For people genetically predisposed to obesity, eating fried food can have twice the effect on body mass index than it can on people with a lower genetic predisposition, a new study finds.
There has been a worldwide increase in obesity over the past 30 years. This epidemic is usually believed to have been caused by modern changes in lifestyle and diet. However, the new study, which is published in the BMJ, argues that the genetic component of obesity is being overlooked.
The researchers behind the new study examined the interactions between the frequency of fried food consumption - a known driver for obesity - and 32 genetic variants associated with obesity.
The researchers used questionnaires to assess the diets of 6,379 men and 31,049 women. These questionnaires recorded how often the people in the study ate fried foods, both at home and out of the home.
Data on the participants' body mass index (BMI) and lifestyle factors, such as how much exercise they get and whether they smoke, were also analyzed. The researchers also calculated the genetic risk scores of the people in the study.
High genetic risk scores increased obesity risk for participants who ate fried food
In the participants who had the highest genetic risk scores, the difference in BMI between people who ate fried foods four or more times each week and those who ate fried foods less than once a week was 1 kilogram per square meter (kg/m2) in women and 0.7 kg/m2 in men.
In the participants who had the lowest genetic risk scores, these differences were 0.5 kg/m2 in women and 0.4 kg/m2 in men.
This shows that those with a genetic predisposition to obesity were significantly more likely to become obese if they frequently ate fried food, compared with people less genetically predisposed to obesity.
But the interaction between fried food and genes could be more complex. As well as genetic predisposition influencing the extent to which people who frequently eat fried food might become obese, the researchers also believe that eating fried food could itself modify the genetic influences on obesity.
"Our findings indicate that genetic risk of obesity could be mitigated by simply changing an eating habit," says study author Frank Hu, professor of nutrition and epidemiology at Harvard School of Public Health in Boston, MA.
Cause and effect is not conclusive in this kind of study
However, the researchers stress that their findings could have been influenced by other unknown factors, despite adjusting their results for diet and lifestyle factors. For instance, the study did not capture information about the types of oil used in frying, the type of frying or its temperature. These factors could have influenced the results.
Also, because participants were self-reporting what they ate and how often, the data might not be entirely accurate. Furthermore, the participants were mostly middle-aged or older people of European descent, so the findings of this study might not apply to other ethnic groups.
"This work provides formal proof of interaction between a combined genetic risk score and environment in obesity," write Prof. Alexandra Blakemore and Dr. Jessica Buxton, of Imperial College London, UK, in a linked editorial. They add, though, that the results "are unlikely to influence public health advice, since most of us should be eating fried food more sparingly anyway."
Recently, Medical News Today also reported on another study from the BMJ that investigated whether living or working near fast food shops could contribute to obesity.