Fried foods may magnify genetic obesity risk

Frequent consumption of fried foods may exacerbate a genetic predisposition to obesity, according to results from a large cohort study that found a significant interaction between fried food consumption and genetic risk.

The study, published March 19 in BMJ (doi: 10.1136/bmj.g1610), looked at fried food consumption in three separate study populations: two cohorts of 9,263 and 6,379 U.S. men, and a cohort of 21,421 U.S. women, all of European ancestry.

© American Heart Association

The researchers, led by Qibin Qi, Ph.D., of the Harvard School of Public Health in Boston, compared subjects’ intake of fried foods, as assessed by questionnaires, with genetic obesity risk scores and body mass index. In the two smaller cohorts, the association between high fried food consumption and BMI was nearly double among those in the top tertile of genetic risk for obesity compared with those in the lowest tertile, suggesting that the degree of association between fried food consumption and BMI varied among people with different genetic predispositions.

In those two cohorts, the differences in BMI among those who consumed fried foods four or more times a week and those who consumed them less than once week were 1.0 in women and 0.7 in men who had the highest genetic risk profile. Among subjects in the lowest tertile of risk, the differences were 0.5 among women and 0.4 among men. The gene-diet interaction was replicated in the third, all-female cohort (P less than .001).

Genetic risk was measured by each individual’s load of 32 known BMI-associated variants. In the combined three cohorts, totalling 37,063 subjects, the differences in BMI per 10 risk alleles were 1.1, 1.6, and 2.2, respectively, for fried food consumption less than once, one to three times, and four or more times a week (P less than .001). The odds ratios for obesity per 10 risk alleles were 1.61, 2.12, and 2.72 across the three categories of fried food consumption (P = .002).

A variant of the FTO (fat mass and obesity–associated) gene, shown in previous studies to be linked to BMI and to appetite, was seen as having the strongest interaction with fried food consumption in this study.

Dr. Qi and colleagues could not explain the observed interaction between genes and fried food in particular, but noted that their results did not differ significantly after adjustment for confounders that included other dietary and lifestyle factors such as sweetened beverage intake, physical activity, and television watching.

The results, Dr. Qi and colleagues wrote, suggest for the first time that "individuals with a greater genetic predisposition to adiposity might be more susceptible to the adverse influence of overconsumption of fried food on adiposity," and that "overconsumption of fried foods might magnify genetic effects on adiposity."

The researchers noted as limitations of their study its observational design, its use of a single ethnic category and an all-female replication cohort, and the possibility of confounding by unknown factors.

The study was funded by the National Institutes of Health, with support from Merck for genotyping. One of the cohort studies used in this analysis had received genotyping support from Amgen. None of its authors disclosed conflicts of interest related to their research.

Frequent consumption of fried foods may exacerbate a genetic predisposition to obesity, according to results from a large cohort study that found a significant interaction between fried food consumption and genetic risk.

The study, published March 19 in BMJ (doi: 10.1136/bmj.g1610), looked at fried food consumption in three separate study populations: two cohorts of 9,263 and 6,379 U.S. men, and a cohort of 21,421 U.S. women, all of European ancestry.

© American Heart Association

The researchers, led by Qibin Qi, Ph.D., of the Harvard School of Public Health in Boston, compared subjects’ intake of fried foods, as assessed by questionnaires, with genetic obesity risk scores and body mass index. In the two smaller cohorts, the association between high fried food consumption and BMI was nearly double among those in the top tertile of genetic risk for obesity compared with those in the lowest tertile, suggesting that the degree of association between fried food consumption and BMI varied among people with different genetic predispositions.

In those two cohorts, the differences in BMI among those who consumed fried foods four or more times a week and those who consumed them less than once week were 1.0 in women and 0.7 in men who had the highest genetic risk profile. Among subjects in the lowest tertile of risk, the differences were 0.5 among women and 0.4 among men. The gene-diet interaction was replicated in the third, all-female cohort (P less than .001).

Genetic risk was measured by each individual’s load of 32 known BMI-associated variants. In the combined three cohorts, totalling 37,063 subjects, the differences in BMI per 10 risk alleles were 1.1, 1.6, and 2.2, respectively, for fried food consumption less than once, one to three times, and four or more times a week (P less than .001). The odds ratios for obesity per 10 risk alleles were 1.61, 2.12, and 2.72 across the three categories of fried food consumption (P = .002).

A variant of the FTO (fat mass and obesity–associated) gene, shown in previous studies to be linked to BMI and to appetite, was seen as having the strongest interaction with fried food consumption in this study.

Dr. Qi and colleagues could not explain the observed interaction between genes and fried food in particular, but noted that their results did not differ significantly after adjustment for confounders that included other dietary and lifestyle factors such as sweetened beverage intake, physical activity, and television watching.

The results, Dr. Qi and colleagues wrote, suggest for the first time that "individuals with a greater genetic predisposition to adiposity might be more susceptible to the adverse influence of overconsumption of fried food on adiposity," and that "overconsumption of fried foods might magnify genetic effects on adiposity."

The researchers noted as limitations of their study its observational design, its use of a single ethnic category and an all-female replication cohort, and the possibility of confounding by unknown factors.

The study was funded by the National Institutes of Health, with support from Merck for genotyping. One of the cohort studies used in this analysis had received genotyping support from Amgen. None of its authors disclosed conflicts of interest related to their research.

Frequent consumption of fried foods may exacerbate a genetic predisposition to obesity, according to results from a large cohort study that found a significant interaction between fried food consumption and genetic risk.

The study, published March 19 in BMJ (doi: 10.1136/bmj.g1610), looked at fried food consumption in three separate study populations: two cohorts of 9,263 and 6,379 U.S. men, and a cohort of 21,421 U.S. women, all of European ancestry.

© American Heart Association

The researchers, led by Qibin Qi, Ph.D., of the Harvard School of Public Health in Boston, compared subjects’ intake of fried foods, as assessed by questionnaires, with genetic obesity risk scores and body mass index. In the two smaller cohorts, the association between high fried food consumption and BMI was nearly double among those in the top tertile of genetic risk for obesity compared with those in the lowest tertile, suggesting that the degree of association between fried food consumption and BMI varied among people with different genetic predispositions.

In those two cohorts, the differences in BMI among those who consumed fried foods four or more times a week and those who consumed them less than once week were 1.0 in women and 0.7 in men who had the highest genetic risk profile. Among subjects in the lowest tertile of risk, the differences were 0.5 among women and 0.4 among men. The gene-diet interaction was replicated in the third, all-female cohort (P less than .001).

Genetic risk was measured by each individual’s load of 32 known BMI-associated variants. In the combined three cohorts, totalling 37,063 subjects, the differences in BMI per 10 risk alleles were 1.1, 1.6, and 2.2, respectively, for fried food consumption less than once, one to three times, and four or more times a week (P less than .001). The odds ratios for obesity per 10 risk alleles were 1.61, 2.12, and 2.72 across the three categories of fried food consumption (P = .002).

A variant of the FTO (fat mass and obesity–associated) gene, shown in previous studies to be linked to BMI and to appetite, was seen as having the strongest interaction with fried food consumption in this study.

Dr. Qi and colleagues could not explain the observed interaction between genes and fried food in particular, but noted that their results did not differ significantly after adjustment for confounders that included other dietary and lifestyle factors such as sweetened beverage intake, physical activity, and television watching.

The results, Dr. Qi and colleagues wrote, suggest for the first time that "individuals with a greater genetic predisposition to adiposity might be more susceptible to the adverse influence of overconsumption of fried food on adiposity," and that "overconsumption of fried foods might magnify genetic effects on adiposity."

The researchers noted as limitations of their study its observational design, its use of a single ethnic category and an all-female replication cohort, and the possibility of confounding by unknown factors.

The study was funded by the National Institutes of Health, with support from Merck for genotyping. One of the cohort studies used in this analysis had received genotyping support from Amgen. None of its authors disclosed conflicts of interest related to their research.