Evidence map›Paper›PMID 38508868›Full record

ArticleInternational journal of epidemiology2024

Alcohol consumption and the risk of all-cause and cause-specific mortality-a linear and nonlinear Mendelian randomization study.

Nigussie Assefa Kassaw, Ang Zhou, Anwar Mulugeta, Sang Hong Lee, Stephen Burgess, Elina Hyppönen

Abstract read
In one paragraph

Article in International journal of epidemiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–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

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3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

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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

6 authors.

Nigussie Assefa KassawAustralian Centre for Precision Health, University of South Australia, Adelaide, Australia.ORCID 0000-0001-5420-0671
Ang ZhouAustralian Centre for Precision Health, University of South Australia, Adelaide, Australia.ORCID 0000-0001-7088-0777
Anwar MulugetaAustralian Centre for Precision Health, University of South Australia, Adelaide, Australia.
Sang Hong LeeAustralian Centre for Precision Health, University of South Australia, Adelaide, Australia.
Stephen BurgessMedical Research Council Biostatistics Unit, University of Cambridge, Cambridge, UK.ORCID 0000-0001-5365-8760
Elina HyppönenAustralian Centre for Precision Health, University of South Australia, Adelaide, Australia.

Funding

Department of Health NIHR203312Medical Research Council MC_UU_00002/7Wellcome Trust 100114Wellcome Trust 225790Wellcome Trust 225790/Z/22/Z
6 · The paper itself

Abstract

backgroundMany observational studies support light-to-moderate alcohol intake as potentially protective against premature death. We used a genetic approach to evaluate the linear and nonlinear relationships between alcohol consumption and mortality from different underlying causes.

methodsWe used data from 278 093 white-British UK Biobank participants, aged 37-73 years at recruitment and with data on alcohol intake, genetic variants, and mortality. Habitual alcohol consumption was instrumented by 94 variants. Linear Mendelian randomization (MR) analyses were conducted using five complementary approaches, and nonlinear MR analyses by the doubly-ranked method.

resultsThere were 20 834 deaths during the follow-up (median 12.6 years). In conventional analysis, the association between alcohol consumption and mortality outcomes was 'J-shaped'. In contrast, MR analyses supported a positive linear association with premature mortality, with no evidence for curvature (Pnonlinearity ≥ 0.21 for all outcomes). The odds ratio [OR] for each standard unit increase in alcohol intake was 1.27 (95% confidence interval [CI] 1.16-1.39) for all-cause mortality, 1.30 (95% CI 1.10-1.53) for cardiovascular disease, 1.20 (95% CI 1.08-1.33) for cancer, and 2.06 (95% CI 1.36-3.12) for digestive disease mortality. These results were consistent across pleiotropy-robust methods. There was no clear evidence for an association between alcohol consumption and mortality from respiratory diseases or COVID-19 (1.32, 95% CI 0.96-1.83 and 1.46, 95% CI 0.99-2.16, respectively; Pnonlinearity ≥ 0.21).

conclusionHigher levels of genetically predicted alcohol consumption had a strong linear association with an increased risk of premature mortality with no evidence for any protective benefit at modest intake levels.

Indexed as

Cardiovascular DiseasesMendelian Randomization AnalysisAlcohol DrinkingCausalityCause of DeathGenome-Wide Association StudyHumansPolymorphism, Single NucleotideAlcohol consumptiondoubly-ranked methodMendelian randomizationmortalitynonlinear analysis

Identifiers

PMID38508868
PMCPMC10951973

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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.