Hormones and Sexual Health
Sexual function, libido, hormonal influences on sexuality, and sexual wellness optimization
14 insights across 1 source
#351 ‒ Male fertility: optimizing reproductive health, diagnosing and treating infertility, and navigating testosterone replacement therapy
Evaluation of male infertility follows a stepwise approach: 1) history and physical exam, 2) semen analysis to document azoospermia or oligospermia, and 3) hormonal testing (eg, pituitary and gonadal hormones) to distinguish primary testicular failure from secondary hypothalamic‑pituitary causes, because spermatogenesis is regulated by the brain via the hypothalamic–pituitary–testicular axis with negative feedback.
Hormonal evaluation helps determine whether absent sperm production is due to intrinsic testicular failure (primary) or lack of central stimulation (secondary).
Spermatogonial stem cells (the basal stem cells in the seminiferous tubule) exhibit unusually high plasticity and, under experimental conditions, can behave like embryonic stem cells — able to produce cell types from all three germ layers.
This refers to demonstrated multipotent/pluripotent potential in laboratory settings; it does not imply routine clinical use but highlights the unique developmental plasticity of male germline stem cells.
Spermatogonial stem cells divide mitotically throughout life, then enter meiosis at puberty; meiosis halves chromosome number and shuffles chromosomes (recombination), creating novel genetic combinations and opportunities for new mutations.
This process explains why new (de novo) genetic variants in offspring often originate in the paternal germline and why paternal age influences mutation burden.
A standard semen analysis reports multiple distinct parameters—ejaculate volume, sperm concentration (number per mL), motility (percent moving and quality of forward progression), morphology (shape), and semen fluid properties (liquefaction time, agglutination/clumping, viscosity)—because each provides different information about male reproductive function.
Round cells (described separately) and fluid characteristics are part of a full analysis, not just count and motility.
Semen analysis should be interpreted as a composite profile—patterns across parameters matter more than any single nonzero abnormality; except for azoospermia (zero sperm), individual abnormal values often do not reliably predict fertility on their own.
Think of the analysis like a 'poker hand'—the combination and severity of abnormal parameters guide diagnosis and management.
The epididymis is a ~10‑day post‑testicular transit during which sperm mature and acquire epigenetic modifications (changes in gene regulation, not DNA sequence); this transit appears to include selection mechanisms that lower aneuploidy in the final ejaculate.
Epididymal maturation involves biochemical and epigenetic changes and physical selection, contributing to sperm quality control before ejaculation.
Human females are born with a finite ovarian reserve: very large numbers of oocytes are present prenatally and fall sharply by birth and across life — commonly cited figures include about 5 million oocytes at conception and ~1 million at birth, with only a small fraction ever ovulated.
Numeric values reflect commonly quoted estimates from reproductive biology and were stated conversationally in the source; actual counts vary and decline with age.
Oocytes are arrested in an early stage of meiosis (prophase I) for years to decades and only complete meiosis if stimulated to mature at ovulation; this prolonged arrest contributes to age‑related declines in egg quality.
Each menstrual cycle recruits multiple ovarian follicles but typically only one follicle completes maturation and ovulates; the non‑ovulated follicles undergo atresia (degeneration), so many oocytes are wasted each cycle.
Male germ cells (sperm) are produced continuously throughout adult life, so the male germline generates many more cell divisions over time and is a major source of new mutations and environment-responsive epigenetic changes that can influence offspring (paternal‑line transgenerational effects).
Transgenerational effects via sperm are an active area of research; evidence includes mechanistic and animal-model studies and some human epidemiology.
Sperm carry not only DNA mutations but also environment-responsive epigenetic marks, and changes in sperm can be transmitted to offspring — i.e., paternal exposures can have transgenerational effects.
Epigenetic marks include DNA methylation, histone modifications, and small RNAs in sperm that can be altered by environmental factors and influence offspring phenotype.
The presence of 'round cells' on semen analysis (usually reported numerically) represents either leukocytes (suggesting infection/inflammation) or immature germ cells; a commonly used threshold is fewer than 1,000,000 round cells (per ejaculate or per mL depending on lab) as within normal limits.
High numbers of round cells prompt further evaluation for infection or abnormal spermatogenesis; verify whether the lab reports per mL or per ejaculate when applying the numeric threshold.
Because men continuously produce sperm from spermatogonial stem cells throughout life, paternal germline-mediated effects of environmental exposures can accumulate across the lifespan and potentially affect offspring conceived later in life.
Contrast with the female germline, where oocytes are largely formed prenatally; continuous spermatogenesis makes the paternal germline a dynamic interface with the environment.
Genetic changes (mutations) and epigenetic changes are distinct: mutations alter DNA sequence, while epigenetic modifications change gene regulation without changing sequence; both can occur in sperm and have different implications for offspring health.
Epigenetic changes may be reversible and responsive to environment, whereas mutations are permanent sequence changes; both contribute to heritable variation but via different mechanisms.