Evidence map›Paper›PMID 21593077›Full record

SynthesisInternational journal of epidemiology2011

Genetic variation at CHRNA5-CHRNA3-CHRNB4 interacts with smoking status to influence body mass index.

Rachel M Freathy, Gbenga R Kazeem, Richard W Morris, Paul C D Johnson, Lavinia Paternoster, Shah Ebrahim, Andrew T Hattersley, Anita Hill, Aroon D Hingorani, Claus Holst and 18 more

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in International journal of epidemiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 5 pooled it
7.2field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 5 syntheses or guidelines pooled it, 127 citations in OpenAlex.

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12 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

28 authors at 9 institutions in 1 country.

Rachel M FreathyThe MRC Centre for Causal Analyses in Translational Epidemiology, Department of Social Medicine, University of Bristol, Bristol, UK.
Gbenga R Kazeem
Richard W Morris
Paul C D Johnson
Lavinia Paternoster
Shah Ebrahim
Andrew T Hattersley
Anita Hill
Aroon D Hingorani
Claus Holst
Barbara J Jefferis
Sofia I I Kring
Vincent Mooser
Sandosh Padmanabhan
Martin Preisig
Susan M Ring
Naveed Sattar
Mark N Upton
Peter Vollenweider
Gerard Waeber
Thorkild I A Sørensen
Timothy M Frayling
Graham Watt
Debbie A Lawlor
Peter H Whincup
Federica Tozzi
George Davey Smith
Marcus Munafò
GlaxoSmithKline (United Kingdom) · GBBritish Heart Foundation · GBSt George's, University of London · GBLondon School of Hygiene & Tropical Medicine · GBUniversity of Bristol · GBUniversity of Exeter · GBUniversity College London · GBPeninsula College of Medicine and Dentistry · GBUniversity of Glasgow · GB

Funding

British Heart Foundation FS05/125British Heart Foundation RG/08/013/25942Department of HealthMedical Research Council G0500070Medical Research Council G0600705Medical Research Council G0802736Medical Research Council G9815508Wellcome Trust 085541/Z/08/ZWellcome Trust 092731Wellcome Trust WT084762
6 · The paper itself

Abstract

backgroundCigarette smoking is associated with lower body mass index (BMI), and a commonly cited reason for unwillingness to quit smoking is a concern about weight gain. Common variation in the CHRNA5-CHRNA3-CHRNB4 gene region (chromosome 15q25) is robustly associated with smoking quantity in smokers, but its association with BMI is unknown. We hypothesized that genotype would accurately reflect smoking exposure and that, if smoking were causally related to weight, it would be associated with BMI in smokers, but not in never smokers.

methodsWe stratified nine European study samples by smoking status and, in each stratum, analysed the association between genotype of the 15q25 SNP, rs1051730, and BMI. We meta-analysed the results (n = 24,198) and then tested for a genotype × smoking status interaction.

resultsThere was no evidence of association between BMI and genotype in the never smokers {difference per T-allele: 0.05 kg/m(2) [95% confidence interval (95% CI): -0.05 to 0.18]; P = 0.25}. However, in ever smokers, each additional smoking-related T-allele was associated with a 0.23 kg/m(2) (95% CI: 0.13-0.31) lower BMI (P = 8 × 10(-6)). The effect size was larger in current [0.33 kg/m(2) lower BMI per T-allele (95% CI: 0.18-0.48); P = 6 × 10(-5)], than in former smokers [0.16 kg/m(2) (95% CI: 0.03-0.29); P = 0.01]. There was strong evidence of genotype × smoking interaction (P = 0.0001).

conclusionsSmoking status modifies the association between the 15q25 variant and BMI, which strengthens evidence that smoking exposure is causally associated with reduced BMI. Smoking cessation initiatives might be more successful if they include support to maintain a healthy BMI.

Indexed as

Body Mass IndexAdultAgedBody CompositionClinical Trials as TopicFemaleGenotypeHumansMaleMiddle AgedNerve Tissue ProteinsPolymorphism, Single NucleotideReceptors, NicotinicSmokingWeight GainCHRNA5 protein, humanNerve Tissue ProteinsReceptors, Nicotinic

Identifiers

PMID21593077
PMCPMC3235017
OpenAlexW2147916435

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.