Male Infertility — Symptoms, Causes & Treatment | MyMedicPlus

Male infertility is defined as the inability of a couple to achieve natural conception after 12 months of regular (2-3 times weekly) unprotected sexual intercourse, attributable to male reproductive factors. Male factor infertility contributes to approximately 40-50% of all infertility cases — either as the sole cause (30%) or as a contributing factor alongside female infertility (20%). Infertility affects approximately 1 in 7 couples globally, meaning male factor infertility impacts roughly 1 in 20 men of reproductive age. The main pathological categories are: spermatogenic disorders (impaired sperm production — the most common category, accounting for 60-70% of male factor infertility) resulting in oligozoospermia (low sperm count), asthenozoospermia (reduced motility), teratozoospermia (abnormal morphology), or azoospermia (complete absence of sperm); obstructive azoospermia (normal spermatogenesis but ductal blockage preventing sperm egress — 15-20% of azoospermic men); hormonal dysfunction (hypogonadotrophic hypogonadism — insufficient FSH and LH stimulation of the testis); and sexual or ejaculatory disorders. The WHO 2021 reference criteria for normal semen analysis are: total sperm count ≥39 million per ejaculate, concentration ≥16 million/mL, total motility ≥42%, progressive motility ≥30%, and normal forms ≥4% (Kruger strict criteria). Simultaneous evaluation of both partners prevents diagnostic delay.

Varicocele — dilated, tortuous pampiniform plexus veins within the scrotum, graded I-III on clinical examination and confirmed by scrotal Doppler ultrasound — is the most common identifiable and surgically correctable cause, found in 15% of all men, 35-40% of men with primary infertility, and 80% of men with secondary infertility (previously fertile). Varicocele impairs fertility through elevated testicular temperature, oxidative stress, and hypoxia. Cryptorchidism (undescended testes) — if not corrected surgically by age 2 — causes progressive seminiferous tubule damage and carries a 4-6x increased testicular cancer risk. Prior orchitis from mumps virus (particularly post-pubertal) causes testicular atrophy and azoospermia in 13-30% of affected men. Sexually transmitted infections (Chlamydia trachomatis, Neisseria gonorrhoeae) cause obstructive epididymitis and ductal scarring. Genetic causes: Klinefelter syndrome (47,XXY — the most common chromosomal cause, affecting 1 in 650 males) causes primary testicular failure with azoospermia in most; Y-chromosome microdeletions (AZFa, AZFb, AZFc regions) are found in 5-10% of non-obstructive azoospermia; cystic fibrosis mutations (CFTR) cause congenital bilateral absence of the vas deferens (CBAVD). Hypogonadotrophic hypogonadism (Kallmann syndrome, hyperprolactinaemia, pituitary tumours) causes low FSH/LH and correctable with hormonal stimulation. Chemotherapy (particularly alkylating agents) and pelvic radiotherapy cause dose-dependent spermatogenic damage. Exogenous testosterone and anabolic steroids suppress LH/FSH via hypothalamic-pituitary feedback, causing testicular atrophy and azoospermia — reversible after 6-24 months of cessation.

The primary and defining symptom of male infertility is failure to achieve pregnancy after 12 months of regular unprotected intercourse. Most men with male factor infertility have no other symptoms — abnormalities are detected only on semen analysis. Symptoms related to underlying causes include: scrotal heaviness, discomfort, or a visible 'bag of worms' above the testis in varicocele; small, soft testes (testicular volume below 15mL) with absent virilisation, gynaecomastia, and tall stature (disproportion of limbs to trunk) in Klinefelter syndrome (47,XXY); reduced libido, erectile dysfunction, fatigue, and reduced secondary sexual characteristics (beard growth, body hair, muscle mass) in hypogonadism from low testosterone; galactorrhoea with sexual dysfunction and visual field defects in hyperprolactinaemia from pituitary adenoma; absence of scrotal vas deferens bilaterally in CBAVD (often with a history of frequent chest infections or a known CFTR mutation for cystic fibrosis); cloudy urine after orgasm indicating retrograde ejaculation into the bladder (seen in diabetes mellitus, post-prostatectomy, and autonomic neuropathy); and a dull testicular ache or a firm testicular lump (testicular cancer — most common cancer in men aged 15-35 — requires urgent scrotal ultrasound).

Semen analysis is the cornerstone investigation, assessed by the WHO 2021 reference values: volume ≥1.4 mL, total sperm count ≥39 million per ejaculate, concentration ≥16 million/mL, total motility ≥42%, progressive motility ≥30%, vitality ≥54% live spermatozoa, and normal morphology ≥4% (Kruger strict criteria). Two semen samples collected 2-7 days after sexual abstinence, 4 weeks apart, are recommended for diagnosis. Hormone panel: serum FSH (elevated in primary testicular failure; low or inappropriately normal in hypogonadotrophic hypogonadism), LH, total testosterone (morning sample), prolactin (elevated in pituitary adenoma), and thyroid function (hypothyroidism impairs spermatogenesis). Elevated FSH with azoospermia strongly predicts non-obstructive azoospermia. Scrotal Doppler ultrasound characterises varicocele grade (I-III), testicular volume (normal above 15 mL), echogenicity (atrophy, microlithiasis, masses), and epididymal abnormalities. Genetic testing in azoospermia or severe oligozoospermia (count below 5 million/mL): karyotype (detects Klinefelter 47,XXY and chromosomal inversions), Y-chromosome microdeletion analysis (AZFa deletion — no sperm on TESE; AZFc deletion — sperm retrieval possible in 50-70%), and CFTR mutation analysis in bilateral absent vas deferens. Post-ejaculatory urine analysis diagnoses retrograde ejaculation. Testicular biopsy is occasionally performed to distinguish obstructive from non-obstructive azoospermia when hormones are inconclusive.

Treatment is directed at the underlying cause. Varicocele repair: microsurgical sub-inguinal varicocelectomy (the gold standard for palpable varicocele with abnormal semen parameters) improves total motile sperm count in 60-70% of men and is associated with significant improvement in natural conception rates (NNT approximately 8 couples treated per additional pregnancy). Hormonal stimulation for hypogonadotrophic hypogonadism: human chorionic gonadotrophin (hCG, replacing LH) and FSH injections induce spermatogenesis in 90-95% of patients after 6-18 months — achieving pregnancy in 70-80% of couples, one of the most successful treatments in male infertility. Obstructive azoospermia: percutaneous epididymal sperm aspiration (PESA) or microsurgical epididymal sperm aspiration (MESA) retrieves sperm for intracytoplasmic sperm injection (ICSI) — live birth rates of 40-60% per ICSI cycle. Microsurgical vasovasostomy (vasectomy reversal) within 10 years of vasectomy achieves patency in 90-95% and pregnancy in 50-75%. Non-obstructive azoospermia (primary testicular failure): microdissection TESE (microTESE) under optical microscopy identifies focal areas of active spermatogenesis and retrieves sperm in 40-60% of cases, including Klinefelter syndrome men (sperm retrieval in 50-72%); retrieved sperm is cryopreserved for ICSI. Assisted reproduction: intrauterine insemination (IUI) for mild oligoasthenoteratozoospermia; ICSI for severe male factor or failed IVF — the gold-standard ART treatment for male infertility achieving live birth rates of 20-40% per transfer in women under 38.

Untreated male infertility causes significant and well-documented psychological distress including depression, anxiety, loss of self-esteem, and sexual dysfunction — affecting both the man and his partner, and placing substantial strain on couple relationships. The psychological impact of infertility is comparable in severity to that of serious physical illness diagnosis. Beyond reproductive consequences, several underlying causes of male infertility carry independent health implications: Klinefelter syndrome (47,XXY) confers significantly elevated lifetime risks of breast cancer (20-50x the male baseline), osteoporosis (from hypogonadism), metabolic syndrome, type 2 diabetes, venous thromboembolism, and autoimmune diseases — requiring lifelong testosterone replacement and multidisciplinary surveillance. Non-obstructive azoospermia and testicular failure are strongly associated with testicular germ cell tumour risk, warranting annual testicular self-examination and periodic ultrasound surveillance. Varicocele, if untreated, causes progressive testicular damage and declining semen parameters over time. Male factor infertility may also represent a 'sentinel' marker of underlying systemic disease — hypogonadism raises cardiovascular risk; young men with poor semen quality have significantly higher all-cause and cancer-specific mortality independent of fertility outcomes.

Lifestyle optimisation is central to male fertility preservation: cessation of anabolic androgenic steroids and exogenous testosterone (which suppress the hypothalamic-pituitary-gonadal axis causing testicular atrophy and azoospermia) — recovery of spermatogenesis typically takes 6-24 months after stopping but may be incomplete. Smoking cessation improves sperm count, motility, and morphology — tobacco is a known testicular toxin increasing oxidative stress. Limiting alcohol (under 14 units weekly), avoiding recreational drugs (cannabis reduces sperm quality; cocaine and opioids suppress testosterone), and reducing caffeine to under 3 cups daily benefit semen parameters. Maintaining scrotal temperature: avoid hot baths, saunas, hot tubs, and tight underwear; avoid prolonged laptop use on the lap; semen quality is sensitive to elevated testicular temperature. Achieving healthy BMI (18.5-25) reduces hyperestrogenism from peripheral adipose aromatisation and improves testosterone levels. Surgical orchidopexy for undescended testes before age 2 optimises subsequent fertility and reduces testicular cancer risk. Timely treatment of sexually transmitted infections (STIs) — particularly Chlamydia trachomatis — prevents obstructive epididymitis and ductal scarring. Fertility preservation (sperm cryopreservation) before cancer chemotherapy, pelvic radiotherapy, or any gonadotoxic treatment is strongly recommended for all men of reproductive age and is a NICE-endorsed standard of care.

Both partners should seek assessment from a GP if they have been trying to conceive without success for 12 months (6 months if the female partner is aged over 35). Male fertility assessment — a semen analysis — should be performed simultaneously with female investigations from the start, as male factors contribute to approximately 50% of infertility cases. Seek earlier assessment for: a known history of undescended testes, previous testicular surgery or torsion, previous groin or scrotal surgery, known varicocele, or symptoms of hypogonadism (fatigue, reduced libido, erectile dysfunction). See a urologist or andrologist promptly for: a new scrotal lump (testicular cancer is the most common cancer in men aged 15–35 and can cause infertility); scrotal pain and swelling; or absent or undescended testes noted on self-examination. Men with confirmed azoospermia (no sperm) should be referred to a specialist andrologist or reproductive endocrinologist for hormonal assessment, genetic testing (karyotype, Y microdeletion), and consideration of surgical sperm retrieval (TESA/TESE).