Abstract: Stress is one of the commonest and underappreciated causes of reproductive frailty in women. The stress system leads to adaptive responses via mobilization of hormonal systems. Adaptability and resistance to stress are fundamental to life. The response to stressors depends on the type of stressor, the timing and duration of stress, the genetic predisposition, personality characteristics, and the way of coping with stress. In pregnancy, maternal stress is known to disturb fetal glucocorticoid environment. In utero stress exposure is a significant predictor of subsequent adult telomere length. In humans, maternal exposure to prenatal psychosocial stress could be associated with decreased insulin sensitivity in the offspring assessed during young adulthood as well as in animals in intrauterine growth restriction (IUGR) cases. Some of the metabolic consequences of IUGR can be mitigated by ensuring early appropriate catchup growth, while avoiding excessive weight gain if relative hypercortisolism is not installed. The effect of maternal stress on fetuses regarding fetal HPA axis responsiveness (increased or decreased) remains under investigation. Animal studies confirmed that increase in stress hormones and pro-inflammatory cytokines in the fetal compartment during sensitive or critical developmental windows can impact the structure and function of the brain and peripheral targets which are related to body composition, energy balance homeostasis, and metabolic function (i.e. adipose tissue, pancreas, and liver). Maternal stress and depression are associated with structural and functional changes of brain parts such as hippocampus. In utero stress modifies epigenetically components of the HPA axis which can be transmitted transgenerationally. Epigenetic changes result in altered gene expression, ultimately affecting the risk for mental disorders.