The bright side of being blue: depression as an adaptation for analyzing complex problems.
The bright side of being blue: depression as an adaptation for analyzing complex problems.
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DOI：
10.1037/a0016242
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发表时间：
2009-07
影响因子：
5.4
通讯作者：
Thomson, J. Anderson, Jr.
中科院分区：
文献类型：
--
作者：
Andrews, Paul W.;Thomson, J. Anderson, Jr.
抑郁症是寻求帮助的主要情绪问题。抑郁的人通常有严重的，复杂的问题，沉思是一个共同的特征。抑郁症患者通常认为他们的沉思能让他们洞察自己的问题，但临床医生通常认为抑郁性沉思是病态的，因为它很难破坏和干扰专注于其他事情的能力。大量的证据表明，抑郁性沉思涉及对事件相关问题的分析。由于分析是耗时的，需要持续的处理，中断会干扰问题的解决。分析性反刍（AR）假说认为，抑郁是一种适应，是对复杂问题的反应，其功能是最大限度地减少对反刍的干扰，并维持对复杂问题的分析。它通过给予与情节相关的问题优先使用有限的处理资源，通过减少参与分散注意力的活动（快感缺失）的欲望，以及通过产生心理变化来减少对分散注意力的刺激的暴露来实现这一点。因为处理资源是有限的，所以不能集中精力处理其他事情是一种必须做出的权衡，以维持对触发问题的分析。AR假说得到了来自多个层面的证据的支持，包括基因、神经递质及其受体、神经生理学、神经解剖学、神经能量学、药理学、认知和行为以及治疗效果。此外，我们解决和解释令人困惑的发现在认知和行为遗传学文献抑郁症。在这个过程中，我们挑战了抑郁症中血清素传递低的信念。最后，我们讨论了理解和治疗抑郁症的假设的影响。
Depression ranks as the primary emotional problem for which help is sought. Depressed people often have severe, complex problems, and rumination is a common feature. Depressed people often believe that their ruminations give them insight into their problems, but clinicians often view depressive rumination as pathological because it is difficult to disrupt and interferes with the ability to concentrate on other things. Abundant evidence indicates that depressive rumination involves the analysis of episode-related problems. Because analysis is time consuming and requires sustained processing, disruption would interfere with problem-solving. The analytical rumination (AR) hypothesis proposes that depression is an adaptation that evolved as a response to complex problems and whose function is to minimize disruption of rumination and sustain analysis of complex problems. It accomplishes this by giving episode-related problems priority access to limited processing resources, by reducing the desire to engage in distracting activities (anhedonia), and by producing psychomotor changes that reduce exposure to distracting stimuli. Because processing resources are limited, the inability to concentrate on other things is a tradeoff that must be made to sustain analysis of the triggering problem. The AR hypothesis is supported by evidence from many levels, including genes, neurotransmitters and their receptors, neurophysiology, neuroanatomy, neuroenergetics, pharmacology, cognition and behavior, and the efficacy of treatments. In addition, we address and provide explanations for puzzling findings in the cognitive and behavioral genetics literatures on depression. In the process, we challenge the belief that serotonin transmission is low in depression. Finally, we discuss implications of the hypothesis for understanding and treating depression.
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影响因子：
6.7
作者：
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通讯作者：
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