Gösta Dahlén

BACKGROUND: The extent to which serum lipid levels are affected by genetic and environmental factors remains a point of controversy. We examined both genetic and environmental influences on serum lipid levels in twins reared either together or apart who participated in the Swedish Adoption/Twin Study of Aging. METHODS: We studied 302 pairs of twins (mean age, 65.6 years; range, 52 to 86); 146 pairs had been reared apart. We simultaneously compared the twins on the basis of both zygosity and rearing status, which allowed joint estimation of genetic and environmental influences on serum lipid levels. Genetic influence was expressed in terms of heritability, the proportion of the population variation attributable to genetic variation (a value of 1.0 indicates that all of the population variation is attributable to genetic variation). The serum lipids and apolipoproteins measured included total cholesterol, high-density lipoprotein cholesterol, apolipoproteins A-I and B, and triglycerides. RESULTS: Structural-equation analyses revealed substantial heritability for the serum levels of each lipid measured, ranging from 0.28 to 0.78. Comparisons of the twins reared together with those reared apart suggested that the environment of rearing had a substantial impact on the level of total cholesterol (accounting for 0.15 to 0.36 of the total variance). Sharing the same environment appeared to affect the other lipid measures much less, however, than did genetic factors and unique environmental factors not shared by twins. Comparisons of younger with older twins suggested that heritability for apolipoprotein B and triglyceride levels decreased with age. CONCLUSIONS: The effect of genetic factors on the serum levels of some but not all lipids appears to decrease with age. Early rearing environment appears to remain an important factor in relation to levels of total cholesterol later in life, but it has less effect on other serum lipids and apolipoproteins in the elderly.

Certain properties of the atypical serum lipoprotein, referred to as pre‐ β 1 ‐lipoprotein, suggested that it might be identical to the lipoprotein carrying the Lp(a) antigen: Lp(a) lipoprotein. Both lipoprotein phenomena are under genetic control and occur in a certain proportion of healthy people. Pre‐ β 1 ‐lipoprotein occurs more frequently in patients with coronary heart disease (CHD) than in the healthy population. The present study of Finnish CHD patients was undertaken to investigate whether a close relationship could be revealed between pre‐ β 1 ‐lipoprotein and Lp(a) lipoprotein, as well as between Lp(a) lipoprotein and CHD. Both expectations were realised, and we conclude that pre‐ β 1 ‐lipoprotein is very closely related, if not identical to Lp(a) lipoprotein. If the present results are confirmed in future studies, serum analysis for Lp(a) lipoprotein/pre‐ β 1 ‐lipoprotein may become a useful tool for the identification in early life of members of a subpopulation which is particularly at risk for developing CHD.