Having certain genes that carry a predilection for excess weight and obesity may also make individuals more susceptible to gaining weight from eating fried food, according to researchers.
Among individuals in the highest tertile for genetic obesity risk, those who consumed fried food four or more times per week versus one time per week had a difference in body mass index (BMI) of 1.0 for women and 0.7 for men, Qibin Qi, PhD, of Harvard Medical School of Public Health in Boston and colleagues reported in BMJ.
Among those in the lowest tertile of genetic risk, the corresponding BMI differences were 0.5 for women and 0.4 for men.
Previous research has found an association between fried food consumption, obesity and chronic disease, but no studies have looked at how an individual’s genetic make-up may modify this risk factor.
So Qi and colleagues analyzed data from three cohorts of patients: 9,623 women from the Nurses’ Health Study, 6,379 men from the Health Professionals Follow-up Study and 21,421 women from the Women’s Genome Study. All participants had genotype data available as well as responses to periodic dietary questionnaires. Genetic risk scores were based on 32 known BMI-associated variants.
When the researchers combined the three cohorts and assessed BMI per 10 risk alleles the following differences in BMI were identified: 1.1 among those who consumed fried food less than once per week vs. 1.6 for fried food one to three times per week and 2.2 for fried food more than three times per week (P<0.001 for interaction).
The researchers also assessed obesity risk per 10 risk alleles and determined the following odds ratios:
- 1.61 (95% CI 1.40 to 1.87) for fried food less than once a week
- 2.12 (95% CI 1.73 to 2.59) for fried food one to three times a week
- 2.72 (95% CI 2.12 to 3.48) for fried food more than three times a week
The study is the first to suggest that individuals with a greater genetic predisposition to adiposity may be more susceptible to adverse outcomes from fried food consumption.
“Our findings further emphasize the importance of reducing consumption of fried foods in the prevention of obesity,” particularly in those with a known genetic predisposition for adiposity, the researchers wrote.
In an accompanying editorial, Alexandra Blakemore, PhD, and Jessica Buxton, PhD, both of Imperial College in London, said the study “provides formal proof of interaction between a combined genetic risk score and environment in obesity.”
They added that although the findings are not likely to change public health advice in the near future, it may lead to more individualized approaches to treating people with obesity.
Study limitations include the potential for confounding from unknown factors, the potential for errors in food frequency questionnaires and the single-sex study design for each of the cohorts.
Furthermore lack of information about factors including whether fried food was consumed at home or in restaurants, which type of oil was used, the type of frying and temperature used and the number of times frying oil was reused, limit the depth of the analyses.
Because study participants were predominantly middle-aged adults of European ancestry, it is unknown if the findings can be generalized to other demographics and ethnic groups.