Kaye W H, Weltzin T E
Western Psychiatric Institute and Clinic, University of Pittsburgh, Pa. 15213.
J Clin Psychiatry. 1991 Dec;52 Suppl:41-8.
Brain serotonin activity contributes to satiety. Theoretically, binging behavior is consistent with reduced serotonin function, whereas anorexia nervosa is consistent with increased serotonin activity. Brain serotonin abnormalities could also contribute to psychopathologic behaviors such as dysphoric mood, disturbance of impulse control, and obsessionality, as well as neuroendocrine disturbances. In fact, disturbances of serotonin have been found in acutely ill anorexia nervosa patients. Tryptophan, an essential amino acid found in the diet, is the precursor of serotonin. Thus serotonin disturbances could be secondary to dietary abnormalities. However, disturbances of serotonin activity appear to persist after long-term weight recovery from anorexia nervosa. While speculative, it is possible that increased serotonin activity could contribute to the pathogenesis of restricted eating and obsessional behaviors in this illness. Physiologic and pharmacologic evidence suggest that patients with normal weight bulimia have reduced serotonin activity when acutely ill. Such disturbances, even if secondary to dietary abnormalities, may still contribute to dysphoric mood and binging behavior.
大脑血清素活性有助于产生饱腹感。从理论上讲,暴饮暴食行为与血清素功能降低相一致,而神经性厌食症则与血清素活性增加相一致。大脑血清素异常也可能导致诸如烦躁情绪、冲动控制障碍和强迫观念等心理病理行为,以及神经内分泌紊乱。事实上,在急性发病的神经性厌食症患者中已发现血清素紊乱。色氨酸是饮食中一种必需氨基酸,是血清素的前体。因此,血清素紊乱可能继发于饮食异常。然而,从神经性厌食症长期体重恢复后,血清素活性紊乱似乎仍然存在。虽然只是推测,但血清素活性增加可能在这种疾病的限制性饮食和强迫行为的发病机制中起作用。生理和药理学证据表明,体重正常的贪食症患者在急性发病时血清素活性降低。这种紊乱即使继发于饮食异常,仍可能导致烦躁情绪和暴饮暴食行为。