Evidence map›Paper›PMID 26291580›Full record

ArticleJournal of clinical epidemiology2016

Beyond Mendelian randomization: how to interpret evidence of shared genetic predictors.

Stephen Burgess, Adam S Butterworth, John R Thompson

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical epidemiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 5 pooled it
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
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  11. The Causal Effect of Adult Height on Late-Life Handgrip Strength: The Singapore Chinese Health Study.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024
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  14. Ethnic-specific associations between body mass index and gastric cancer: a Mendelian randomization study in European and Korean populations.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024
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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Stephen BurgessCardiovascular Epidemiology Unit, Department of Public Health and Primary Care, 2 Worts Causeway, Cambridge CB1 8RN, UK; Homerton College, University of Cambridge, Hills Road, Cambridge CB2 8PH, UK. Electronic address: sb452@medschl.cam.ac.uk.
Adam S ButterworthCardiovascular Epidemiology Unit, Department of Public Health and Primary Care, 2 Worts Causeway, Cambridge CB1 8RN, UK.
John R ThompsonDepartment of Health Sciences, Adrian Building, University Road, Leicester, LE1 7RH, UK.

Funding

British Heart Foundation RG/08/014/24067British Heart Foundation SP/08/007/23628Medical Research Council MC_UU_00002/7Medical Research Council MR/L003120/1Wellcome TrustWellcome Trust 100114
6 · The paper itself

Abstract

objectiveMendelian randomization is a popular technique for assessing and estimating the causal effects of risk factors. If genetic variants which are instrumental variables for a risk factor are shown to be additionally associated with a disease outcome, then the risk factor is a cause of the disease. However, in many cases, the instrumental variable assumptions are not plausible, or are in doubt. In this paper, we provide a theoretical classification of scenarios in which a causal conclusion is justified or not justified, and discuss the interpretation of causal effect estimates.

resultsA list of guidelines based on the 'Bradford Hill criteria' for judging the plausibility of a causal finding from an applied Mendelian randomization study is provided. We also give a framework for performing and interpreting investigations performed in the style of Mendelian randomization, but where the choice of genetic variants is statistically, rather than biologically motivated. Such analyses should not be assigned the same evidential weight as a Mendelian randomization investigation.

conclusionWe discuss the role of such investigations (in the style of Mendelian randomization), and what they add to our understanding of potential causal mechanisms. If the genetic variants are selected solely according to statistical criteria, and the biological roles of genetic variants are not investigated, this may be little more than what can be learned from a well-designed classical observational study.

Indexed as

Mendelian Randomization AnalysisData Interpretation, StatisticalGenetic VariationAetiologyCausal inferenceGenetic predictorsGenetic variantsInstrumental variableMendelian randomizationTranslational Genetics

Identifiers

PMID26291580
PMCPMC4687951

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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.