Fried foods may interact with genes to influence body weight, say experts
Eating fried foods more than four times a week had twice as much of an effect on Body Mass Index (BMI) for those with the highest genetic risk scores compared to those with lower scores, according to new research from Harvard Medical School.
It is well known that both fried food consumption and genetic variants are associated with adiposity (fatness), but the researchers from the Harvard School of Public Health, Brigham and Women’s Hospital, and Harvard Medical School said the interaction between these two risk factors in relation to BMI and obesity had not previously been examined.
The research was undertaken by Lu Qi, Assistant Professor at Harvard Medical School of Public Health and Brigham and Women’s Hospital and Harvard Medical School, and colleagues.
The research, published in the British Medical Journal on 18 March 2014, analysed interactions between fried food consumption and genetic risk associated with obesity in over 37,000 men and women taking part in three large US health trials.
The researchers used food frequency questionnaires to assess fried food consumption (both at home and away from home) and a genetic risk score based on 32 known genetic variants associated with BMI and obesity.
Three categories of fried food consumption were identified: less than once a week, one to three times a week, and four or more times a week. Genetic risk scores ranged from zero to 64, and those with a higher score had a higher BMI.
Height and body weight were assessed at the start of the trials, and weight was requested at each follow-up questionnaire. Lifestyle information, such as physical activity and smoking, was also collected. The researchers found consistent interactions between fried food consumption and genetic risk scores on BMI.
Among participants in the highest third of the genetic risk score, the differences in BMI between individuals who consumed fried foods four or more times a week and those who consumed less than once a week were 1kg/m2 in women and 0.7kg/m2 in men.
For participants in the lowest third of the genetic risk score, the differences were 0.5kg/m2 in women and 0.4kg/m2 in men.
Results show importance of genes in obesity
The researchers stressed that their results could also have been affected by other unmeasured or unknown factors, despite the careful adjustments that were made for several diet and lifestyle factors.
However, they said the results indicate that the association between fried food consumption and adiposity may vary according to differences in genetic predisposition, and vice versa — the genetic influences on adiposity may be modified by fried food consumption.
“Our findings emphasise the importance of reducing fried food consumption in the prevention of obesity, particularly in individuals genetically predisposed to adiposity,” Professor Lu Qi said.
“This work provides formal proof of interaction between a combined genetic risk score and environment in obesity,” wrote Professor Alexandra Blakemore and Dr Jessica Buxton from the Imperial College in London in an editorial that accompanied the publication of the study results.
Professor Blakemore and Dr Buxton stressed in the editorial that genetic information could be very valuable for treating ‘monogenic’ forms of obesity, caused by changes in a single gene and that it would be a “great shame” to assumed genetics could be ignored in the management of obesity. They called for further studies “providing clinically useful prediction for individuals and enabling stratification of patients for appropriate care and treatment”.