Advances in our understanding of the physiological mechanisms subserving reproduction and those mediating responses to stress now permit us to understand in detail at least one mechanism by which stress compromises fertility. In women, stress, as evidenced by an increase in cortisol secretion, suppresses hypothalamic gonadotropin-releasing hormone (GnRH) input to the pituitary-ovarian axis. If the decrement in GnRH drive is chronic, anovulation results. Episodic decrements in the GnRH pulse generator likely result in luteal inadequacy or oligo-ovulation. The more complete the suppression of GnRH, the more likely is the reproductive compromise to be clinically recognizable. Profound and persistent loss of GnRH input manifests as amenorrhea, whereas episodic or less profound interruptions in GnRH secretion can be clinically occult and present only as decrements in luteal phase progesterone secretion by the corpus luteum in the face of preserved menstrual cycle intervals, i.e., so-called luteal phase defects. Recognition of stress-induced compromise of ovarian function expands therapeutic options because, at least in theory, stress management and reduction will lead to return of GnRH drive, resumption of ovulation and menses, and restoration of fertility.
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