Companion to LH — drives sperm production in men and follicle maturation in women. The fertility marker.
FSH stimulates Sertoli cells in the testes (sperm production) and ovarian follicle maturation. Like LH, it's secreted by the pituitary and suppressed by gonadal steroid feedback (testosterone, estrogen, inhibin B).
Men with elevated FSH despite normal testosterone often have impaired spermatogenesis — the testes need more pituitary signal to produce sperm. Women's FSH rises with declining ovarian reserve, making it a key fertility marker.
FSH is influenced by: testicular/ovarian function (inhibin B from Sertoli/granulosa cells suppresses FSH; loss of these cells raises FSH), pituitary health, age (rises significantly in women approaching menopause; modest rise in men), exogenous steroids (suppress), HCG (suppresses), enclomiphene/clomiphene (raise via SERM mechanism).
For fertility-conscious men on TRT, monitoring FSH is critical — TRT alone usually crushes FSH and impairs spermatogenesis. HCG protects testicular function but doesn't replace FSH directly; some protocols add HMG (which contains FSH) for fertility preservation. Enclomiphene raises FSH alongside LH — the most fertility-friendly axis-restoring approach.
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Start tracking →Informational only — not medical advice. Reference ranges vary by lab and individual context. Work with a licensed provider to interpret your specific results.