Chronic anxiety, depression and physical exertion-related stress consistently activate the hypothalamic-pituitary-adrenal axis. Almost each component of this activated axis, such as CRH, ACTH, β-endorphin and glucocorticoids exerts profound inhibitory effects on the hypothalamic-pituitary-ovarian axis and subsequently leads to reproductive failure in females. The pulsatile secretion of GnRH and the response of gonadotrophs to GnRH stimulation are severely impaired. Increased levels of glucocorticoids moreover inhibit gonadal axis at the hypothalamic, pituitary and ovarian levels and concurrently result in deficient ovarian steroidogenesis, amenorrhea, anovulation, defective endometrial decidualization and implantation, abnormal fetal outcome and delayed parturition. Stress-associated growth hormone deficiency with a corresponding deficiency of insulin-like growth factor-1 at the level of the pituitary, ovary and uterine endometrium also leads to defective reproductive outcome in females. Moreover, stress-related imbalance between prooxidant and antioxidant forces may cause damage to the released ovum, embryo fragmentation, implantation failure or abortion.