Athletic amenorrhea: energy deficit or psychogenic challenge?

Abstract

Athletic women are at risk for developing ovulatory dysfunction, which presents variably as menstrual irregularity or absence. Initially characterized as an isolated disruption of hypothalamic gonadotropin-releasing hormone (GnRH) release, athletic amenorrhea, a form of hypogonadotropic hypogonadism, is invariably accompanied by additional neuroendocrine aberrations, including activation of adrenal and suppression of thyroidal axes. Exercise may elicit intermittent or chronic metabolic stress owing to increased energy expenditure and/or insufficient or imbalanced nutrient intake. In addition, athletic activities are motivated by or serve as psychogenic stressors. Prior studies dichotomized stressors as metabolic or psychogenic. Not only is this a false dichotomy because all stressors have both a metabolic and a psychogenic component, but also stressors act synergistically rather than in isolation to compromise GnRH drive and endocrine homeostasis. To ameliorate reproductive and endocrine consequences of stress, then, requires identification and amelioration of all relevant stressors. Formal psychosocial support helps individuals to develop better coping strategies and make appropriate lifestyle changes. Our research has shown that cognitive behavior therapy restores reproductive and endocrine balance.

Figure 1

Diagram showing the major neuroendocrine alterations produced by the synergistic combination of metabolic and psychogenic stress. The proximate cause of athletic amenorrhea is reduced GnRH drive leading to reduced LH and FSH and secondary compromise of ovarian activity and hypoestrogenism. Athletic amenorrhea is a variant of functional hypothalamic anovulation (FHA) and concomitant neuroendocrine alterations include hypothalamic-pituitary-adrenal axis activation leading to increased circulatory and cerebrospinal fluid levels of cortisol and hypothalamic-pituitary-thyroidal suppression leading to variable degrees of hypothyroxinemia.