Precision Nutrition and Omega-3 Polyunsaturated Fatty Acids: A Case for Personalized Supplementation Approaches for the Prevention and Management of Human Diseases

Nutrients

Susan Sergeant¹  Lindsay M. Reynolds²  Michael C. Seeds³  Floyd H. Chilton⁴  Rahul Dutta⁵  Rasika A. Mathias⁶ 

[1] Department of Biochemistry, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA;Department of Epidemiology and Prevention, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA;Department of Internal Medicine, Section on Molecular Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA;Department of Physiology and Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA;Department of Urology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA;GeneSTAR Research Program, General Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA;

关键词: omega-3 fatty acids;    polyunsaturated fatty acids;    gene-diet interaction;    human disease;    inflammation;    fatty acid desaturase genes;    arachidonic acid;    eicosanoids;    endocannabinoids;   

DOI  :  10.3390/nu9111165

来源: DOAJ

【 摘 要 】

Background: Dietary essential omega-6 (n-6) and omega-3 (n-3) 18 carbon (18C-) polyunsaturated fatty acids (PUFA), linoleic acid (LA) and α-linolenic acid (ALA), can be converted (utilizing desaturase and elongase enzymes encoded by FADS and ELOVL genes) to biologically-active long chain (LC; >20)-PUFAs by numerous cells and tissues. These n-6 and n-3 LC-PUFAs and their metabolites (ex, eicosanoids and endocannabinoids) play critical signaling and structural roles in almost all physiologic and pathophysiologic processes. Methods: This review summarizes: (1) the biosynthesis, metabolism and roles of LC-PUFAs; (2) the potential impact of rapidly altering the intake of dietary LA and ALA; (3) the genetics and evolution of LC-PUFA biosynthesis; (4) Gene–diet interactions that may lead to excess levels of n-6 LC-PUFAs and deficiencies of n-3 LC-PUFAs; and (5) opportunities for precision nutrition approaches to personalize n-3 LC-PUFA supplementation for individuals and populations. Conclusions: The rapid nature of transitions in 18C-PUFA exposure together with the genetic variation in the LC-PUFA biosynthetic pathway found in different populations make mal-adaptations a likely outcome of our current nutritional environment. Understanding this genetic variation in the context of 18C-PUFA dietary exposure should enable the development of individualized n-3 LC-PUFA supplementation regimens to prevent and manage human disease.

【 授权许可】

Unknown