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During lactation, the act of suckling by the infant generates sensory impulses from the nipples that travel via somatic nerves to the mother's spinal cord and then to the hypothalamus. These nervous signals trigger the secretion of prolactin from the anterior pituitary gland. Prolactin levels, which are already elevated during pregnancy (10-20 times the normal non-pregnant level), are further sustained by each episode of suckling.

The critical mechanism behind lactational amenorrhea is that these same nervous signals - either directly, or indirectly through the sustained elevation of prolactin - inhibit the secretion of Gonadotropin-Releasing Hormone (GnRH) by the hypothalamus. The suppression of GnRH, in turn, reduces the output of the pituitary gonadotropic hormones: Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH).

Since LH and FSH are essential for follicular development, ovulation, and the production of estrogen and progesterone by the ovaries, their deficiency means that the normal monthly ovarian cycle cannot be reinstated. Without ovulation and the cyclical hormonal changes that follow, menstruation does not occur - resulting in amenorrhea. This suppression typically persists for many months after delivery, for as long as the mother is nursing. However, in some mothers who nurse only part of the time, the pituitary may eventually secrete sufficient gonadotropins to re-establish the menstrual cycle even while nursing continues.