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dc.contributor.authorBrandkvist, Maria Charlotta
dc.contributor.authorBjørngaard, Johan Håkon
dc.contributor.authorØdegård, Rønnaug
dc.contributor.authorÅsvold, Bjørn Olav
dc.contributor.authorSund, Erik
dc.contributor.authorVie, Gunnhild Åberge
dc.date.accessioned2020-04-14T07:37:17Z
dc.date.available2020-04-14T07:37:17Z
dc.date.created2019-09-13T14:45:57Z
dc.date.issued2019
dc.identifier.citationBMJ. British Medical Journal. 2019, 366 1-8.en_US
dc.identifier.issn1756-1833
dc.identifier.urihttps://hdl.handle.net/11250/2650874
dc.description.abstractObjectives: To 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. Design: Longitudinal study. Setting: General population of Nord-Trøndelag County, Norway. Participants: 118 959 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 measure: BMI. Results: Obesity 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/m2 (95% confidence interval 1.03 to 1.37 kg/m2) higher BMI than those who were least genetically predisposed in the 1960s compared with 2.09 kg/m2 (1.90 to 2.27 kg/m2) in the 2000s. For women of the same age, the corresponding differences in BMI were 1.77 kg/m2 (1.56 to 1.97 kg/m2) and 2.58 kg/m2 (2.36 to 2.80 kg/m2). Conclusions: This 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.en_US
dc.language.isoengen_US
dc.publisherBMJ Publishing Groupen_US
dc.rightsNavngivelse-Ikkekommersiell 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/deed.no*
dc.titleQuantifying the impact of genes on body mass index during the obesity epidemic: Longitudinal findings from the HUNT Studyen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.pagenumber1-8en_US
dc.source.volume366en_US
dc.source.journalBMJ. British Medical Journalen_US
dc.identifier.doi10.1136/bmj.l4067
dc.identifier.cristin1724540
dc.relation.projectStiftelsen Kristian Gerhard Jebsen: SKGJ-MED-015en_US
dc.relation.projectNorges forskningsråd: 250335en_US
dc.description.localcodeCopyright © 2019 Author(s). This is an open access article distributed under the terms of the Creative Commons CC-BY-NC 4.0License (http://creativecommons.org/licenses/by-nc/4.0/)en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2


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Navngivelse-Ikkekommersiell 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse-Ikkekommersiell 4.0 Internasjonal