Literature DB >> 29882082

Extending Causality Tests with Genetic Instruments: An Integration of Mendelian Randomization with the Classical Twin Design.

Camelia C Minică1, Conor V Dolan2, Dorret I Boomsma2, Eco de Geus2, Michael C Neale2,3.   

Abstract

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.

Entities:  

Keywords:  Causality; Mendelian randomization; Pleiotropy; Twin design

Mesh:

Year:  2018        PMID: 29882082      PMCID: PMC6028857          DOI: 10.1007/s10519-018-9904-4

Source DB:  PubMed          Journal:  Behav Genet        ISSN: 0001-8244            Impact factor:   2.805


  59 in total

1.  Power and instrument strength requirements for Mendelian randomization studies using multiple genetic variants.

Authors:  Brandon L Pierce; Habibul Ahsan; Tyler J Vanderweele
Journal:  Int J Epidemiol       Date:  2010-09-02       Impact factor: 7.196

2.  A test of the equal environment assumption (EEA) in multivariate twin studies.

Authors:  Eske M Derks; Conor V Dolan; Dorret I Boomsma
Journal:  Twin Res Hum Genet       Date:  2006-06       Impact factor: 1.587

3.  Genetic pleiotropy in depression and coronary artery disease.

Authors:  Eco J C de Geus
Journal:  Psychosom Med       Date:  2006 Mar-Apr       Impact factor: 4.312

Review 4.  Avoiding bias from weak instruments in Mendelian randomization studies.

Authors:  Stephen Burgess; Simon G Thompson
Journal:  Int J Epidemiol       Date:  2011-03-16       Impact factor: 7.196

5.  Testing hypotheses about direction of causation using cross-sectional family data.

Authors:  A C Heath; R C Kessler; M C Neale; J K Hewitt; L J Eaves; K S Kendler
Journal:  Behav Genet       Date:  1993-01       Impact factor: 2.805

Review 6.  The Finnish Twin Cohort Study: an update.

Authors:  Jaakko Kaprio
Journal:  Twin Res Hum Genet       Date:  2013-01-08       Impact factor: 1.587

7.  Are extended twin family designs worth the trouble? A comparison of the bias, precision, and accuracy of parameters estimated in four twin family models.

Authors:  Matthew C Keller; Sarah E Medland; Laramie E Duncan
Journal:  Behav Genet       Date:  2009-12-16       Impact factor: 2.805

8.  Major depression and generalized anxiety disorder. Same genes, (partly) different environments?

Authors:  K S Kendler; M C Neale; R C Kessler; A C Heath; L J Eaves
Journal:  Arch Gen Psychiatry       Date:  1992-09

Review 9.  Mendelian Randomization: New Applications in the Coming Age of Hypothesis-Free Causality.

Authors:  David M Evans; George Davey Smith
Journal:  Annu Rev Genomics Hum Genet       Date:  2015-04-22       Impact factor: 8.929

10.  Mendelian randomisation and causal inference in observational epidemiology.

Authors:  Nuala A Sheehan; Vanessa Didelez; Paul R Burton; Martin D Tobin
Journal:  PLoS Med       Date:  2008-08-26       Impact factor: 11.069

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  12 in total

1.  Notes on Three Decades of Methodology Workshops.

Authors:  Hermine H Maes
Journal:  Behav Genet       Date:  2021-02-14       Impact factor: 2.805

2.  Onset of regular cannabis use and adult sleep duration: Genetic variation and the implications of a predictive relationship.

Authors:  Evan A Winiger; Spencer B Huggett; Alexander S Hatoum; Michael C Stallings; John K Hewitt
Journal:  Drug Alcohol Depend       Date:  2019-08-30       Impact factor: 4.492

3.  Investigating the causal risk factors for self-harm by integrating Mendelian randomisation within twin modelling.

Authors:  Kai Xiang Lim; Olakunle Ayokunmi Oginni; Kaili Rimfeld; Jean-Baptiste Pingault; Frühling Rijsdijk
Journal:  Behav Genet       Date:  2022-09-14       Impact factor: 2.965

4.  How humans can contribute to Mendelian randomization analyses.

Authors:  Stephen Burgess; George Davey Smith
Journal:  Int J Epidemiol       Date:  2019-06-01       Impact factor: 7.196

5.  Associations of coffee genetic risk scores with consumption of coffee, tea and other beverages in the UK Biobank.

Authors:  Amy E Taylor; George Davey Smith; Marcus R Munafò
Journal:  Addiction       Date:  2017-09-29       Impact factor: 6.526

6.  Avoiding dynastic, assortative mating, and population stratification biases in Mendelian randomization through within-family analyses.

Authors:  George Davey Smith; Bjørn Olav Åsvold; Gibran Hemani; Neil M Davies; Ben Brumpton; Eleanor Sanderson; Karl Heilbron; Fernando Pires Hartwig; Sean Harrison; Gunnhild Åberge Vie; Yoonsu Cho; Laura D Howe; Amanda Hughes; Dorret I Boomsma; Alexandra Havdahl; John Hopper; Michael Neale; Michel G Nivard; Nancy L Pedersen; Chandra A Reynolds; Elliot M Tucker-Drob; Andrew Grotzinger; Laurence Howe; Tim Morris; Shuai Li; Adam Auton; Frank Windmeijer; Wei-Min Chen; Johan Håkon Bjørngaard; Kristian Hveem; Cristen Willer; David M Evans; Jaakko Kaprio
Journal:  Nat Commun       Date:  2020-07-14       Impact factor: 14.919

7.  Bias in Mendelian randomization due to assortative mating.

Authors:  Fernando Pires Hartwig; Neil Martin Davies; George Davey Smith
Journal:  Genet Epidemiol       Date:  2018-07-03       Impact factor: 2.135

8.  Fetal Origins of Mental Disorders? An Answer Based on Mendelian Randomization.

Authors:  Subhi Arafat; Camelia C Minică
Journal:  Twin Res Hum Genet       Date:  2018-12       Impact factor: 1.587

9.  Investigating the association between family connectedness and self-control in adolescence in a genetically sensitive design.

Authors:  Yayouk E Willems; Odilia M Laceulle; Meike Bartels; Catrin Finkenauer
Journal:  Eur Child Adolesc Psychiatry       Date:  2020-02-05       Impact factor: 4.785

10.  Empirical comparisons of multiple Mendelian randomization approaches in the presence of assortative mating.

Authors:  Camelia C Minică; Dorret I Boomsma; Conor V Dolan; Eco de Geus; Michael C Neale
Journal:  Int J Epidemiol       Date:  2020-08-01       Impact factor: 7.196

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