Evidence map›Paper›PMID 23911805›Full record

ReviewPhysiology & behavior2013

Biological mechanisms that promote weight regain following weight loss in obese humans.

Christopher N Ochner, Dulce M Barrios, Clement D Lee, F Xavier Pi-Sunyer

Abstract readReview
In one paragraph

Review in Physiology & behavior, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
5.8field-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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 185 citations in OpenAlex.

  1. ZumbaInternational journal of environmental research and public health · 2020
    Pooled it
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  8. Obesity in Living Kidney Donors from Risk to Ethics: Bridging Gaps in Evaluation and Management.Clinical journal of the American Society of Nephrology : CJASN · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Do Weight Suppression and Body Mass Index Predict Daily Body Image and Eating Urges in Non-Clinical Adults?European eating disorders review : the journal of the Eating Disorders Association · 2026
    Article
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26 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

4 authors at 2 institutions in 1 country.

Christopher N OchnerNew York Obesity Nutrition Research Center, St. Luke's Roosevelt Hospital, Columbia University College of Physicians and Surgeons, New York, NY, USA; Mount Sinai Adolescent Health Center, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: christopher.ochner@mountsinai.org.
Dulce M Barrios
Clement D Lee
F Xavier Pi-Sunyer
Columbia University · USIcahn School of Medicine at Mount Sinai · US

Funding

RESEARCH TRAININGP30DK026687 · NIDDK · ST. LUKE'S-ROOSEVELT INST FOR HLTH SCIS · PI Anthony W Ferrante, DYMPNA GALLAGHER · 1986 to 2026
$33.0M
CTSA: K12 COMPONENTKL2RR024157 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2006 to 2011
$8.9M
NCRR NIH HHS KL2 RR024157NCRR NIH HHS KL2RR024157NIDDK NIH HHS P30 DK026687NIDDK NIH HHS P30DK26687
6 · The paper itself

Abstract

Weight loss dieting remains the treatment of choice for the vast majority of obese individuals, despite the limited long-term success of behavioral weight loss interventions. The reasons for the near universal unsustainability of behavioral weight loss in [formerly] obese individuals have not been fully elucidated, relegating researchers to making educated guesses about how to improve obesity treatment, as opposed to developing interventions targeting the causes of weight regain. This article discusses research on several factors that may contribute to weight regain following weight loss achieved through behavioral interventions, including adipose cellularity, endocrine function, energy metabolism, neural responsivity, and addiction-like neural mechanisms. All of these mechanisms are engaged prior to weight loss, suggesting that these so called "anti-starvation" mechanisms are activated via reductions in energy intake, rather than depletion of energy stores. Evidence suggests that these mechanisms are not necessarily part of a homeostatic feedback system designed to regulate body weight, or even anti-starvation mechanisms per se. Although they may have evolved to prevent starvation, they appear to be more accurately described as anti-weight loss mechanisms, engaged with caloric restriction irrespective of the adequacy of energy stores. It is hypothesized that these factors may combine to create a biological disposition that fosters the maintenance of an elevated body weight and works to restore the highest sustained body weight, thus precluding the long-term success of behavioral weight loss. It may be necessary to develop interventions that attenuate these biological mechanisms in order to achieve long-term weight reduction in obese individuals.

Indexed as

Adipose TissueBehavior, AddictiveDiet, ReducingEndocrine GlandsEnergy MetabolismHumansObesityRecurrenceWeight GainWeight LossAdiposeBMIBrainDietEndocrineMetabolicMetabolismNeural

Identifiers

PMID23911805
PMCPMC3797148
OpenAlexW2065853269

What OpenQuestion holds

Textmetadata
LicenceTDM
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.