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. 2019 Jul 3:366:l4067.
doi: 10.1136/bmj.l4067.

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

Maria Brandkvist  1   2 , Johan Håkon Bjørngaard  3 , Rønnaug Astri Ødegård  2   4   5 , Bjørn Olav Åsvold  6   7   8 , Erik R Sund  8   9 , Gunnhild Åberge Vie  3
Affiliations

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

Maria Brandkvist et al. BMJ. .

Abstract

Objectives: 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.

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Conflict of interest statement

Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf and declare: GÅV reports grants from the Research Council of Norway during the conduct of the study. MB reports grants from the Liaison Committee for Education, Research and Innovation in Central Norway during the conduct of the study; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.

Figures

Fig 1
Fig 1
Flowchart of study participants and criteria for inclusion in study sample. *Linkage to data from tuberculosis screening programme 1963-75 required participation in any part of Nord-Trøndelag Health Study. †Of 52 699 people with body mass index (BMI) measured in 1963-75, 48 959 had another valid BMI measurement before age 80. Of the 71 541 people with BMI measured in 1984-86, 43 723 had BMI measured also in 1995-97 and 27 536 had BMI measured also in 2006-08. Of these, 25 253 had BMI measured in 1984-86, 1995-97, and 2006-08. Of 1695 people who had BMI measured in 2000-01, 1664 had valid BMI measurements in 1995-97. 36 292 people had BMI measured in 1995-97 and 2006-08. ‡Of the 26 113 people with genetic data and BMI measured in 1966-69, 26 082 also had another valid BMI measurement before age 80. Of the 41 281 people with genetic data and BMI measured in 1984-86, 38 888 also had a valid BMI measurement in 1995-97 and 26 927 also had BMI measured in 2006-08. Of these, 24 714 had BMI measured in 1984-86, 1995-97, and 2006-08. 35 408 people had genetic data and BMI measured before age 80 in 1995-97 and 2006-08
Fig 2
Fig 2
Body mass index (BMI) trajectories with 95% confidence intervals for women and men by birth cohort. Estimates from a linear mixed model of participants in the Nord-Trøndelag Health Study, Norway. The most recent cohorts are observed at the youngest ages (on left of graph)
Fig 3
Fig 3
Estimated body mass index (BMI) by top (most susceptible, shown in blue) and bottom fifth (least susceptible, shown in orange) of genetic risk score by age and time point for 31 823 men and 35 482 women who participated in the Nord-Trøndelag Health Study, Norway
See this image and copyright information in PMC

Comment in

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