Not only does genetic predisposition to obesity have a role in people’s risk of excess weight, it also interacts with an ever-more “obesogenic” environment to increase the population average body mass index (BMI), new research from Norway has shown. The authors of the study*, published today by The BMJ, said their results indicate that we need more effective obesity prevention strategies that would benefit the population as a whole and that could be particularly advantageous among people with a genetic predisposition to obesity. However, experts argued that an exclusive focus on population-wide preventive strategies is unlikely to make a noticeable difference in reversing the obesity epidemic, given that most BMI variation is between individuals rather than populations, and that we are still unable to explain much of this interindividual variation in BMI.
Researchers led from the Norwegian University of Science and Technology, in Trondheim, studied the trajectories of BMI in Norway over five decades, with the aim of assessing the differential influence of the “obesogenic” environment on BMI according to genetic predisposition. Using data covering 67,305 participants aged 13-80 years in the longitudinal population-based Nord-Trøndelag Health Study (HUNT), they analysed the association between genetic predisposition and BMI.
They found that the prevalence of obesity started to increase in Norway between the mid-1980s and mid-1990s and, compared with older birth cohorts, people born after 1970 had a substantially higher BMI already in young adulthood. They also reported that BMI differed substantially between the highest and lowest fifths of genetic susceptibility for all ages at each decade, and that the difference increased gradually from the 1960s to the 2000s. For example, among 35-year-old men, the most genetically predisposed had 1.20kg/m2 higher BMI than those who were least genetically predisposed in the 1960s, compared with a difference in BMI of 2.09kg/m2 in the 2000s; for 35-year-old women, the differences in BMI were 1.77 and 2.58 respectively.
The study authors commented that their results provide evidence that genetically predisposed people are at greater risk of a higher BMI and that genetic predisposition interacts with the “obesogenic” environment resulting in the higher BMI in recent decades.
They concluded: “Regardless of BMI being a heritable trait, secular trends have increased BMI for both genetically predisposed and genetically non-predisposed people. 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.”
The authors of an accompanying editorial** pointed out that the study might have overlooked two aspects of global trends in BMI. The first is that the overall increase in mean BMI over time has been accompanied by increasing dispersion over time both within and across countries, and variability in BMI also seems to differ systematically across different subgroups at any one time. And the second is that much of the research assessing the contribution to BMI of genetic, behavioural, social, and environmental characteristics has also relied on average associations; and BMI polygenic risk score is known to explain only 3-4% of the variation in BMI.
They concluded: “Substantial heterogeneities in BMI, both over time and across different population groups, the fact that the bulk of the variation in BMI is between individuals (and not between populations), and our inability to explain much of this interindividual variation in BMI together suggest that an exclusive focus on population-wide preventive strategies is unlikely to make a noticeable difference in reversing the obesity epidemic.
“Future research should aim to identify more clearly the sources of within population variation to inform better strategies for improving the health of both populations and individuals. Further, it is necessary to consider both mean BMI and the variation in BMI when deciding where best to target these strategies.”
*Brandkvist M, Bjørngaard JK, Ødegård RA, et al. Quantifying the impact of genes on body mass index during the obesity epidemic: longitudinal findings from the HUNT Study. BMJ 2019; 366: l4067 doi: 10.1136/bmj.l4067
**Kim R, Lee DH, Subramanian SV. Editorial: Understanding the obesity epidemic. BMJ 2019; 366: l4409 doi: 10.1136/bmj.l4409