Evidence map›Paper›PMID 38853248›Full record

ArticleBMC medicine2024

How do lifestyle factors modify the association between genetic predisposition and obesity-related phenotypes? A 4-way decomposition analysis using UK Biobank.

Mengrong Zhang, Joey Ward, Rona J Strawbridge, Carlos Celis-Morales, Jill P Pell, Donald M Lyall, Frederick K Ho

Abstract read
In one paragraph

Article in BMC medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

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

17 citing papers in PubMed.

  1. Effects of obesity on brain health and cognition.Nature reviews. Neurology · 2026
    Review
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  10. The Genetic Blueprint of Obesity: From Pathogenesis to Novel Therapies.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Review
  11. Article
  12. Article
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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

7 authors.

Mengrong ZhangSchool of Health and Wellbeing, University of Glasgow, Clarice Pears Building, 90 Byers Road, Glasgow, G12 8TB, UK.
Joey WardSchool of Health and Wellbeing, University of Glasgow, Clarice Pears Building, 90 Byers Road, Glasgow, G12 8TB, UK.
Rona J StrawbridgeSchool of Health and Wellbeing, University of Glasgow, Clarice Pears Building, 90 Byers Road, Glasgow, G12 8TB, UK.
Carlos Celis-MoralesSchool of Cardiovascular and Metabolic Sciences, University of Glasgow, Glasgow, UK.
Jill P Pell *School of Health and Wellbeing, University of Glasgow, Clarice Pears Building, 90 Byers Road, Glasgow, G12 8TB, UK.
Donald M Lyall *School of Health and Wellbeing, University of Glasgow, Clarice Pears Building, 90 Byers Road, Glasgow, G12 8TB, UK.
Frederick K Ho *School of Health and Wellbeing, University of Glasgow, Clarice Pears Building, 90 Byers Road, Glasgow, G12 8TB, UK. Frederick.Ho@glasgow.ac.uk.ORCID 0000-0001-7190-9025

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity and central obesity are multifactorial conditions with genetic and non-genetic (lifestyle and environmental) contributions. There is incomplete understanding of whether lifestyle modifies the translation from respective genetic risks into phenotypic obesity and central obesity, and to what extent genetic predisposition to obesity and central obesity is mediated via lifestyle factors.

methodsThis is a cross-sectional study of 201,466 (out of approximately 502,000) European participants from UK Biobank and tested for interactions and mediation role of lifestyle factors (diet quality; physical activity levels; total energy intake; sleep duration, and smoking and alcohol intake) between genetic risk for obesity and central obesity. BMI-PRS and WHR-PRS are exposures and obesity and central obesity are outcomes.

resultsOverall, 42.8% of the association between genetic predisposition to obesity and phenotypic obesity was explained by lifestyle: 0.9% by mediation and 41.9% by effect modification. A significant difference between men and women was found in central obesity; the figures were 42.1% (association explained by lifestyle), 1.4% (by mediation), and 40.7% (by modification) in women and 69.6% (association explained by lifestyle), 3.0% (by mediation), and 66.6% (by modification) in men.

conclusionsA substantial proportion of the association between genetic predisposition to obesity/central obesity and phenotypic obesity/central obesity was explained by lifestyles. Future studies with repeated measures of obesity and lifestyle would be needed to clarify causation.

Indexed as

Biological Specimen BanksGenetic Predisposition to DiseaseLife StyleObesityPhenotypeAdultAgedCross-Sectional StudiesFemaleHumansMaleMiddle AgedObesity, AbdominalUK BiobankUnited KingdomBMI-PRSCentral obesityObesityTotal lifestyle factorsWHR-PRS

Identifiers

PMID38853248
PMCPMC11163778

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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.