in either direction.

What is clearer is that much of the testosterone association travels with body weight. When CPAP studies were pooled, testosterone did not significantly change. The authors of that meta-analysis concluded their review does not support a direct interaction between sleep apnoea and testosterone, and that strategies other than CPAP should be considered for hypogonadism in these men.

Untreated sleep apnoea is still worth diagnosing and treating. The reasons are cardiovascular and they are more serious than the fertility question.

One controlled comparison, published in Frontiers in Endocrinology in 2025, is the study this page rests on. It enrolled 108 men aged 20 to 40 newly diagnosed with OSA by full-night polysomnography at a single Chinese hospital, and 84 men attending the same hospital for fertility evaluation as controls.

• Sperm concentration 90.0 versus 129.3 million per ml.
• Total motility 68.6% versus 71.0%; progressive motility 63.8% versus 66.6%.
• Testosterone 13.1 versus 21.8 nmol/L.
• All differences p<0.01, with a stepwise decline in semen parameters as OSA severity increased, and apnoea-hypopnoea index independently associated with concentration and motility on multivariable analysis.

Two things about that study limit what it can be used for. It is cross-sectional, so it shows association and not cause. And the men with OSA also had significantly higher body weight and BMI than the controls — which is the confounder that runs through this entire literature, because obesity is independently associated with both sleep apnoea and reduced fertility. NICE NG257 1.9.3 states that men with a BMI of 30 kg/m2 or over have an increased risk of reduced fertility.

Note also that the comparison group were men attending a fertility evaluation, not men from the general population, so the 129.3 million per ml figure is not a population norm.

Pooled, it has not been shown to. A 2019 systematic review searched to June 2018 and included 10 prospective cohort studies and 2 randomised studies, n = 388 men. Pooled, CPAP use was not associated with a significant change in total testosterone, mean difference 1.08 (95% CI -0.48 to 2.64), and there was no significant change in free testosterone, SHBG, FSH, LH or prolactin either. A subgroup analysis splitting men by whether they were hypogonadal or eugonadal at baseline confirmed the overall result.

That is a meaningful negative. If sleep apnoea were suppressing testosterone directly, relieving the apnoea should raise it. The more likely reading is that weight is doing much of the work in both directions.

This is the most useful part of the topic, because the gaps are larger than the findings:

• No study has measured whether diagnosing or treating sleep apnoea changes time to pregnancy, clinical pregnancy or live birth. Not a trial, not a cohort. Any page saying treatment improves fertility outcomes is asserting something nobody has measured.
• CPAP has not been shown to raise testosterone in pooled data, so the mechanism most often described — apnoea suppresses testosterone, CPAP restores it — is not supported at the treatment end.
• The semen findings come from a single cross-sectional comparison of 108 men with 84 controls at one hospital, in which the two groups differed in body weight. That is a starting point, not a settled result.
• Sleep duration is a different exposure from sleep apnoea, and the largest study of it is also mostly null. In a Danish cohort of young men, n = 1,055, deviation from 6-9 hours of sleep was associated with higher DNA stainability (5%, 95% CI -1% to 13%); in the same cohort, higher testosterone (3%, 95% CI 0% to 7%) and, still in that cohort, higher free androgen index (6%, 95% CI 0% to 13%) — confidence intervals touching or crossing zero, and in the opposite direction to the one usually claimed. Sperm concentration and motility were not among the parameters where a difference was found.
• Claims that sleep apnoea causes PCOS, anovulation or miscarriage are not supported by anything cited here. Sleep apnoea and PCOS share obesity and insulin resistance as risk factors, which is a different statement.
• No supplement, antioxidant or hormone has been shown to correct anything attributable to sleep apnoea. NICE NG257 1.24.6 (2026) states: do not offer supplements, antioxidants or medical treatments to improve sperm DNA integrity (fragmentation).

Because the cardiovascular evidence is strong, and it does not depend on the fertility question at all. Across 10 cohort studies, n = 36,347 subjects, the pooled relative risk of cardiovascular disease compared with no or normal OSA was 1.13 (95% CI 1.02 to 1.24) for mild, pooled 1.26 (95% CI 1.15 to 1.39) for moderate-to-severe and pooled 1.41 (95% CI 1.22 to 1.63) for severe disease, rising continuously with apnoea-hypopnoea index across those cohorts.

This is not a small condition in India either. Pooled across 8 studies and 11,009 subjects, the prevalence of OSA in Indian adults at an apnoea-hypopnoea index of 5 or more was 11% (95% CI 7% to 15%), 13% in males, with moderate-to-severe disease at 5%. The authors estimated that on those figures around 104 million working-age Indians have OSA, of whom 47 million have moderate-to-severe disease.

So the honest framing is this: if loud snoring, witnessed breathing pauses, gasping awakenings or heavy daytime sleepiness are present, that is worth investigating on its own merits. Fertility is not the argument for doing it.

1. If the symptoms above are present, ask for a sleep assessment. Diagnosis is by polysomnography, or in some cases a home sleep apnoea test. Treat it as a cardiovascular and daytime-safety question.
2. Have the semen analysis done on its own terms, not as a test for sleep apnoea. There is no semen finding that identifies apnoea, and no apnoea finding that predicts a semen result in an individual.
3. Weight sits behind both. NICE NG257 1.9.3 records the increased risk of reduced fertility at a BMI of 30 kg/m2 or over in men, and weight is also the strongest modifiable driver of OSA severity.
4. Allow about three months before re-reading a semen analysis. One cycle of sperm production was measured at a mean 64 plus or minus 8 days, range 42 to 76, in 11 men, and NICE NG257 1.17.4 sets the repeat confirmatory analysis at ideally three months after the first for that reason.

Being pointed at your weight when you are already doing everything you were told to do is a hard thing to hear, and it is not the same as being told this is your fault.

Verified live pages on adjacent parts of this topic:

• The Impact of Sleep on Couple Fertility
• Male Fertility and Weight: Is There a Link?
• Testosterone Therapy: What It Does, and What It Costs Fertility
• Semen Analysis Report: How to Read Yours, Line by Line
• Male Fertility and Lifestyle: What Has Actually Been Measured