Stress in early pregnancy: maternal neuro-endocrine-immune responses and effects.

Stress profoundly compromises reproduction, particularly when experienced in early gestation. One outcome is pregnancy failure: although glucocorticoids have adverse effects it is not clear what their role in pregnancy failure is. However, secretion of vital hormones such as progesterone and prolactin are reduced and this unbalances the delicate and important pregnancy-protective cytokine milieu. Complex interaction between glucocorticoids, progesterone/prolactin and the immune system evidently precipitate the loss, although early loss may confer reproductive advantage by preserving maternal energy stores and facilitating ongoing maternal care for other offspring. If pregnancy failure is not induced another, perhaps more profound, outcome of maternal stress is fetal programming. Much is known about the role of elevated glucocorticoids during late gestation in fetal programming, but in early gestation their role is less clear, though likely. Other key pregnancy hormones and immune factors also contribute to fetal programming. Undoubtedly integrated action of glucocorticoids, progesterone/prolactin and the immune system is crucial for optimal pregnancy outcome and is highly susceptible to environmental conditions.