Beck Aaron T
Department of Psychiatry, University of Pennsylvania, 3535 Market St., Rm. 2032, Philadelphia, PA 19104, USA.
Am J Psychiatry. 2008 Aug;165(8):969-77. doi: 10.1176/appi.ajp.2008.08050721. Epub 2008 Jul 15.
Although the cognitive model of depression has evolved appreciably since its first formulation over 40 years ago, the potential interaction of genetic, neurochemical, and cognitive factors has only recently been demonstrated. Combining findings from behavioral genetics and cognitive neuroscience with the accumulated research on the cognitive model opens new opportunities for integrated research. Drawing on advances in cognitive, personality, and social psychology as well as clinical observations, expansions of the original cognitive model have incorporated in successive stages automatic thoughts, cognitive distortions, dysfunctional beliefs, and information-processing biases. The developmental model identified early traumatic experiences and the formation of dysfunctional beliefs as predisposing events and congruent stressors in later life as precipitating factors. It is now possible to sketch out possible genetic and neurochemical pathways that interact with or are parallel to cognitive variables. A hypersensitive amygdala is associated with both a genetic polymorphism and a pattern of negative cognitive biases and dysfunctional beliefs, all of which constitute risk factors for depression. Further, the combination of a hyperactive amygdala and hypoactive prefrontal regions is associated with diminished cognitive appraisal and the occurrence of depression. Genetic polymorphisms also are involved in the overreaction to the stress and the hypercortisolemia in the development of depression--probably mediated by cognitive distortions. I suggest that comprehensive study of the psychological as well as biological correlates of depression can provide a new understanding of this debilitating disorder.
尽管抑郁症的认知模型自40多年前首次提出以来已经有了显著发展，但基因、神经化学和认知因素之间的潜在相互作用直到最近才得到证实。将行为遗传学和认知神经科学的研究结果与对认知模型的累积研究相结合，为综合研究带来了新的机遇。借鉴认知心理学、人格心理学和社会心理学的进展以及临床观察结果，对原始认知模型的扩展在连续阶段纳入了自动思维、认知扭曲、功能失调信念和信息加工偏差。发展模型将早期创伤经历和功能失调信念的形成确定为易感事件，而将后期生活中一致的应激源确定为促发因素。现在有可能勾勒出与认知变量相互作用或平行的可能的基因和神经化学途径。杏仁核高度敏感与一种基因多态性以及消极认知偏差和功能失调信念模式相关，所有这些都构成了抑郁症的危险因素。此外，杏仁核过度活跃和前额叶区域活动不足的组合与认知评估能力下降和抑郁症的发生有关。基因多态性也参与了抑郁症发展过程中对应激的过度反应和高皮质醇血症——可能是由认知扭曲介导的。我认为，对抑郁症的心理和生物学相关性进行全面研究可以为这种使人衰弱的疾病提供新的认识。
