MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Department of Psychology and Neuroscience, Duke University, Durham, NC, USA; Department of Psychiatry and Behavioral Sciences, Duke University, Durham, NC, USA.
Brain Behav Immun. 2018 Jan;67:211-217. doi: 10.1016/j.bbi.2017.08.025. Epub 2017 Sep 1.
Childhood victimization is an important risk factor for later immune-related disorders. Previous evidence has demonstrated that childhood victimization is associated with elevated levels of inflammation biomarkers measured decades after exposure. However, it is unclear whether this association is (1) already detectable in young people, (2) different in males and females, and (3) confounded by genetic liability to inflammation. Here we sought to address these questions.
Participants were 2232 children followed from birth to age 18years as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Childhood victimization was measured prospectively from birth to age 12years. Inflammation was measured through C-reactive protein (CRP) levels in dried blood spots at age 18years. Latent genetic liability for high inflammation levels was assessed through a twin-based method.
Greater exposure to childhood victimization was associated with higher CRP levels at age 18 (serum-equivalent means were 0.65 in non-victimized Study members, 0.74 in those exposed to one victimization type, and 0.81 in those exposed to poly-victimization; p=0.018). However, this association was driven by a significant association in females (serum-equivalent means were 0.75 in non-victimized females, 0.87 in those exposed to one type of victimization, and 1.19 in those exposed to poly-victimization; p=0.010), while no significant association was observed in males (p=0.19). Victimized females showed elevated CRP levels independent of latent genetic influence, as well as childhood socioeconomic status, and waist-hip ratio and body temperature at the time of CRP assessment.
Childhood victimization is associated with elevated CRP levels in young women, independent of latent genetic influences and other key risk factors. These results strengthen causal inference about the effects of childhood victimization on inflammation levels in females by accounting for potential genetic confounding.
儿童期受虐是导致日后免疫相关疾病的一个重要危险因素。既往证据表明，儿童期受虐与暴露数十年后炎症生物标志物水平升高有关。然而，目前尚不清楚这种关联是否（1）在年轻人中已经可以检测到，（2）在男性和女性中有所不同，以及（3）是否受到炎症遗传易感性的混杂。本研究旨在解决这些问题。
本研究纳入了 2232 名儿童，他们自出生起至 18 岁均作为环境风险（E-Risk）纵向双胞胎研究的一部分被随访。儿童期受虐通过从出生到 12 岁的前瞻性测量进行评估。炎症通过 18 岁时干血斑中的 C 反应蛋白（CRP）水平来衡量。通过基于双胞胎的方法评估高炎症水平的潜在遗传易感性。
与未受虐的研究参与者相比，更多的儿童期受虐经历与 18 岁时更高的 CRP 水平相关（血清等效均值分别为未受虐者 0.65，单一受虐类型暴露者 0.74，多类型受虐者 0.81；p=0.018）。然而，这种关联主要存在于女性中（血清等效均值分别为未受虐女性 0.75，单一受虐类型暴露女性 0.87，多类型受虐女性 1.19；p=0.010），而在男性中则无显著关联（p=0.19）。受虐女性的 CRP 水平升高独立于潜在的遗传影响，以及儿童期社会经济地位、CRP 评估时的腰围-臀围比和体温。
儿童期受虐与年轻女性 CRP 水平升高有关，独立于潜在的遗传影响和其他关键危险因素。这些结果通过考虑潜在的遗传混杂因素，增强了儿童期受虐对女性炎症水平影响的因果推断。
