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Genetic Variants in the FADS Gene: Implications for Dietary Recommendations for Fatty Acid Intake

  • Cardiovascular Disease (JH Goedecke, Section Editor)
  • Published:
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Abstract

Unequivocally, genetic variants within the fatty acid desaturase (FADS) cluster are determinants of long chain polyunsaturated fatty acid (LC-PUFA) levels in circulation, cells, and tissues. A recent series of papers have addressed these associations in the context of ancestry; evidence clearly supports that the associations are robust to ethnicity. However, ~80 % of African Americans carry two copies of the alleles associated with increased levels of arachidonic acid compared with only ~45 % of European Americans, raising important questions of whether gene-PUFA interactions induced by a modern western diet are differentially driving the risk of diseases of inflammation in diverse populations, and are these interactions leading to health disparities. We highlight an important aspect thus far missing in the debate regarding dietary recommendations; we contend that current evidence from genetics strongly suggest that an individual’s, or at the very least the population from which an individual is sampled, genetic architecture must be factored into dietary recommendations currently in place.

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Abbreviations

ALA:

α-linolenic acid

ARA:

Arachidonic acid

COX:

Cyclooxygenase

DGLA:

Dihomo γ-linolenic acid

DHA:

Docosahexaenoic acid

EPA:

Eicosapentaenoic acid

ETA:

Eicosatetraenoic acid

CAD:

Coronary artery disease

CVD:

Cardiovascular disease

GLA:

γ-linolenic acid

GWAS:

Genome wide association study

IMT:

Intima-media thickness

LA:

Linoleic acid

Lc:

Long chain

LD:

Linkage disequilibrium

LTB4:

Leukotriene B4

C18:

18 carbon

MWD:

Modern western diet

NSAID:

Non-steroidal anti-inflammatory drug

PC:

Phosphatidylcholine

PE:

Phosphatidylethanolamine

PI:

Phosphatidylinositol

PS:

Phosphatidylserine

PLA2 :

Phospholipase A2

PUFA:

Polyunsaturated fatty acid

SDA:

Stearidonic acid

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Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance

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Acknowledgments

This work was supported by a grant from the National Institutes of Health, P50 AT002782.

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Conflict of Interest

Rasika A. Mathias declares that she has no conflict of interest.

Vrindarani Pani declares that she has no conflict of interest.

Floyd H. Chilton is an unpaid consultant for Gene Smart Health and receives no compensation or equity in this role. This information has been disclosed to Wake Forest University Health Sciences (WFUHS) and outside sponsors, as appropriate, and is institutionally managed.

All authors have necessary ethics training.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

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Authors and Affiliations

  1. Division of Allergy and Clinical Immunology, Department of Medicine, The Johns Hopkins University, 5501 Hopkins Bayview Circle, Baltimore, MD, 21224, USA

    Rasika A. Mathias & Vrindarani Pani

  2. The Center for Botanical Lipids and Inflammatory Disease Prevention, Wake Forest School of Medicine, Winston-Salem, NC, 27157, USA

    Floyd H. Chilton

  3. Department of Physiology/Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC, 27157, USA

    Floyd H. Chilton

  4. Molecular Medicine and Translational Sciences, Wake Forest School of Medicine, Winston-Salem, NC, 27157, USA

    Floyd H. Chilton

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  1. Rasika A. Mathias
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Correspondence to Rasika A. Mathias.

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Mathias, R.A., Pani, V. & Chilton, F.H. Genetic Variants in the FADS Gene: Implications for Dietary Recommendations for Fatty Acid Intake. Curr Nutr Rep 3, 139–148 (2014). https://doi.org/10.1007/s13668-014-0079-1

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