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Fatty acid desaturase genetic variations and dietary omega-3 fatty acid intake associate with arterial stiffness
Author(s) -
Magnus Bäck,
Constance Xhaard,
Raphaël Rouget,
Quentin Thuillier,
Oscar Plunde,
Susanna C. Larsson,
Nicolas Girerd,
João Pedro Ferreira,
JeanMarc Boivin,
Erwan Bozec,
Ludovic Mercklé,
Faı̈ez Zannad,
Axelle Hoge,
Michèle Guillaume,
Claire DandineRoulland,
Édith Le Floch,
Delphine BacqDaian,
JeanFrançois Deleuze,
Laurie Van Den Berghe,
JulieAnne Nazare,
Martine Laville,
Christiane Branlant,
Isabelle BehmAnsmant,
Sandra Wagner,
Patrick Rossignol
Publication year - 2022
Publication title -
european heart journal open
Language(s) - English
Resource type - Journals
ISSN - 2752-4191
DOI - 10.1093/ehjopen/oeac016
Subject(s) - arterial stiffness , pulse wave velocity , polyunsaturated fatty acid , fads2 , eicosapentaenoic acid , medicine , endocrinology , population , genotype , physiology , biology , fatty acid , docosahexaenoic acid , blood pressure , genetics , biochemistry , environmental health , gene
Aims Long-chain polyunsaturated fatty acids (PUFAs) generate diverse bioactive lipid mediators, which tightly regulate vascular inflammation. The effects of omega-3 PUFA supplementation in cardiovascular prevention however remain controversial. In addition to direct dietary intake, fatty acid desaturases (FADS) determine PUFA levels. Increased arterial stiffness represents an independent predictor of mortality and cardiovascular events. The aim of the present study was to determine the association of PUFA intake, FADS1 genotype, and FADS expression with arterial stiffness. Methods and results A cross-sectional population-based cohort study of 1464 participants without overt cardiovascular disease was conducted. Dietary intake was assessed using a food frequency questionnaire. Arterial stiffness was assessed by carotid–femoral pulse wave velocity (cfPWV), and the FADS1 locus variant was determined. Blood cell transcriptomics was performed in a subset of 410 individuals. Pulse wave velocity was significantly associated with the FADS1 locus variant. Differential associations between PWV and omega-3 PUFA intake were observed depending on the FADS1 genotype. High omega-3 PUFA intake attenuated the FADS1 genotype-dependent associations. Carriers of the minor FADS1 locus variant exhibited increased expression of FADS2, which is associated with PWV. Conclusion Taken together, these findings point to FADS1 genotype-dependent associations of omega-3 PUFA intake on subclinical cardiovascular disease. These findings may have implications for identifying responders and non-responders to omega-3 PUFA supplementation and open up for personalized dietary counselling in cardiovascular prevention.

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