Evidence map›Paper›PMID 28352118›Full record

ReviewEuropean journal of clinical nutrition2017

Body composition and susceptibility to type 2 diabetes: an evolutionary perspective.

J C K Wells

Abstract readReview
PubMed Publisher
In one paragraph

Review in European journal of clinical nutrition, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
8.1field-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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Beyond Deterministic Fetal Programming: Intrauterine Exposures and the Multifactorial Origins of Adiposity.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  2. Review
  3. Article
  4. Fat-Free Mass: Friend or Foe to Metabolic Health?Journal of cachexia, sarcopenia and muscle · 2025
    Review
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  8. Review
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  13. Review
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  16. Review
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  18. Developmental plasticity as adaptation: adjusting to the external environment under the imprint of maternal capital.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
  19. Article
  20. Article
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

1 author at 1 institution in 1 country.

J C K WellsChildhood Nutrition Research Centre, UCL Great Ormond Street Institute of Child Health, London, UK.
University College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes is rapidly increasing in prevalence worldwide, in concert with epidemics of obesity and sedentary behavior that are themselves tracking economic development. Within this broad pattern, susceptibility to diabetes varies substantially in association with ethnicity and nutritional exposures through the life-course. An evolutionary perspective may help understand why humans are so prone to this condition in modern environments, and why this risk is unequally distributed. A simple conceptual model treats diabetes risk as the function of two interacting traits, namely 'metabolic capacity' which promotes glucose homeostasis, and 'metabolic load' which challenges glucose homoeostasis. This conceptual model helps understand how long-term and more recent trends in body composition can be considered to have shaped variability in diabetes risk. Hominin evolution appears to have continued a broader trend evident in primates, towards lower levels of muscularity. In addition, hominins developed higher levels of body fatness, especially in females in relative terms. These traits most likely evolved as part of a broader reorganization of human life history traits in response to growing levels of ecological instability, enabling both survival during tough periods and reproduction during bountiful periods. Since the emergence of Homo sapiens, populations have diverged in body composition in association with geographical setting and local ecological stresses. These long-term trends in both metabolic capacity and adiposity help explain the overall susceptibility of humans to diabetes in ways that are similar to, and exacerbated by, the effects of nutritional exposures during the life-course.

Indexed as

Body CompositionAdiposityDiabetes Mellitus, Type 2Genetic Predisposition to DiseaseHumansObesityPrevalenceRisk FactorsSedentary Behavior

Identifiers

PMID28352118
OpenAlexW2597805022

What OpenQuestion holds

Textmetadata
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.