Evidence map›Paper›PMID 25400997›Full record

ReviewWorld journal of gastrointestinal pathophysiology2014

Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma.

Leo Alexandre, Elizabeth Long, Ian Lp Beales

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

Review in World journal of gastrointestinal pathophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
6.7field-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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Review
  6. Review
  7. Associations between body mass index and gastroesophageal cancer incidence and mortality: novel insights from a nationwide registry-based cohort study.Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus · 2025
    Article
  8. Article
  9. Review
  10. Mitochondrial CaScientific reports · 2024
    Article
  11. Article
  12. Dietary fat and lipid metabolism in the tumor microenvironment.Biochimica et biophysica acta. Reviews on cancer · 2023
    Review
  13. Impact of Morbid Obesity on Post-esophagectomy Leak Rate: a NSQIP Analysis.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Leo AlexandreLeo Alexandre, Elizabeth Long, Ian LP Beales, Norwich Medical School, University of East Anglia, Norwich, Norfolk NR4 7TJ, United Kingdom.
Elizabeth LongLeo Alexandre, Elizabeth Long, Ian LP Beales, Norwich Medical School, University of East Anglia, Norwich, Norfolk NR4 7TJ, United Kingdom.
Ian Lp BealesLeo Alexandre, Elizabeth Long, Ian LP Beales, Norwich Medical School, University of East Anglia, Norwich, Norfolk NR4 7TJ, United Kingdom.
University of East Anglia · GB

Funding

Department of Health DRF-2013-06-115
6 · The paper itself

Abstract

In recent decades there has been a dramatic rise in the incidence of esophageal adenocarcinoma (EAC) in the developed world. Over approximately the same period there has also been an increase in the prevalence of obesity. Obesity, especially visceral obesity, is an important independent risk factor for the development of gastro-esophageal reflux disease, Barrett's esophagus and EAC. Although the simplest explanation is that this mediated by the mechanical effects of abdominal obesity promoting gastro-esophageal reflux, the epidemiological data suggest that the EAC-promoting effects are independent of reflux. Several, not mutually exclusive, mechanisms have been implicated, which may have different effects at various points along the reflux-Barrett's-cancer pathway. These mechanisms include a reduction in the prevalence of Helicobacter pylori infection enhancing gastric acidity and possibly appetite by increasing gastric ghrelin secretion, induction of both low-grade systemic inflammation by factors secreted by adipose tissue and the metabolic syndrome with insulin-resistance. Obesity is associated with enhanced secretion of leptin and decreased secretion of adiponectin from adipose tissue and both increased leptin and decreased adiponectin have been shown to be independent risk factors for progression to EAC. Leptin and adiponectin have a set of mutually antagonistic actions on Barrett's cells which appear to influence the progression of malignant behaviour. At present no drugs are of proven benefit to prevent obesity associated EAC. Roux-en-Y reconstruction is the preferred bariatric surgical option for weight loss in patients with reflux. Statins and aspirin may have chemopreventative effects and are indicated for their circulatory benefits.

Indexed as

AdiposeBarrett’s esophagusBody mass indexReflux

Identifiers

PMID25400997
PMCPMC4231518
OpenAlexW1968520358

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.