Testes

The testes are paired oval glands held outside the body in the scrotum. Each is roughly 4-5 cm long and 3 cm wide, and together they run two biochemically distinct operations in very close quarters: continuous sperm production and continuous testosterone synthesis. Both are controlled by the pituitary, both are sensitive to temperature, and both decline with age and poor health.

At a glance

What it does

Produces sperm and testosterone. Sperm carry half the genetic material needed to make a baby. Testosterone drives male development during puberty, maintains male secondary sex characteristics through adulthood, and shows up as a major modulator of libido, muscle mass, bone density, mood, and cognition in both sexes. The testes also produce small amounts of estradiol via aromatase.

Anatomy

Each testis is packed with seminiferous tubules — long, coiled channels where sperm production happens. Between the tubules sits interstitial tissue containing Leydig cells, which make testosterone. Inside the tubules, Sertoli cells scaffold the sperm maturation process, nurse developing germ cells, and create the blood-testis barrier that keeps the immune system from recognizing sperm as foreign.

Sperm mature and acquire motility in the epididymis, a tightly coiled tube sitting on top of each testis. From there they travel up the vas deferens at ejaculation, mix with seminal vesicle and prostate fluid, and exit via the urethra.

Leydig cells — the testosterone engine

Leydig cells sit in the interstitium and respond to LH from the pituitary. When LH binds, cholesterol is pulled into mitochondria and converted step-by-step to testosterone via the steroidogenic cascade (pregnenolone to progesterone to androstenedione to testosterone). Output is pulsatile and follows a diurnal rhythm — highest in the early morning, lowest in the evening — which is why morning labs matter for accurate measurement.

A small fraction of testosterone is converted locally or downstream to dihydrotestosterone (DHT, via 5-alpha-reductase) or to estradiol (via aromatase). This conversion is why androgen pharmacology is more complex than "testosterone up, testosterone down."

Sertoli cells — the sperm factory

Sertoli cells respond to FSH from the pituitary and to local testosterone. They create the blood-testis barrier by tight junctions between adjacent cells, walling off developing sperm from the bloodstream. Germ cells start at the basal side of the tubule, pass through the barrier, and mature as they move toward the lumen. Full spermatogenesis takes about 74 days from stem cell to mature sperm — which is why sperm-related interventions take months to show effects.

Sertoli cells also produce inhibin B, which feeds back to the pituitary to suppress FSH. This is the loop that keeps sperm output in homeostasis.

Why they hang outside the body

Spermatogenesis is temperature-sensitive and works poorly at core body temperature. The testes sit in the scrotum because that organ runs 2-4 degrees C cooler. The cremaster muscle pulls them up when cold and relaxes to drop them when hot. Cryptorchidism — undescended testes — destroys spermatogenesis if not corrected early in childhood. Frequent hot tubs, laptops on laps, and fever all reduce sperm counts temporarily; tight underwear probably does not, despite the folklore.

Aging and decline

Total testosterone declines with age, but the story is more nuanced than popular framing. Healthy aging without metabolic disease produces roughly a 1-2% drop per year in total T after 30. Most of the "crashing testosterone" picture in modern men is driven by obesity, insulin resistance, poor sleep, alcohol, and medications — reversible contributors stacked on top of the small biological decline.

SHBG climbs with age, so free (bioavailable) testosterone drops faster than total testosterone. By 60-70, roughly 20% of men meet clinical hypogonadism criteria. Sperm count and quality also decline with age — slower than the female fertility drop-off, but real, with paternal age influencing miscarriage risk and some rare genetic conditions.

When it goes wrong

Primary hypogonadism — testicular failure itself — raises LH and FSH as the pituitary shouts at unresponsive testes. Causes include Klinefelter syndrome (47,XXY), mumps orchitis, trauma, torsion, chemotherapy, and radiation. Secondary hypogonadism — the pituitary failing to stimulate otherwise-healthy testes — shows low LH/FSH alongside low T, and is commonly driven by obesity, opioids, anabolic steroid cycles, pituitary lesions, or functional suppression from illness.

Testicular torsion is a urological emergency — the cord twists, blood supply cuts off, and viability drops within hours. Testicular cancer is rare but overrepresented in young men (15-35) and has excellent cure rates with early detection.

Interactions

Exogenous testosterone — anabolic steroids or TRT — shuts down LH and FSH, which collapses both endogenous production and spermatogenesis. Coming off without a proper restart protocol can leave men with months to years of suppressed function. Alcohol is testicularly toxic in a dose-dependent way, both directly and via increased aromatase activity. Chronic opioid use crashes testosterone through central suppression. Obesity raises aromatase activity in adipose tissue, converting testosterone to estradiol and shifting the ratio.

Honest take

Sources

• Bhasin et al., Endocrine Society Clinical Practice Guideline (2018) — testosterone therapy in men with hypogonadism.
• Sharpe, Endocrinology and Metabolism Clinics of North America — environmental and lifestyle effects on the testis.
• Jarow et al., American Urological Association — guidelines on evaluation of the azoospermic male.