近日,美国一项新研究指出,抑郁症能提高人体免疫系统对抗各种传染病和攻击的能力,在人类历史发展演变过程具有重要意义。研究提案大纲发表在《分子精神病学》(Molecular Psychiatry)刊物上。
以往对抑郁症研究的焦点大部分集中在该心理疾病所致社会和行为的方面。然而,心理学家们认为抑郁症在肥胖,心血管疾病,糖尿病,哮喘,癌症等慢性疾病群体中,以及在吸烟,体能活动不足及酗酒人群中更加盛行可能另有原因。
埃默里大学精神病学和行为科学的研究人员认为一些抑郁行为在人类历史进化方面存在优势,能帮助我们的祖先们对抗传染性疾病。抑郁和其所致的基因变异能帮助那时代的人适应那时的生存环境并与疾病对抗中存活下来,特别是年轻的孩子,虽然抑郁行为不利于适应社交关系。
抑郁症常与炎症以及免疫反应过度相联系,有抑郁情绪的个体往往炎症发病很高,即使人体没有反抗传染病也会炎症发作。但炎症高发并不是抑郁症的必然结果。
“抑郁会导致基因变异,最终会影响免疫功能。我们需要重新思考为什么抑郁症像是嵌入基因组里的。”研究的共同作者安德鲁. 米勒博士表示。
在人类历史中,先祖们需要在对抗人类历史早期的大敌——传染病中存活下来并将他们的基因传递给下一代,与传染病抗衡中得以存活是他们传递基因的关键性因素。而基因演化过程中融合了一些抑郁症状和生理反应比如发热,疲劳,不活跃,社交回避和食欲不振等能遏制和减少传染病所致的死亡率。
作者还表示他们的理论为压力为什么是导致抑郁症的风险因素提供了新的解释。这些压力可以被认为免疫反应机制对身体预见受伤进行准备时的“副产品”。
该理论也为个体对各种抑郁症治疗方案怎样反应,以及某种通常被用于治疗自然免疫疾病的药物是否对治疗某些抑郁症有效给出一些建议。(生物谷Bioon.com)
doi:10.1016/j.cell.2011.10.017
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The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)
C L Raison and A H Miller
Given the manifold ways that depression impairs Darwinian fitness, the persistence in the human genome of risk alleles for the disorder remains a much debated mystery. Evolutionary theories that view depressive symptoms as adaptive fail to provide parsimonious explanations for why even mild depressive symptoms impair fitness-relevant social functioning, whereas theories that suggest that depression is maladaptive fail to account for the high prevalence of depression risk alleles in human populations. These limitations warrant novel explanations for the origin and persistence of depression risk alleles. Accordingly, studies on risk alleles for depression were identified using PubMed and Ovid MEDLINE to examine data supporting the hypothesis that risk alleles for depression originated and have been retained in the human genome because these alleles promote pathogen host defense, which includes an integrated suite of immunological and behavioral responses to infection. Depression risk alleles identified by both candidate gene and genome-wide association study (GWAS) methodologies were found to be regularly associated with immune responses to infection that were likely to enhance survival in the ancestral environment. Moreover, data support the role of specific depressive symptoms in pathogen host defense including hyperthermia, reduced bodily iron stores, conservation/withdrawal behavior, hypervigilance and anorexia. By shifting the adaptive context of depression risk alleles from relations with conspecifics to relations with the microbial world, the Pathogen Host Defense (PATHOS-D) hypothesis provides a novel explanation for how depression can be nonadaptive in the social realm, whereas its risk alleles are nonetheless represented at prevalence rates that bespeak an adaptive function.