Interaction of genetics risk score and fatty acids quality indices on healthy and unhealthy obesity phenotype.

Abstract

Background: The growth in obesity and rates of abdominal obesity in developing countries is due to the dietary transition, meaning a shift from traditional, fiber-rich diets to Westernized diets high in processed foods, sugars, and unhealthy fats. Environmental changes, such as improving the quality of dietary fat consumed, may be useful in preventing or mitigating the obesity or unhealthy obesity phenotype in individuals with a genetic predisposition, although this has not yet been confirmed. Therefore, in this study, we investigated how dietary fat quality indices with metabolically healthy obesity (MHO) or metabolically unhealthy obesity (MUO) based on the Karelis criterion interact with genetic susceptibility in Iranian female adults.

Methods: In the current cross-sectional study, 279 women with overweight or obesity participated. Dietary intake was assessed using a 147-item food frequency questionnaire and dietary fat quality was assessed using the cholesterol-saturated fat index (CSI) and the ratio of omega-6/omega-3 (N6/N3) essential fatty acids. Three single nucleotide polymorphisms-MC4R (rs17782313), CAV-1 (rs3807992), and Cry-1(rs2287161) were genotyped by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique and were combined to produce the genetic risk score (GRS). Body composition was evaluated using a multi-frequency bioelectrical impedance analyzer. Participants were divided into MHO or MUO phenotypes after the metabolic risk assessment based on the Karelis criteria.

Results: We found significant interactions between GRS and N6/N3 in the adjusted model controlling for confounding factors (age, body mass index, energy, and physical activity) (β = 2.26, 95% CI: 0.008 to 4.52, P = 0.049). In addition, we discovered marginally significant interactions between GRS and N6/N3 in crude (β = 1.92, 95% CI: -0.06 to 3.91, P = 0.058) and adjusted (age and energy) (β = 2.00, 95% CI: -0.05 to 4.05, P = 0.057) models on the MUH obesity phenotype. However, no significant interactions between GRS and CSI were shown in both crude and adjusted models.

Conclusion: This study highlights the importance of personalized nutrition and recommends further study of widely varying fat intake based on the findings on gene-N6/N3 PUFA interactions.