Guisinger Shan
Psychol Rev. 2003 Oct;110(4):745-61. doi: 10.1037/0033-295X.110.4.745.
Anorexia nervosa (AN) is commonly attributed to psychological conflicts, attempts to be fashionably slender, neuroendocrine dysfunction, or some combination of these factors. Considerable research reveals these theories to be incomplete. Psychological and societal factors account for the decision to diet but not for the phenomenology of the disorder; theories of biological defects fail to explain neuroendocrine findings that suggest coordinated physiological mechanisms. This article presents evidence that AN's distinctive symptoms of restricting food, denial of starvation, and hyperactivity are likely to be evolved adaptive mechanisms that facilitated ancestral nomadic foragers leaving depleted environments; genetically susceptible individuals who lose too much weight may trigger these archaic adaptations. This hypothesis accounts for the occurrence of AN-like syndromes in both humans and animals and is consistent with changes observed in the physiology, cognitions, and behavior of patients with AN.
神经性厌食症（AN）通常被归因于心理冲突、追求时尚苗条的尝试、神经内分泌功能障碍或这些因素的某种组合。大量研究表明这些理论并不完整。心理和社会因素可以解释节食的决定，但无法解释该疾病的症状表现；生物缺陷理论无法解释那些表明存在协调生理机制的神经内分泌研究结果。本文提出证据表明，神经性厌食症独特的限制饮食、否认饥饿和多动症状可能是进化而来的适应性机制，这些机制曾帮助古代游牧觅食者离开枯竭的环境；那些基因易感性个体体重过度减轻时，可能会触发这些古老的适应性反应。这一假设解释了人类和动物中类似神经性厌食症综合征的出现，并且与神经性厌食症患者在生理、认知和行为方面观察到的变化相一致。
