Ovulation Induction

Ovulation induction aims to produce one ovulation in a woman who is not ovulating; controlled ovarian stimulation aims to grow many follicles for retrieval. The first works by lifting estrogen's negative feedback so endogenous FSH rises - clomiphene citrate blocks hypothalamic estrogen receptors, letrozole blocks aromatase and lowers estradiol at source. The second bypasses the hypothalamus entirely with injected gonadotropins. In both, a separate agent then triggers final oocyte maturation.

The trigger exploits receptor promiscuity: hCG shares the LH receptor and has a far longer half-life, so one injection substitutes for the physiological surge, with retrieval timed roughly 36 hours later. In antagonist cycles a GnRH agonist can trigger instead, releasing endogenous LH and sharply cutting hyperstimulation risk. For anovulatory PCOS, the PPCOS II trial published in 2014 found letrozole produced higher live birth rates than clomiphene, displacing decades of practice.

The distinction changes both the goal and the risk. Induction succeeds when a single follicle ovulates, and more than one is a failure that raises the multiple pregnancy rate. Stimulation is judged on oocyte yield, and its characteristic harm, ovarian hyperstimulation syndrome, scales with follicle number and with hCG exposure - which is why the choice of trigger is a safety decision rather than a technicality.

The misuse worth naming is hCG appearing outside fertility care as a general hormone product. In men it is used as an LH mimic to preserve testicular function; in women, without follicular monitoring, it triggers ovulation blind. Neither resembles the approved trigger indication, which assumes ultrasound tracking of follicle number and size, and the old hCG weight-loss protocol was ruled unsupported by the FDA long ago and remains so.