Childhood victimization and inflammation in young adulthood: A genetically sensitive cohort study.
Childhood victimization and inflammation in young adulthood: A genetically sensitive cohort study.
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DOI：
10.1016/j.bbi.2017.08.025
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发表时间：
2018-01
期刊：
影响因子：
--
通讯作者：
Danese A
中科院分区：
文献类型：
--
作者：
Baldwin JR;Arseneault L;Caspi A;Fisher HL;Moffitt TE;Odgers CL;Pariante C;Ambler A;Dove R;Kepa A;Matthews T;Menard A;Sugden K;Williams B;Danese A
童年受害预示 18 岁时 CRP 水平升高。儿童受害与 CRP 水平之间的关联针对女性。 CRP 水平的潜在遗传影响并不能解释女性中的这种关联。童年受害是后来发生免疫相关疾病的重要危险因素。先前的证据表明，儿童受害与接触后几十年后测量的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）男性和女性之间存在差异，（3）与炎症的遗传倾向相混淆。在这里，我们试图解决这些问题。作为环境风险（E-Risk）纵向双胞胎研究的一部分，参与者是 2232 名从出生到 18 岁的儿童。对从出生到 12 岁的儿童期受害情况进行了前瞻性测量。通过 18 岁时干燥血斑中的 C 反应蛋白 (CRP) 水平来测量炎症情况。通过基于双胞胎的方法评估了高炎症水平的潜在遗传倾向。童年受害经历越多，18 岁时 CRP 水平越高（非受害研究成员的血清当量平均值为 0.65，接触过一种受害类型的成员为 0.74，接触多重受害的成员为 0.81；p = 0.018）。然而，这种关联是由女性中的显着关联驱动的（未受害女性的血清当量平均值为 0.75，遭受一种类型受害的女性为 0.87，遭受多重受害的女性为 1.19；p = 0.010），而在男性中没有观察到显着关联（p = 0.19）。受害女性的 CRP 水平升高，与潜在遗传影响、儿童社会经济状况、CRP 评估时的腰臀比和体温无关。童年受害与年轻女性 CRP 水平升高有关，与潜在遗传影响和其他关键风险因素无关。这些结果通过考虑潜在的遗传混杂因素，加强了关于童年受害对女性炎症水平影响的因果推断。
Childhood victimization predicted elevated levels of CRP at age 18. The association between child victimization and CRP levels was specific to females. Latent genetic influences on CRP levels did not explain the association in females. 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 18 years as part of the Environmental Risk (E-Risk) Longitudinal Twin Study. Childhood victimization was measured prospectively from birth to age 12 years. Inflammation was measured through C-reactive protein (CRP) levels in dried blood spots at age 18 years. 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.
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影响因子：
37.8
作者：
Dehghan A;Dupuis J;Barbalic M;Bis JC;Eiriksdottir G;Lu C;Pellikka N;Wallaschofski H;Kettunen J;Henneman P;Baumert J;Strachan DP;Fuchsberger C;Vitart V;Wilson JF;Paré G;Naitza S;Rudock ME;Surakka I;de Geus EJ;Alizadeh BZ;Guralnik J;Shuldiner A;Tanaka T;Zee RY;Schnabel RB;Nambi V;Kavousi M;Ripatti S;Nauck M;Smith NL;Smith AV;Sundvall J;Scheet P;Liu Y;Ruokonen A;Rose LM;Larson MG;Hoogeveen RC;Freimer NB;Teumer A;Tracy RP;Launer LJ;Buring JE;Yamamoto JF;Folsom AR;Sijbrands EJ;Pankow J;Elliott P;Keaney JF;Sun W;Sarin AP;Fontes JD;Badola S;Astor BC;Hofman A;Pouta A;Werdan K;Greiser KH;Kuss O;Meyer zu Schwabedissen HE;Thiery J;Jamshidi Y;Nolte IM;Soranzo N;Spector TD;Völzke H;Parker AN;Aspelund T;Bates D;Young L;Tsui K;Siscovick DS;Guo X;Rotter JI;Uda M;Schlessinger D;Rudan I;Hicks AA;Penninx BW;Thorand B;Gieger C;Coresh J;Willemsen G;Harris TB;Uitterlinden AG;Järvelin MR;Rice K;Radke D;Salomaa V;Willems van Dijk K;Boerwinkle E;Vasan RS;Ferrucci L;Gibson QD;Bandinelli S;Snieder H;Boomsma DI;Xiao X;Campbell H;Hayward C;Pramstaller PP;van Duijn CM;Peltonen L;Psaty BM;Gudnason V;Ridker PM;Homuth G;Koenig W;Ballantyne CM;Witteman JC;Benjamin EJ;Perola M;Chasman DI
通讯作者：
Chasman DI
DOI：
10.1176/appi.ajp.2016.16030333
发表时间：
2017-04-01
期刊：
The American journal of psychiatry
影响因子：
--
作者：
Danese A;Moffitt TE;Arseneault L;Bleiberg BA;Dinardo PB;Gandelman SB;Houts R;Ambler A;Fisher HL;Poulton R;Caspi A
通讯作者：
Caspi A
DOI：
10.1073/pnas.1218253109
发表时间：
2012-12-11
影响因子：
11.1
作者：
Cole, Steven W.;Conti, Gabriella;Suomi, Stephen J.
通讯作者：
Suomi, Stephen J.
影响因子：
11
作者：
Baumeister D;Akhtar R;Ciufolini S;Pariante CM;Mondelli V
通讯作者：
Mondelli V
影响因子：
--
作者：
Danese, Andrea;Moffitt, Terrie E.;Harrington, HonaLee;Milne, Barry J.;Polanczyk, Guilherme;Pariante, Carmine M.;Poulton, Richie;Caspi, Avshalom
通讯作者：
Caspi, Avshalom