Gene:environment interaction in lipid metabolism and effect on coronary heart disease risk.
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.
Talmud
Philippa J
PJ
Cardiovascular Genetics, British Heart Foundation Laboratories, Rayne Building, Royal Free and University College London Medical School, London, UK. p.talmud@ucl.ac.uk
Humphries
Steve E
SE
D001057:Apolipoproteins E / Q000235:genetics*; D043303:Aryldialkylphosphatase; D003327:Coronary Disease / Q000209:etiology*; D004777:Environment; D004950:Esterases / Q000235:genetics*; D005982:Glutathione Transferase / Q000235:genetics*; D006801:Humans; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*
D001057:Apolipoproteins E; D005982:Glutathione Transferase; D004950:Esterases; D043303:Aryldialkylphosphatase