Evidence map›Paper›PMID 27460712›Full record

ReviewObesity (Silver Spring, Md.)2016

Body mass index: Has epidemiology started to break down causal contributions to health and disease?

Laura J Corbin, Nicholas J Timpson

Abstract readReview
In one paragraph

Review in Obesity (Silver Spring, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Genetics of Severe Obesity.Current diabetes reports · 2018
    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.

Laura J CorbinMRC Integrative Epidemiology Unit (IEU) at the University of Bristol, Bristol, UK.
Nicholas J TimpsonMRC Integrative Epidemiology Unit (IEU) at the University of Bristol, Bristol, UK.

Funding

Medical Research Council MC_UU_12013/3Wellcome Trust 202802Wellcome Trust 202802/Z/16/Z
6 · The paper itself

Abstract

objectivesTo review progress in understanding the methods and results concerning the causal contribution of body mass index (BMI) to health and disease.

methodsIn the context of conventional evidence focused on the relationship between BMI and health, this review considers current literature on the common, population-based, genetic contribution to BMI and how this has fed into the developing field of applied epidemiology.

resultsTechnological and analytical developments have driven considerable success in identifying genetic variants relevant to BMI. This has enabled the implementation of Mendelian randomization to address questions of causality. The product of this work has been the implication of BMI as a causal agent in a host of health outcomes. Further breakdown of causal pathways by integration with other "omics" technologies promises to deliver additional benefit.

conclusionsGaps remain in our understanding of BMI as a risk factor for health and disease, and while promising, applied genetic epidemiology should be considered alongside alternative methods for assessing the impact of BMI on health. Potential limitations, relating to inappropriate or nonspecific measures of obesity and the improper use of genetic instruments, will need to be explored and incorporated into future research aiming to dissect BMI as a risk factor.

Indexed as

Body Mass IndexMendelian Randomization AnalysisBody WeightGenetic VariationHumansObesityPhenotypeRisk Factors

Identifiers

PMID27460712
PMCPMC5972005

What Socratic 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 Socratic graph.