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How genetics and fried foods inflate body weight

Genetic makeup can inflate the effects of bad diet

Eating fried food more than four times a week had twice the effect on BMI for those with the highest genetic risk scores, compared with lower scores according to a paper published in the British Medical Journal. The findings demonstrate that our genetic makeup can inflate the effects of bad diet.

"Our findings emphasize the importance of reducing fried food consumption in the prevention of obesity, particularly in individuals genetically predisposed to adiposity," said lead researcher Lu Qi, Assistant Professor at Harvard School of Public Health and Brigham and Women's Hospital and Harvard Medical School.

The research team 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 (9,623 women from the Nurses’ Health Study; 6,379 men from the Health Professionals Follow-up Study; and a replication cohort of 21,421 women from the Women’s Genome Health Study).

They 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 0 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.

Outcomes

The researchers found consistent interactions between fried food consumption and genetic risk scores on BMI (p≤0.001 for interaction).

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 1.0kg/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.

The authors stress that their results may have been affected by other unmeasured or unknown factors, despite carefully adjusting for several diet and lifestyle factors.

However, they say they 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.

"This work provides formal proof of interaction between a combined genetic risk score and environment in obesity," write Professor Alexandra Blakemore and Dr Jessica Buxton at Imperial College London in an editorial. However, the results "are unlikely to influence public health advice, since most of us should be eating fried food more sparingly anyway."

In contrast, they stress that genetic information can be very valuable for treating 'monogenic' forms of obesity, caused by changes in a single gene. They say that it would therefore be "a great shame" to assume that genetics can be ignored in the management of obesity, and call for further studies "providing clinically useful predictions for individuals and enabling stratification of patients for appropriate care and treatment."

To access the article, please click here

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