Evidence map›Paper›PMID 28921935›Full record

ArticleAddiction (Abingdon, England)2018

Assessing causal relationships using genetic proxies for exposures: an introduction to Mendelian randomization.

Srinivasa Vittal Katikireddi, Michael J Green, Amy E Taylor, George Davey Smith, Marcus R Munafò

Open access · hybridAbstract read
In one paragraph

Article in Addiction (Abingdon, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 4 pooled it
3.3field-weighted citation impact, top 8% of its field
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

33 citing papers in PubMed, 4 syntheses or guidelines pooled it, 64 citations in OpenAlex.

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  5. Calcium and Vitamin D Supplementation Are Not Associated With Risk of Incident Ischemic Cardiac Events or Death: Findings From the UK Biobank Cohort.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018
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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

5 authors at 2 institutions in 1 country.

Srinivasa Vittal KatikireddiMRC/CSO Social and Public Health Sciences Unit, University of Glasgow, Glasgow, UK.ORCID 0000-0001-6593-9092
Michael J GreenMRC/CSO Social and Public Health Sciences Unit, University of Glasgow, Glasgow, UK.
Amy E TaylorMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.ORCID 0000-0003-1853-0563
George Davey SmithMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
Marcus R MunafòMRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
University of Bristol · GBMRC/CSO Social and Public Health Sciences Unit · GB

Funding

Chief Scientist Office SCAF/15/02Chief Scientist Office SPHSU13Chief Scientist Office SPHSU15Medical Research Council MC_UU_00011/7Medical Research Council MC_UU_12013/1Medical Research Council MC_UU_12013/6Medical Research Council MC_UU_12017/13Medical Research Council MC_UU_12017/15
6 · The paper itself

Abstract

BACKGROUND AND

aimsStudying the consequences of addictive behaviours is challenging, with understanding causal relationships from observational data being particularly difficult. For example, people who smoke or drink excessively are often systematically different from those who do not, are less likely to participate in research and may misreport their behaviours when they do. Furthermore, the direction of causation between an addictive behaviour and outcome may be unclear. Mendelian randomization (MR) offers potential solutions to these problems.

methodsWe describe MR's principles and the criteria under which it is valid. We identify challenges and potential solutions in its application (illustrated using two applied examples) and describe methodological extensions in its application.

resultsMR is subject to certain assumptions, and requires the availability of appropriate genetic data, large sample sizes and careful design and conduct. However, it has already been applied successfully to the addiction literature. The relationship between alcohol consumption (proxied by a variant in the ADH1B gene) and cardiovascular risk has been investigated, finding that alcohol consumption increases risk, with no evidence of a cardioprotective effect at moderate consumption levels. In addition, heaviness of smoking (proxied by a variant in the CHRNA5-A3-B4 gene cluster) and risk of depression and schizophrenia have been investigated, with no evidence of a causal effect of smoking on depression but some evidence of a causal effect on schizophrenia.

conclusionsMendelian randomization analyses are already producing robust evidence for addiction-related practice and policy. As genetic variants associated with addictive behaviours are identified, the potential for Mendelian randomization analyses will grow. Methodological developments are also increasing its applicability.

Indexed as

CausalityMendelian Randomization AnalysisAlcohol DehydrogenaseAlcohol DrinkingCardiovascular DiseasesDepressive DisorderGenetic Predisposition to DiseaseGenetic VariationHumansNerve Tissue ProteinsReceptors, NicotinicSchizophreniaSmokingADH1B protein, humanAlcohol DehydrogenaseCHRNA5 protein, humanCHRNB4 protein, humanNerve Tissue ProteinsReceptors, NicotinicAddictive behaviourcausalityeconometric modelsepidemiological methodsgenetic epidemiologyMendelian randomization analysis

Identifiers

PMID28921935
PMCPMC5873430
OpenAlexW2755389687

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.