Circulating fatty acids, genetic susceptibility and hypertension: a prospective cohort study.

Abstract

Combining genetic risk factors and plasma fatty acids (FAs) can be used as an effective method of precision medicine to prevent hypertension risk. A total of 195,250 participants in the UK Biobank cohort were included in this study from 2006-2010. Polygenic risk scores (PRSs) were calculated for hypertension using single-nucleotide polymorphisms (SNPs). Concentrations of plasma FAs, including polyunsaturated fatty acids (PUFAs), monounsaturated fatty acids (MUFAs) and saturated fatty acids (SFAs), were tested by nuclear magnetic resonance. The Cox model was used to test for the main effects of PRS, different plasma FAs and their joint effects on hypertension. Relative excess risk due to interaction (RERI) and the attributable proportion due to interaction (AP) were used to test the additive interaction. Plasma PUFAs, n-3 PUFAs, MUFAs and SFAs were related to the risk of hypertension (PUFAs: HR, 0.878; 95% CI, 0.868-0.888; MUFAs: HR, 1.13; 95% CI, 1.123-1.150; SFAs: HR, 1.086; 95% CI, 1.074-1.098; n-3 PUFAs: HR, 0.984; 95% CI, 0.973-0.995). Moreover, an additive interaction was found between PRS and plasma FAs, which could contribute to an approximately 10-18% risk of hypertension, and the associations between high plasma MUFAs and a high PRS of hypertension were the strongest positive [RERI: 0.178 (95% CI: 0.062, 0.294), AP: 0.079 (95% CI: 0.027, 0.130)]. Increased plasma MUFAs or SFAs and decreased plasma PUFAs or n-3 PUFAs were associated with hypertension risk, especially among people at high genetic risk.