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      A framework for the investigation of pleiotropy in two‐sample summary data Mendelian randomization

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          Abstract

          Mendelian randomization (MR) uses genetic data to probe questions of causality in epidemiological research, by invoking the Instrumental Variable (IV) assumptions. In recent years, it has become commonplace to attempt MR analyses by synthesising summary data estimates of genetic association gleaned from large and independent study populations. This is referred to as two‐sample summary data MR. Unfortunately, due to the sheer number of variants that can be easily included into summary data MR analyses, it is increasingly likely that some do not meet the IV assumptions due to pleiotropy. There is a pressing need to develop methods that can both detect and correct for pleiotropy, in order to preserve the validity of the MR approach in this context. In this paper, we aim to clarify how established methods of meta‐regression and random effects modelling from mainstream meta‐analysis are being adapted to perform this task. Specifically, we focus on two contrastin g approaches: the Inverse Variance Weighted (IVW) method which assumes in its simplest form that all genetic variants are valid IVs, and the method of MR‐Egger regression that allows all variants to violate the IV assumptions, albeit in a specific way. We investigate the ability of two popular random effects models to provide robustness to pleiotropy under the IVW approach, and propose statistics to quantify the relative goodness‐of‐fit of the IVW approach over MR‐Egger regression. © 2017 The Authors. Statistics in Medicine Published by JohnWiley & Sons Ltd

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          'Mendelian randomization': can genetic epidemiology contribute to understanding environmental determinants of disease?

          Associations between modifiable exposures and disease seen in observational epidemiology are sometimes confounded and thus misleading, despite our best efforts to improve the design and analysis of studies. Mendelian randomization-the random assortment of genes from parents to offspring that occurs during gamete formation and conception-provides one method for assessing the causal nature of some environmental exposures. The association between a disease and a polymorphism that mimics the biological link between a proposed exposure and disease is not generally susceptible to the reverse causation or confounding that may distort interpretations of conventional observational studies. Several examples where the phenotypic effects of polymorphisms are well documented provide encouraging evidence of the explanatory power of Mendelian randomization and are described. The limitations of the approach include confounding by polymorphisms in linkage disequilibrium with the polymorphism under study, that polymorphisms may have several phenotypic effects associated with disease, the lack of suitable polymorphisms for studying modifiable exposures of interest, and canalization-the buffering of the effects of genetic variation during development. Nevertheless, Mendelian randomization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to understanding and preventing the adverse effects on human health of modifiable exposures.
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            Mendelian randomization as an instrumental variable approach to causal inference.

            In epidemiological research, the causal effect of a modifiable phenotype or exposure on a disease is often of public health interest. Randomized controlled trials to investigate this effect are not always possible and inferences based on observational data can be confounded. However, if we know of a gene closely linked to the phenotype without direct effect on the disease, it can often be reasonably assumed that the gene is not itself associated with any confounding factors - a phenomenon called Mendelian randomization. These properties define an instrumental variable and allow estimation of the causal effect, despite the confounding, under certain model restrictions. In this paper, we present a formal framework for causal inference based on Mendelian randomization and suggest using directed acyclic graphs to check model assumptions by visual inspection. This framework allows us to address limitations of the Mendelian randomization technique that have often been overlooked in the medical literature.
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              Explaining heterogeneity in meta-analysis: a comparison of methods.

              Exploring the possible reasons for heterogeneity between studies is an important aspect of conducting a meta-analysis. This paper compares a number of methods which can be used to investigate whether a particular covariate, with a value defined for each study in the meta-analysis, explains any heterogeneity. The main example is from a meta-analysis of randomized trials of serum cholesterol reduction, in which the log-odds ratio for coronary events is related to the average extent of cholesterol reduction achieved in each trial. Different forms of weighted normal errors regression and random effects logistic regression are compared. These analyses quantify the extent to which heterogeneity is explained, as well as the effect of cholesterol reduction on the risk of coronary events. In a second example, the relationship between treatment effect estimates and their precision is examined, in order to assess the evidence for publication bias. We conclude that methods which allow for an additive component of residual heterogeneity should be used. In weighted regression, a restricted maximum likelihood estimator is appropriate, although a number of other estimators are also available. Methods which use the original form of the data explicitly, for example the binomial model for observed proportions rather than assuming normality of the log-odds ratios, are now computationally feasible. Although such methods are preferable in principle, they often give similar results in practice. Copyright 1999 John Wiley & Sons, Ltd.
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                Author and article information

                Contributors
                jack.bowden@bristol.ac.uk
                Journal
                Stat Med
                Stat Med
                10.1002/(ISSN)1097-0258
                SIM
                Statistics in Medicine
                John Wiley and Sons Inc. (Hoboken )
                0277-6715
                1097-0258
                23 January 2017
                20 May 2017
                : 36
                : 11 ( doiID: 10.1002/sim.v36.11 )
                : 1783-1802
                Affiliations
                [ 1 ] MRC Integrative Epidemiology UnitUniversity of Bristol U.K.
                [ 2 ] Center for BiomedicineEURAC research BolzanoItaly
                [ 3 ] Population Health and Occupational DiseaseNHLI, Imperial College LondonU.K.
                [ 4 ] Department of Health SciencesUniversity of Leicester LeicesterU.K.
                Author notes
                [*] [* ] Correspondence to: Jack Bowden, MRC Integrative Epidemiology Unit, Oakfield House, BS8 2BN.

                E‐mail: jack.bowden@ 123456bristol.ac.uk

                Article
                SIM7221 sim.7221
                10.1002/sim.7221
                5434863
                28114746
                fe64a201-5c28-44cb-8317-081f811e1cae
                © 2017 The Authors. Statistics in Medicine Published by JohnWiley & Sons Ltd

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 22 May 2016
                : 12 October 2016
                : 10 December 2016
                Page count
                Figures: 9, Tables: 4, Pages: 20, Words: 13800
                Funding
                Funded by: MRC Methodology Research Fellowship
                Award ID: MR/N501906/1
                Funded by: MRC Integrative Epidemiology Unit at the University of Bristol
                Award ID: MCUU12013/1
                Categories
                Research Article
                Research Articles
                Custom metadata
                2.0
                sim7221
                sim7221-hdr-0001
                20 May 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.0.9 mode:remove_FC converted:17.05.2017

                Biostatistics
                instrumental variables,mendelian randomization,meta‐analysis,mr‐egger regression,pleiotropy

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