Evidence map›Paper›PMID 31270083›Full record

ArticleBMJ (Clinical research ed.)2019

Quantifying the impact of genes on body mass index during the obesity epidemic: longitudinal findings from the HUNT Study.

Maria Brandkvist, Johan Håkon Bjørngaard, Rønnaug Astri Ødegård, Bjørn Olav Åsvold, Erik R Sund, Gunnhild Åberge Vie

Abstract read
In one paragraph

Article in BMJ (Clinical research ed.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 5 pooled it
–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

48 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Are There Any Effective Behavior Change Strategies for Communicating Genetic Risk in Obesity Prevention and Body Weight Reduction Interventions?Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Maria BrandkvistDepartment of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Postboks 8905, 7491 Trondheim, Norway maria.brandkvist@ntnu.no.ORCID http://orcid.org/0000-0002-3916-7313
Johan Håkon BjørngaardDepartment of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Postboks 8905, 7491 Trondheim, Norway.
Rønnaug Astri ØdegårdDepartment of Paediatrics, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway.
Bjørn Olav ÅsvoldK.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Erik R SundHUNT Research Centre, Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Levanger, Norway.
Gunnhild Åberge VieDepartment of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Postboks 8905, 7491 Trondheim, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo study the trajectories of body mass index (BMI) in Norway over five decades and to assess the differential influence of the obesogenic environment on BMI according to genetic predisposition.

designLongitudinal study.

settingGeneral population of Nord-Trøndelag County, Norway.

participants118 959 people aged 13-80 years who participated in a longitudinal population based health study (Nord-Trøndelag Health Study, HUNT), of whom 67 305 were included in analyses of association between genetic predisposition and BMI.

main outcome measureBMI.

resultsObesity increased in Norway starting between the mid-1980s and mid-1990s and, compared with older birth cohorts, those born after 1970 had a substantially higher BMI already in young adulthood. BMI differed substantially between the highest and lowest fifths of genetic susceptibility for all ages at each decade, and the difference increased gradually from the 1960s to the 2000s. For 35 year old men, the most genetically predisposed had 1.20 kg/m

conclusionsThis study provides evidence that genetically predisposed people are at greater risk for higher BMI and that genetic predisposition interacts with the obesogenic environment resulting in higher BMI, as observed between the mid-1980s and mid-2000s. Regardless, BMI has increased for both genetically predisposed and non-predisposed people, implying that the environment remains the main contributor.

Indexed as

Body Mass IndexGenetic Predisposition to DiseaseObesityAdolescentAdultAgedAged, 80 and overFemaleHumansLinear ModelsLongitudinal StudiesMaleMiddle AgedNorwayPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID31270083
PMCPMC6607203

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.