Winning Ashley, Glymour M Maria, McCormick Marie C, Gilsanz Paola, Kubzansky Laura D
From the Department of Social and Behavioral Sciences (Winning, McCormick, Gilsanz, Kubzansky), Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Department of Epidemiology & Biostatistics (Glymour), School of Medicine, University of California San Francisco, San Francisco, California.
Psychosom Med. 2016 Nov/Dec;78(9):1019-1030. doi: 10.1097/PSY.0000000000000409.
Prior research on the relationship between early adversity and adult chronic disease has often relied on retrospective reports of a limited range of exposures and has not considered childhood psychological distress as a mediator. We investigate whether distress in childhood is one pathway by which early social disadvantage leads to greater cardiometabolic risk in middle adulthood.
Data are from the 1958 British Birth Cohort study (sample n = 6027). We created an early social disadvantage index based on 16 exposures related to family and socioeconomic hardship from birth to age 7. Childhood psychological distress was ascertained from internalizing and externalizing symptoms at ages 7, 11, and 16 years. Cardiometabolic risk was assessed with a Z-standardized score derived from 9 immune, cardiovascular, and metabolic biomarkers measured at age 45. We used linear regression models and formal tests of mediation to assess relationships between disadvantage, distress, and subsequent cardiometabolic risk.
Higher social disadvantage predicted increased adult cardiometabolic risk (β = 0.05; 95% CI = 0.03-0.07). Mediation analyses revealed a significant direct (path c'; β = 0.03; 95% CI = 0.01-0.05) and indirect (path ab; β = 0.02; 95% CI = 0.01-0.02) effect of social disadvantage on cardiometabolic risk, adjusting for potential confounders. Child psychological distress accounted for 37% (95% CI = 34-46%) of the observed association.
Results suggest childhood distress may be one factor on the pathway linking early disadvantage to higher risk of developing cardiometabolic diseases. Such results may point to the importance of blocking the translation of psychosocial to biological risk during a potentially sensitive developmental window.
先前关于早期逆境与成人慢性病之间关系的研究通常依赖于对有限范围暴露的回顾性报告,且未将儿童期心理困扰视为中介因素。我们调查儿童期困扰是否是早期社会劣势导致中年期心脏代谢风险增加的一种途径。
数据来自1958年英国出生队列研究(样本n = 6027)。我们基于从出生到7岁与家庭和社会经济困难相关的16种暴露因素创建了一个早期社会劣势指数。通过7岁、11岁和16岁时的内化和外化症状来确定儿童期心理困扰。心脏代谢风险通过45岁时测量的9种免疫、心血管和代谢生物标志物得出的Z标准化分数进行评估。我们使用线性回归模型和中介的正式检验来评估劣势、困扰与随后的心脏代谢风险之间的关系。
较高的社会劣势预示着成人心脏代谢风险增加(β = 0.05;95%CI = 0.03 - 0.07)。中介分析显示,在调整潜在混杂因素后,社会劣势对心脏代谢风险有显著的直接效应(路径c';β = 0.03;95%CI = 0.01 - 0.05)和间接效应(路径ab;β = 0.02;95%CI = 0.01 - 0.02)。儿童心理困扰占观察到的关联的37%(95%CI = 34 - 46%)。
结果表明,儿童期困扰可能是将早期劣势与患心脏代谢疾病的较高风险联系起来的途径中的一个因素。这些结果可能表明在一个潜在敏感的发育窗口期间阻断心理社会风险向生物风险转化的重要性。