ArticlePLoS genetics2016
G = E: What GWAS Can Tell Us about the Environment.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 59 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Systematic review of Mendelian randomization studies on risk of cancer.BMC medicine · 2022Pooled it
- Leveraging polygenic risk scores to infer causal directions in genotype-by-environment interactions between complex traits.Human genetics · 2026Article
- Personality Genomics.Annual review of psychology · 2026Review
- How exposomic tools complement and enrich genomic research.Cell genomics · 2025Review
- Comparison of caffeine consumption behavior with plasma caffeine levels as exposure measures in drug-target mendelian randomization.American journal of epidemiology · 2024Article
- Association Between Glaucoma and Brain Structural Connectivity Based on Diffusion Tensor Tractography: A Bidirectional Mendelian Randomization Study.Brain sciences · 2024Article
- An approach to identify gene-environment interactions and reveal new biological insight in complex traits.Nature communications · 2024Article
- MRSamePopTest: introducing a simple falsification test for the two-sample mendelian randomisation 'same population' assumption.BMC research notes · 2024Article
- Exploring the causal links between cigarette smoking, alcohol consumption, and aneurysmal subarachnoid hemorrhage: a two-sample Mendelian randomization analysis.Frontiers in nutrition · 2024Article
- A new Approach to Identify Gene-Environment Interactions and Reveal New Biological Insight in Complex traits.Research square · 2023Article
- Exploring the Lifetime Effect of Children on Wellbeing Using Two-Sample Mendelian Randomisation.Genes · 2023Article
- Why we need families in genomic research on developmental psychopathology.JCPP advances · 2023Article
- Gene-environment interactions and their impact on human health.Genes and immunity · 2023Review
- A genetically informed Registered Report on adverse childhood experiences and mental health.Nature human behaviour · 2023Article
- Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes.Journal of child psychology and psychiatry, and allied disciplines · 2022Review
- Article
- Association of Obsessive-Compulsive Disorder and Obsessive-Compulsive Symptoms With Substance Misuse in 2 Longitudinal Cohorts in Sweden.JAMA network open · 2022Article
- Enrichment analyses identify shared associations for 25 quantitative traits in over 600,000 individuals from seven diverse ancestries.American journal of human genetics · 2022Article
- Genetic Risk for Smoking: Disentangling Interplay Between Genes and Socioeconomic Status.Behavior genetics · 2022Article
- Lack of Support for the Genes by Early Environment Interaction Hypothesis in the Pathogenesis of Schizophrenia.Schizophrenia bulletin · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
As our understanding of genetics has improved, genome-wide association studies (GWAS) have identified numerous variants associated with lifestyle behaviours and health outcomes. However, what is sometimes overlooked is the possibility that genetic variants identified in GWAS of disease might reflect the effect of modifiable risk factors as well as direct genetic effects. We discuss this possibility with illustrative examples from tobacco and alcohol research, in which genetic variants that predict behavioural phenotypes have been seen in GWAS of diseases known to be causally related to these behaviours. This consideration has implications for the interpretation of GWAS findings.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.