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00019616-199511000-00005MiscellaneousThe EndocrinologistThe Endocrinologist© Lippincott-Raven Publishers.5November 1995 p 416–421Stress and AmenorrheaHistorical Note: PDF OnlyBerga, Sarah L. M.D.Division of Reproductive Endocrinology, Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine, Magee-Womens Hospital, Pittsburgh, PA 15213.AbstractAdvances 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.Stress and AmenorrheaBerga Sarah L. M.D.Historical Note: PDF OnlyHistorical Note: PDF Only65p 416-421