Evaluating the contribution of genetics and familial shared environment to common disease using the UK Biobank.
Evaluating the contribution of genetics and familial shared environment to common disease using the UK Biobank.
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DOI：
10.1038/ng.3618
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发表时间：
2016-09
期刊：
影响因子：
30.8
通讯作者：
Tenesa A
中科院分区：
文献类型：
--
作者：
Muñoz M;Pong-Wong R;Canela-Xandri O;Rawlik K;Haley CS;Tenesa A
全基因组关联研究已经发现了许多潜在的疾病易感性位点，但大多数导致疾病易感性的遗传因素仍然未知。在这里，我们提供的证据表明，部分缺失的遗传力可以解释为高估的遗传力。我们利用英国生物样本库中1，555，906名欧洲白色个体的疾病家族史，估计了12种复杂人类疾病的遗传性。使用简单的基于家庭的统计模型的估计值与专门考虑共享家庭环境因素的结构方程模型（SEM）的估计值相比，平均膨胀了约47%。此外，使用SNP数据的遗传力平均解释了44.2%的基于简单家庭的疾病估计值，平均解释了57.3%的SEM估计遗传力，并几乎解释了高血压的所有SEM遗传力。我们的研究结果表明，遗传和家庭环境作出重大贡献的家族聚集性疾病。
Genome-wide association studies have detected many loci underlying susceptibility to disease, but most of the genetic factors that contribute to disease susceptibility remain unknown. Here we provide evidence that part of the missing heritability can be explained by an overestimation of heritability. We estimated the heritability of twelve complex human diseases using family history of disease in 1,555,906 white European individuals from the UK Biobank. Estimates using simple family-based statistical models were inflated on average by ~47% comparing with those from Structural Equation Models (SEM) that specifically accounted for shared familial environmental factors. In addition, heritabilities using SNP data explained an average of 44.2% of the simple family-based estimates across diseases and an average of 57.3% of SEM estimated heritability and accounted for almost all of the SEM heritability for hypertension. Our results show that both genetics and familial environment make substantial contributions to familial clustering of disease.
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