Stress and reproduction

The adverse effects of stress on reproductive function are well documented. The common pathway of stress related stimuli of whatever type(psychogenic, infectious, or physical exercise) is the hypothalamo-pituitary-adrenal axis (HPA), resulting; via corticotropic releasing factor, vasopressin and endorphin and activation of the sympathetic system, in a decrease in the activity of the hypothalamic GnRH pulse generator, leading eventually to an almost complete arrest of LH pulses. Although stress affects reproductive function in both sexes, female reproductive function is more susceptible to stress; hence reliable data on the influence of stress on fertility are essentially available in women. The spectrum of the hypothalamo-puituitary-gonadal (HPG) responses to HPA activation in women varies from abnormal luteal phase,irregular cycles to finally, chronic anovulation. Even short duration stress in the midfollicular phase may interfere with fecundity. Impairment of ovarian function by psychogenic stress occurs generally within the context of anorexia nervosa, malnutrition and depression and is generally multifactorial. Increased vulnerability to stress is associated with a poor outcome of in vitro fertilization-embryo transfer whereas during pregnancy, psychological stress is associated with preterm delivery. Also strenuous physical exercise impairs ovarian function, the frequency and severity depending on the intensity and type, nutrition and menstrual pattern before starting training: In males, depression does not seem to have significant effects on testosterone levels but other psychic stresses generally induce decreased T levels and appear to have negative effects on sperm density and motility. Severe prolonged physical stress is accompanied by a decrease in T levels and may be accompanied by a decrease of most sperm parameters.