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Cardiovascular disease (CVD) risk is the result of complex interactions between genetic and environmental factors. During the past few decades, much attention has focused on plasma lipoproteins as CVD risk factors. The current evidence supports the concept that gene-environment interactions modulate plasma lipid concentrations and potentially CVD risk. The findings from studies examining gene-diet interactions and lipid metabolism have been highly promising. Several loci (i.e., APOA1, APOA4, APOE, and LIPC) are providing proof-of-concept for the potential application of genetics in the context of personalized nutritional recommendations for CVD prevention. (1)


  • Gene name: APOA1
  • Name: apolipoprotein A-I
  • Chromosome: 11; Location: 11q23-q24
  • Gene type: protein coding
  • Organism: Homo sapiens
  • Gene aliases: MGC117399

This gene encodes apolipoprotein A-I, which is the major protein component of high density lipoprotein (HDL) in plasma. The protein promotes cholesterol efflux from tissues to the liver for excretion, and it is a cofactor for lecithin cholesterolacyltransferase (LCAT) which is responsible for the formation of most plasma cholesteryl esters. This gene is closely linked with two other apolipoprotein genes on chromosome 11. Defects in this gene are associated with HDL deficiencies, including Tangier disease, and with systemic non-neuropathic amyloidosis.


  • Official Symbol: APOA4
  • Name: apolipoprotein A-IV
  • Chromosome: 11; Location: 11q23
  • Gene type: protein coding
  • Gene name: APOA4
  • Gene description: apolipoprotein A-IV
  • Organism: Homo sapiens

Apoliprotein (apo) A-IV gene contains 3 exons separated by two introns. A sequence polymorphism has been identified in the 3'UTR of the third exon. The primary translation product is a 396-residue preprotein which after proteolytic processing is secreted its primary site of synthesis, the intestine, in association with chylomicron particles. Although its precise function is not known, apo A-IV is a potent activator of lecithin-cholesterol acyltransferase in vitro.



Genetic interactions with diet influence the risk of cardiovascular disease.

Am J Clin Nutr. 2006 Feb;83(2):443S-446S. Ordovas JM.

  • Single-nucleotide polymorphisms are an integral component of the evolutionary process that over millennia have resulted from the interaction between the environment and the human genome. Relatively recent changes in diet have upset this interaction with respect to the nutritional environment, but nutritional science is beginning to better understand the interaction between genes and diet, with the resulting potential to influence cardiovascular disease risk by dietary modification. Single-nucleotide polymorphisms in several genes have been linked to differential effects in terms of lipid metabolism; however, even a simple model of benefit and risk is difficult to interpret in terms of dietary advice to carriers of the various alleles because of conflicting interactions between different genes. The n-3 family of polyunsaturated fatty acids is underrepresented in our modern diet; much of the benefit of polyunsaturated fatty acids found in studies of various polymorphisms seems to be linked to increased n-3 polyunsaturated fatty acid intake. The nascent science of nutrigenomics faces many challenges; more and better research is needed to clarify the picture, rebut scepticism, and re-invigorate the discussion concerning genetic polymorphism and its interaction with diet.


1. Corella D, Ordovas JM.SINGLE NUCLEOTIDE POLYMORPHISMS THAT INFLUENCE LIPID METABOLISM: Interaction with Dietary Factors. Annu Rev Nutr. 2005;25:341-90.