The more likely explanation is that the rise in obesity stems from interactions between genes and other factors, such as diet, lifestyle, and physical activity, whose patterns have shifted toward a more pro-obesity, or obesogenic, environment.
These were the conclusions that researchers in Norway came to after conducting a longitudinal study spanning over 4 decades of data from more than 100,000 people.
They report their findings in a recent BMJ paper.
An important message from the study is that it appears that environments that increasingly favor obesity contribute more to the obesity epidemic than genetic factors.
Lead author Maria Brandkvist of the Department of Public Health and Nursing at the Norwegian University of Science and Technology in Trondheim comments on this point in an opinion article that accompanies the study paper, saying:
“Although previous research suggested that genetic vulnerability had larger consequences after the onset of the obesity epidemic than before, our dataset provides convincing results [to the contrary], with a large sample size and range of years of assessments and ages.”
Example of effect of obesogenic environment
Brandkvist illustrates with one example that their dataset revealed.
In the 1960s, a 35-year-old man of average height with pro-obesity genes would, on average, weigh around 3.9 kilograms (kg) more than his counterparts without pro-obesity genes.
“If the same man remained 35 years old but lived in Norway today,” Brandkvist explains, “his vulnerable genes would make him more than 6.8 kg heavier.”
In addition, both the obesity-predisposed man and his nonpredisposed peers “would have gained an extra 7.1 kg simply as a result of living in our obesogenic environment,” she adds.
In other words, she explains, “This man’s 13.9 kg excess weight is caused mostly by today’s unhealthy lifestyle, but also by how his genes interplay with the environment.”
Changing influence of genes
In their study paper, the researchers note that even though worldwide obesity has nearly tripled over the last 4 decades, scientists are still unclear about the causes of the epidemic.
While many similar studies have also concluded that the causes likely result from interactions between genes and environment, they have relied mainly on short age spans and follow-ups and self-reported body weight.
What has also remained unclear is how the influence of genes changes as environments become more favorable to obesity.
So, they investigated trends in BMI in Norway between the 1960s and the 2000s. They also assessed the impact of the environment on BMI according to genetic differences.
They used data on 118,959 people in the Nord-Trøndelag Health Study (HUNT), whose ages ranged from 13 to 80 years. The HUNT researchers had measured their height and weight several times between 1963 and 2008.
Of these participants, the analysis that searched for links between genetic susceptibility and BMI took in data on 67,305 individuals.
The results showed a distinct rise in BMI over the decade preceding the mid-1990s. In addition, individuals born from 1970 onwards appeared to develop higher BMIs in earlier adulthood than their older peers.
The researchers then ranked the participants in five equal groups by genetic predisposition to obesity. They found, for each decade, a significant difference in BMI between those with the highest and those with the lowest genetic predisposition.
Also, the difference in BMI between those with the most and those with the least genetic predisposition rose gradually over the 5 decades between the 1960s and the 2000s.
Average is not enough to understand obesity
In a linked editorial, Prof. S. V. Subramanian of the Department of Social and Behavioral Sciences at Harvard T.H. Chan School of Public Health in Boston, MA, and two colleagues from other research centers in the United States comment on the study.
They suggest that the findings highlight a need to focus on more than average changes in BMI to understand the obesity epidemic.
“This focus on average changes in BMI,” they write, “has underpinned the case for population-wide approaches to obesity prevention and treatment, either by modifying the ‘obesogenic environment’ or by advocating whole population changes in behavior, such as increasing physical activity and reducing consumption of high energy food.”
They argue that such an approach not only overlooks the fact that BMI varies significantly within a population, but it also falsely assumes that variation is “constant across different populations and over time.”
If public health efforts continue to work under these assumptions, then they are “unlikely to make a noticeable difference in reversing the obesity epidemic.”
They urge researchers to try and find out what causes the BMI variations within populations so that strategies for health improvement can help individuals as well as populations. They conclude:
“Further, it is necessary to consider both mean BMI and the variation in BMI when deciding where best to target these strategies.”
