Treatment of dyslipidemia: genetic interactions with diet and drug therapy.
Coronary heart disease (CHD) is multifactorial, and its manifestation is determined by multiple gene loci and their interaction with a cohort of environmental factors. Variation at several candidate gene loci has already been shown to have a significant effect over the spectrum of plasma lipid levels observed in the population. Moreover, some variants are known to influence the interindividual variability in response to dietary and pharmacologic interventions aimed to reduce atherogenic lipoproteins. The continuous progress in this area of research is getting us closer to the development of genetic screening panels that will allow a more precise assessment of individual CHD risk and response to therapeutic interventions.
Ordovas
J M
JM
Lipid Metabolism Laboratory, JM-USDA-Human Nutrition Research Center on Aging at Tufts University, Department of Medicine, New England Medical Center, Boston, MA, USA.
Schaefer
E J
EJ
D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D001053:Apolipoproteins / Q000235:genetics; D002352:Carrier Proteins / Q000235:genetics; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters / Q000235:genetics; D018752:Diet, Fat-Restricted; D006023:Glycoproteins; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006949:Hyperlipidemias / Q000097:blood / Q000235:genetics* / Q000628:therapy*; D008055:Lipids / Q000097:blood / Q000235:genetics
D000924:Anticholesteremic Agents; D001053:Apolipoproteins; C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters; D006023:Glycoproteins; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids