Evidence map›Paper›PMID 26625858›Full record

ArticleDiabetologia2016

Innate biology versus lifestyle behaviour in the aetiology of obesity and type 2 diabetes: the GLACIER Study.

Alaitz Poveda, Robert W Koivula, Shafqat Ahmad, Inês Barroso, Göran Hallmans, Ingegerd Johansson, Frida Renström, Paul W Franks

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Morbidity and mortality associated with obesity.Annals of translational medicine · 2017 · on this map
    Review
  7. Article
  8. 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

8 authors at 3 institutions in 3 countries.

Alaitz PovedaGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Clinical Research Center Building 91, Level 10, Jan Waldenströms gata 35, SE-20502, Malmö, Sweden.
Robert W KoivulaGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Clinical Research Center Building 91, Level 10, Jan Waldenströms gata 35, SE-20502, Malmö, Sweden.
Shafqat AhmadGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Clinical Research Center Building 91, Level 10, Jan Waldenströms gata 35, SE-20502, Malmö, Sweden.
Inês BarrosoWellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK.
Göran HallmansDepartment of Biobank Research, Umeå University, Umeå, Sweden.
Ingegerd JohanssonDepartment of Odontology, Umeå University, Umeå, Sweden.
Frida RenströmGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Clinical Research Center Building 91, Level 10, Jan Waldenströms gata 35, SE-20502, Malmö, Sweden.
Paul W FranksGenetic and Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, Clinical Research Center Building 91, Level 10, Jan Waldenströms gata 35, SE-20502, Malmö, Sweden. paul.franks@med.lu.se.
Lund University · SEUmeå University · SEWellcome/MRC Institute of Metabolic Science · GB

Funding

Wellcome Trust WT098051
6 · The paper itself

Abstract

aims/hypothesisWe compared the ability of genetic (established type 2 diabetes, fasting glucose, 2 h glucose and obesity variants) and modifiable lifestyle (diet, physical activity, smoking, alcohol and education) risk factors to predict incident type 2 diabetes and obesity in a population-based prospective cohort of 3,444 Swedish adults studied sequentially at baseline and 10 years later.

methodsMultivariable logistic regression analyses were used to assess the predictive ability of genetic and lifestyle risk factors on incident obesity and type 2 diabetes by calculating the AUC.

resultsThe predictive accuracy of lifestyle risk factors was similar to that yielded by genetic information for incident type 2 diabetes (AUC 75% and 74%, respectively) and obesity (AUC 68% and 73%, respectively) in models adjusted for age, age(2) and sex. The addition of genetic information to the lifestyle model significantly improved the prediction of type 2 diabetes (AUC 80%; p = 0.0003) and obesity (AUC 79%; p < 0.0001) and resulted in a net reclassification improvement of 58% for type 2 diabetes and 64% for obesity. CONCLUSIONS/

interpretationThese findings illustrate that lifestyle and genetic information separately provide a similarly high degree of long-range predictive accuracy for obesity and type 2 diabetes.

Indexed as

Life StyleBlood GlucoseDiabetes Mellitus, Type 2ExerciseHumansLogistic ModelsObesityProspective StudiesBlood GlucoseEnvironmentGenesObesityPredictorsType 2 diabetes

Identifiers

PMID26625858
PMCPMC4742501
OpenAlexW2183780835

What OpenQuestion holds

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LicenceCC BY
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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.