Variation in the serum concentrations of VLDL, IDL, LDL, and HDL was studied in 192 survivors of myocardial infarction under the age of 50 living in the north-east Scotland; 250 relatives, mostly first degree; and 259 unrelated individuals, comprising mostly spouses and their relatives. Serum lipoprotein concentrations have been compared in samples taken at different times after the incident. The average value of samples taken within 24 hours is similar to the mean scores for LDL and VLDL of repeat samples taken, on average, 9 months later. VLDL levels are substantially increased in regular cigarette smokers in both sexes, especially in males, HDL levels tend to be lower, though not significantly so. The frequency of persons who are or have been regular cigerette smokers is higher in index cases than in controls. About a quarter of the variance of VLDL in males is accounted for by multiple regression on measures of body fatness, that is, relative weight and subscapular skinfold thickness. In females only about 10% of the variance is thus accounted for, and only in males do LDL levels show correlated changes with fatness. There are no significant differences for either relative body weight or subscapular skinfold thickness between the means of first degree relatives or survivors of infarction and controls. The concentrations of VLDL and LDL in first degree relatives of survivors of infarction are significantly higher than the control means. HDL shows no significant difference. The evidence for genetic variation in serum lipoprotein is based on the polygenic model and the analysis of the correlation between parents and offspring and the correlation between sibs. From the pooled regression on single parents, heritabilities for HDL, LDL, and VLDL work out at 0.67 ± 0.21, 0.36 ± 0.18, and 0.23 ± 0.20, respectively. The lower heritability of VLDL is consistent with the variance of repeat measurements on the same control individuals, which is much higher for VLDL than for LDL or HDL. The high correlation between VLDL and measures of fatness, for which heritability estimates are statistically insignificant, as well as the association between raised VLDL concentration and smoking, also provide confirmatory evidence of the major importance of non-genetic causes in the variation of VLDL. The results are discussed in relation to the origin of the effects of smoking, variation in proneness to coronary disease, and the biological significance of differences in HDL concentration.
