Department of Biological Psychology, Vrije Universiteit Amsterdam, Transitorium 2B03, Van der Boechorststraat 1, 1081 BT, Amsterdam, The Netherlands.
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, 1-156, P.O. Box 980126, Richmond, VA, 23298-0126, USA.
Behav Genet. 2018 Jul;48(4):337-349. doi: 10.1007/s10519-018-9904-4. Epub 2018 Jun 7.
Although experimental studies are regarded as the method of choice for determining causal influences, these are not always practical or ethical to answer vital questions in health and social research (e.g., one cannot assign individuals to a "childhood trauma condition" in studying the causal effects of childhood trauma on depression). Key to solving such questions are observational studies. Mendelian Randomization (MR) is an influential method to establish causality in observational studies. MR uses genetic variants to test causal relationships between exposures/risk factors and outcomes such as physical or mental health. Yet, individual genetic variants have small effects, and so, when used as instrumental variables, render MR liable to weak instrument bias. Polygenic scores have the advantage of larger effects, but may be characterized by horizontal pleiotropy, which violates a central assumption of MR. We developed the MR-DoC twin model by integrating MR with the Direction of Causation twin model. This model allows us to test pleiotropy directly. We considered the issue of parameter identification, and given identification, we conducted extensive power calculations. MR-DoC allows one to test causal hypotheses and to obtain unbiased estimates of the causal effect given pleiotropic instruments, while controlling for genetic and environmental influences common to the outcome and exposure. Furthermore, the approach allows one to employ strong instrumental variables in the form of polygenic scores, guarding against weak instrument bias, and increasing the power to detect causal effects of exposures on potential outcomes. Beside allowing to test pleiotropy directly, incorporating in MR data collected from relatives provide additional within-family data that resolve additional assumptions like random mating, the absence of the gene-environment interaction/covariance, no dyadic effects. Our approach will enhance and extend MR's range of applications, and increase the value of the large cohorts collected at twin/family registries as they correctly detect causation and estimate effect sizes even in the presence of pleiotropy.
虽然实验研究被认为是确定因果影响的首选方法,但在回答健康和社会研究中的重要问题时,这些方法并不总是可行或合乎道德的(例如,在研究童年创伤对抑郁的因果影响时,不能将个体分配到“童年创伤状况”中)。解决此类问题的关键是观察性研究。孟德尔随机化(MR)是一种在观察性研究中建立因果关系的有影响力的方法。MR 使用遗传变异来检验暴露/风险因素与身体或心理健康等结果之间的因果关系。然而,个体遗传变异的影响较小,因此,当用作工具变量时,MR 容易受到弱工具偏差的影响。多基因分数具有较大的优势,但可能具有水平 pleiotropy,这违反了 MR 的一个中心假设。我们通过将 MR 与因果关系双胞胎模型相结合,开发了 MR-Doc 双胞胎模型。该模型允许我们直接测试 pleiotropy。我们考虑了参数识别问题,并在给定识别的情况下,进行了广泛的功效计算。MR-Doc 允许在存在多效工具的情况下测试因果假设并获得因果效应的无偏估计,同时控制与结果和暴露共同的遗传和环境影响。此外,该方法允许使用多基因分数形式的强工具变量,防止弱工具偏差,并增加检测暴露对潜在结果的因果效应的能力。除了允许直接测试 pleiotropy 之外,将从亲属那里收集的 MR 数据纳入其中,可以提供更多的家庭内数据,从而解决了随机交配、不存在基因-环境相互作用/协方差、没有二元效应等额外假设。我们的方法将增强和扩展 MR 的应用范围,并增加双胞胎/家庭登记处收集的大量队列的价值,因为它们即使在存在 pleiotropy 的情况下也能正确检测因果关系并估计效应大小。