Evidence map›Paper›PMID 36394061›Full record

ReviewLife metabolism2022

Obesity: an evolutionary context.

John R Speakman, Joel K Elmquist

Open access · diamondAbstract readReview
In one paragraph

Review in Life metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
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  5. Review
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  11. MTCH2 Suppresses Thermogenesis by Regulating Autophagy in Adipose Tissue.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Effects ofFrontiers in physiology · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Obesity and cardiovascular health.European journal of preventive cardiology · 2024
    Review
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

2 authors at 2 institutions in 3 countries.

John R SpeakmanShenzhen Key Laboratory of Metabolic Health, Center for Energy Metabolism and Reproduction, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Joel K ElmquistDepartments of Internal Medicine and Pharmacology, Center for Hypothalamic Research, University of Texas Southwestern, Dallas, TX, USA.
The University of Texas Southwestern Medical Center · USUniversity of Aberdeen · GB

Funding

Ventromedial Hypothalamic Regulation of Metabolic Changes Induced by ExerciseP01DK119130 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WASSERMAN, DAVID H · 2019 to 2023
$10.0M
Metabolic Benefits of Leptin ReductionR01DK127274 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST, PHILIPP E SCHERER · 2021 to 2026
$5.1M
SF1 neurons and sympathetic regulation of glucose homeostasisR01DK100659 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2014 to 2026
$4.8M
Interactions of Leptin and the Melanocortin SystemR01DK118725 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2018 to 2026
$3.5M
NIDDK NIH HHS P01 DK119130NIDDK NIH HHS R01 DK100659NIDDK NIH HHS R01 DK118725NIDDK NIH HHS R01 DK127274
6 · The paper itself

Abstract

People completely lacking body fat (lipodystrophy/lipoatrophy) and those with severe obesity both show profound metabolic and other health issues. Regulating levels of body fat somewhere between these limits would, therefore, appear to be adaptive. Two different models might be contemplated. More traditional is a set point (SP) where the levels are regulated around a fixed level. Alternatively, dual-intervention point (DIP) is a system that tolerates fairly wide variation but is activated when critically high or low levels are breached. The DIP system seems to fit our experience much better than an SP, and models suggest that it is more likely to have evolved. A DIP system may have evolved because of two contrasting selection pressures. At the lower end, we may have been selected to avoid low levels of fat as a buffer against starvation, to avoid disease-induced anorexia, and to support reproduction. At the upper end, we may have been selected to avoid excess storage because of the elevated risks of predation. This upper limit of control seems to have malfunctioned because some of us deposit large fat stores, with important negative health effects. Why has evolution not protected us against this problem? One possibility is that the protective system slowly fell apart due to random mutations after we dramatically reduced the risk of being predated during our evolutionary history. By chance, it fell apart more in some people than others, and these people are now unable to effectively manage their weight in the face of the modern food glut. To understand the evolutionary context of obesity, it is important to separate the adaptive reason for storing some fat (i.e. the lower intervention point), from the nonadaptive reason for storing lots of fat (a broken upper intervention point). The DIP model has several consequences, showing how we understand the obesity problem and what happens when we attempt to treat it.

Indexed as

adaptiveadiposityBMIbody fatdual-intervention point modelevolutionleptin resistancemetabolic programmingobesityselectionset-point model

Identifiers

PMID36394061
PMCPMC9642988
OpenAlexW4225147609

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.