Conceptualizing the role of estrogens and serotonin in the development and maintenance of bulimia nervosa.

Serotonergic dysregulation is thought to underlie much of the pathology in bulimia nervosa (BN). The purpose of this review is to expand the serotonergic model by incorporating specific and nonspecific contributions of estrogens to the development and maintenance of bulimic pathology in order to guide research from molecular genetics to novel therapeutics for BN. Special emphasis is given to the organizing theory of general brain arousal which allows for integration of specific and nonspecific effects of these systems on behavioral endpoints such as binge eating or purging as well as arousal states such as fear, novelty seeking, or sex. Regulation of the serotonergic system by estrogens is explored, and genetic, epigenetic, and environmental estrogen effects on bulimic pathology and risk factors are discussed. Genetic and neuroscientific research support this two-system conceptualization of BN with both contributions to the developmental and maintenance of the disorder. Implications of an estrogenic-serotonergic model of BN are discussed as well as guidelines and suggestions for future research and novel therapeutic targets.

血清素能失调被认为是神经性贪食症（BN）大部分病理的基础。本综述的目的是通过纳入雌激素对贪食症病理的发生和维持的特异性和非特异性作用来扩展血清素能模型，以便指导从分子遗传学到神经性贪食症新疗法的研究。特别强调了大脑整体唤醒的组织理论，该理论考虑了这些系统对行为终点（如暴饮暴食或催吐）以及唤醒状态（如恐惧、寻求新奇或性）的特异性和非特异性影响。探讨了雌激素对血清素能系统的调节，并讨论了遗传、表观遗传和环境雌激素对贪食症病理和风险因素的影响。遗传和神经科学研究支持这种神经性贪食症的双系统概念化，两者都对该疾病的发生和维持有作用。讨论了神经性贪食症的雌激素 - 血清素能模型的意义，以及对未来研究和新治疗靶点的指导方针和建议。