Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases

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...

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Main Authors: Floyd H. Chilton, Robert C. Murphy, Bryan A. Wilson, Susan Sergeant, Hannah Ainsworth, Michael C. Seeds, Rasika A. Mathias
Format: Article
Language:English
Published: MDPI AG 2014-05-01
Series:Nutrients
Subjects:
Online Access:http://www.mdpi.com/2072-6643/6/5/1993
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spelling doaj-37aeb5da49cb44e0aee1c31b579c1edb2020-11-25T01:01:43ZengMDPI AGNutrients2072-66432014-05-01651993202210.3390/nu6051993nu6051993Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human DiseasesFloyd H. Chilton0Robert C. Murphy1Bryan A. Wilson2Susan Sergeant3Hannah Ainsworth4Michael C. Seeds5Rasika A. Mathias6The Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest School of Medicine, Winston-Salem, NC 27157, USADepartment of Pharmacology, University of Colorado Denver, Aurora, CO 80045, USAMolecular Medicine and Translational Sciences, Wake Forest School of Medicine, Winston-Salem, NC 27157, USAThe Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest School of Medicine, Winston-Salem, NC 27157, USAMolecular Medicine and Translational Sciences, Wake Forest School of Medicine, Winston-Salem, NC 27157, USAThe Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest School of Medicine, Winston-Salem, NC 27157, USADivision of Allergy and Clinical Immunology, Department of Medicine, The Johns Hopkins University, Baltimore, MD 21224, USAThe “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.http://www.mdpi.com/2072-6643/6/5/1993polyunsaturated fatty acidsnutritiongenetic variantsfatty acid desaturase (FADS)single nucleotide polymorphismsarachidonic acideicosanoidsinflammationcardiovascular disease
collection DOAJ
language English
format Article
sources DOAJ
author Floyd H. Chilton
Robert C. Murphy
Bryan A. Wilson
Susan Sergeant
Hannah Ainsworth
Michael C. Seeds
Rasika A. Mathias
spellingShingle Floyd H. Chilton
Robert C. Murphy
Bryan A. Wilson
Susan Sergeant
Hannah Ainsworth
Michael C. Seeds
Rasika A. Mathias
Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases
Nutrients
polyunsaturated fatty acids
nutrition
genetic variants
fatty acid desaturase (FADS)
single nucleotide polymorphisms
arachidonic acid
eicosanoids
inflammation
cardiovascular disease
author_facet Floyd H. Chilton
Robert C. Murphy
Bryan A. Wilson
Susan Sergeant
Hannah Ainsworth
Michael C. Seeds
Rasika A. Mathias
author_sort Floyd H. Chilton
title Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases
title_short Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases
title_full Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases
title_fullStr Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases
title_full_unstemmed Diet-Gene Interactions and PUFA Metabolism: A Potential Contributor to Health Disparities and Human Diseases
title_sort diet-gene interactions and pufa metabolism: a potential contributor to health disparities and human diseases
publisher MDPI AG
series Nutrients
issn 2072-6643
publishDate 2014-05-01
description 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.
topic polyunsaturated fatty acids
nutrition
genetic variants
fatty acid desaturase (FADS)
single nucleotide polymorphisms
arachidonic acid
eicosanoids
inflammation
cardiovascular disease
url http://www.mdpi.com/2072-6643/6/5/1993
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