Abstract
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.
Highlights
Modern humans emerged from Africa ~200,000 years ago and spread across the earth over the past 100,000 years
>1000-fold from 1909 to 1999 and contributes to ~7% of daily energy of the modern Western diet (MWD) [1]. This progressive increase in the ingestion of vegetable oils has led to a 3-fold increase in dietary linoleic acid (LA) content of the MWD [1,3,24,25,26], as well as an estimated 40% reduction in total n-3 long chain (≥20 carbon; LC-) polyunsaturated fatty acids (PUFA) levels, and a large shift in the ratio of dietary n-6/n-3 C18 PUFAs consumed from ~5:1 to >10:1 [1,27]
From the work of George and Mildred Burr almost 100 years ago [28,29], which was extended by the studies of Ralph Holman [30,31], it became clear that n-3 and n-6 18 carbon (18C-)PUFAs were essential for human health
Summary
Modern humans emerged from Africa ~200,000 years ago and spread across the earth over the past 100,000 years. Changes in food type (quality) and quantity in the MWD have been largely driven by technological changes in food production and processing to provide high-calorie and appealing food (high in sugars, refined grains and oils) to large urban populations [1,4] These have led to detrimental shifts in nutrient metabolism leading to gene-diet interactions responsible for more obesity and localized and systemic inflammation [2]. The objectives of this review are first to point out how lifestyle variables and our current dietary PUFA exposure together with ancestral-based genetic variation in the LC-PUFA biosynthetic pathway gives rise to distinct molecular profiles (levels of LC-PUFAs, LC-PUFA metabolites, inflammatory and other disease biomarkers) that enhance disease risk for certain individuals and populations These gene-diet interactions may be important to health in western countries as dietary n-6 and n-3 18C PUFAs comprise almost 10% of daily calories in the MWD. The second objective of the review is to describe how an understanding of PUFA-based gene-diet interactions can provide a scientific basis for the development of specific dietary and supplement strategies with n-3 LC-PUFAs to prevent and manage human diseases
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