Yu Zhi, Huang Tao, Zheng Yan, Wang Tiange, Heianza Yoriko, Sun Dianjianyi, Campos Hannia, Qi Lu
Division of Rheumatology, Allergy and Immunology, Brigham and Women's Hospital, Boston, MA.
Epidemiology Domain, Saw Swee Hock School of Public Health, and.
Am J Clin Nutr. 2017 May;105(5):1198-1203. doi: 10.3945/ajcn.116.148106. Epub 2017 Mar 22.
Previous studies have indicated that the cardioprotective effects of long-chain (LC) n-3 (ω-3) polyunsaturated fatty acids (PUFAs) may vary across various ethnic populations. Emerging evidence has suggested that the gene-environment interaction may partly explain such variations. Proprotein convertase subtilisin/kexin type 9 (PCSK9) was shown to have a mutually regulating relation with LC n-3 PUFAs and also to reduce the risk of cardiovascular diseases (CVDs). Therefore, we hypothesized that certain genetic variants may modify the association between LC n-3 PUFA intake and CVD risk. We determined whether a variant (rs11206510), which has been identified for early onset myocardial infarction (MI), modified the association of LC n-3 PUFAs with nonfatal MI risk in Costa Rican Hispanics. We analyzed cross-sectional data from 1932 case subjects with a first nonfatal MI and 2055 population-based control subjects who were living in Costa Rica to examine potential gene-environment interactions. Two-sided values <0.05 were considered significant. We observed a significant interaction between the rs11206510 genotype and LC n-3 PUFA intake on nonfatal MI risk (-interaction = 0.012). The OR of nonfatal MI was 0.84 (95% CI: 0.72, 0.98) per 0.1% increase in total energy intake from LC n-3 PUFAs in protective-allele (C-allele) carriers, whereas the corresponding OR (95% CI) in non-C-allele carriers was 1.02 (95% CI: 0.95, 1.10). Similar results were observed when we examined the association between docosahexaenoic acid, which is one type of LC n-3 PUFA, and nonfatal MI risk (-interaction = 0.003). LC n-3 PUFA intake is associated with a lower risk of nonfatal MI in C-allele carriers of rs11206510 ( = 799) but not in non-C-allele carriers ( = 3188).
先前的研究表明，长链（LC）n-3（ω-3）多不饱和脂肪酸（PUFA）的心脏保护作用可能因不同种族人群而有所不同。新出现的证据表明，基因-环境相互作用可能部分解释了这种差异。前蛋白转化酶枯草溶菌素/kexin 9型（PCSK9）已被证明与LC n-3 PUFA存在相互调节关系，并且还能降低心血管疾病（CVD）的风险。因此，我们假设某些基因变异可能会改变LC n-3 PUFA摄入量与CVD风险之间的关联。我们确定了一个已被确定与早发性心肌梗死（MI）相关的变异（rs11206510）是否会改变哥斯达黎加西班牙裔人群中LC n-3 PUFA与非致命性MI风险之间的关联。我们分析了来自1932例首次发生非致命性MI的病例受试者和2055例居住在哥斯达黎加的基于人群的对照受试者的横断面数据，以研究潜在的基因-环境相互作用。双侧P值<0.05被认为具有统计学意义。我们观察到rs11206510基因型与LC n-3 PUFA摄入量之间在非致命性MI风险上存在显著相互作用（P相互作用=0.012）。在保护性等位基因（C等位基因）携带者中，每增加0.1%来自LC n-3 PUFA的总能量摄入，非致命性MI的OR为0.84（95%CI：0.72，0.98），而非C等位基因携带者中的相应OR（95%CI）为1.02（95%CI：0.95，1.10）。当我们研究二十二碳六烯酸（一种LC n-3 PUFA）与非致命性MI风险之间的关联时，观察到了类似的结果（P相互作用=0.003）。rs11206510的C等位基因携带者（n = 799）中，LC n-3 PUFA摄入量与较低的非致命性MI风险相关，但在非C等位基因携带者（n = 3188）中并非如此。
