Danese Andrea, Pariante Carmine M, Caspi Avshalom, Taylor Alan, Poulton Richie
Medical Research Council Social, Genetic, and Developmental Psychiatry Centre and Department of Psychological Medicine, Institute of Psychiatry, King's College London, London SE5 8AF, United Kingdom.
Proc Natl Acad Sci U S A. 2007 Jan 23;104(4):1319-24. doi: 10.1073/pnas.0610362104. Epub 2007 Jan 17.
Stress in early life has been associated with insufficient glucocorticoid signaling in adulthood, possibly affecting inflammation processes. Childhood maltreatment has been linked to increased risk of adult disease with potential inflammatory origin. However, the impact of early life stress on adult inflammation is not known in humans. We tested the life-course association between childhood maltreatment and adult inflammation in a birth cohort followed to age 32 years as part of the Dunedin Multidisciplinary Health and Development Study. Regression models were used to estimate the effect of maltreatment on inflammation, adjusting for co-occurring risk factors and potential mediating variables. Maltreated children showed a significant and graded increase in the risk for clinically relevant C-reactive protein levels 20 years later, in adulthood [risk ratio (RR)=1.80, 95% confidence interval (CI)=1.26-2.58]. The effect of childhood maltreatment on adult inflammation was independent of the influence of co-occurring early life risks (RR=1.58, 95% CI=1.08-2.31), stress in adulthood (RR=1.64, 95% CI=1.12-2.39), and adult health and health behavior (RR=1.76, 95% CI=1.23-2.51). More than 10% of cases of low-grade inflammation in the population, as indexed by high C-reactive protein, may be attributable to childhood maltreatment. The association between maltreatment and adult inflammation also generalizes to fibrinogen and white blood cell count. Childhood maltreatment is a previously undescribed, independent, and preventable risk factor for inflammation in adulthood. Inflammation may be an important developmental mediator linking adverse experiences in early life to poor adult health.
早年生活中的压力与成年期糖皮质激素信号不足有关,这可能会影响炎症过程。童年期受虐与成年疾病风险增加有关,这些疾病可能源于炎症。然而,早年生活压力对成年人炎症的影响在人类中尚不清楚。作为达尼丁多学科健康与发展研究的一部分,我们对一个出生队列进行了跟踪研究,直至其32岁,以测试童年期受虐与成年炎症之间的生命历程关联。我们使用回归模型来估计虐待对炎症的影响,并对同时出现的风险因素和潜在中介变量进行了调整。受虐儿童在20年后成年时,临床相关C反应蛋白水平升高的风险显著且呈梯度增加[风险比(RR)=1.80,95%置信区间(CI)=1.26 - 2.58]。童年期受虐对成年炎症的影响独立于同时出现的早年风险因素的影响(RR = 1.58,95% CI = 1.08 - 2.31)、成年期压力(RR = 1.64,95% CI = 1.12 - 2.39)以及成年健康和健康行为(RR = 1.76,95% CI = 1.23 - 2.51)。以高C反应蛋白为指标,人群中超过10%的低度炎症病例可能归因于童年期受虐。虐待与成年炎症之间的关联也适用于纤维蛋白原和白细胞计数。童年期受虐是成年期炎症的一个此前未被描述的、独立的且可预防的风险因素。炎症可能是一个重要的发育中介因素,将早年的不良经历与成年后的健康不佳联系起来。