近日,，美國(guó)一項(xiàng)新研究指出，抑郁癥能提高人體免疫系統(tǒng)對(duì)抗各種傳染病和攻擊的能力,，在人類歷史發(fā)展演變過(guò)程具有重要意義,。研究提案大綱發(fā)表在《分子精神病學(xué)》（Molecular Psychiatry）刊物上。
以往對(duì)抑郁癥研究的焦點(diǎn)大部分集中在該心理疾病所致社會(huì)和行為的方面,。然而,，心理學(xué)家們認(rèn)為抑郁癥在肥胖，心血管疾病,，糖尿病,，哮喘，癌癥等慢性疾病群體中,，以及在吸煙,，體能活動(dòng)不足及酗酒人群中更加盛行可能另有原因。
埃默里大學(xué)精神病學(xué)和行為科學(xué)的研究人員認(rèn)為一些抑郁行為在人類歷史進(jìn)化方面存在優(yōu)勢(shì),，能幫助我們的祖先們對(duì)抗傳染性疾病,。抑郁和其所致的基因變異能幫助那時(shí)代的人適應(yīng)那時(shí)的生存環(huán)境并與疾病對(duì)抗中存活下來(lái)，特別是年輕的孩子,，雖然抑郁行為不利于適應(yīng)社交關(guān)系,。
抑郁癥常與炎癥以及免疫反應(yīng)過(guò)度相聯(lián)系,，有抑郁情緒的個(gè)體往往炎癥發(fā)病很高，即使人體沒(méi)有反抗傳染病也會(huì)炎癥發(fā)作,。但炎癥高發(fā)并不是抑郁癥的必然結(jié)果,。
“抑郁會(huì)導(dǎo)致基因變異，最終會(huì)影響免疫功能,。我們需要重新思考為什么抑郁癥像是嵌入基因組里的,。”研究的共同作者安德魯. 米勒博士表示。
在人類歷史中,，先祖?zhèn)冃枰趯?duì)抗人類歷史早期的大敵——傳染病中存活下來(lái)并將他們的基因傳遞給下一代,，與傳染病抗衡中得以存活是他們傳遞基因的關(guān)鍵性因素,。而基因演化過(guò)程中融合了一些抑郁癥狀和生理反應(yīng)比如發(fā)熱,，疲勞，不活躍,，社交回避和食欲不振等能遏制和減少傳染病所致的死亡率,。
作者還表示他們的理論為壓力為什么是導(dǎo)致抑郁癥的風(fēng)險(xiǎn)因素提供了新的解釋。這些壓力可以被認(rèn)為免疫反應(yīng)機(jī)制對(duì)身體預(yù)見(jiàn)受傷進(jìn)行準(zhǔn)備時(shí)的“副產(chǎn)品”,。
該理論也為個(gè)體對(duì)各種抑郁癥治療方案怎樣反應(yīng),，以及某種通常被用于治療自然免疫疾病的藥物是否對(duì)治療某些抑郁癥有效給出一些建議。（生物谷Bioon.com）
doi:10.1016/j.cell.2011.10.017
PMC:
PMID:
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.
