Obesity is a complex condition, but the food industry and its products have been targeted as a major culprit by many. The new research, published in the American Journal of Clinical Nutrition, indicates that genes for body mass index may be responsible for less than one per cent of obesity.
European researchers, led by Ruth Loos from Addenbrooke’s Hospital in Cambridge, UK, performed a genetic survey of over 20,000 people participating in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohort.
In an accompanying editorial, Claude Bouchard from the Pennington Biomedical Research Center in Baton Rouge, Louisiana said the new findings extend previously understanding on the role of genetics in obesity.
“The obesity epidemic we are facing today unfolded over the past few decades and can clearly not be explained by changes in the frequency of risk alleles,” wrote Bouchard. “It is more likely due to a changing social and physical environment that encourages consumption and discourages expenditure of energy, behaviors that are poorly compatible with the genome that we have inherited.”
Bouchard goes on to say that a key unanswered question is “whether it will ever be possible to take advantage of the advances in our understanding of the genetic basis of obesity to identify the individuals at risk of becoming obese before they gain a large amount of body weight and adiposity”.
Study details
Loos and her co-workers genotyped 12 single nucleotide polymorphisms (SNPs) in 20,431 people aged between 39 and 79 and their “obesity risk” was calculated. The results showed that the variations had an effect on body mass index (BMI) of only between 0.058 and 0.329 kg/m2, and between 0.094 and 0.866 kg for weight.
While the genetic influences were found to have a cumulative effect, the researchers discovered that “their predictive value for obesity risk is limited”.
“All SNPs combined explained 0.9 per cent of BMI variation,” they wrote.
Independent comment
In the editorial, Bouchard added that the “gains that we are making in our understanding of the genetic architecture of obesity should lead to new and exciting research on the biology and behavior of energy balance regulation.
“There is no better place to start than to identify the true gene associated with each significant SNP instead of being satisfied with the closest positional gene,” he added.
Source: American Journal of Clinical Nutrition
Study: January 2010, Volume 91, Pages 184-190
“Cumulative effects and predictive value of common obesity-susceptibility variants identified by genome-wide association studies”
Authors: Li S, Zhao JH, Luan J, et al..
Editorial: January 2010, Volume 91, Pages 5-6
“Defining the genetic architecture of the predisposition to obesity: a challenging but not insurmountable task”
Author: C. Bouchard