Abstract
The “modern western” diet (MWD) has increased the onset and progression of chronic human diseases as qualitatively and quantitatively maladaptive dietary components give rise to obesity and destructive gene-diet interactions. There has been a three-fold increase in dietary levels of the omega-6 (n-6) 18 carbon (C18), polyunsaturated fatty acid (PUFA) linoleic acid (LA; 18:2n-6), with the addition of cooking oils and processed foods to the MWD. Intense debate has emerged regarding the impact of this increase on human health. Recent studies have uncovered population-related genetic variation in the LCPUFA biosynthetic pathway (especially within the fatty acid desaturase gene (FADS) cluster) that is associated with levels of circulating and tissue PUFAs and several biomarkers and clinical endpoints of cardiovascular disease (CVD). Importantly, populations of African descent have higher frequencies of variants associated with elevated levels of arachidonic acid (ARA), CVD biomarkers and disease endpoints. Additionally, nutrigenomic interactions between dietary n-6 PUFAs and variants in genes that encode for enzymes that mobilize and metabolize ARA to eicosanoids have been identified. These observations raise important questions of whether gene-PUFA interactions are differentially driving the risk of cardiovascular and other diseases in diverse populations, and contributing to health disparities, especially in African American populations.
Highlights
Perhaps at no time in human history has the human diet changed so dramatically and rapidly than in the past 75 years in developed countries
Free fatty acids are activated by conjugation with Coenzyme A (CoA) by gene products derived from up to five genes before incorporation into and remodelling through various phospholipids by enzymes differing in both LCPUFA and phospholipid acceptor specificities
Higher levels of arachidonic acid (ARA) within circulating and cellular glycerolipids enhance the synthesis of elevated levels of ARA-derived pro-inflammatory eicosanoids and other cardiovascular disease (CVD) biomarkers; and third, the modern western diet (MWD) combined with specific genetic variants in the fatty acid desaturase (FADS) cluster observed more often African ancestry populations are associated with higher incidences of human disease
Summary
Perhaps at no time in human history has the human diet changed so dramatically and rapidly than in the past 75 years in developed countries. Three decades of research show that high intakes of refined carbohydrates, added sugars and a radical change in the nature of ingested fats, and animal-source foods have dramatically escalated obesity in the developed and developing world [1]. As challenging as obesity and gene-diet interactions have been for overall populations of developed countries such as the US, they manifest themselves in a negative way for certain populations and ethnic groups [10,11,12,13,14,15]. This review discusses how the combination of dramatic increases in levels of certain dietary PUFAs together with diet-gene interactions within PUFA pathways may be driving chronic diseases and health disparities
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