Recurrent Implantation Failure by Jason M. Franasiak & Richard T. Scott Jr

Author:Jason M. Franasiak & Richard T. Scott Jr.
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

Stress does more than inhibit GnRH drive. The “ stress response complex” includes CRH, ACTH, GH, PRL, oxytocin, vasopressin, norepinephrine, and epinephrine [39]. Physical or mental stress causes acute release of CRH secretion centrally, leading to pituitary secretion of ACTH and other pro-opiomelanocortin (POMC)-related peptides such as beta-endorphin [40]. Both animal models and human studies demonstrate a direct antagonistic effect of CRH on GnRH pulsatility [41]. In one study, prolonged and intermittent infusion of CRH into the third cerebral ventricle of follicular phase ewes resulted in a significant decrease in GnRH mRNA levels in the hypothalamus. Conversely, institution of a CRH signaling blockade through administration of CRH receptor antagonists results in an increase in GnRH transcriptional activity. Michopoulos et al. showed that administration of a CRH antagonist to monkeys reversed the GABAergic activation caused by the stress of subordination [32]. Modification of the stress response may restore physiologic HPO activity and is associated with restoration of other neuroendocrine and metabolic aberrations. A randomized controlled trial of 16 women treated with cognitive behavior therapy (CBT) versus observation showed that CBT not only restored normal ovulatory function but also simultaneously reduced nocturnal cortisol secretion [32, 42]; this RCT provides additional validation of the notion that FHA is caused by stress. Additionally, other neuroendocrine and metabolic components such as TSH and leptin levels were increased in CBT-treated women compared to controls. This study not only underscores the effect of stress on reproductive function, it also highlights the therapeutic importance of active stress management for stress-induced infertility.

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