Gene: environment interaction in lipid metabolism and effect on coronary heart disease risk.
CURR OPIN LIPIDOL
149 - 154.
Both genetic and environmental factors influence coronary heart disease, therefore studies of coronary heart disease risk are often confounded by gene: gene and gene: environment interactions. Such interactions imply that at the molecular level there is synergy between the gene products or with the by-products of the environmental insult, resulting in a greater than additive effect on risk. Genetic risk is thus modifiable in an environment-specific manner, This review focuses on recently reported effects of smoking (environmental factor) on the impact of variation in the genes for glutathione S-transferase, paraoxonase and apolipoprotein E on the risk of coronary heart disease and effects on intermediate lipid traits. We end on a cautionary note for the need for repeat studies to confirm these reported gene: environment effects. Curr Opin Lipidol 13:149-154, (C) 2002 Lippincott Williams Wilkins.
|Title:||Gene: environment interaction in lipid metabolism and effect on coronary heart disease risk|
|Keywords:||HUMAN PARAOXONASE GENE, APOLIPOPROTEIN-E POLYMORPHISM, APOE-DEFICIENT MICE, MYOCARDIAL-INFARCTION, DENSITY-LIPOPROTEIN, ARTERY-DISEASE, GLN-ARG192 POLYMORPHISM, ALZHEIMERS-DISEASE, CIGARETTE-SMOKE, PLASMA-LIPIDS|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science|
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