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

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/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).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.

A descriptive study of ten-year longitudinal changes in weight and waist circumference in the multi-ethnic rural Northern Norway. The SAMINOR Study, 2003-2014

“…It is in this context relevant that studies suggest that genetic predisposition interacts with the obesogenic environment. This results in higher BMI in later birth cohorts compared to earlier cohorts less exposed to environmental obesogenic factors [19,20].…”

La interacción de nuestros genes con el ambiente obesogénico

“…Este enfoque fue el que adoptaron Brandkvist y Cols., en un reciente artículo publicado en el British Medical Journal 4 . El estudio incluyó a 118.959 noruegos con edades entre 13 a 80 años, para quienes había datos disponibles de IMC y obesidad entre los años 1963 y 2008.…”

“…Asumiendo que las características genéticas de la población, es decir la frecuencia de los polimorfismos en el ADN, no han cambiado significa-tivamente en este lapso de tiempo, los investigadores estudiaron 97 variantes genéticas asociadas a la obesidad y crearon un score de riesgo genético (personas con menor a mayor predisposición genética). Los autores de este trabajo también estimaron que el ambiente obesogénico apareció por primera vez en Noruega alrededor de los años 80, por lo que posterior a esta fecha, el ambiente fue transformándose en forma gradual en un entorno pro-obesidad, característico de países de alto ingreso económico y común en los países occidentalizados 4 .…”

“…Sin embargo, en el año 2008, donde ya existía un marcado ambiente obesogénico, estas diferencias se hicieron más notorias, siendo de 2,1 kg/m 2 para hombres (equivalente a 6,1 kg de peso corporal) y en 2,6 kg/m 2 para mujeres (equivalente a 7,5 kg de peso corporal). Si bien el IMC aumentó entre los años 1960 y 2008 en la totalidad de la población noruega, este aumento fue más pronunciado en la población con mayor predisposición genética a la obesidad frente a un ambiente obesogénico 4 .…”

Genetic risk of obesity as a modifier of associations between neighbourhood environment and body mass index: an observational study of 335,046 UK Biobank participants

“…Some recent studies have examined interactions between genetic risk and birth cohort as a means of capturing exposure to an increasingly obesogenic environment in very broad terms, [7][8][9] but there has been limited investigation of specific features of the environment that might plausibly interact with genetic risk, [10][11][12][13][14] despite a number of 'socio-ecological' environmental factors long being recognised in social epidemiology as potentially important determinants of weight status.…”