Chronic anxiety, depression or physical exertion-associated stress consistently activates the hypothalamic-pituitary-adrenal (HPA) axis. Each individual component of the HPA axis, such as CRH, ACTH, β-endorphin or glucocorticoid exerts deleterious effect on the hypo-thalamic-pituitary-gonadal (HPG) axis and subsequently leads to reproductive failure. Gonadotropin-releasing hormone (GnRH) secretion and the response of gonadotrophs to GnRH stimulation are severely impaired. Moreover, failure of gonadal response to gonad-otropin concurrently results in deficient steroidogenesis, anovulation, defective endometrial decidualization and implantation, abnormal fetal outcome and delayed parturition. In male, a consistent testosterone deficiency due to stress-linked altered functioning of the HPG axis has also been documented. Stress-associated growth hormone (GH) deficiency with a corresponding deficiency of insulin-like growth factor-1 (IGF-1) at the level of the hypothalamus, pituitary, ovary, and uter-ine endometrium leads to defective reproductive outcome and lactation. GH or IGF-1 deficiency also impairs testosterone biosynthesis, spermatogenesis, sperm maturation and erectile process.