Abstract
Background: Fried food consumption has been associated with obesity; little is known about whether genetic background modifies this association. Methods: We analyzed interactions between a genetic risk score (GRS) based on 32 BMI-associated variants and fried food consumption on body mass index (BMI) and obesity in 9623 women from the Nurses’ Health Study (NHS) and 6379 men from the Health Professionals Follow-up Study (HPFS) and in a replication cohort of 21426 women from the Women’s Genome Health Study (WGHS). Results: An interaction between fried food consumption and the GRS on BMI was identified in both NHS and HPFS (P for interaction≤0.001). Among participants in the highest tertile of the GRS, the differences in BMI between individuals who consumed fried foods ≥4times/week and those consumed <1time/week amounted to 1.0 in women and 0.7 kg/m2 in men, whereas the corresponding differences were 0.5 and 0.4 kg/m2 in the lowest tertile of the GRS. The gene-diet interaction was replicated in the WGHS (P for interaction<0.001). Viewed differently, the genetic association with adiposity was strengthened with higher consumption of fried foods. In the combined three cohorts, the differences in BMI per 10 risk alleles were 1.2, 1.6, and 2.4 kg/m2 for fried food consumption<1, 1-3 and ≥4times/week (P for interaction<0.001) (Figure); and the odds ratios (95% CI) for obesity per 10 risk alleles were 1.60 (1.38-1.84), 2.13 (1.74-2.60) and 2.65 (2.08-3.39) across the three categories of consumption (P for interaction=0.002). In addition, we found that the individual variants in genes highly expressed or known to act in the central nervous system showed significant interactions, with the FTO variant showing the strongest result (P for interaction<0.001). Conclusion: Fried food consumption may interact with genetic background in relation to obesity, highlighting the particular importance of reducing fried food consumption in individuals genetically predisposed to obesity.
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