Evidence map›Paper›PMID 22065844›Full record

ReviewDisease models & mechanisms2011

Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity.

John R Speakman, David A Levitsky, David B Allison, Molly S Bray, John M de Castro, Deborah J Clegg, John C Clapham, Abdul G Dulloo, Laurence Gruer, Sally Haw and 15 more

Abstract readReview
In one paragraph

Review in Disease models & mechanisms, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed, 3 pooled it
–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

142 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Short-term variability in body weight predicts long-term weight gain.The American journal of clinical nutrition · 2015
    Trial
  10. International Society of Sports Nutrition position stand: diets for body weight reduction.Journal of the International Society of Sports Nutrition · 2026
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Hypothalamic obesity.Reviews in endocrine & metabolic disorders · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review

82 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

25 authors.

John R SpeakmanInstitute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen, Scotland, AB39 2PN, UK. J.Speakman@abdn.ac.uk
David A Levitsky
David B Allison
Molly S Bray
John M de Castro
Deborah J Clegg
John C Clapham
Abdul G Dulloo
Laurence Gruer
Sally Haw
Johannes Hebebrand
Marion M Hetherington
Susanne Higgs
Susan A Jebb
Ruth J F Loos
Simon Luckman
Amy Luke
Vidya Mohammed-Ali
Stephen O'Rahilly
Mark Pereira
Louis Perusse
Tom N Robinson
Barbara Rolls
Michael E Symonds
Margriet S Westerterp-Plantenga

Funding

Training Interventions and Genetics of Exercise Response (TIGER)R01DK062148 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BRAY, MOLLY · 2003 to 2014
$6.0M
Medical Research Council G0600717Medical Research Council G0900554Medical Research Council G9824984Medical Research Council MC_U105960389Medical Research Council MC_U106188470NIDDK NIH HHS R01 DK062148
6 · The paper itself

Abstract

The close correspondence between energy intake and expenditure over prolonged time periods, coupled with an apparent protection of the level of body adiposity in the face of perturbations of energy balance, has led to the idea that body fatness is regulated via mechanisms that control intake and energy expenditure. Two models have dominated the discussion of how this regulation might take place. The set point model is rooted in physiology, genetics and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain. This model is consistent with many of the biological aspects of energy balance, but struggles to explain the many significant environmental and social influences on obesity, food intake and physical activity. More importantly, the set point model does not effectively explain the 'obesity epidemic'--the large increase in body weight and adiposity of a large proportion of individuals in many countries since the 1980s. An alternative model, called the settling point model, is based on the idea that there is passive feedback between the size of the body stores and aspects of expenditure. This model accommodates many of the social and environmental characteristics of energy balance, but struggles to explain some of the biological and genetic aspects. The shortcomings of these two models reflect their failure to address the gene-by-environment interactions that dominate the regulation of body weight. We discuss two additional models--the general intake model and the dual intervention point model--that address this issue and might offer better ways to understand how body fatness is controlled.

Indexed as

Gene-Environment InteractionModels, BiologicalAdiposityFeeding BehaviorHumans

Identifiers

PMID22065844
PMCPMC3209643

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.