Neurobiology of anorexia and bulimia nervosa
Neurobiology of anorexia and bulimia nervosa
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DOI：
10.1016/j.physbeh.2007.11.037
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发表时间：
2008-04-22
影响因子：
2.9
通讯作者：
Kaye, Walter
中科院分区：
文献类型：
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作者：
Kaye, Walter
神经性厌食症（AN）和神经性贪食症（BN）是一种病因不明的相关疾病，最常见于女性青春期开始。AN和BN具有独特且令人困惑的症状，例如限制进食或暴饮暴食行为，身体形象扭曲，否认消瘦和抵抗治疗。这些通常是慢性和复发性疾病，而AN的死亡率是所有精神疾病中最高的。缺乏对这种疾病的发病机制的了解阻碍了有效干预措施的发展，特别是对于AN。AN和BN患者的一贯特征是完美主义，强迫症和焦虑情绪。AN患者倾向于具有高度的约束力，情感和情感表达的收缩，ahendonia和禁欲主义，而BN患者倾向于更冲动和寻求感觉。这些症状通常开始于儿童时期，在进食障碍发作之前，并在恢复后持续存在，这表明它们是产生发展ED的脆弱性的特征。越来越多的人认识到神经生物学脆弱性对AN和BN的发病机制有重大贡献。相当多的证据表明，改变大脑5-羟色胺（5-HT）功能有助于食欲，情绪和冲动控制AN和BN的失调。使用5-HT特异性配体的脑成像研究表明，当人们生病时，5-HT功能会发生紊乱，并在AN和BN恢复后持续存在。这可能是一个特质相关的5-HT神经元调制障碍早于AN的发病，并有助于焦虑，强迫症和抑制的发病前症状。这种烦躁的气质可能涉及情绪和奖励途径的固有失调，这些途径也介导了进食的享乐方面，从而使这些个体容易受到食欲行为的干扰。限制食物摄入可能会成为强有力的强化，因为它提供了一个暂时的喘息从烦躁的情绪。有几个因素可能作用于这些脆弱性，导致AN在青春期开始。首先，青春期相关的女性性腺类固醇或年龄相关的变化可能会加剧5-HT失调。其次，压力和/或文化和社会压力可能会增加焦虑和强迫性气质。AN患者可能会发现，通过减少血浆色氨酸的可用性，减少饮食摄入是一种调节大脑5-HT功能活动和焦虑情绪的方法。AN患者进入一个恶性循环，这是这种疾病慢性化的原因，因为热量限制会导致烦躁情绪的短暂缓解。然而，营养不良和体重减轻反过来又会改变许多神经肽和单胺功能，这可能是为了节省能量，但也会加剧烦躁情绪。总之，这篇文章回顾了脑化学和神经影像学的发现，这些发现为理解这些困难和令人沮丧的疾病的精神病理学提供了新的线索。(C)2007年爱思唯尔公司All rights reserved.
Anorexia nervosa (AN) and bulimia nervosa (BN) are related disorders of unknown etiology that most commonly begin during adolescence in women. AN and BN have unique and puzzling symptoms, such as restricted eating or binge-purge behaviors, body image distortions, denial of emaciation, and resistance to treatment. These are often chronic and relapsing disorders, and AN has the highest death rate of any psychiatric disorder. The lack of understanding of the pathogenesis of this illness has hindered the development of effective interventions, particularly for AN. Individuals with AN and BN are consistently characterized by perfectionism, obsessive-compulsiveness, and dysphoric mood. Individuals with AN tend to have high constraint, constriction of affect and emotional expressiveness, ahendonia and asceticism, whereas individuals with BN tend to be more impulsive and sensation seeking. Such symptoms often begin in childhood, before the onset of an eating disorder, and persist after recovery, suggesting they are traits that create a vulnerability for developing an ED. There is growing acknowledgement that neurobiological vulnerabilities make a substantial contribution to the pathogenesis of AN and BN. Considerable evidence suggests that altered brain serotonin (5-HT) function contributes to dysregulation of appetite, mood, and impulse control in AN and BN. Brain imaging studies, using 5-HT specific ligands, show that disturbances of 5-HT function occur when people are ill, and persist after recovery from AN and BN. It is possible that a trait-related disturbance of 5-HT neuronal modulation predates the onset of AN and contributes to premorbid symptoms of anxiety, obsessionality, and inhibition. This dysphoric temperament may involve an inherent dysregulation of emotional and reward pathways which also mediate the hedonic aspects of feeding, thus making these individuals vulnerable to disturbed appetitive behaviors. Restricting food intake may become powerfully reinforcing because it provides a temporary respite from dysphoric mood. Several factors may act on these vulnerabilities to cause AN to start in adolescence. First, puberty-related female gonadal steroids or age-related changes may exacerbate 5-HT dysregulation. Second, stress and/or cultural and societal pressures may contribute by increasing anxious and obsessional temperament. Individuals with AN may discover that reduced dietary intake, by reducing plasma tryptophan availability, is a means by which they can modulate brain 5-HT functional activity and anxious mood. People with AN enter a vicious cycle which accounts for the chronicity of this disorder because caloric restriction results in a brief respite from dysphoric mood. However, malnutrition and weight loss, in turn, produce alterations in many neuropeptides and monoamine function, perhaps in the service of conserving energy, but which also exaggerates dysphoric mood. In summary, this article reviews findings in brain chemistry and neuroimaging that shed new light on understanding the psychopathology of these difficult and frustrating disorders. (C) 2007 Elsevier Inc. All rights reserved.