心理科学进展, 2018, 26(6): 1041-1053 doi: 10.3724/SP.J.1042.2018.01041

研究前沿

抑郁症起源的三类理论视角 *

陈子晨, 张慧娟, 汪新建, 吕小康,

南开大学周恩来政府管理学院社会心理学系, 天津 300350

Three theoretical perspectives on the origin of depression

CHEN Zichen, ZHANG Huijuan, WANG Xinjian, LV Xiaokang,

Department of Social Psychology, Nankai University, Tianjin 300350, China

通讯作者: 吕小康, E-mail: xkdog@126.com

收稿日期: 2017-07-3   网络出版日期: 2018-06-10

基金资助: * 教育部哲学社会科学研究重大课题攻关项目.  15JZD 030
南开大学亚洲研究中心项目.  AS1719

Received: 2017-07-3   Online: 2018-06-10

摘要

生物医学取向下的抑郁症研究多着重探究具体的致病基因和神经病理机制,致力于对抑郁症的直接致病原因进行解释和干预。关于抑郁症起源的理论医学研究则以基于实证结果的理论推导为基本方式,力图从终极意义上探讨抑郁症的历史原因。这些理论视角基本可归为三类:进化适应视角认为抑郁症起源于应对进化压力的适应机制, 主要体现为社会性适应假说和个体性适应假说; 功能失调视角认为抑郁症起源于正常心境和情绪功能的失调, 主要体现为错配解释和基因分布解释; 社会文化视角则认为抑郁症起源于社会文化的建构, 主要体现为社会文化建构观点和知识发展观点。三种理论观点下的抑郁症在内涵和本质上存在本质主义和建构主义的不同倾向, 如何发展出更具综合性的解释框架还有待理论整合和实证依据。

关键词: 抑郁症 ; 精神疾病 ; 精神病学 ; 理论医学

Abstract

Biomedical approaches to study depression focus on the explanation and intervention of the proximate cause of depression by exploring specific pathogenic genes and neuropathological mechanisms, while the theoretical medical studies of the origin of depression discuss the ultimate historical cause of depression, mainly through theoretical reasoning based on empirical results. Those theories can be classified into three perspectives. First is the evolutionary adaptation perspective, which suggested that depression originates from the adaptive mechanisms coping with evolutionary pressure, represented by the social adaptation hypothesis and the individual adaptation hypothesis. Second is the functional disorder perspective, which assumes that depression originates from the dysfunction of normal moods and emotions, represented by the mismatch explanation and gene distribution explanation. Third is the social culture perspective, which believed that depression originates from social-cultural constructed concepts, represented by the social-cultural construction viewpoint and knowledge development viewpoint. There are different tendencies of the meaning and essence of depression under three perspectives, either of essentialism or constructivism. Theoretical integration and evidence base are needed for developing more comprehensive interpretation frameworks.

Keywords: depression ; mental disorder ; psychiatry ; theoretical medicine

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本文引用格式

陈子晨, 张慧娟, 汪新建, 吕小康. 抑郁症起源的三类理论视角 * . 心理科学进展[J], 2018, 26(6): 1041-1053 doi:10.3724/SP.J.1042.2018.01041

CHEN Zichen, ZHANG Huijuan, WANG Xinjian, LV Xiaokang. Three theoretical perspectives on the origin of depression. Advances in Psychological Science[J], 2018, 26(6): 1041-1053 doi:10.3724/SP.J.1042.2018.01041

1 前言

抑郁症指一类以低落心境为核心的情绪障碍, 主要表现包括悲伤、空虚或易激惹, 同时伴随着多种认知和躯体症状, 严重影响患者的正常功能(American Psychiatric Association, 2013, p. 155)。在诸多精神障碍中, 抑郁症相对较高的发病率使其广受关注。而抑郁症的成因也是一直以来困扰学界的热点问题。一种疾病的成因问题实际上包含两个层次, 一个层次是所谓的“直接原因”, 即疾病的病因和病理机制, 它能解释个体如何患上该疾病并表现出相应症状(Drysdale et al., 2017); 另一个层次则可以被称作“终极原因”, 即疾病的起源, 它解释的是该疾病如何出现并存在于特定人群中。比如, 对于“精神障碍为何发生”这个问题, 直接原因可能指出, 是脑神经或内分泌系统的某种不平衡状态和特定环境刺激的结合导致了该障碍。而终极原因则会指出, 某种精神障碍及其机制起源于人类进化或文明发展史的特定状态, 它在自然或社会文化环境中的“适应性”使其能够在人类种群中留存至今。对精神障碍的理解和干预固然需要对直接原因进行解释, 但对精神障碍起源的探究则有助于了解其更深层的产生基础, 从而催生更准确的认知和更有针对性的干预。

到目前为止, 精神病学研究还没有建立起一个公认的模型来解释抑郁症的起源。当下抑郁症成因的实证研究多数致力于探究具体的遗传或神经病理机制, 以生物医学取向为主导, 已经形成一整套的病理机制假说及与之相匹配的治疗程序(汤明明, 林文娟, 2013; 蒙杰, 位东涛, 王康程, 邱江, 2016; 曹衍淼, 王美萍, 曹丛, 张文新, 2016; 靳宇倡, 丁美月, 2017)。这可以视为是对抑郁症“直接原因”的解释与干预(Kamenov, Cabello, Coenen, & Ayuso-Mateos, 2015)。而关于抑郁症起源的研究则以理论推导为主要方法, 可以称为是一种“理论医学”。理论医学虽暂时不能对抑郁症的治疗起到立竿见影的效果, 但它擅长从长时距的生物进化和历史社会变迁视角来理解抑郁症的起源, 或能为抑郁症的产生提供一种综合性的解释框架。

关于抑郁症起源的理论医学重点在于解释以下问题: 抑郁症作为一种造成普遍认知、行为和社会功能损伤的精神障碍是如何产生的, 又为何能够一直存在于人类群体中, 并且维持较高的发病率。已有不少研究者综合病因、病理、进化和文化上的证据, 提出多种不同的假说和模型。这些假说和模型虽然在细节上各有特色, 但其基本取向或说理论视角大致可归为三类: (1)进化适应视角, 认为抑郁症起源于应对进化压力的适应机制; (2)功能失调视角, 认为抑郁症起源于正常心境和情绪功能的失调; (3)社会文化视角, 认为抑郁症起源于社会文化的建构。需要注意的是, 这里所说的理论视角并不是关于抑郁症的理论本身, 而是具体假说和模型以之为基础的理论倾向和立场。某个学者在提出具体假说或模型时, 可能不会直接声明自身采取的理论视角, 但其倾向通常会在假说或模型的内容和形式中显露出来。以下分别对三类理论视角进行介绍和评述。

2 进化适应视角

2.1 进化适应视角的基本观点

进化适应视角的理论主要采用适应主义的观点来回答抑郁症起源的问题, 认为抑郁症是一种适应机制, 其症状从结果上说能让个体更好地应对进化过程中的特定选择压力, 因此才在人类种群中存留至今(Liu et al., 2014; Miller & Raison, 2016)。抑郁症的核心症状, 即低落的心境和情绪, 虽然让人不愉快甚至痛苦, 但也是一种普遍存在的适应机制。正常人的抑郁或低落心境通常是对不利情景和生存风险的应激反应, 比如亲友伤亡、遭遇失败等。当应激出现时, 心境和情绪系统会激活一系列免疫、心理、注意、认知和生理变化, 帮助机体增强对环境的适应(Nesse & Ellsworth, 2009; Nettle, 2009; Nettle & Bateson, 2012)。从结果来说, 低落的情绪和心境状态能让个体节奏变缓, 保存能量, 回避风险, 向他人寻求帮助, 而这些都有助于个体从损失和伤害中恢复(Hagen, 2011)。

适应主义者认为, 作为疾病的抑郁症可能也是从类似的适应过程演化而来的。在进化医学视角下, 损害有时是由正常的防御机制引起的。比如, 发烧在临床上被视为一种有害的疾病症状, 因为它会造成新陈代谢、性功能和社会功能等方面的损害, 但它本质上其实是特定免疫系统的适应反应。抑郁症可能也是一种较为强烈的心理—生理适应反应, 虽然它对生活的很多方面都具有破坏性, 但是就像发烧、疲劳、恶心或疼痛, 正是这些破坏性特征帮助我们回避了潜在的健康风险。按照这种思路, 进化适应视角对抑郁症起源的分析一般包括以下几个方面: 第一, 寻找进化环境中有哪些重复发生的状况和抑郁症状的出现相关; 第二, 找到和这些状况相对应的主要选择压力; 第三, 确定抑郁状态有哪些特征可以使抑郁个体在这些压力状况下比其它个体具有更好的生存或繁衍机会。简单来说, 适应主义的抑郁症起源理论就是要解释, 各类看似“有害”的抑郁症症状可能对个体的生存繁衍具有什么积极意义。传统的适应主义假说主要关注于抑郁症和社会性应激的相关性, 认为抑郁症是人类应对社会负性事件的一种特殊适应机制, 这类假说可以称为“社会性适应假说”。而另一种“个体性适应假说”则专注于抑郁症的某些症状对于个体的适应意义, 比如分析性沉思假说。

2.2 社会性适应假说

社会性适应假说认为, 抑郁症起源于个体在应对社会性压力中产生的适应机制。根据人际关系的维度, 社会性的选择压力又可以分成两种类型: 亲和维度的压力(如失去亲密伙伴、被群体排斥)和权力维度的压力(如竞争失败、地位下降) (Allen & Badcock, 2006)。抑郁症在这两种社会性压力下的表现可分别由抑郁的依恋理论和社会竞争假说加以解释(Gilbert, 2006)。依恋理论认为, 抑郁状态可以视为一种应对重要人际关系丧失的特殊依恋反应。人类在漫长的进化过程中继承了应对各种发展环境的依恋模式, 但由于个体所经历的成长事件和家庭教养等发展环境上的差异, 不同的个体在应对压力时会运用不同的依恋模型, 并在此基础上逐渐形成稳定的人际应对模式(Simpson & Belsky, 2008)。如果个体在成长环境中发现, 表达悲伤和低落的情绪更容易获得父母的爱护, 那么在以后的成长过程中, 个体就更容易对类似的人际压力事件产生同样的反应, 表现出更高的抑郁症易感性(Mezulis, Hyde, & Abramson, 2006)。

抑郁症的社会竞争假说则认为抑郁的作用在于传递服从, 使个体在遭受挫折后免受来自主导者更进一步的威胁, 本质上是个体接受挫折的一个过程(Price, Sloman, Gardner, Gilbert, & Rohde, 1994)。在进化过程中, 具有社会性的生物对资源的获取很大程度上依赖于其在群体中的地位或等级, 而竞争失败造成的地位下降则是一种重大适应压力。抑郁症中典型的退缩和屈服性表现可能就起源于对社会地位下降的适应。抑郁者在面对竞争时, 会倾向于接受较低的地位和回报, 从而回避进一步冲突(Kupferberg et al., 2016)。因为如果个体在未来的争斗中难以取胜, 那么展示屈服姿态并避免争斗将有助于降低受伤或死亡的风险, 利于其生存和繁衍(Price, Gardner, & Erickson, 2004; Taylor, Gooding, Wood, & Tarrier, 2011)。

Hagen (1999, 2002)与Watson和Andrews (2002)提出的“社会导航假说”则认为, 成人的抑郁状态传达了恳求帮助的信号, 通过唤起亲密社会伙伴的同情心来获得额外的人际资源。抑郁症患者在认知和行为方面的有害变化, 不仅对其本人是一种伤害, 还可能让他们的亲密社会伙伴也遭受损失。因此, 抑郁症造成的有害社会后果在某种程度上会推动抑郁者的社会伙伴投入更多的资源, 以帮助抑郁者结束抑郁状态, 避免自身和群体损失的扩大。另外, 有些抑郁症状还可能是迫使社会成员不得不伸出援手的强迫或威胁性手段(Watson & Andrews, 2002)。而这可以解释抑郁症中常出现的自伤和自杀倾向的适应意义。自伤和自杀倾向有可能是对亲密社会伙伴进行胁迫性资源索取的一种极端化表现(Andrews, 2006)。

2.3 个体性适应假说

个体性适应假说认为, 抑郁症起源于极端自然选择压力下进化而来的特有认知模式。此类理论中较典型的一种就是“分析性沉思假说”。沉思是抑郁症等情绪和心境障碍中的一种独特现象, 指个体反复关注自身的抑郁症状及造成抑郁的原因和结果, 特别是聚焦于其中的消极感受和负面信念。普遍认为沉思对于抑郁症的发展、维持和复发起着重要作用, 而且很难被抑制, 是一种需要干预的有害风险因素(Barbic, Durisko, & Andrews, 2014; Smith & Alloy, 2008)。但与这种传统理解不同, Andrews和Thomson (2009)的分析性沉思假说认为抑郁性沉思是一种具有进化意义的思维模式。在这种思维模式下, 个体的注意力主要分配在细节上, 信息处理速度缓慢而深刻(Lerner, Li, Valdesolo, & Kassam, 2015)。沉思和其它支持沉思的抑郁症状(比如重复和闯入性思维、失眠等)共 同形成一种应对复杂生存繁衍问题的适应机制(Andrews & Thomson, 2009)。抑郁者对一般的快感来源(比如性、饮食)失去兴趣, 而将注意力和认知资源完全置于对最紧迫问题的分析上。虽然抑郁状态下的处理风格对解决复杂问题有所助益, 但通常而言, 这种缓慢而需要努力的思维也较容易引起疲劳和注意力分散, 这就是抑郁性沉思的代价。不过适应主义的理论家认为, 其在进化过程中的适应作用足够平衡其带来的代价(Watson & Andrews, 2002; Andrews & Thomson, 2009)。

另外, 还有些理论家认为, 抑郁症是一种独特的风险策略调整机制。抑郁症的重要表现之一是负面认知偏差, 包括消极的归因方式、负性自我图式、夸大任务难度等。这些症状可以说是负性心境调节系统在更极端风险情境下的一种延伸。各种负性事件广义上其实都可以理解为提醒个体未来出现重大适应性风险(如社会排斥或生存状况恶化)的一种信号, 包括负性人际经验(比如丧失或拒绝)、重要目标的失败、失去社会等级或地位、以及对社会状况缺乏控制感(比如羞辱或困窘经验)等(Allen & Badcock, 2003)。一旦风险应对机制被激活, 抑郁症状会同时影响风险感知和决策行为, 让个体减少高风险的活动, 同时回避对繁衍产生威胁的冒险行为。风险感知的变化让个体对风险信号过度敏感。因为个体越能警觉地保存现有资源并减少风险, 就越可能在已出现危机的环境中生存下去(Allen & Badcock, 2003; Sloman, Gilbert, & Hasey, 2003)。行为决策上的变化则让个体更倾向于风险规避, 比如, 退缩和社会孤立有助于个体回避可能造成危险的社会互动, 在有害条件或糟糕状况下减少风险(Nettle, 2009)。

但也有批评指出, 适应主义的理论似乎高估了临床性抑郁症状的适应功能。比如对于沉思, 有研究显示抑郁状态整体上还是更多地降低了社会问题解决能力。抑郁者常有负性自我认知, 并且缺乏自信, 他们即使知道某种特定的行动有效果, 也难以有动力去进行该活动; 而且沉思者还倾向于将问题难度估计过大, 更容易觉得无法成功解决问题(Donaldson & Lam, 2004)。将沉思作为一种压力反应的人更容易患抑郁障碍, 也有更长的抑郁阶段(Nolen-Hoeksema, Wisco, & Lyubomirsky, 2008)。综合正反两方面的证据来看, 在抑郁的严重性和抑郁提升社会问题解决能力之间可能是一种曲线关系, 较轻度的抑郁能够提升社会推理和思维任务的表现, 但在重度抑郁症患者身上, 这种优势就不复存在(Lee, Harkness, Sabbagh, & Jacobson, 2005)。

3 功能失调视角

3.1 功能失调视角的基本观点

在功能失调视角下, 抑郁症起源于机体正常功能的失调。抑郁症的本质是心境系统的功能障碍, 其原因是心境相关的生理或心理机能出现了“故障”。当个体面临应激时, 心境系统激活的心理生理变化强度过大, 或持续时间过长, 超过适应环境的需要就会造成损害(Wolpert, 2008)。功能失调视角与进化适应视角的共同点在于, 二者都认为在抑郁症的起源中, 适应性的负性心境和情绪起着关键作用。而它们最大的区别则是, 进化适应视角认为抑郁症本身就是通过自然选择而保留下来的一种特殊适应机制, 具有损害性的生理、认知、行为症状也具有一定的适应意义; 功能失调视角则认为只有抑郁状态的一些核心机制(比如低落心境)才具有适应功能, 作为疾病的抑郁症则是这些适应机制发生失调的结果(Keller & Nesse, 2005; Nettle & Bateson, 2012)。

对于抑郁症起源的问题, 功能失调视角的理论家关注于解释两个问题: 1)失调的机制本来具有的功能从何而来, 即正常抑郁状态或低落心境的起源; 2)正常的心境功能为何发生失调而变成一种精神障碍或疾病, 即人类种群中抑郁症易感性的起源。功能主义者对第一个问题的回答基本一致, 都是解释抑郁情绪或低落心境的积极作用, 这方面和适应主义者的观点有诸多重合, 此处不再赘述。功能失调视角的重点在于解释第二个问题。这个问题的具体表述有多种形式, 比如, “正常的抑郁状态与异常的临床抑郁之间是连续的关系吗?”或“为什么正常的反应会变得过度化而成为一种障碍?”, 但其本质都是在探究失调的原因。对此, 功能失调视角的理论主要有两种不同的解释路径: 1)错配解释(Varga, 2012, 2016), 认为抑郁症来源于古代留存下来的反应机制和现代环境中应激的不匹配; 2)基因分布解释, 认为抑郁症是正常情绪机制的相关基因在种群中的特定分布状态导致的极端情况。

3.2 错配解释

错配解释是功能失调视角结合了进化论证据和适应主义观点的一种理论假说, 也可称为进化遗存(evolutionary vestige)假说。这种解释认为, 抑郁症可能衍生自人类祖先时代的适应机制, 其与现代环境的不匹配导致了功能的失调。

在进化医学中可以找到很多错配类型的假说, 比如“节俭基因” (thrifty genotype)能促使能量更有效地转化为脂肪储存起来, 这在食物匮乏的古代环境中曾起到适应作用, 但是在当前物质丰富的社会经济环境中却会导致肥胖症这样的健康风险(Wells, 2012); “卫生假说” (hygiene hypothesis)的衍生观点认为, 哮喘和过敏反应等疾病的流行原因可能是免疫反应的进化结果和现代生活环境的错配(Brooks, Pearce, & Douwes, 2013)。抑郁症起源的错配解释也套用了类似的逻辑路径。与生理结构一样, 人类心理中也包括很多适应不同进化年代的系统, 其中不少如今仍在意识阈限之下运行(Stevens & Price, 1996)。而抑郁症的相关机制就属于其中之一, 它所应对的特定问题通常出现于古代人类的小社会群体中。是人类社会过快的发展导致遗传下来的抑郁反应与现代环境“错误匹配”, 使其反而变成了有害生存的“不良适应”, 成为一种流行率颇高的“疾病” (Baptista, Aldana, Angeles, & Beaulieu, 2008)。

在远古人类的小群体中, 个体面临着较大的生存风险, 同时强烈依赖群体和稳定的人际关系。因此当竞争失败、遭遇挫折等负性事件发生时, 接受损失、回避风险是比较有利的策略。抑郁状态下的低落心境、社会回避行为、食欲减退等症状能够节省能量和资源、应对失败、挫折和风险, 创造了更好的生存繁衍机会(Nesse & Williams, 1995; Price et al., 1994)。但在现代变化更快、群体规模更大的社会中, 这种自动激活的遗传机制就不再适应环境了(Nesse & Williams, 1995)。在当前全球化的背景下, 相互竞争的同辈群体人数更多, 之间的联系却不像小群体中那样紧密, 竞争和变化也更加频繁。对于社会失败的过度敏感和退缩反应不能再让个体保持稳定的地位, 反而降低了其社会功能, 导致繁殖成功率的下降(Nesse & Williams, 1995; Stevens & Price, 2000)。因此, 抑郁症既是一种适应, 也可被视为一种“疾病”。

有一种较新的理论, 病原体宿主防御假说(Pathogen host defense hypothesis)在抑郁症起源的问题上也采用了错配解释。但与以往的错配解释主要关注社会环境的错配不同, 病原宿主防御假说则提出, 抑郁症来自于人类与病原体环境的错配(Raison & Miller, 2013)。该理论的病因基础是抑郁症的炎症假说, 即认为病理性的抑郁状态可能是一种神经炎症反应。在进化史中漫长的狩猎—采集年代, 人类无法存活到成年的主要原因之一就是感染。轻微外伤都很可能发展为致命的感染。这种选择压力让人类和微生物之间的互动成为重要的进化动力(Fumagalli et al., 2011), 逐渐塑造了一种由感染所激活的综合适应机制, 其中包括生理上的炎症反应以及心理和行为上的抑郁状态。低落心境下的社会回避等症状形成了一种“疾病行为模式”, 降低了个体的病原体暴露风险, 起到了促炎症和抗病菌的效果。在古代病菌环境中, 这种炎症性抑郁倾向能够帮助个体恢 复创伤、降低受伤机会和交叉感染风险, 提高生存率。但在现代较为卫生的环境中, 这种优势就不复存在, 甚至可能变成劣势(Messay, Lim, & Marsland, 2012; Miller & Raison, 2016; Raison & Miller, 2013)。

还有一种理论与主要的错配解释相似而略有不同, 它关注于中性等位基因在抑郁症起源中的作用。现代人类的生存环境与进化环境有着巨大差异, 而新环境和古代基因组中某些中性等位基因的交互可能导致各种类似抑郁症的障碍(Di Rienzo & Hudson, 2005; Keller & Miller, 2006)。中性等位基因指的是既不给予适应代价也没有好处的基因。在古代环境中, 这些基因可能没有特殊的适应意义, 但也不会减少繁衍机会, 因而没有被自然选择淘汰掉。而到了现代环境, 这些基因可能就会造成适应不良的结果。在远古时期较为简单的社会关系模式下, 抑郁倾向可能不会造成太多负面影响, 或至少不会降低性成熟之前的生存率以及繁殖几率, 因此也就能将相关基因传递下来。而现代环境则凸显出了抑郁症的负面效果, 使其成为一种功能失调反应。但是, 该理论也不能完全解释像重度抑郁这类障碍的高流行率和遗传性, 因为古代中性等位基因变异应该很稀少, 而遗传漂变完全可能在种群中使稀少的基因变异消失(Keller & Miller, 2006)。鉴于目前对抑郁症的相关基因研究还没有非常明确的结果, 这种理论所假设的进化遗传过程也很难得到证实。

3.3 基因分布解释

基因选择解释认为抑郁症对患病个体生存是不利因素, 但却可能有利于相关易感基因通过自然选择留存下来。自然选择可能是通过一个多层次的过程来实现的, 其直接选择的对象是个体的表现型, 本质则是群体基因池中基因频率的定向改变。因此, 抑郁症的产生原因可能不仅来自于个体的适应过程, 而且还源于人类群体中相关基因的表达以及基因分布在进化史中的长期变化。如果说错配解释是以纵向视角(进化环境和选择压力随时间的变化)来说明抑郁功能失调的起源, 那么基因分布解释就是以横向视角(同一时间上的种群基因分布)来回答这个问题。

该类理论一般是通过基因的统计或数学模型做出推论。比如, Nettle (2004)的个体差异解释认为疾病现象除了有其适应来源, 还可能产生自相关基因在群体中的不均匀分布。典型的例子比如男性的身高, 身高较高一般意味着更大的体型, 是有利于繁衍的特质。但如果身高超过特定高度, 难产、肌肉骨骼疾病以及其它健康问题的风险也会随之升高(Nettle, 2004; Gage, 2002)。因此, 男性身高的社会竞争和择偶优势与其带来的婴儿及成年期健康风险相制衡, 导致身高的最优适应状态处于一个中间值。每一代种群的平均身高都会大致维持在最优的适应状态, 而个体的实际身高则形成一个围绕适应状态的正态分布, 其中就有少数男性恰好遗传了更为极端的基因型, 表现为身高过高或过矮, 并造成相应的健康问题。

人类情绪系统中的异常可能也与身高类似。虽然情绪系统本身是所有人都具有的适应机制, 但同样的人际事件在某些个体身上会引发更强烈或长久的情绪反应。抑郁状态下对社会风险的过敏会给个体带来繁衍优势, 而当其强度超过某个水平, 造成精神障碍的风险就超过了其优势带来的边际收益。如同身高, 情绪系统的敏感性围绕最适水平呈正态分布, 使种群的每一代中总有一部分人处于分布的首端或末端。而处于高敏感端的人对抑郁症等情绪障碍就有更高的易感性。同时, 控制情绪系统反应的神经生物学机制非常复杂, 能引起它发生变化的基因数量可能比影响身高的基因要多得多。如果一个特质的相关基因数量很多, 其变异目标也会很多, 明显的基因变异也可能维持下来(Houle, 1998)。因此, 抑郁症作为种群分布中的极端值, 其流行率可能比病理性的身高过高或过矮更多, 也更容易保留下来。

还有一些类似理论则提出, 抑郁症主要起源于自然选择的平衡, 即导致更高抑郁症风险的基因和其它方面的好处有关。比如, 有研究指出, 导致MDD风险的等位基因可能在易感个体的健康手足身上带来一些优势(Power et al., 2013)。虽然抑郁症个体的生存几率下降, 但是其携带同样等位基因的亲属得到了更高的生存机会, 两者的平衡就保持了种群基因池中抑郁症易感基因的比例。另一方面, 使个体在有害环境下易感生物学功能障碍的等位基因, 也可能让个体在更适当的环境中生存得更好(Ellis & Boyce, 2008, 2011)。一种抑郁风险相关的等位基因在恶劣环境中可能导致抑郁症, 但在支持性环境中也可能激发更多的积极反应(Brody, Chen, Beach, Philibert, & Kogan, 2009)。某些条件下具有适应优势的基因型在其它条件下可能会导致更高的抑郁症风险。比如, 脑源性神经营养因子(brain-derived neurotrophic factor, BDNF)基因Val66Met多态性的一种基因型在青少年中可预测更高的抑郁风险, 但在成人阶段则相反(Hilt, Sander, Nolen-Hoeksema, & Simen, 2007; Stone, McGeary, Palmer, & Gibb, 2013); 而5-羟色胺转运体基因连锁多态性区域(serotonin-transporter- linked polymorphic region, 5-HTTLPR)、MAOA (monoamine oxidase A, 单胺氧化酶A)基因对抑郁风险的预测则存在性别差异(曹衍淼, 王美萍, 曹丛, 陈光辉, 张文新, 2013)。甚至对于抑郁症中最严重的一类症状, 即自伤、自杀行为也可做出类似推论: 这些自我毁灭的举动从结果上说“淘汰”掉了那些遭遇不幸或处于不利状况的个体(比如在竞争中失败的个体), 将资源保留给其生存状况更好的亲属; 或可以阻止受伤及患病的个体将病原体传染给其他人, 从而提高种群的平均生存率(Aubin, Berlin, & Kornreich, 2013; Tanaka & Kinney, 2011)。

4 社会文化视角

4.1 社会文化视角的基本观点

社会文化视角主要以建构主义的态度来看待抑郁症问题, 认为所谓的“抑郁症”是人们在特定社会文化背景下建构出来的一个知识概念。需要注意的是, 在抑郁症起源问题上的社会文化视角并不是病因学的社会文化视角。后者是指个体患上抑郁症的原因可能包含社会或文化的因素(陈子晨, 汪新建, 2015), 而前者是指人们对“抑郁症”这种疾病的定义和认识本身就具有社会文化性质(吕小康, 汪新建, 2012)。对抑郁症病因的社会文化因素进行探讨在抑郁症的相关理论中并不少见, 现代医学向生物-心理-社会模式的转变已经让健康和疾病问题的社会文化属性成为一个不可忽视的因素。但是, 从社会文化视角探寻疾病起源的观点却不太常见, 因为这涉及到对疾病本体的质疑。而且这种质疑通常超出对该疾病本身的讨论, 而是成为一种对研究和定义该疾病的医学或精神病学理论的探讨, 即所谓“元理论”。

在此意义上, 社会文化视角与前两种视角产生了一个根本的区别, 就是对于抑郁症本体论的认识。社会文化视角的核心观点之一是质疑“抑郁症”作为一个疾病实体的客观实在性。功能失调视角和进化适应视角对抑郁症的定义基本都属于本质主义(essentialist)观点, 即认为客观存在着一个被人称之为“抑郁症”的疾病实体, 独立于我们对它的识别和分类(de Jonge, Wardenaar, & Wichers, 2015)。而与之不同, 社会文化视角采用的是建构主义(constructivist)观点, 即认为自然中并不存在“抑郁症”实体, 它只是由特定社会文化背景下的医学和精神病学理论将一系列自然现象对象化后所描绘出来的人造范畴。该视角下的理论主要包括以下两种类型: (1)社会文化建构观点, 主张“抑郁症”是社会文化建构出来的概念; (2)知识发展观点, 主张“抑郁症”是医学知识发展不完善时期的暂时性概念。

4.2 社会文化建构观点

社会文化建构观点是社会文化视角最主要的表现形式, 其核心主张认为“抑郁症”是产生自特定社会文化形塑的概念。在医学人类学等交叉学科领域的理论视野下, 像抑郁症这样的精神疾病从来都不是单纯的客观科学概念, 而是由现实中的社会疾苦和个人痛苦共同建构而成的经验综合体, 因此需要用能够体现社会背景和文化渊源的术语和框架来对其进行认识(Patel, 2017; White, Orr, Read, & Jain, 2017)。社会结构的变化和文化的特殊观念, 塑造和定义了所谓“抑郁症”的行为表现。“抑郁症”的核心是超乎正常范围的忧郁、悲伤或低落的心境, 在不同的社会文化背景下, 有一系列生理心理表现可能与这个核心症状同时出现。人们选择其中特定的一些表现与这个核心联系在一起, 构成了有着文化特征的疾病概念。这种症状群的选择和划分有时候是根据该文化背景中常见的组合, 有时是由先前的某些历史观念衍生而来。同样一种表现在不同文化背景下可能得到不同的归类, 而当前我们所谈论的“抑郁症”就是西方现代精神医学对这类症状群的划分和 定义。

“抑郁症” (depression)一词作为精神疾病术语出现于19世纪, 可以说只有一个短暂的历史, 但作为其前身的“忧郁症” (melancholia)则有着更为漫长的过去。古希腊时期的希波克拉底是第一个提出“忧郁”概念的人, 他认为忧郁是一种体液决定的气质类型或负性情绪体验, 这种状态下的个体失去了体验快乐的能力。在漫长的中世纪, “忧郁者”一直作为一个独特的文化形象存在着。而到了18世纪之后, 随着精神医学走向专业化, 各种学术理论又开始包裹在忧郁这个文化象征的内核之上, 使其演变为一个科学化的精神疾病概念。福柯在其著名的精神医学史批判中对此进行了详尽的论述: 忧郁症成为与躁狂相对的概念, 虽然体液或躯体失调的病因论调逐渐被排除, 但物质性的隐喻仍然保留在神经系统或精神动力理论中, 形成忧郁症的核心特征, 即个体精神和行为表现上的沉重、低落和迟缓(米歇尔·福柯, 2005, pp. 379-398)。从19世纪开始, “抑郁”一词越来越多地出现在对忧郁症的讨论中, 指称其中的心境或情绪症状。随着“躁狂—抑郁”作为心境障碍两极的分类越来越得到认可, “忧郁症”这个概念反而不断衰落, 直到在疾病名称上彻底被抑郁症所替代(Jackson, 2008)。

社会文化建构观的另一个重要观点则来自于凯博文(Arthur Kleinman)对中国人的神经衰弱和抑郁所做的医学人类学分析(Kleinman, 1982)。其中, 凯博文将抑郁视为一种和精神问题躯体化相对应的“心理化”表达方式。一些跨文化的文献研究显示, 西方社会的躯体化报告率较低, 而包括中国在内的许多东方社会及其他现代化程度较低的社会则拥有更高的躯体化报告率。与此同时, 西方社会的抑郁症发病率却远远地高于非西方社会。凯博文在田野调查中发现, 很多被诊断为神经衰弱的中国患者, 经过进一步详细问诊也表达出躯体主诉之外的更多心理痛苦。如果按照西方流行的诊断标准, 这些患者的症状表现完全可以诊断为抑郁症。凯博文认为, 这种区别源于西方现代化进程导致的社会文化发展。西方人已经习惯了将内心世界展露出来的“心理化”疾病表达方式, 也更接受直接向心理治疗师或咨询师求助, 表达内心情感; 而多数非西方的传统社会则更习惯隐藏内心感受的“躯体化”疾病表达模式(吕小康, 汪新建, 2013)。现代西方的医学模式主要关注抑郁症所引起的情绪和心理症状, 抑郁者的躯体症状被认为是心理冲突的衍生症状, 这种看法也影响了公众对自身体验的判断。“抑郁症”概念中对躯体化的忽视和对心理化的强调随着工业文明的全球化扩展到世界其它地区。从这个角度说, 抑郁症只是西方文化影响下人们对于某类精神疾病的习惯性表达(凯博文, 2008)。

近些年来, 凯博文等人尤其看重从“社会痛苦” (social suffering)的理论视角来看待抑郁症。其所谓的“社会痛苦”实质是一种批判性的建构论观点, 将抑郁症及其他造成社会成员不同程度身心痛苦的现象置于全球化、理性化、工业化的现代性背景加以考察和批判, 强调产生身心疾病的社会决定因素(social determinants), 如个体的早年经历、教育、经济状况、就业机会、住房条件和环境状况等(Kuah-Pearce, Kleinman, & Harrison, 2014; Wilkinson, 2014; Wilkinson & Kleinman, 2016; 布尔迪厄, 2017)。在方法论上, 这种观点强调以医学人类学的视角对人类遭受的身心苦楚加以切身化的体验与描述, 认为精神疾病治疗应具备“文化胜任力” (cultural competence)以了解多元文化中不同个体的文化背景、治疗需求和价值体系, 对其痛苦应给予足够的人性的关爱(caring), 而不仅仅是生物学意义上的医学治疗, 并应注重从全球或区域性政策干预的角度加以解决(Aggarwal, Cedeño, Guarnaccia, Kleinman, & Lewis- Fernández, 2016; Kohrt, Mendenhall, & Brown, 2016; Napier et al., 2014)。因此, 这是一种兼具批判性与行动性的视角, 强调主观体验、强调人性关爱、强调社会行动, 这与之前生物医学模式下的抑郁症治疗模式形成了鲜明的对比。

4.3 知识发展观点

社会文化视角的一种非典型模式是知识发展观点。与社会文化建构假说不同, 知识发展观点从医学和精神病学专业知识发展的角度看待抑郁症起源的问题。这一类观点认为, “抑郁症”是当前医学对病理过程的不成熟理解所塑造的暂时性分类, 随着相关知识的发展这个术语可能不再和某个确定的病因模型相联系。知识发展观点对抑郁症的定义持解构主义的态度。在此视角下, “抑郁症”是一种有待解决的医学谜题(汪新建, 陈子晨, 2014)。医学史中经常出现这种情况: 随着技术的发展和病因的确定, 更准确的疾病实体名称替代了宽泛定义的临床综合征, 原有的疾病名称就变成一种模糊的症状描述(比如“水肿”或“消耗性疾病”等术语); 或者新的研究发现了病理过程中隐藏的决定因素, 原有的疾病分类不再指向一个统一的病因, 而是被新的理解所取代(比如部分“消化性溃疡”病例被确定为幽门螺旋杆菌感染) (Patten, 2015)。

知识发展观点的重点之一是指出“抑郁症”现有定义的不完善之处。当前诊断标准中的“抑郁症”是一种并不精确的临床综合征。不同版本的诊断手册描述的“抑郁症”是略有差异的一系列症状的组合, 除了低落心境这种核心症状, 还可能包括快感缺乏、体重变化、睡眠障碍、精神运动性失调、疲劳、无望感、罪恶感以及自杀观念等症状中的几种(陈子晨, 汪新建, 2013)。这类诊断标准其实只是对表面现象的描述, 而无法指示症状之间的联系以及潜在的病因。因而, 当人们谈论“抑郁症”的时候, 可能指的根本不是一个疾病实体。这种模糊而不断变化的定义在临床实践上也引起了很多问题, 比如会错误地扩大精神障碍诊断的范畴, 或忽略患者可能存在的真实生理问题(Frances, 2013; Wakefield, 2013)。因此有学者建议, 也许应当解构或淘汰当前的范畴, 建立更有效的分类(Weinberger & Goldberg, 2014)。比如, 美国国立精神卫生研究所(National Institute of Mental Health, NIMH)计划开展的研究领域标准(Research Domain Criteria, RDoC)项目, 就提出或可打破原有的分类框架, 将诊断建立在一些更基础的病理模块上(如工作记忆不足或快感缺乏), 这也许有助于临床工作者更精确地描述和认识每个具体的“抑郁症”个案(Insel, 2014)。

另一方面, 随着医学检验技术和病理研究的深入, 精神障碍领域也出现了一些从心理到生理的诊断分类转变。研究者对慢性疲劳综合征(chronic fatigue syndrome, 简称CFS)的重新认识就是一个典型例子。很长一段时间, 学界的主流观点认为CFS是一种源于心理因素的心身疾病。而近年来, 研究者才发现CFS其实很可能是一种由细胞化学反应异常或酶功能障碍导致的生理疾病(Fluge et al., 2016; Nagy-Szakal et al., 2017)。 这种由新技术引发的转变对知识发展观点的支持者是一种鼓舞。在抑郁症起源的问题上, 有不少热门的假说认为“抑郁症”的本质可能也是某种目前医学还不了解的生理疾病。比如脑肠轴(gut-brain axis)理论认为微生物菌群可能是抑郁症及其它一些精神障碍的决定因素(Foster & Neufeld, 2013); 前文提到过的炎症假说则认为炎症细胞因子是导致抑郁症的关键原因(Felger & Lotrich, 2013; Maes et al., 2009)。但无论对病因的推论落在哪个领域中, 持知识发展观点的假说对抑郁症的起源都有着相同的看法: “抑郁症”只是源自知识不完善的一种妥协性概念, 是专业文化建构的产物。而这些假说也等待着科学知识的进一步发展来证实它们对“抑郁症”真实本质的推测。

5 总结与展望

总体而言, 抑郁症起源的三种理论视角之间既存在共性, 也存在分歧。一方面, 这些视角之间并不是完全互斥的, 更多地是讨论问题的角度不同, 有时它们之间还可以形成互补。比如说, 在功能失调视角下, 抑郁症本身不具有适应性, 而是正常心境功能的异常化, 但它同时也承认发生异常的机制本身可能起源于进化适应; 又或者, 进化适应视角将抑郁症视为一种适应机制, 着重强调其对生存的良性作用, 其实形成了对过去“抑郁症”现象中正常与异常划分的一种质疑, 而这恰好契合了社会文化视角的观点, 即“抑郁症”是专业知识建构的产物。由此可见, 对于解释抑郁症起源这种复杂的问题, 三种理论视角并没有高下优劣之分, 而是都能贡献有洞见的观点。甚至一种具体的抑郁症理论可以同时从三种视角出发, 分析抑郁症起源问题的不同阶段和层次。

但另一方面, 如果详细考察这三种理论视角暗含的基本假设, 就会发现, 它们在几个最根本的问题上存在分歧。这就决定了没有一种理论可以将三种视角完全融合在一起。三种理论视角的分歧主要表现在以下几个方面(见表1): 第一, 如前所述, 三者在抑郁症的本体问题上认识不同。如果一种理论认同抑郁症是确定的疾病实体, 那么它就很难完全同意文化建构的观点。第二, 对于抑郁症是否是一种疾病, 三者的回答也不完全一致。这关系到如何划分抑郁症中正常与异常的界线。第三, 对于“抑郁症”这个概念所指称的现象究竟是什么, 三者的看法仍然不同。其中, 进化适应视角和功能失调视角的最大分歧之一, 就是在于临床意义的抑郁是否是一种适应, 但何谓“临床意义的抑郁”也并不清晰, 而这恰恰又是社会文化视角批判的重点。这三个主要分歧结合在一起就造成了三种理论视角共同面临的一个重大局限, 即不同的理论有时候讨论的根本就不是同一个问题。每个理论都重新定义一遍自己所讨论的对象, 以至于其它派别的理论既无法找到反驳方法, 也无法转换角度进行分析。既然无从对话, 就更谈不上相互融合。

表1   抑郁症起源三种理论视角的主要分歧

理论视角 如何认识抑郁症的? 抑郁症是否是一种客观存在的疾病实体? “抑郁症”现象的本质是什么?
进化适应视角 本质主义 是一种不完全是疾病的实体 进化产物、适应
功能失调视角 本质主义 是一种疾病实体 功能失调、疾病
社会文化视角 建构主义 不是一种疾病实体 一系列由文化联系在一起的生理心理表现

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从以上分歧可以看出, 三种理论视角各有其长处, 同时也有一些共同的局限之处亟待解决。为了推动这个极具潜力的理论领域进一步发展, 以下两个方向值得重点关注。

第一, 抑郁症起源理论需要明确讨论对象的范畴, 在抑郁症的基本认识论上建立一定的共识。只有这样, 不同的理论之间才可以对话, 厘清异同之处。要解决这个问题, 必须先明确抑郁症的定义和标准, 然后在正常和异常之间划定界线。目前最大的问题在于, 现有的分类标准(比如DSM等诊断手册)本来就已经广受争议(Frances, 2013), 而无论适应主义的视角还是社会文化视 角, 都更注重抑郁症中“正常”的一面, 最后难免成为对现有诊断标准的抨击(Durisko, Mulsant, & Andrews, 2015)。反过来, 抑郁症起源的解释应该可以担负起定义界线的作用。虽然从起源角度确定正常和异常的界线, 可能比当前以表面现象进行划分更加困难(Nettle & Bateson, 2012)。未来的理论或许可以先划定一个讨论对象的范围, 搁置正常还是异常的标准判断问题, 纯粹描述抑郁症现象从自然产生到人类认识的过程, 这样一种路径也许能够将适应主义和功能主义视角对自然起源、变异的描述和社会文化视角对概念生成的分析结合在一起。

第二, 不同的抑郁症起源理论可以相互取长补短, 构建更具系统性的理论体系, 并为相应的实践干预模式提供指导。正因为讨论的层次不同, 目前的多数解释只是一些和抑郁症现象相关的零散推论和假说, 它们只能从已有研究中寻求间接的支持, 而较少产生可以通过科学方法进行检验的预测。不同视角的理论多少都能找到一些实证研究和统计数据的支持, 但同时其反对者又多少能够在其它研究中发现一些否定性的证据。导致这个问题的根源可能恰恰又要回到上一个问题, 即不同理论讨论的对象有时并不一致。在这种情况下, 各种理论的假说也许都有其正确性, 比如社会文化视角指出了当前根据一系列综合症定义的“抑郁症”也许根本就不是同一种现象或“疾病”, 进化适应视角指出了这种现象在人类种群中起源的合理性, 而功能失调视角则能说明群体中遗传下来的抑郁易感性如何导致个体层面上出现被认知为“抑郁症”的一系列症状。因此, 如果能在统一讨论对象的基础上, 以一个系统性的理论框架将不同视角的优势结合到一起, 或许能够进一步加深对抑郁症起源的认识。

The authors have declared that no competing interests exist.
作者已声明无竞争性利益关系。

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DSM-Ⅳ是使用最广泛的精神障碍诊断标准之一,但其中的躯体形式障碍诊断标准在临床实践中存在应用性低,标准模糊,分类重叠等问题。因此DSM-5针对这些问题将其修改为躯体症状障碍,删去医学无法解释症状的要求,增加心理标准,合并和简化亚型,以改善该诊断标准的临床应用。本文分析了DSM-5躯体症状障碍修订的主要内容和原因,并讨论了新标准在未来面临的问题和可能的进展。

陈子晨, 汪新建 . ( 2015).

躯体化的心身交互机制及其中的文化因素

心理科学进展, 23( 5), 849-857.

URL     [本文引用: 1]

基于神经生物学的心身交互作用是当前躯体化病理机制的一个研究重 点。在生理-心理的功能连续体中,认知学习、感觉监控、注意、记忆过程等都会影响躯体症状的呈现。文化则会通过这些过程塑造个体对症状的归因和解释,引发 躯体症状的呈现和扩大,最终通过不同文化特有的民族生理学模式形成具有文化特异性的疑病焦虑和医学无法解释症状。

靳宇倡, 丁美月 . ( 2017).

产后抑郁的预测因素及神经生理机制

心理科学进展, 25( 7), 1145-1161.

URL     [本文引用: 1]

产后抑郁是产后时期出现的抑郁症状,对女性及其后代甚至家人都会造成严重的负面影响。产后抑郁稳定的预测因素是遗传基因、依恋风格、童年负性生活经历和激素水平的变化;涉及的脑区和神经网络集中在前额叶皮层、扣带回、杏仁核和海马等脑区及相应神经网络。未来应在探索综合的预测模型、男性伴侣的对照试验和基于大脑可塑性特征的干预模式等方面展开深入研究。

凯博文 . ( 2008). 苦痛和疾病的社会根源: 现代中国的抑郁、神经衰弱和病痛 (郭金华译). 上海: 上海三联书店.

[本文引用: 1]

吕小康, 汪新建 . ( 2012).

意象思维与躯体化症状: 疾病表达的文化心理学途径

心理学报, 44( 2), 276-284.

URL     [本文引用: 1]

意象思维是中国人的传统思维模 式,它通过观物取象和取象比类的方式认知世界、推演联系。这种思维模式塑造了中国人特有的身心不分而非两分的身体观、疾病观和治疗观。在中国人的观念中, 身体不仅仅是一具生理躯体,还具有气、阴阳、五行等本土概念所体现的弥合物质与精神、联结生理与心理的模糊性与开放性。人们在表达疾病感觉时通常不分生理 与心理,任何一方面出现不适感觉即可认为自己生病,在面对心理医生时也倾向于同时报告躯体状况与心理感觉,从而使得临床报告出现较高的躯体化报告率。这正 是文化心理影响疾病表达的体现。这也使得疾病不仅是一种医学现象,也是一种文化现象;医学不仅需要生理知识,也需要人文知识。

吕小康, 汪新建 . ( 2013).

因果判定与躯体化: 精神病学标准化的医学社会学反思

社会学研究, ( 3), 29-46.

[本文引用: 1]

蒙杰, 位东涛, 王康程, 邱江 . ( 2016).

抑郁症的影像遗传学研究: 探索基因与环境的交互作用

心理科学, 39( 2), 490-496.

URL     [本文引用: 1]

抑郁症具有中等的遗传度。通过影像遗传学方法探讨抑郁相关基因的多态性对神经活动的影响,发现编码五羟色胺、促肾上腺素释放激素受体、多巴胺等神经递质或受体的基因多态性会影响杏仁核、前扣带等情绪加工脑区的功能或结构,且多数基因与压力生活经历发生交互作用。表明基因与环境的交互作用在抑郁症发病机理中扮演重要角色。未来的研究应拓展遗传和神经影像分析方法,重视环境因素的测量,通过整合遗传、神经影像及环境变量构建抑郁病理模型。

米歇尔·福柯. ( 2005). 古典时代疯狂史 (林志明译). 北京: 生活·读书·新知三联书店.

汤明明, 林文娟 . ( 2013).

缰核在抑郁症中的作用: 研究和治疗的新途径

心理科学进展, 21( 7), 1213-1219.

URL     [本文引用: 1]

缰核是哺乳动物神经系统中连接前脑和中脑的重要节点,这一古老的核团因其与抑郁症的密切联系,近来获得国内外研究者的关注.缰核接受来自边缘系统、基底神经节等的传入信号,向下投射到中脑5-羟色胺系统和多巴胺系统.在应激条件下缰核免疫活动增强,向下游的投射信号增强,以此调节单胺类递质释放,参与抑郁症的发病机制,并且参与抗抑郁治疗的起效途径.这些证据提示缰核在抑郁症中具有重要作用,将成为研究和治疗的新途径.未来研究应从缰核与上下游核团的神经联系、与丘脑-垂体-肾上腺轴的相互影响、以及与免疫激活的交互作用等方面进一步探索,为研究抑郁症病理机制和治疗方法提供线索.

汪新建, 陈子晨 . ( 2014).

“医学无法解释症状”的界定: 躯体化诊断的本土视角

南京师大学报(社会科学版), 60( 2), 110-116.

URL     [本文引用: 1]

医学无法解释症状是指无法通过实验医学的生理性病因进行合理解释的功能性躯体症状,也是躯体化等躯体性心理障碍诊断标准的核心条件之一。医学无法解释症状的界定及其历史变迁反映了西方医学体系中普通医学和精神病学的二元分裂。而从本土身心合一和整体医学观的视角看,医学专科的二元分裂并不是天然存在的。这种差异也成为躯体化诊断在中国产生不适应性的原因之一。

Aggarwal N. K., Cedeño K., Guarnaccia P., Kleinman A., & Lewis-Fernández R . ( 2016).

The meanings of cultural competence in mental health: An exploratory focus group study with patients, clinicians, and administrators

SpringerPlus, 5, 384.

URL     PMID:4814393      [本文引用: 1]

Cultural competence training is mandatory in the United States of America to alleviate minority health disparities though few studies have examined perceptions across stakeholders. We conducted separate focus groups with patients, clinicians, and administrators from the psychiatry department at one community hospital and compared responses to hospital policies. Stakeholders defined cultural competence through group-based or person-centered traits despite policies recommended person-centered approaches. Administrators and clinicians named clinician techniques for psycho-education whereas patients named these techniques for enlistment in treatment planning as equals. All groups named patient cultural views and institutional challenges as barriers to care, but only patients and administrators additionally named clinician biases as possible barriers. We discuss these discrepant perceptions and possible solutions to improve research, practice, and policy on cultural competence in mental health.

Allen, N. B., & Badcock, P. B. T . ( 2003).

The social risk hypothesis of depressed mood: Evolutionary, psychosocial, and neurobiological perspectives

Psychological Bulletin, 129( 6), 887-913.

URL     PMID:14599287      [本文引用: 2]

Abstract The authors hypothesize that depressed states evolved to minimize risk in social interactions in which individuals perceive that the ratio of their social value to others, and their social burden on others, is at a critically low level. When this ratio reaches a point where social value and social burden are approaching equivalence, the individual is in danger of exclusion from social contexts that, over the course of evolution, have been critical to fitness. Many features of depressed states can be understood in relation to mechanisms that reduce social risk in such circumstances, including (a) hyper-sensitivity to signals of social threat from others, (b) sending signals to others that reduce social risks, and (c) inhibiting risk-seeking (e.g., confident, acquisitive) behaviors. These features are discussed in terms of psychosocial and neurobiological research on depressive phenomena.

Allen, N. B., & Badcock, P. B. T . ( 2006).

Darwinian models of depression: A review of evolutionary accounts of mood and mood disorders

Progress in Neuro-Psychopharmacology and Biological Psychiatry, 30( 5), 815-826.

URL     PMID:16647176      [本文引用: 1]

Over the last ten years, there has been increased interest in the evolutionary origins of depressive phenomena. The current article provides a review of the major schools of thought that have emerged in this area. First, we consider important Darwinian explanations of depressed mood, including an integrative social risk hypothesis recently proposed by the authors. According to the social risk hypothesis, depression represents an adaptive response to the perceived threat of exclusion from important social relationships that, over the course of evolution, have been critical to maintaining an individual's fitness prospects. We argue, moreover, that in the ancestral environment, depression minimized the likelihood of exclusion by inducing: (i) cognitive hypersensitivity to indicators of social risk/threat; (ii) signaling behaviours that reduce social threat and elicit social support; and (iii) a generalized reduction in an individual's propensity to engage in risky, appetitive behaviours. Neurobiological support for this argument is also provided. Finally, we review three models that endeavour to explain the relationship between the adaptations that underlie depressed mood and clinically significant, depressed states, followed by a consideration of the merits of each.

American Psychiatric Association. ( 2013).

DSM-5: Diagnostic and statistical manual of mental disorders (fifth edition)

Washington, DC: American Psychiatric Association.

[本文引用: 1]

Andrews, P. W . ( 2006).

Parent-offspring conflict and cost-benefit analysis in adolescent suicidal behavior

Human Nature, 17( 2), 190-211.

URL     PMID:26181414      [本文引用: 1]

Data on birth order and parent-offspring relations for 1,601 adolescents participating in the National Longitudinal Study of Adolescent Health were used to test hypotheses about the role of adolescent suicidal behavior in parent-offspring conflict. Among adolescents highly dissatisfied with their mothers, the odds that middleborns would make at least one suicide attempt was 23% that of first- and lastborns (p<.001), but their odds of receiving medical treatment for their attempts was 8.5 times greater than the odds for first- and lastborns (p=.032). The results are tentatively interpreted as supporting the hypothesis that adolescents use suicide attempts to leverage investment from their parents.

Andrews, P. W., & Thomson. J. A . ( 2009).

The bright side of being blue: Depression as an adaptation for analyzing complex problems

Psychological Review, 116( 3), 620-654.

URL     PMID:2734449      [本文引用: 3]

Abstract Depression is the primary emotional condition for which help is sought. Depressed people often report persistent rumination, which involves analysis, and complex social problems in their lives. Analysis is often a useful approach for solving complex problems, but it requires slow, sustained processing, so disruption would interfere with problem solving. The analytical rumination hypothesis proposes that depression is an evolved response to complex problems, whose function is to minimize disruption and sustain analysis of those problems by (a) giving the triggering problem prioritized access to processing resources, (b) reducing the desire to engage in distracting activities (anhedonia), and (c) producing psychomotor changes that reduce exposure to distracting stimuli. As processing resources are limited, sustained analysis of the triggering problem reduces the ability to concentrate on other things. The hypothesis is supported by evidence from many levels-genes, neurotransmitters and their receptors, neurophysiology, neuroanatomy, neuroenergetics, pharmacology, cognition, behavior, and efficacy of treatments. In addition, the hypothesis provides explanations for puzzling findings in the depression literature, challenges the belief that serotonin transmission is low in depression, and has implications for treatment. Copyright (c) 2009 APA, all rights reserved.

Aubin H. J., Berlin I., & Kornreich C . ( 2013).

The evolutionary puzzle of suicide

International Journal of Environmental Research & Public Health, 10( 12), 6873-6886.

URL     PMID:24351787      [本文引用: 1]

Abstract Mechanisms of self-destruction are difficult to reconcile with evolution's first rule of thumb: survive and reproduce. However, evolutionary success ultimately depends on inclusive fitness. The altruistic suicide hypothesis posits that the presence of low reproductive potential and burdensomeness toward kin can increase the inclusive fitness payoff of self-removal. The bargaining hypothesis assumes that suicide attempts could function as an honest signal of need. The payoff may be positive if the suicidal person has a low reproductive potential. The parasite manipulation hypothesis is founded on the rodent-Toxoplasma gondii host-parasite model, in which the parasite induces a "suicidal" feline attraction that allows the parasite to complete its life cycle. Interestingly, latent infection by T. gondii has been shown to cause behavioral alterations in humans, including increased suicide attempts. Finally, we discuss how suicide risk factors can be understood as nonadaptive byproducts of evolved mechanisms that malfunction. Although most of the mechanisms proposed in this article are largely speculative, the hypotheses that we raise accept self-destructive behavior within the framework of evolutionary theory.

Baptista T., Aldana E., Angeles F., & Beaulieu S . ( 2008).

Evolution theory: An overview of its applications in psychiatry

Psychopathology, 41( 1), 17-27.

URL     PMID:17952017      [本文引用: 1]

Objectives: (1) Describe the concept, mechanisms and outcome of evolution; (2) review the current topics in research and clinical psychiatry where evolutionary concepts are explicitly applied. Methods: The authors reviewed relevant textbooks of evolution, evolutionary psychiatry/psychology and articles in scientific journals, and discussed these topics in a college course at McGill University School of Medicine, Montreal, Canada. Results: (1) Most natural scientists agree that evolution has occurred in all living beings. However, the mechanisms and outcomes of evolution are controversial. (2) In the first three quarters of the 20th century, several authors provided theories about human psychology based on ethological concepts. The so-called evolutionary psychology/psychiatry developed more recently, and it explores the adaptive/nonadaptive features of psychopathology and mental disorders. In the 1990s a concept of mental disorder (as a harmful dysfunction) based on evolutionary theory has been developed. Conclusions: Evolution is a pivotal concept in biology with relevant applications in psychiatry. We suggest encouraging the interaction between psychiatric educators and researchers in evolutionary psychiatry and biology in order to improve the education of psychiatric residents in this subject.

Barbic S. P., Durisko Z., & Andrews P. W . ( 2014).

Measuring the bright side of being blue: A new tool for assessing analytical rumination in depression

PLoS One, 9( 11), e112077.

URL     PMID:25397902      [本文引用: 1]

Background Diagnosis and management of depression occurs frequently in the primary care setting. Current diagnostic and management of treatment practices across clinical populations focus on eliminating signs and symptoms of depression. However, there is debate that some interventions may pathologize normal, adaptive responses to stressors. Analytical rumination (AR) is an example of an adaptive response of depression that is characterized by enhanced cognitive function to help an individual focus on, analyze, and solve problems. To date, research on AR has been hampered by the lack of theoretically-derived and psychometrically sound instruments. This study developed and tested a clinically meaningful measure of AR. Methods Using expert panels and an extensive literature review, we developed a conceptual framework for AR and 22 candidate items. Items were field tested to 579 young adults; 140 of whom completed the items at a second time point. We used Rasch measurement methods to construct and test the item set; and traditional psychometric analyses to compare items to existing rating scales. Results Data were high quality (<1% missing; high reliability: Cronbach's alpha = 0.92, test-retest intraclass correlations >0.81; evidence for divergent validity). Evidence of misfit for 2 items suggested that a 20-item scale with 4-point response categories best captured the concept of AR, fitting the Rasch model (2 = 95.26; df = 76, p = 0.07), with high reliability (rp = 0.86), ordered response scale structure, and no item bias (gender, age, time). Conclusion Our study provides evidence for a 20-item Analytical Rumination Questionnaire (ARQ) that can be used to quantify AR in adults who experience symptoms of depression. The ARQ is psychometrically robust and a clinically useful tool for the assessment and improvement of depression in the primary care setting. Future work is needed to establish the validity of this measure in people with major depression.

Brody G. H., Chen Y. F., Beach S. R. H., Philibert R. A., & Kogan S. M . ( 2009).

Participation in a family-centered prevention program decreases genetic risk for adolescents' risky behaviors

Pediatrics, 124( 3), 911-917.

URL     PMID:19706565      [本文引用: 1]

OBJECTIVE: The present research addressed the following important question in pediatric medicine: can participation in an efficacious preventive intervention ameliorate the risk that a genetic vulnerability factor is hypothesized to confer on increases in risk behaviors across preadolescence? METHODS: As part of the Strong African American Families preventive intervention study, data were collected from 641 black families in rural Georgia, assigned randomly to the prevention or control condition. The prevention condition consisted of 7 consecutive meetings at community facilities, with separate parent and youth skill-building curricula and a family curriculum. Each meeting included separate, concurrent sessions for parents and youths, followed by a joint parent-youth session in which families practiced skills they learned in the separate sessions. Involvement in risk behaviors was assessed when the youths were 11 (pretest), 12 (posttest), and 14 (long-term follow-up) years of age. A genetic vulnerability factor, that is, a variable-nucleotide repeat polymorphism in the promoter region of the SLC6A4 gene (5HTT), was assessed 2 years after the long-term follow-up assessment. RESULTS: Youths at genetic risk who were assigned to the control condition displayed greater increases in risk behaviors across the 29 months that separated the pretest and long-term follow-up assessments, compared with youths at genetic risk who were assigned to the Strong African American Families condition and youths without genetic risk who were assigned to either condition. CONCLUSION: This is the first study to demonstrate that participation in an efficacious preventive intervention can ameliorate a genetic risk for increasing involvement in health-compromising risk behaviors across preadolescence.

Brooks C., Pearce N., & Douwes J . ( 2013).

The hygiene hypothesis in allergy and asthma: An update

Current Opinion in Allergy & Clinical Immunology, 13( 1), 70-77.

URL     PMID:23103806      [本文引用: 1]

Purpose of review;It has been hypothesized that increased cleanliness, reduced family size, and subsequent decreased microbial exposure could explain the increases in global asthma prevalence. This review considers the recent evidence for and against the 'hygiene hypothesis'.Recent findings;Recent evidence does not provide unequivocal support for the hygiene hypothesis: the hygiene hypothesis specifically relates to atopic asthma, but some of the protective effects (e. g. farm exposures) appear to apply to both atopic and nonatopic asthma; asthma prevalence has begun to decline in some western countries, but there is little evidence that they have become less clean; Latin American countries with high infection rates have high asthma prevalence and the hygiene hypothesis relates to early-life exposures, but exposures throughout life may be important.Summary;There is a considerable body of evidence which warrants scepticism about the hygiene hypothesis. However, these anomalies contradict the 'narrow' version of it in which microbial pressure early in life protects against atopic asthma by suppressing T-helper 2 immune responses. It is possible that a more general version of the hygiene hypothesis is still valid, but the aetiologic mechanisms involved are currently unclear.

de Jonge P., Wardenaar K. J., & Wichers M . ( 2015).

What kind of thing is depression?

Epidemiology and Psychiatric Sciences, 24( 4), 312-314.

URL     PMID:25864453      [本文引用: 1]

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Di Rienzo, A., & Hudson, R. R . ( 2005).

An evolutionary framework for common diseases: The ancestral-susceptibility model

Trends in Genetics, 21( 11), 596-601.

URL     PMID:16153740      [本文引用: 1]

Unlike rare mendelian diseases, which are due to new mutations (i.e. derived alleles), several alleles that increase the risk to common diseases are ancestral. Moreover, population genetics studies suggest that some derived alleles that protect against common diseases became advantageous recently. These observations can be explained within an evolutionary framework in which ancestral alleles reflect ancient adaptations to the lifestyle of ancient human populations, whereas the derived alleles were deleterious. However, with the shift in environment and lifestyle, the ancestral alleles now increase the risk of common diseases in modern populations. In this article, we develop an explicit evolutionary model and use population genetics simulations to investigate the expected haplotype structure and type of disease-association signals of ancestral risk alleles.

Donaldson, C., & Lam, D. (2004).

Rumination, mood and social problem-solving in major depression

Psychological Medicine, 34( 7), 1309-1318.

URL     PMID:15697057      [本文引用: 1]

Ruminating when depressed is thought to lower mood and impair problem-solving, while distraction is thought to alleviate mood and assist problem-solving. The present study investigates each of these proposals using both naturally occurring and experimentally induced rumination and distraction in a sample of patients with major depression.Thirty-six patients with major depression and 36 control participants were randomly allocated to either a rumination or distraction induction condition. Levels of trait rumination and distraction were measured at baseline, mood and problem-solving were measured before and after the inductions.In terms of trait measures, depressed patients with higher levels of trait rumination reported poorer mood and gave less effective problem solutions than those who were less ruminative. Trait distraction was not associated with mood or problem-solving. In terms of induced responses, depressed patients who were made to ruminate experienced a deterioration in their mood and gave poorer problem solutions. For those receiving the distraction induction, mood improved in all patients and problem-solving improved in patients who were not naturally ruminating at a high level. Neither induction had an impact on mood or problem-solving in control participants.Treatment for depression associated with adverse life events may need to target rumination as well as problem-solving deficits if interventions are to be effective. The differential effects of self-applied versus experimentally induced distraction require further investigation. Future research will need to consider that high levels of trait rumination may interfere with the impact of experimental inductions.

Drysdale A. T., Grosenick L., Downar J., Dunlop K., Mansouri F., Meng Y., … Liston C . ( 2017).

Resting-state connectivity biomarkers define neurophysiological subtypes of depression

Nature Medicine, 23( 1), 28-38.

URL     PMID:5624035      [本文引用: 1]

Using functional MRI in a large multisite sample of more that 1,000 patients, four distinct neurophysiological biotypes of depression are defined. These biotypes are used to develop diagnostic classifiers that distinguish patients with depression from controls in separate multisite validation and replication cohorts, and can predict patient responsiveness to therapy.

Durisko Z., Mulsant B. H., & Andrews P. W . ( 2015).

An adaptationist perspective on the etiology of depression

Journal of Affective Disorders, 172, 315-323.

URL     PMID:25451432      [本文引用: 1]

Major depressive disorder (MDD) presents with a variety of symptoms and responds to a wide range of treatment interventions. Diagnostic criteria collapse multiple syndromes with distinct etiologies into the same disorder. MDD is typically understood as a malfunction of neurotransmission or brain circuitry regulating mood, pleasure and reward, or executive function. However, research from an evolutionary perspective suggests that the - ormal functioning of adaptations may also generate symptoms meeting diagnostic criteria. Functioning adaptations may be an underappreciated etiological pathway to MDD. Many adaptive functions for depressive symptoms have been suggested: biasing cognition to avoid losses, conserving energy, disengaging from unobtainable goals, signaling submission, soliciting resources, and promoting analytical thinking. We review the potential role of these adaptive functions and how they can lead to specific clusters of depressive symptoms. Understanding MDD from such a perspective reduces the heterogeneity of cases and may help to select the best intervention for each patient. We discuss the implications of different adaptive and maladaptive etiological pathways for the use of antidepressants and various modes of psychotherapy. In particular, instances of MDD caused by functioning adaptations may benefit most from treatments that support the adaptive function, or that target the precipitating causal stressor. We conclude that an evolutionary approach to the study of MDD may be one of the more promising approaches to reduce its heterogeneity and to better match patients and treatment.

Ellis, B. J., & Boyce, W. T . ( 2008).

Biological sensitivity to context

Current Directions in Psychological Science, 17( 3), 183-187.

URL     [本文引用: 1]

Ellis, B. J., & Boyce, W. T . ( 2011).

Differential susceptibility to the environment: Toward an understanding of sensitivity to developmental experiences and context

Development and Psychopathology, 23( 1), 1-5.

URL     PMID:21262035      [本文引用: 1]

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Felger, J. C., & Lotrich, F. E . ( 2013).

Inflammatory cytokines in depression: Neurobiological mechanisms and therapeutic implications

Neuroscience, 246, 199-229.

URL     PMID:3741070      [本文引用: 1]

Abstract Mounting evidence indicates that inflammatory cytokines contribute to the development of depression in both medically ill and medically healthy individuals. Cytokines are important for development and normal brain function, and have the ability to influence neurocircuitry and neurotransmitter systems to produce behavioral alterations. Acutely, inflammatory cytokine administration or activation of the innate immune system produces adaptive behavioral responses that promote conservation of energy to combat infection or recovery from injury. However, chronic exposure to elevated inflammatory cytokines and persistent alterations in neurotransmitter systems can lead to neuropsychiatric disorders and depression. Mechanisms of cytokine behavioral effects involve activation of inflammatory signaling pathways in the brain that results in changes in monoamine, glutamate, and neuropeptide systems, and decreases in growth factors, such as brain-derived neurotrophic factor. Furthermore, inflammatory cytokines may serve as mediators of both environmental (e.g. childhood trauma, obesity, stress, and poor sleep) and genetic (functional gene polymorphisms) factors that contribute to depression's development. This review explores the idea that specific gene polymorphisms and neurotransmitter systems can confer protection from or vulnerability to specific symptom dimensions of cytokine-related depression. Additionally, potential therapeutic strategies that target inflammatory cytokine signaling or the consequences of cytokines on neurotransmitter systems in the brain to prevent or reverse cytokine effects on behavior are discussed. Copyright 2013 IBRO. Published by Elsevier Ltd. All rights reserved.

Fluge Ø., Mella O., Bruland O., Risa K., Dyrstad S. E., Alme K., … Tronstad K. J . ( 2016).

Metabolic profiling indicates impaired pyruvate dehydrogenase function in myalgic encephalopathy/chronic fatigue syndrome

The Journal of Clinical Investigation Insight, 1( 21), e89376.

URL     PMID:28018972      [本文引用: 1]

Abstract Myalgic encephalopathy/chronic fatigue syndrome (ME/CFS) is a debilitating disease of unknown etiology, with hallmark symptoms including postexertional malaise and poor recovery. Metabolic dysfunction is a plausible contributing factor. We hypothesized that changes in serum amino acids may disclose specific defects in energy metabolism in ME/CFS. Analysis in 200 ME/CFS patients and 102 healthy individuals showed a specific reduction of amino acids that fuel oxidative metabolism via the TCA cycle, mainly in female ME/CFS patients. Serum 3-methylhistidine, a marker of endogenous protein catabolism, was significantly increased in male patients. The amino acid pattern suggested functional impairment of pyruvate dehydrogenase (PDH), supported by increased mRNA expression of the inhibitory PDH kinases 1, 2, and 4; sirtuin 4; and PPAR未 in peripheral blood mononuclear cells from both sexes. Myoblasts grown in presence of serum from patients with severe ME/CFS showed metabolic adaptations, including increased mitochondrial respiration and excessive lactate secretion. The amino acid changes could not be explained by symptom severity, disease duration, age, BMI, or physical activity level among patients. These findings are in agreement with the clinical disease presentation of ME/CFS, with inadequate ATP generation by oxidative phosphorylation and excessive lactate generation upon exertion.

Foster, J. A., & Neufeld, K. A. M . ( 2013).

Gut-brain axis: How the microbiome influences anxiety and depression

Trends in Neurosciences, 36, 305-312.

URL     [本文引用: 1]

Frances, A. (2013).

The new crisis of confidence in psychiatric diagnosis

Annals of Internal Medicine, 159 ( 10), 720.

URL     PMID:24247686      [本文引用: 2]

The American Psychiatric Association has released the long-awaited fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). This commentary notes that the DSM-5 "introduced several high-prevalence diagnoses at the fuzzy boundary with normality" and recommends that "physicians ... use the DSM-5 cautiously, if at all."

Fumagalli M., Sironi M., Pozzoli U., Ferrer-Admettla A., Pattini L., & Nielsen R . ( 2011).

Signatures of environmental genetic adaptation pinpoint pathogens as the main selective pressure through human evolution

PLoS Genetics, 7( 11), e1002355.

URL     [本文引用: 1]

Gage, T. B . ( 2002).

Birth-weight-specific infant and neonatal mortality: Effects of heterogeneity in the birth cohort

Human Biology, 74( 2), 165-184.

URL     [本文引用: 1]

Gilbert, P. (2006).

Evolution and depression: Issues and implications

Psychological Medicine, 36( 3), 287-297.

URL     PMID:16236231      [本文引用: 1]

Abstract Depression is well recognized to be rooted in the down-regulation of positive affect systems. This paper reviews some of the social and non-social theories that seek to explain the potential adaptive advantages of being able to tone down positive affect, and how dysfunctions in such affect control can occur in some contexts. Common to most evolutionary theories of depression is the view that loss of control over aversive events and/or major resources/rewards exert downward pressure on positive affect. Social theories, however, suggest that it is loss of control over the social environment that is particularly depressogenic. Two evolutionary theories (the attachment-loss, and the defeat-loss theories) are briefly reviewed and their interaction considered. It is suggested that phenotypes for toning down positive affect, in the face of loss of control, may become more severe in the context of socially hostile, unsupportive and/or excessively competitive environments. The paper briefly considers how human competencies for self-evaluation in relation to others, rumination, self-criticism, and modern social contexts can accentuate dysfunctional expressions of affect regulation.

Hagen, E. H . ( 1999).

The functions of postpartum depression

Evolution & Human Behavior, 20( 5), 325-359.

[本文引用: 1]

Hagen, E. H . ( 2002).

Depression as bargaining: The case postpartum

Evolution & Human Behavior, 23( 5), 323-336.

URL     [本文引用: 1]

It was recently hypothesized that depression might function, in part, as a bargaining strategy when cooperation imposes a net cost, but there are social constraints on defection [Evol. Hum. Behav. 20 (1999) 325.]. If so, such social constraints should be associated with depression, and depression in one partner should be associated with increased investment by other partners. Several predictions of this hypothesis were tested using postpartum depression (PPD) as a model for depression in general. The depression levels, abortion attitudes, additional mating opportunities, and investment in childrearing of 240 mothers and fathers with a new child were measured using self-report instruments. Mothers were also asked whether the new child was planned and whether it was wanted. Perceived constraints on abortion correlated significantly with PPD levels, but, as predicted, only for mothers with an unplanned or unwanted child. Contrary to predictions, perceived constraints imposed by family and friends did not correlate with PPD levels. Sexual opportunities correlated significantly with PPD levels, but, as predicted, only for men. As predicted, PPD levels in one spouse correlated significantly with increased investment in childrearing as reported by the other spouse. PPD levels correlated positively with parity for older women with few future reproductive opportunities, as predicted.

Hagen, E. H . ( 2011).

Evolutionary theories of depression: A critical review

Canadian Journal of Psychiatry, 56( 12), 716-726.

URL     [本文引用: 1]

Hilt L. M., Sander L. C., Nolen-Hoeksema S., & Simen A. A . ( 2007).

The BDNF Val66met polymorphism predicts rumination and depression differently in young adolescent girls and their mothers

Neuroscience Letters, 429( 1), 12-16.

URL     PMID:17959306      [本文引用: 1]

A single nucleotide polymorphism (SNP) in the brain-derived neurotrophic factor (BDNF) gene Val66Met has been associated with depression. However, the relationship between this SNP and depression has been mixed, especially when comparing studies of child and adult depression. We examined whether Val66Met would predict depression differentially in mothers versus their daughters. We also examined whether rumination, the tendency to brood and repetitively think about negative information, might serve as a mediator in the path between genotype and depressive symptoms. Participants included 200 individuals (100 mother-aughter pairs) from a high-risk population. The BDNF Val66Met polymorphism was examined in DNA samples from the mothers and daughters, and measures of depressive symptoms and rumination were also obtained. Among the young adolescent girls (ages 10-14), the Val/Val genotype was associated with more depressive symptoms and higher rumination scores compared to the Val/Met genotype. Furthermore, rumination mediated the relationship between genotype and depressive symptoms. However, in the mothers with adult-onset depression the Val/Met genotype was associated with more depressive symptoms, and rumination again mediated the relationship between genotype and depression. Rumination may be an endophenotype in the pathway from the BDNF Val66Met polymorphism to depression. Future work should further explore this mechanism and pursue explanations for its effects at different times in development.

Houle, D. (1998).

How should we explain variation in the genetic variance of traits?

Genetica, 102-103, 241-253.

URL     PMID:9720283      [本文引用: 1]

Recent work has called attention to large differences among traits in the amount of standardized genetic variance they possess. There are four general factors which could play a role in causing this variation: mutation, elimination of deleterious variation, selection of favorable alleles, and balancing selection. Three factors could directly influence the mutational variability of traits: canalization, the mutational target size, and the timing of trait expression. Here I carry out simple tests of the importance of some of these factors using data from Drosophila melanogaster. I compiled information from the literature on the mutational and standing genetic variances in outbred populations, inferred the relative mutational target size of each trait, its a timing of expression, and used models of life history to calculate fitness sensitivities for each trait. Mutation variation seems to play an important role, as it is highly correlated with standing variance. The target size hypothesis was supported by a significant correlation between mutational variance and inferred target size. There was also a significant relationship between the timing of trait expression and mutational variance. These hypotheses are confounded by a correlation between timing and target size. The elimination and canalization hypotheses were not supported by these data, suggesting that they play a quantitatively less important role in determining overall variances. Additional information concerning the pleiotropic consequences of mutations would help to validate the fitness sensitivities used to test the elimination and canalization hypotheses.

Insel, T. R . ( 2014).

The NIMH research domain criteria (RDoC) project: Precision medicine for psychiatry

American Journal of Psychiatry, 171( 4), 395-397.

URL     [本文引用: 1]

Jackson, S. W . ( 2008).

A history of melancholia and depression

In E. R. Wallace & J. Gach (Eds.). History of psychiatry and medical psychology(pp. 443-460). New York: Springer.

URL     [本文引用: 1]

In the terms melancholia and depression and their cognates, we have well over two millennia of the Western world’s ways of referring to a goodly number of different dejected states. At any particular

Kamenov K., Cabello M., Coenen M., & Ayuso-Mateos J. L . ( 2015).

How much do we know about the functional effectiveness of interventions for depression? A systematic review

Journal of Affective Disorders, 188, 89-96.

URL     PMID:26344753      [本文引用: 1]

Abstract BACKGROUND: Functional difficulties are determined as one of the reasons for the public health priority given to depression. However, previous literature shows that the evidence on treatment effectiveness in depression does not reflect all relevant functional areas affected. This paper aimed to review recent literature and identify which areas are addressed and what are the gaps in the measurement of treatment effectiveness in depression. METHODS: Electronic search was performed in PsycINFO, PubMed, Web of science, and the Cochrane Central Register of Controlled Trials. A content item analysis of outcome measures was performed. RESULTS: Two hundred and fourty-seven studies were included. The functional areas addressed in the measurement process did not vary across studies assessing psychotherapeutic, pharmacological or alternative interventions. The content analysis revealed that 80% of the areas covered by instruments represented symptomatology. Many functional areas were insufficiently covered, whereas others like handling stress, solving problems, maintaining daily routine, problems in education, or participation in community, political or religious life were not addressed at all. LIMITATIONS: Only articles in English were included and the time frame was limited. CONCLUSIONS: More than 10 years after the first global burden of disease studies have been published evidence on the treatment effectiveness in depression is still based primarily on symptoms. Many important functional areas remain unexplored. Consequently the effectiveness of well recognized interventions might be overestimated. Future steps should include use of comprehensive tools, provision of detailed information on functional areas instead of global scores of instruments, and design of functional impairment oriented therapies. Copyright 2015 Elsevier B.V. All rights reserved.

Keller, M. C., & Miller, G. (2006).

Resolving the paradox of common, harmful, heritable mental disorders: Which evolutionary genetic models work best?

Behavioral & Brain Sciences, 29( 4), 405-452.

[本文引用: 2]

Keller, M. C., & Nesse, R. M . ( 2005).

Is low mood an adaptation? Evidence for subtypes with symptoms that match precipitants

Journal of Affective Disorders, 86( 1), 27-35.

URL     PMID:15820268      [本文引用: 1]

Abstract BACKGROUND: Although severe depression is dysfunctional, the capacity to experience normal low mood may be useful in certain fitness-threatening situations. Moreover, if specific kinds of situations recurred often enough in the course of evolution, natural selection may have shaped partially differentiated subtypes of low mood that are parallel to the subtypes of anxiety that protect against different kinds of danger. To test this hypothesis, we examined how symptoms of low mood differ depending upon the precipitating situation, and whether these differences match expectations of symptoms useful in each kind of situation. METHOD: 337 subjects who experienced a period of low mood within the last year wrote accounts describing perceived causes of their low mood and they filled out the CES-D depression inventory. Seven symptom scales were derived from analysis of CES-D data. Independent judges blindly coded the accounts into one of six precipitant categories. RESULTS: Different untoward situations were associated with different symptoms that were predicted to be useful in those situations. Social losses (death of a loved one, romantic breakups, and social isolation) were associated with greater crying and arousal. Failure to reach a goal, stress, and winter seasons were associated with more fatigue and pessimism. DISCUSSION: These results suggest that natural selection shaped not only a generic state of low mood but also partially differentiated subtypes shaped to cope with specific situations that were associated with fitness losses among our ancestors.

Kleinman, A. (1982).

Neurasthenia and depression: A study of somatization and culture in China

Culture, Medicine and Psychiatry, 6( 2), 117-190.

URL     PMID:7116909      [本文引用: 1]

The author reviews conceptual and empirical issues regarding the interaction of neurasthenia, somatization and depression in Chinese culture and in the West. The historical background of neurasthenia and its current status are discussed, along with the epidemiology and phenomenology of somatization and depression. Findings are presented from a combined clinical and anthropological field study of 100 patients with neurasthenia in the Psychiatry Outpatient Clinic at the Hunan Medical College. Eighty-seven of these patients made the DSM-III criteria of Major Depressive Disorder; diagnoses of anxiety disorders were also frequent. Forty-four patients were suffering from chronic pain syndromes previously undiagnosed, and cases of culture-bound syndromes also were detected. For three-quarters of patients the social significances and uses of their illness behavior chiefly related to work. Although from the researchers' perspective 70% of patients with Major Depressive Disorder experienced substantial improvement and 87% some improvement in symptoms when treated with antidepressant medication, fewer experienced decreased help seeking, and a much smaller number perceived less social impairment and improvement in illnes problems (the psychosocial accompaniment of disease including maladaptive coping and work, family and school problems). These findings are drawn on to advance medical anthropology and cultural psychiatry theory and research regarding somatization in Chinese culture, the United States and cross culturally. The author concludes that though neurasthenia can be understood in several distinctive ways, it is most clinically useful to regard it as bioculturally patterned illness experience (a special form of somatization) related to either depression and other diseases or to culturally sanctioned idioms of distress and psychosocial coping.

Kohrt B. A., Mendenhall E., & Brown P. J . ( 2016).

How anthropological theory and methods can advance global mental health

The Lancet Psychiatry, 3( 5), 396-398.

URL     PMID:27155506      [本文引用: 1]

The following article identifies new areas for engaged medical anthropological research on health insurance in low- and middle-income countries (LMICs). Based on a review of the literature and pilot research, we identify gaps in how insurance is understood, administered, used, and abused. We provide a historical overview of insurance as an emerging global health panacea and then offer brief assessments of three high-profile attempts to provide universal health coverage. Considerable research on health insurance in LMICs has been quantitative and focused on a limited set of outcomes. To advance the field, we identify eight productive areas for future ethnographic research that will add depth to our understanding of the social life and impact of health insurance in LMICs. Anthropologists can provide unique insights into shifting health and financial practices that accompany insurance coverage, while documenting insurance programs as they evolve and respond to contingencies.

Kuah-Pearce K. E., Kleinman A., & Harrison E . ( 2014).

Social suffering and the culture of compassion in a morally divided China

Anthropology & Medicine, 21( 1), 1-7.

URL     PMID:24524752      [本文引用: 1]

Abstract This collection of essays opens a critical examination of compassionate acts responding to social suffering in the intensely complex moral context of a rapidly changing and globalizing China. Jeanne Shea describes self-compassion among older women in China as a post-revolutionary response to changing opportunities and resistance to consumerism. Khun Eng Kuah-Pearce's essay frames the Buddhist organizations as NGOs and shows compassion being mobilized and its acts being spiritual-philanthropic, not political. The next three papers illuminate the complexity of mobility in a moral sea of changing values. Even as modernity facilitates movement of people away from suffering, the grinding of entangled moral experiences within the mobile group can be the cause of suffering. Shu-Min Huang critiques 'cultural petrification' as the diasporic Yunnan Chinese community in Thailand attempt to preserve the cultural forms and procedures of the world they left behind. Likewise, Richard Madsen shows that the idea of a universalized cultural heritage fails in the face of the 'micro-ecologies'. And yet the modern impulse to universalize beyond China has important implications for transnational compassion and cooperation. The work of the humanitarian organization M decins Sans Fronti res in China, discussed by Kuah-Pearce and Guiheux, challenges the universality of global humanitarian actions. Following the series of essays threaded across intersections of compassion, suffering, and a morally-divided China, the collection closes by looking at the West. Iain Wilkinson discusses the origins of social suffering as a focus of the social sciences, as well as the difficulties of making engaged compassion its task in a morally-divided world.

Kupferberg A., Hager O. M., Fischbacher U., Brändle L. S., Haynes M., & Hasler G . ( 2016).

Testing the social competition hypothesis of depression using a simple economic game

The British Journal of Psychiatry Open, 2( 2), 163-169.

URL     PMID:27703769      [本文引用: 1]

Price’s social competition hypothesis interprets the depressive state as an unconscious, involuntary losing strategy, which enables individuals to yield and accept defeat in competitive situations. We investigated whether patients who suffer from major depressive disorder (MDD) would avoid competition more often than either patients suffering from borderline personality disorder (BPD) or healthy controls. In a simple paper-folding task healthy participants and patiens with MDD and BPD were matched with two opponents, one with an unknown diagnosis and one who shared their clinical diagnosis, and they had to choose either a competitive or cooperative payment scheme for task completion. When playing against an unknown opponent, but not the opponent with the same diagnosis, the patients with depression chose the competitive payment scheme statistically less often than healthy controls and patients diagnosed with BPD. The competition avoidance against the unknown opponent is consistent with Price’s social competition hypothesis. G.H. received research support, consulting fees and speaker honoraria from Lundbeck, AstraZeneca, Servier, Eli Lilly, Roche and Novartis. 08 The Royal College of Psychiatrists 2016. This is an open access article distributed under the terms of the Creative Commons Non-Commercial, No Derivatives (CC BY-NC-ND) licence.

Lee L., Harkness K. L., Sabbagh M. A., & Jacobson J. A . ( 2005).

Mental state decoding abilities in clinical depression

Journal of Affective Disorders, 86( 2-3), 247-258.

URL     [本文引用: 1]

Lerner J. S., Li Y., Valdesolo P., & Kassam K. S . ( 2015).

Emotion and decision making

Annual Review of Psychology, 66( 1), 799-823.

URL     [本文引用: 1]

Liu R. T., Alloy L. B., Mastin B. M., Choi J. Y., Boland E. M., & Jenkins A . ( 2014).

Vulnerability-specific stress generation: An examination of depressogenic cognitive vulnerability across multiple domains

Anxiety Stress & Coping, 27( 6), 695-711.

URL     PMID:24679143      [本文引用: 1]

Abstract BACKGROUND AND OBJECTIVES: Although there is supporting evidence for the stress generation hypothesis (i.e., the tendency for depression-prone individuals to experience more negative dependent events influenced by their behaviors and characteristics), additional research is required to advance current understanding of the specific types of dependent events relevant to this effect. The present study elaborated on the stress generation hypothesis, in which the content of negative dependent events experienced by individuals is contingent upon, and matches, the nature of their particular vulnerabilities. This extension was tested within the context of Cole's competency-based model of depression. DESIGN: Participants (n=185) were assessed at two time-points separated by a four-month interval. METHODS: Self-perceived competence in academic, social, and appearance domains at the initial time-point were examined in relation to negative life events prospectively occurring over the four-month follow-up period, assessed using the "contextual threat" method. RESULTS: Partial support was obtained for vulnerability-specific stress generation. Stress-generation specificity was found for self-perceived competence in appearance and academic domains, but not for self-perceived social competence. CONCLUSIONS: The current findings are consistent with the possibility of a more complex relation between self-perceived social competence and domain-congruent stress generation. Individuals may be more likely to experience negative dependent events in domains matching their specific vulnerabilities.

Maes M., Yirmyia R., Noraberg J., Brene S., Hibbeln J., Perini G., … Maj M . ( 2009).

The inflammatory & neurodegenerative (I&ND) hypothesis of depression: Leads for future research and new drug developments in depression

Metabolic Brain Disease, 24( 1), 27-53.

URL     [本文引用: 1]

Messay B., Lim A., & Marsland A. L . ( 2012).

Current understanding of the bi-directional relationship of major depression with inflammation

Biology of Mood & Anxiety Disorders, 2, 4.

URL     PMID:3384230      [本文引用: 1]

Consistent evidence links major depression and its affective components to negative health outcomes. Although the pathways of these effects are likely complex and multifactorial, recent evidence suggests that innate inflammatory processes may play a role. An overview of current literature suggests that pathways between negative moods and inflammation are bi-directional. Indeed, negative moods activate peripheral physiologic mechanisms that result in an up regulation of systemic levels of inflammation. Conversely, peripheral inflammatory mediators signal the brain to affect behavioral, affective and cognitive changes that are consistent with symptoms of major depressive disorder. It is likely that these pathways are part of a complex feedback loop that involves the nervous, endocrine, and immune systems and plays a role in the modulation of peripheral inflammatory responses to central and peripheral stimuli, in central responses to peripheral immune activation and in the maintenance of homeostatic balance. Further research is warranted to fully understand the role of central processes in this feedback loop, which likely contributes to the pathophysiology of mental and physical health.

Mezulis A. H., Hyde J. S., & Abramson L. Y . ( 2006).

The developmental origins of cognitive vulnerability to depression: Temperament, parenting, and negative life events in childhood as contributors to negative cognitive style

Developmental Psychology, 42( 6), 1012-1025.

URL     PMID:17087538      [本文引用: 1]

Cognitive models of depression have been well supported with adults, but the developmental origins of cognitive vulnerability are not well understood. The authors hypothesized that temperament, parenting, and negative life events in childhood would contribute to the development of cognitive style, with withdrawal negativity and negative parental feedback moderating the effects of negative life events to predict more depressogenic cognitive styles. These constructs were assessed in 289 children and their parents followed longitudinally from infancy to 5th grade; a subsample (n = 120) also participated in a behavioral task in which maternal feedback to child failure was observed. Results indicated that greater withdrawal negativity in interaction with negative life events was associated with more negative cognitive styles. Self-reported maternal anger expression and observed negative maternal feedback to child's failure significantly interacted with child's negative events to predict

Miller, A. H., & Raison, C. L . ( 2016).

The role of inflammation in depression: From evolutionary imperative to modern treatment target

Nature Reviews Immunology, 16( 1), 22-34.

URL     [本文引用: 2]

Nagy-Szakal D., Williams B. L., Mishra N., Che X. Y., Lee B., Bateman L., … Lipkin W. I . ( 2017).

Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome

Microbiome, 5( 1), 44.

URL     PMID:28441964      [本文引用: 1]

Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is characterized by unexplained persistent fatigue, commonly accompanied by cognitive dysfunction, sleeping disturbances, orthostatic intolerance, fever, lymphadenopathy, and irritable bowel syndrome (IBS). The extent to which the gastrointestinal microbiome and peripheral inflammation are associated with ME/CFS remains unclear. We pursued rigorous clinical characterization, fecal bacterial metagenomics, and plasma immune molecule analyses in 50 ME/CFS patients and 50 healthy controls frequency-matched for age, sex, race/ethnicity, geographic site, and season of sampling. Results: Topological analysis revealed associations between IBS co-morbidity, body mass index, fecal bacterial composition, and bacterial metabolic pathways but not plasma immune molecules. IBS co-morbidity was the strongest driving factor in the separation of topological networks based on bacterial profiles and metabolic pathways. Predictive selection models based on bacterial profiles supported findings from topological analyses indicating that ME/CFS subgroups, defined by IBS status, could be distinguished from control subjects with high predictive accuracy. Bacterial taxa predictive of ME/CFS patients with IBS were distinct from taxa associated with ME/CFS patients without IBS. Increased abundance of unclassified Alistipes and decreased Faecalibacterium emerged as the top biomarkers of ME/CFS with IBS; while increased unclassified Bacteroides abundance and decreased Bacteroides vulgatus were the top biomarkers of ME/CFS without IBS. Despite findings of differences in bacterial taxa and metabolic pathways defining ME/CFS subgroups, decreased metabolic pathways associated with unsaturated fatty acid biosynthesis and increased atrazine degradation pathways were independent of IBS co-morbidity. Increased vitamin B6 biosynthesis/salvage and pyrimidine ribonucleoside degradation were the top metabolic pathways in ME/CFS without IBS as well as in the total ME/CFS cohort. In ME/CFS subgroups, symptom severity measures including pain, fatigue, and reduced motivation were correlated with the abundance of distinct bacterial taxa and metabolic pathways. Conclusions: Independent of IBS, ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity. However, our findings indicate that dysbiotic features that are uniquely ME/CFS-associated may be masked by disturbances arising from the high prevalence of IBS co-morbidity in ME/CFS. These insights may enable more accurate diagnosis and lead to insights that inform the development of specific therapeutic strategies in ME/CFS subgroups. Electronic supplementary material The online version of this article (doi:10.1186/s40168-017-0261-y) contains supplementary material, which is available to authorized users.

Napier A. D., Ancarno C., Butler B., Calabrese J., Chater A., Chatterjee H., .. Woolf K . ( 2014).

Culture and health

The Lancet, 384( 9954), 1607-1639.

URL     [本文引用: 1]

Nesse, R. M., & Ellsworth, P. C . ( 2009).

Evolution, emotions, and emotional disorders

American Psychologist, 64( 2), 129-139.

URL     PMID:19203145      [本文引用: 1]

Emotions research is now routinely grounded in evolution, but explicit evolutionary analyses of emotions remain rare. This article considers the implications of natural selection for several classic questions about emotions and emotional disorders. Emotions are special modes of operation shaped by natural selection. They adjust multiple response parameters in ways that have increased fitness in adaptively challenging situations that recurred over the course of evolution. They are valenced because selection shapes special processes for situations that have influenced fitness in the past. In situations that decrease fitness, negative emotions are useful and positive emotions are harmful. Selection has partially differentiated subtypes of emotions from generic precursor states to deal with specialized situations. This has resulted in untidy emotions that blur into each other on dozens of dimensions, rendering the quest for simple categorically distinct emotions futile. Selection has shaped flexible mechanisms that control the expression of emotions on the basis of an individual's appraisal of the meaning of events for his or her ability to reach personal goals. The prevalence of emotional disorders can be attributed to several evolutionary factors.

Nesse, R. M., & Williams, G. C . ( 1995).

Why we get sick

New York: Times Books.

[本文引用: 3]

Nettle, D. (2004).

Evolutionary origins of depression: A review and reformulation

Journal of Affective Disorders, 81( 2), 91-102.

URL     PMID:15306134      [本文引用: 2]

There has been a recent surge of interest in the evolutionary basis of depression. One approach argues that the affective mechanisms that are dysregulated in depression are adaptations, whilst a second approach argues that depression itself is an adaptation. The evidence relating to whether depression could itself be an adaptation is reviewed. Adaptations generally have four hallmarks; they lack heritable variation, show evidence of good design, are evoked by appropriate triggers, and fitness is reduced where they are absent. Depression shows none of these hallmarks. It is characterized by heritability, recurrence, cognitive impairment, and poor social outcome. In an alternative evolutionary formulation, I argue that evolution has produced a continuous population distribution of affective reactivity that is subject to stabilizing selection. Individuals vulnerable to depression are at the upper end of this distribution. This conceptualization, in which depression itself is not selected for, is compatible with the known clinical and epidemiological facts.

Nettle, D. (2009).

An evolutionary model of low mood states

Journal of Theoretical Biology, 257( 1), 100-103.

URL     [本文引用: 2]

Nettle, D., & Bateson, M. (2012).

The evolutionary origins of mood and its disorders

Current Biology, 22( 17), R712-R721.

URL     PMID:22975002      [本文引用: 3]

The term 'mood' in its scientific usage refers to relatively enduring affective states that arise when negative or positive experience in one context or time period alters the individual's threshold for responding to potentially negative or positive events in subsequent contexts or time periods. The capacity for mood appears to be phylogenetically widespread and the mechanisms underlying it are highly conserved in diverse animals, suggesting it has an important adaptive function. In this review, we discuss how moods can be classified across species, and what the selective advantages of the capacity for mood are. Core moods can be localised within a two-dimensional continuous space, where one axis represents sensitivity to punishment or threat, and the other, sensitivity to reward. Depressed mood and anxious mood represent two different quadrants of this space. The adaptive function of mood is to integrate information about the recent state of the environment and current physical condition of the organism to fine-tune its decisions about the allocation of behavioural effort. Many empirical observations from both humans and non-human animals are consistent with this model. We discuss the implications of this adaptive approach to mood systems for mood disorders in humans.

Nolen-Hoeksema S., Wisco B. E., & Lyubomirsky S . ( 2008).

Rethinking rumination

Perspectives on Psychological Science, 3( 5), 400-424.

URL     [本文引用: 1]

Patel, V. (2017).

Talking sensibly about depression

PLoS Medicine, 14( 4), e1002257.

URL     [本文引用: 1]

Patten, S. B . ( 2015).

Medical models and metaphors for depression

Epidemiology and Psychiatric Sciences, 24( 4), 303-308.

URL     PMID:25682806      [本文引用: 1]

The aetiology of depression is not fully understood, which allows many different perspectives on aetiology to be adopted. Researchers and clinicians may be attracted to concepts of aetiology that parallel other diagnoses with which they are familiar. Such parallels may assume the role of informal models or metaphors for depressive disorders. They may even function as informal scientific theories of aetiology, energising research activities by guiding hypothesis generation and organising new knowledge. Parallels between different types of disease may ultimately prove valuable as frameworks supporting the emergence and maturation of new knowledge. However, such models may be counterproductive if their basis, which is likely to lay at least partially in analogy, is unacknowledged or overlooked. This could cause such models to appear more compelling than they really are. Listing examples of situations in which models of depression may arise from, or be strengthened by, parallels to other familiar conditions may increase the accessibility of such models either to criticism or support. However, such a list has not yet appeared in the literature. The present paper was written with the modest goal of stating several examples of models or metaphors for depression.This paper adopted narrative review methods. The intention was not to produce a comprehensive list of such ideas, but rather to identify prominent examples of ways of thinking about depression that may have been invigorated as a result parallels with other types of disease.Eight possible models are identified: depressive disorders as chemical imbalances (e.g., a presumed or theoretical imbalance of normally balanced neurotransmission in the brain), degenerative conditions (e.g., a brain disease characterised by atrophy of specified brain structures), toxicological syndromes (a result of exposure to a noxious psychological environment), injuries (e.g., externally induced brain damage related to stress), deficiency states (e.g., a serotonin deficiency), an obsolete category (e.g., similar to obsolete terms such as 'consumption' or 'dropsy'), medical mysteries (e.g., a condition poised for a paradigm-shifting breakthrough) or evolutionary vestiges (residual components of once adaptive mechanisms have become maladaptive in modern environments).Conceptualisation of depressive disorders may be partially shaped by familiar disease concepts. Analogies of this sort may ultimately be productive (e.g., through generating hypotheses by analogy) or destructive (e.g., by structuring knowledge in incorrect, but intellectually seductive, ways).

Power R. A., Kyaga S., Uher R., MacCabe J. H., Långström N., Landen M., … Svensson A. C . ( 2013).

Fecundity of patients with schizophrenia, autism, bipolar disorder, depression, anorexia nervosa, or substance abuse vs their unaffected siblings

The Journal of the American Medical Association Psychiatry, 70( 1), 22-30.

[本文引用: 1]

Price J. S., Gardner R., Jr., & Erickson M . ( 2004).

Can depression, anxiety and somatization be understood as appeasement displays?

Journal of Affective Disorders, 79( 1-3), 1-11.

URL     PMID:15023475      [本文引用: 1]

Background: No satisfactory basis in normal function characterizes major depression and its co-morbid disorders. Yet these may represent maladaptive expression of adaptive communicational states exhibited normally in many species. Methods: We examined the signal value of depressive and anxious mood states, fatigue syndrome and somatoform disorders and found them to resemble appeasement or submission to conspecifics (members of a same species) as studied in other animals. Moreover, applying game theory formulations of conflict resolution and the triune brain theory of MacLean supported the hypothesis. Limitations: Direct experimental evidence must still test hypotheses that emanate from the presented framework. Conclusions: Implications for this approach include improved understanding and treatment of depression, improved research strategies, and a potential future pathogenesis-focused nosology.

Price J., Sloman L., Gardner R., Gilbert P., & Rohde P . ( 1994).

The social competition hypothesis of depression

British Journal of Psychiatry, 164( 3), 309-315.

URL     [本文引用: 2]

Raison, C. L. & Miller, A. H . ( 2013).

The evolutionary significance of depression in pathogen host defense (PATHOS-D)

Molecular Psychiatry, 18( 1), 15-37.

URL     [本文引用: 2]

Simpson J. A. ,& Belsky, J.( 2008) . Attachment theory within a modern evolutionary framework. In J. Cassidy, & P. R. Shaver (Eds.). Handbook of attachment: Theory, research, and clinical applications (pp. 131-157). New York: Guilford Press.

[本文引用: 2]

Sloman L., Gilbert P., & Hasey G . ( 2003).

Evolved mechanisms in depression: The role and interaction of attachment and social rank in depression

Journal of Affective Disorders, 74( 2), 107-721.

URL     PMID:12706512      [本文引用: 1]

Abstract Evolved mechanisms underpinning attachment and social rank behavior may be the basis for some forms of major depression, especially those associated with chronic stress. We note the heterogeneity of depression, but suggest that some of its core symptoms, such as behavioral withdrawal, low self-esteem and anhedonia, may have evolved in order to regulate behavior and mood and convey sensitivity to threats and safety. Focusing on the evolved mental mechanisms for attachment and social rank helps to make sense of (1) depression's common early vulnerability factors (e.g., attachment disruptions, neglect and abuse), (2) the triggering events (e.g., loss of close relationships, being defeated and/or trapped in low socially rewarding or hostile environments), and (3) the psychological preoccupations of depressed people (e.g., sense of unlovableness, self as inferior and a failure). This focus offers clues as to how these two systems interact and on how to intervene.

Smith, J. M., & Alloy, L. B . ( 2008).

A roadmap to rumination: A review of the definition, assessment, and conceptualization of this multifaceted construct

Clinical Psychology Review, 29( 2), 116-128.

Stevens, A., & Price, J. (1996).

Evolutionary psychiatry: A new beginning

London: Routledge.

[本文引用: 1]

Stevens, A., & Price, J. (2000).

Evolutionary psychiatry: A new beginning (2nd ed.)

New York: Routledge.

[本文引用: 1]

Stone L. B., McGeary J. E., Palmer R. H. C., & Gibb B. E . ( 2013).

Identifying genetic predictors of depression risk: 5-HTTLPR and BDNF Val66met polymorphisms are associated with rumination and co-rumination in adolescents

Frontiers in Genetics, 4, 246.

URL     PMID:3826084      [本文引用: 1]

Abstract BACKGROUND: Despite research supporting moderate heritability of depression, efforts to replicate candidate gene associations to depression have yielded inconsistent results. We tested whether Val66Met and 5-HTTLPR exhibit utility as genetic markers of depression risk, testing for replicable associations to cognitive and interpersonal endophenotypes of depression (rumination and co-rumination), and further exploring developmental and sex moderation. METHOD: In Study I, 228 youth (ages 8-14) of mothers with or without a history of MDD during the child's lifetime were recruited from the community. Replication tests were carried out in Study II, a sample of 87 youth with similar recruitment. RESULTS: In Study I, the Val66Met single-nucleotide polymorphism (SNP) was associated with rumination in adolescents, but not children, such that adolescents homozygous for the Val allele reported higher rumination levels. Further, a cumulative genetic score (CGS) (Val66Val and 5-HTTLPR) predicted higher levels of co-rumination, specifically among adolescent girls. Both genetic associations maintained significance after covarying for current depressive symptomology, and the other endophenotype. Finally, both genetic associations exhibited similar effect sizes in Study II, although results did not reach statistical significance. CONCLUSIONS: RESULTS replicate a previously reported association between the brain derived neurotrophic factor (BDNF) Val allele and rumination in adolescents, and provide preliminary support for a CGS predictive of co-rumination in adolescent girls. The current study indicates that candidate genes may demonstrate utility as consistent genetic markers of depression risk when focused on specific phenotypes, and supports the need to explore potential differential effects of developmental stage and sex. However, given the small sample sizes and possibility of chance findings, these results should be interpreted with caution pending replication.

Tanaka, M., & Kinney, D. K . ( 2011).

An evolutionary hypothesis of suicide: Why it could be biologically adaptive and is so prevalent in certain occupations

Psychological Reports, 108( 3), 977-992.

URL     PMID:21879643      [本文引用: 1]

From an evolutionary perspective, suicide is a puzzle, because it has serious adverse effects, yet is remarkably common and heritable. An hypothesis is proposed to explain this puzzle, by explaining how suicide could be adaptive through reducing risk that individuals will transmit infections to kin. Empirical evidence supports four predictions from the hypothesis. There are well-established mechanisms by which infections and immune factors increase risk for mental disorders that contribute to suicide. Suicide is more prevalent in occupations with greater exposure to infection and immune-compromising factors and at higher latitudes, where key environmental factors increase vulnerability to infection. In several other highly social species, suicide-like behaviors have evolved to reduce transmission of infections. If the hypothesis is correct, detection and treatment of underlying infections and immune dysfunction should help predict and prevent suicidal behavior, while also combating spread of infectious diseases.

Taylor P. J., Gooding P., Wood A. M., & Tarrier N . ( 2011).

The role of defeat and entrapment in depression, anxiety, and suicide

Psychological Bulletin, 137( 3), 391-420.

URL     PMID:21443319      [本文引用: 1]

Abstract Defeat and entrapment are psychological constructs that have played a central role in evolutionary accounts of depression. These concepts have since been implicated in theoretical accounts of anxiety disorders and suicidality. The current article reports on a systematic review of the existing research investigating the links among defeat, entrapment, and psychopathology in the domains of depression, suicidality, posttraumatic stress disorder (PTSD), and other anxiety syndromes. Fifty-one original research articles were identified and critically reviewed. There was strong convergent evidence for a link with depressive symptoms, across a variety of clinical and nonclinical samples. Preliminary support for an association with suicidality was also observed, with effects not readily explainable in terms of comorbid depression. There was strong evidence for an association between defeat and PTSD, although this may have been partly accounted for by comorbid depression. The findings for other anxiety disorders were less consistent. There was, however, evidence that social anxiety in individuals with psychosis may be related to perceptions of entrapment. Overall, there was evidence that perceptions of defeat and entrapment were closely associated with various forms of human psychopathology. These effects were often in the moderate to large range and superseded the impact of other environmental and psychological stressors on psychopathology. We provide a unified theoretical model of how defeat and entrapment may contribute to these different psychopathological conditions. Clinical implications and avenues for future research are discussed. 2011 American Psychological Association

Varga, S. (2012).

Evolutionary psychiatry and depression: Testing two hypotheses

Medicine, Health Care and Philosophy, 15( 1), 41-52.

URL     PMID:21221814      [本文引用: 1]

In the last few decades, there has been a genuine ‘adaptive turn’ in psychiatry, resulting in evolutionary accounts for an increasing number of psychopathologies. In this paper, I explore the advantages and problems with the two main evolutionary approaches to depression, namely the mismatch and persistence accounts . I will argue that while both evolutionary theories of depression might provide some helpful perspectives, the accounts also harbor significant flaws that might question their authority and usefulness as explanations.

Varga, S. (2016). Evolutionary approaches to depression: Prospects and limitations. In A. Alvergne, C. Jenkinson, & C. Faurie (Eds.). Evolutionary thinking in medicine (pp. 347-356). New York: Springer International Publishing.

[本文引用: 1]

Wakefield, J. C . ( 2013).

The DSM-5 debate over the bereavement exclusion: Psychiatric diagnosis and the future of empirically supported treatment

Clinical Psychology Review, 33( 7), 825-845.

URL     PMID:23706392      [本文引用: 1]

Valid diagnostic criteria support generalizations about treatment effectiveness, allowing progress in developing empirically supported treatments. The DSM-5 revision provides an opportunity to consider whether diagnostic changes are increasing validity. In this paper, I first offer broad suggestions for conceptually advancing diagnostic validity while awaiting greater etiological understanding. These include, for example, improving “conceptual validity” (disorder/nondisorder differentiation); extending diagnosis beyond disorders to include mismatches between normal variation and social demands (“psychological justice”); placing disorder etiology in evolutionary context as harmful failure of biologically designed functioning (“harmful dysfunction”); and taking an integrative theoretical approach to human meaning systems. The paper then examines the DSM-5's controversial decision to eliminate the major depression bereavement exclusion (BE), detailing the evidence and attendant debate. Elimination was defended by citing several hypotheses (e.g., excluded cases are similar to other MDD; exclusions risk missing suicidal cases; medication works with excluded cases), all of which were either empirically falsified or based on faulty arguments. Most dramatically, excluded cases were empirically demonstrated to have no more depression on follow-up than those who never had MDD. I conclude that BE elimination undermined rather than increased conceptual validity and usefulness for treatment research. Finally, I draw some general lessons from the DSM-5 BE debacle.

Watson, P. J., & Andrews, P. W . ( 2002).

Toward a revised evolutionary adaptationist analysis of depression: The social navigation hypothesis

Journal of Affective Disorders, 72( 1), 1-14.

URL     [本文引用: 3]

Weinberger, D. R., & Goldberg, T. E . ( 2014).

RDoCs redux

World Psychiatry, 13( 1), 36-38.

URL     [本文引用: 1]

Wells, J. C. K . ( 2012).

The evolution of human adiposity and obesity: Where did it all go wrong?

Disease Models & Mechanisms, 5( 5), 595-607.

URL     PMID:22915021      [本文引用: 1]

Because obesity is associated with diverse chronic diseases, little attention has been directed to the multiple beneficial functions of adipose tissue. Adipose tissue not only provides energy for growth, reproduction and immune function, but also secretes and receives diverse signaling molecules that coordinate energy allocation between these functions in response to ecological conditions. Importantly, many relevant ecological cues act on growth and physique, with adiposity responding as a counterbalancing risk management strategy. The large number of individual alleles associated with adipose tissue illustrates its integration with diverse metabolic pathways. However, phenotypic variation in age, sex, ethnicity and social status is further associated with different strategies for storing and using energy. Adiposity therefore represents a key means of phenotypic flexibility within and across generations, enabling a coherent life-history strategy in the face of ecological stochasticity. The sensitivity of numerous metabolic pathways to ecological cues makes our species vulnerable to manipulative globalized economic forces. The aim of this article is to understand how human adipose tissue biology interacts with modern environmental pressures to generate excess weight gain and obesity. The disease component of obesity might lie not in adipose tissue itself, but in its perturbation by our modern industrialized niche. Efforts to combat obesity could be more effective if they prioritized ‘external’ environmental change rather than attempting to manipulate ‘internal’ biology through pharmaceutical or behavioral means.

White R. G., Orr D. M. R., Read U. M., & Jain S . ( 2017).

Situating global mental health: Sociocultural perspectives

In R. G. White, S. Jain, D. M. R. Orr, & U. M. Read (Eds.), The Palgrave handbook of sociocultural perspectives on global mental health(pp. 1-27). London: Palgrave Macmillan.

URL     [本文引用: 1]

This introductory chapter of The Palgrave Handbook of Sociocultural Perspectives on Global Mental Health highlights how understanding about aberrant behaviours has varied across time, geography and cu

Wilkinson, I. (2014).

On the task of making social inquiry aligned to caregiving: An invitation to debate

Anthropology & Medicine, 21( 1), 87-99.

URL     PMID:24559227      [本文引用: 1]

Abstract This paper is designed as an invitation to debate the value of research and writing on social suffering in relation to practices of caregiving. It offers a brief account of the origins and development of 'social suffering' as a concern for social inquiry. Henry Mayhew and Jane Addams are profiled in terms of their pioneering roles as social researchers heavily preoccupied with problems of social suffering. The contrast between Henry Mayhew's frustrated attempts at caregiving and Jane Addams' success in instituting the pedagogy of caregiving in the work of Hull House is set up for analysis. These examples are used to issue an invitation to readers to question the cultural and institutional circumstances that make possible forms of social inquiry that recognise caregiving both as a means to social understanding and as an aim for social research in practice.

Wilkinson I.,& Kleinman, A. ( 2016) . A passion for society: How we think about human suffering Oakland, California: University of California Press How we think about human suffering. Oakland, California: University of California Press.

[本文引用: 1]

Wolpert, L. (2008).

Depression in an evolutionary context

Philosophy, Ethics, and Humanities in Medicine,3, 8.

URL     PMID:18312654      [本文引用: 1]

Sadness and low levels of depression are adaptive since they lead the individual to try and make up a loss. By contrast, severe or clinical depression is not adaptive, but can be thought of as sadness having become malignant.

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