Title: Impact of Amerind ancestry and FADS genetic variation on omega-3 deficiency and cardiometabolic traits in Hispanic populations.

Authors: Yang, Chaojie; Hallmark, Brian; Chai, Jin Choul; O'Connor, Timothy D; Reynolds, Lindsay M; Wood, Alexis C; Seeds, Michael; Chen, Yii-Der Ida; Steffen, Lyn M; Tsai, Michael Y; Kaplan, Robert C; Daviglus, Martha L; Mandarino, Lawrence J; Fretts, Amanda M; Lemaitre, Rozenn N; Coletta, Dawn K; Blomquist, Sarah A; Johnstone, Laurel M; Tontsch, Chandra; Qi, Qibin; Ruczinski, Ingo; Rich, Stephen S; Mathias, Rasika A; Chilton, Floyd H; Manichaikul, Ani

Published In Commun Biol, (2021 07 28)

Abstract: Long chain polyunsaturated fatty acids (LC-PUFAs) have critical signaling roles that regulate dyslipidemia and inflammation. Genetic variation in the FADS gene cluster accounts for a large portion of interindividual differences in circulating and tissue levels of LC-PUFAs, with the genotypes most strongly predictive of low LC-PUFA levels at strikingly higher frequencies in Amerind ancestry populations. In this study, we examined relationships between genetic ancestry and FADS variation in 1102 Hispanic American participants from the Multi-Ethnic Study of Atherosclerosis. We demonstrate strong negative associations between Amerind genetic ancestry and LC-PUFA levels. The FADS rs174537 single nucleotide polymorphism (SNP) accounted for much of the AI ancestry effect on LC-PUFAs, especially for low levels of n-3 LC-PUFAs. Rs174537 was also strongly associated with several metabolic, inflammatory and anthropomorphic traits including circulating triglycerides (TGs) and E-selectin in MESA Hispanics. Our study demonstrates that Amerind ancestry provides a useful and readily available tool to identify individuals most likely to have FADS-related n-3 LC-PUFA deficiencies and associated cardiovascular risk.

PubMed ID: 34321601

MeSH Terms: No MeSH terms associated with this publication