Hostname: page-component-78c5997874-ndw9j Total loading time: 0 Render date: 2024-11-05T05:36:21.495Z Has data issue: false hasContentIssue false

Twin Studies of Coronary Heart Disease and Its Risk Factors

Published online by Cambridge University Press:  01 August 2014

Kare Berg*
Affiliation:
Institute of Medical Genetics, University of Oslo, and Department of Medical Genetics, City of Oslo
*
Institute of Medical Genetics, University of Oslo, P.O. Box 1036, Blindern, 0315 Oslo 3, Norway

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

The ongoing comprehensive study of the updated population-based Norwegian Twin Panel (like-sexed twin pairs born since 1915) has already given results of interest to the research on coronary heart disease and its risk factors. Significantly more dizygotic (DZ) than monozygotic (MZ) pairs are discordant for death between 40 and 60 years of age. Presumably, several of the cases must have been coronary heart disease deaths. In pairs where both members are alive, concordance rate for coronary heart disease before the age of 60 years is significantly higher in MZ than in DZ pairs. Concordance rate for reported hypertension is significantly higher in MZ than in DZ pairs. These findings are compatible with a significant genetic effect on premature death, coronary heart disease and hypertension.

There is a strong genetic effect on serum level of apoB, apoA-I and apoA-II, a weaker effect on cholesterol level and a doubtful effect on triglyceride level. Genes belonging to several normal genetic polymorphisms may participate in the control of environmentally/dietary caused variability in lipid and lipoprotein parameters. The study of MZ twins that was conducted to detect these effects holds considerable promise for the detection of gene control of many kinds of quantitative parameters. Further work with this twin panel may provide more definite answers to several questions raised during the present investigation. Application of more sophisticated models for twin family analysis on several normal and pathological traits may be very informative. Also, this updated Norwegian Twin Panel should in the long run make it possible to estimate the predictive value for the second member of a twin pair of having a twin contracting coronary heart disease (or any other reasonably frequent disease) by a given age. Finally, the subsample that is subjected to extensive laboratory analyses will provide useful data for genetic linkage analyses since in many cases, offspring of two members of a MZ pair can effectively be considered as one single (more informative) sibship.

Type
Research Article
Copyright
Copyright © The International Society for Twin Studies 1984

References

REFERENCES

1.Berg, K (1981): Twin research in coronary heart disease. In: Gedda, L, Parisi, P, Nance, WE (eds): Twin Research 3: Part C, Epidemiological and Clinical Studies. New York: A.R. Liss, p 117130.Google Scholar
2.Berg, K (1982): The genetics of the hyperlipidemias and coronary artery disease. In Bonné-Tamir, B, Cohen, T, Goodman, RM (eds.): Human Genetics. Part B: Medical Aspects. New York: A.R. Liss, p. 111125.Google Scholar
3.Berg, K (1983): Genetics of coronary heart disease. In Steinberg, AG, Bearn, AG, Motulsky, AG, Childs, B (eds): Progress in Medical Genetics. New Series, Vol. V. Philadelphia: W.B. Saunders, p 3590.Google Scholar
4.Fabsitz, RR, Havlik, R, Feinleib, M, LaRue, CG (1982): Association of genotype and total cholesterol in MZ twins. Clin Genet 21: 418419.Google Scholar
5.Magnus, P, Berg, K, Nance, WE (1983): Predicting zygosity in Norwegian twin pairs born 1915-1960. Clin Genet 24:103112.CrossRefGoogle ScholarPubMed
6.Magnus, P, Berg, K, Borresen, AL, Nance, WE (1981): Apparent influence of marker genotypes on variation in serum cholesterol in monozygotic twins. Clin Genet 19: 6770.Google Scholar
7.Magnus, P, Maartmann-Moe, K, Golden, W, Nance, WE, Berg, K (1981): Genetics of the low density lipoprotein receptor: II. Genetic control of variation in cell membrane low density lipoprotein receptor activity in cultured fibroblasts. Clin Genet 20: 104112.Google Scholar
8.Martin, NG, Rowell, DM, Whitfield, JB (1983): Do the MN and Jk systems influence environmental variability in serum lipid levels? Clin Genet 24:114.Google Scholar