NEW YORK – Both genetic predisposition and an obesogenic environment have contributed to rising body mass indices in recent decades, according to a new study.
Global obesity rates have nearly tripled since the 1970s, but the cause of the epidemic is not clear. Genetic variants explain a small fraction — between 2 percent and 5 percent — of BMI variation, and environmental factors, such as dietary changes and increased sedentary lifestyles, also likely contribute to increased BMIs, according to researchers from the Norwegian University of Science and Technology.
Using longitudinal data collected as part of Norway's Nord-Trødelag Health Study, NTNU researchers examined the interaction between genetic predisposition and BMI over time. As they reported in The BMJ last week, they found that while BMI broadly increased over time in this population, genetically predisposed individuals were more highly affected.
"This reinforces the need for more effective preventive strategies that would benefit the population as a whole and that could prove to be particularly advantageous among people with a genetic predisposition to obesity," NTNU's Gunnhild Åberge Vie and her colleagues wrote in their paper.
The Nord-Trødelag Health (HUNT) study began in the 1980s and has collected height and weight data on 118,959 people. It has also linked back to earlier data collected from some overlapping individuals from a tuberculosis screening program that began in 1963.
From this, the researchers noted upward ticks in BMI in Norway beginning in the mid-1980s to mid-1990s, around the same time that it occurred in other parts of the world.
More than 67,300 individuals from later HUNT study waves, between 1995 and 1997 and between 2006 and 2008, also underwent genotyping. This included 96 of the 97 SNPs linked to increased BMI by the GIANT consortium. Using this genotyping data, the researchers developed a weighted genetic risk score and divided their population into five groups based on their genetic risk of having a high BMI.
People at higher genetic risk of developing obesity, the researchers reported, saw larger BMI gains than people with a lower genetic risk of developing obesity, and that difference increased over time. For instance, in the 1960s, 35-year-old men with a high genetic predisposition to obesity had a 1.20 kg/m2 higher BMI than men of the same age with a low genetic predisposition to obesity. But by the 2000s, that difference became 2.09 kg/m2.
They noted a similar increase in BMI differences between women with high and low genetic predisposition over time.
"Our study suggests that genetic predisposition interacts with the obesogenic environment and this has resulted in higher BMI in recent decades," the researchers wrote.
However, the study has a number of limitations. In an accompanying editorial appearing in The BMJ, a trio of researchers from the Harvard T.H. Chan School of Public Health noted that the study does not take into consideration some recent global trends in BMI. For instance, they noted that in the US, increases in BMI were not uniform across populations, as African American women and women with lower educational attainment tended to experience the highest BMI gains. Additionally, they noted that while a polygenic risk score for BMI only accounts for 3 percent to 4 percent of BMI variation and socioeconomic factors account for about 2 percent of BMI variation, the cause of most of variation in BMI remains unknown.
Still, Vie and her colleagues argued that population-level initiatives toward preventing obesity could not only help the general populace, but also particularly those with a genetic predisposition to obesity.