Pituitary signal driving testosterone production in men + ovulation in women — first marker to move on enclomiphene/HCG protocols.
LH is secreted by the anterior pituitary in pulses every 60–90 minutes. In men, it stimulates Leydig cells to produce testosterone. In women, the mid-cycle LH surge triggers ovulation. Because LH sits upstream of testosterone, it tells you WHERE in the HPG axis a problem lives — low LH + low T points to secondary (pituitary) hypogonadism; high LH + low T points to primary (testicular) failure.
Any exogenous testosterone (TRT) suppresses LH to near zero via negative feedback. Enclomiphene blocks estrogen feedback at the pituitary, raising LH. HCG mimics LH directly. Kisspeptin acts upstream of LH at the hypothalamus.
LH is influenced by: testicular/ovarian feedback (estradiol + testosterone suppress it), opioids (suppress GnRH → suppress LH), high prolactin (suppresses), aging (slowly rises in men, varies in women), body fat (high adiposity lowers via aromatization), stress, and pharmacologic agents — TRT crushes it; HCG, enclomiphene, clomiphene raise it; aromatase inhibitors raise it.
On enclomiphene monotherapy, LH typically rises 2–3× from baseline within 4–6 weeks; this is the marker proving the drug is working. On HCG add-back protocols, LH stays suppressed (HCG IS the LH mimic) but downstream T responds. On TRT alone, LH near-zero is expected and not a problem unless fertility matters. Pair with FSH for full HPG axis read.
Upload any lab PDF and MyProtocolStack maps your values to LH and 40+ other biomarkers. StackAI interprets the trend in context of your protocol.
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.