Evidence map›Paper›PMID 37482774›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2023

Behavioural susceptibility theory: the role of appetite in genetic susceptibility to obesity in early life.

C H Llewellyn, A R Kininmonth, M Herle, Z Nas, A D Smith, S Carnell, A Fildes

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  16. Canine genome-wide association study identifiesScience (New York, N.Y.) · 2025
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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 at 5 institutions in 2 countries.

C H LlewellynResearch Department of Behavioural Science and Health, Institute of Epidemiology and Health Care, University College London, London, WC1E 6BT, UK.ORCID 0000-0002-0066-2827
A R KininmonthResearch Department of Behavioural Science and Health, Institute of Epidemiology and Health Care, University College London, London, WC1E 6BT, UK.ORCID 0000-0002-1145-525X
M HerleSocial, Genetic & Developmental Psychiatry Centre, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, SE5 8AF, UK.ORCID 0000-0003-3220-5070
Z NasResearch Department of Behavioural Science and Health, Institute of Epidemiology and Health Care, University College London, London, WC1E 6BT, UK.
A D SmithMRC Epidemiology Unit, University of Cambridge, Cambridge, CB2 0SL, UK.ORCID 0000-0002-6925-6667
S CarnellDepartment of Psychiatry and Behavioural Sciences, Johns Hopkins University School of Medicine, Baltimore, MD21287, USA.ORCID 0000-0001-6200-3635
A FildesSchool of Psychology, University of Leeds, Leeds, LS2 9JT, UK.ORCID 0000-0002-5452-2512
Department of Health and Social Care · GBJohns Hopkins University · USKing's College London · GBUniversity of Cambridge · GBUniversity of Leeds · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excess weight gained during the early years and, in particular, rapid weight gain in the first 2 years of life, are a major risk factors for adult obesity. The growing consensus is that childhood obesity develops from a complex interaction between genetic susceptibility and exposure to an 'obesogenic' environment. Behavioural susceptibility theory (BST) was developed to explain the nature of this gene-environment interaction, and why the 'obesogenic' environment does not affect all children equally. It hypothesizes that inherited variation in appetite, which is present from birth, determines why some infants and children overeat, and others do not, in response to environmental opportunity. That is, those who inherit genetic variants promoting an avid appetite are vulnerable to overeating and developing obesity, while those who are genetically predisposed to have a smaller appetite and lower interest in food are protected from obesity-or even at risk of being underweight. We review the breadth of research to-date that has contributed to the evidence base for BST, focusing on early life, and discuss implications and future directions for research and theory. This article is part of a discussion meeting issue 'Causes of obesity: theories, conjectures and evidence (Part I)'.

Indexed as

AppetitePediatric ObesityChildFeeding BehaviorGene-Environment InteractionGenetic Predisposition to DiseaseHumansappetitebehavioural susceptibility theoryenvironmentgenesobesity

Identifiers

PMID37482774
PMCPMC10363697
OpenAlexW4385185936

What OpenQuestion holds

Textmetadata
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.