Dataset Information

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

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.

SUBMITTER: Brandkvist M

PROVIDER: S-EPMC6607203 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

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

Brandkvist Maria M Bjørngaard Johan Håkon JH Ødegård Rønnaug Astri RA Åsvold Bjørn Olav BO Sund Erik R ER Vie Gunnhild Åberge GÅ

BMJ (Clinical research ed.) 20190703

<h4>Objectives</h4>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.<h4>Design</h4>Longitudinal study.<h4>Setting</h4>General population of Nord-Trøndelag County, Norway.<h4>Participants</h4>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 ...[more]

PMID: 31270083

Similar Datasets

Project description:BackgroundThe intergenerational resemblance in body mass index may have increased during the development of the obesity epidemic due to changes in environment and/or expression of genetic predisposition.ObjectivesThis study investigates trends in intergenerational correlations of childhood body mass index (BMI; kg/m2) during the emergence of the obesity epidemic.MethodsThe study population was derived from the Copenhagen School Health Records Register, which includes height and weight measurements since birth year 1930. Mothers and fathers with BMIs available at ages 7 (n = 25,923 and n = 20,972) or 13 years (n = 26,750 and n = 21,397), respectively, were linked through the civil registration system introduced in 1968 to their children with BMIs available at age 7 years. Age- and sex-specific BMI z-scores were calculated. Correlations were estimated across eight intervals of child birth years (1952-1989) separately by sex. Trends in these correlations were examined. Whereas the mother-child correlations reflected the biological relationship, a likely decline in the assignment of non-biological fathers through the registration system across time must be considered when interpreting the father-child correlations.ResultsThe BMI correlations between mothers and sons ranged from 0.29-0.36 and they decreased marginally, albeit significantly across time at ages 7-7 years (-0.002/year, p = 0.006), whereas those at 13-7 years remained stable (<0.0004/year, p = 0.96). Mother-daughter correlations ranged from 0.30-0.34, and they were stable at ages 7-7 years (0.0001/year, p = 0.84) and at 13-7 years (0.0004/year, p = 0.56). In contrast, father-son correlations increased significantly during this period, both at ages 7-7 (0.002/year, p = 0.007) and at ages 13-7 years (0.003/year, p<0.001), whereas the increase in father-daughter correlations were insignificant both at ages 7-7 (0.001/year, p = 0.37) and at ages 13-7 years (0.001/year, p = 0.18).ConclusionDuring the obesity epidemics development, the intergenerational resemblance with mothers remained stable, whereas the father-child BMI resemblance increased, possibly reflecting changes in family relationships, and unlikely to have influenced the epidemic.

Project description:BackgroundAccurate obesity classification is important so that appropriate intervention can be instituted to modify metabolic risk factors. Commonly utilized body mass index (BMI) and percentage body fat (PBF) are influenced by lean mass whereas fat mass index (FMI) measures only body fat. This study compares the prevalence of obesity and metabolic risk factors with FMI, BMI and PBF using DXA (dual-energy x-ray absorptiometry).Methods489 women randomly recruited from the electoral roll were stratified into 4 age groups; 40-49, 50-59, 60-69 and 70-79 years from 2000 to 2001. Clinical data and DXA body composition were obtained. Statistical analyses were performed using Medcalc v15 (Ostend, Belgium) with significance level at p = 0.05 (two-tailed).ResultsThere was higher prevalence of obesity using PBF compared to BMI and FMI (p<0.001). This difference was greater from age 50-59 (p<0.05) which may be explained by age-related lean mass loss. PBF over-classified obesity in over 35% of normal and 95% of overweight categories compared to FMI and BMI. BMI has a sensitivity of 78.9% and specificity of 98.3% for obesity using FMI as the standard. BMI under-classified obesity in the overweight category by 14.9% compared to FMI. There was no difference in diabetes, dyslipidemia, hypertension and metabolic syndrome prevalence within the BMI-obesity and FMI-obesity categories (p>0.05).ConclusionPBF classified more obesity than BMI and FMI because of its low pre-determined threshold. The greater difference with PBF compared to BMI and FMI from the 50-59 decade onwards can be attributed to age-related lean mass loss. BMI had the lowest sensitivity for obesity diagnosis. BMI under-classified obesity in the overweight category compared to FMI due to its inability to differentiate lean mass. However, there was no significant difference in the prevalence of metabolic risk factors between BMI and FMI-obesity categories indicating that fat location may influence metabolic dysregulation.

Dataset Information

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

Objectives

Design

Setting

Participants

Main outcome measure

Results

Conclusions

Publications

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets