Predictive genetic testing to control coronary heart disease and hyperlipidemia.
The contribution of genes to the etiology of coronary heart disease (CHD) is highly significant even when monogenic hyperlipidemias are excluded. Previous studies in the area of quantitative genetics and of disease or risk factor association with random genetic markers have, in recent years, been supplemented with studies focused on "candidate genes"--genes whose products are known or suspected to be involved in the atherogenic process, the thrombogenic process, lipid metabolism, or apolipoprotein (apo) structure or function. In 1974, the candidate gene approach led to the detection of a strong association between genetically determined Lp(a) lipoprotein and premature CHD and, in 1976, also led to the detection, in several populations, of the association between lipid levels and genetic types in the normal low density lipoprotein (LDL) polymorphism referred to as the Ag(x) variation. Restriction fragment length polymorphisms in DNA have been uncovered in the genes for several functionally important proteins including apos. Some of these DNA variants have been reported to be associated with CHD or lipid level. Such variants should become useful tools in predictive genetic testing for CHD risk. Most studies on the genetics of risk factors have focused on risk factor level. Because an individual's propensity to develop atherosclerosis could depend not only on absolute lipid levels but also on lipid responses to atherogenic stimuli, we have developed a method to examine if "variability genes" exist. To detect the latter class of genes, we examine within-pair differences in quantitative parameters between monozygotic (MZ) twin pairs possessing and MZ twin pairs lacking the gene under study.(ABSTRACT TRUNCATED AT 250 WORDS)
Berg
K
K
Institute of Medical Genetics, University of Oslo, Norway.
D000818:Animals; D001053:Apolipoproteins / Q000235:genetics; D001161:Arteriosclerosis / Q000175:diagnosis* / Q000235:genetics; D003327:Coronary Disease / Q000175:diagnosis* / Q000235:genetics; D004992:Ethics, Medical; D005819:Genetic Markers; D015186:Hominidae / Q000502:physiology; D006949:Hyperlipidemias / Q000175:diagnosis* / Q000235:genetics; D017270:Lipoprotein(a); D008074:Lipoproteins / Q000502:physiology; D008077:Lipoproteins, LDL / Q000235:genetics / Q000276:immunology; D011973:Receptors, LDL / Q000235:genetics; D012307:Risk Factors
D001053:Apolipoproteins; D005819:Genetic Markers; D017270:Lipoprotein(a); D008074:Lipoproteins; D008077:Lipoproteins, LDL; D011973:Receptors, LDL