Kathe Kelly

Black-white differences in plasma lipoproteins in Cincinnati schoolchildren (one-to-one pair matched by total plasma cholesterol, sex, and age)

The suburban, biethnic Princeton School District provided a suitable population of children (ages 6–17) to test the hypothesis that black schoolchildren have higher high density lipoprotein cholesterol (C-HDL), lower low density lipoprotein cholesterol (C-LDL), and lower triglyceride levels than white schoolchildren when pair-matched by total plasma cholesterol, age, and sex. In 194 black-white pairs of male schoolchildren, black children had higher C-HDL (59.5 ± 13.5 versus 54.8 ± 12.7 mg/dl, p < .001), lower C-LDL (105.7 ± 25.8 versus 108.1 ± 26.7, p < .05), and lower triglyceride (60.7 ± 27.2 versus 71 ± 38.1, p < .001). In 222 black-white pairs of female schoolchildren, black girls had higher C-HDL (57.7 ± 13.1 versus 52.0 ± 11.6 mg/dl, p < .001), lower C-LDL (107.4 ± 24.8 versus 109.6 ± 23.3, p < .05, and lower triglyceride (64.0 ± 24.6 versus 80.2 ± 38.6, p < .001). Mean Quetelet indices (weight/height2) did not differ significantly for the black and white males or females. Since, by matching, the pairs did not differ in age, sex, or total plasma cholesterol, and also did not differ by Quetelet, any differences in C-HDL, C-LDL, and triglyceride can be imputed to racial or other unmeasured, racially related environmental differences in the cholesterol-carrying lipoprotein fractions. Persistence of these black-white differences in lipoproteins into adulthood may be associated with a relatively lower risk of coronary heart disease (CHD) in blacks than in whites, for any given total plasma cholesterol level.

LIPID AND LIPOPROTEIN TRACKING IN CHILDREN

Summary: This study was designed to assess tracking of plasma cholesterol, trigly-ceride, high and low density lipoprotein cholesterols (C-HDL, C-LDL), in 108 children followed over a 4 year period in the Cincinnati Lipid Research Clinics Princeton School Study, with focus on those children initially in the lowest decile for lipids and lipoproteins. For children whose initial lipid-lipoprotein levels were in the lowest decile, 60% (for cholesterol), 33% (for triglyceride), 56% (for C-LDL), and 13% (for C-HDL) remained in the lowest decile after 4 years of follow-up. The difference in total plasma cholesterol, triglyceride, C-LDL, and C-HDL between those children initially in the lowest decile and all others was retained for these specific children during the 4 year follow-up, p ≤ 003. A considerable proportion of the increase in group mean lipid-lipoprotein levels over 4 years could be accounted for by the phenomenon of regression toward the mean, with the exception of C-LDL where the observed means did not increase as one would expect due to regression towards the mean (≤.05), a further example of tight tracking at low C-LDL levels. For children whose initial total plasma, cholesterol, triglyceride, C-LDL, and C-HDL were in the highest decile, 46% (for cholesterol), 27% (for triglyceride), 27% (for C-LDL), and 45% (for C-HDL) remained in the highest decile after 4 years follow-up. For all 108 children, initial plasma cholesterol, triglyceride, C-LDL, and C-HDL were all closely correlated with subsequent measurements 1, 2, and 3 years apart, p ≤.001. Such findings raise the possibility that children who tend to track in the lowest and highest deciles for cholesterol and C-LDL may mature to become adults respectively at reduced and increased coronary heart disease (CHD) risk. Children who tend to track in the lowest and highest deciles for C-HDL may also mature to become adults respectively at increased and reduced CHD risk. Although the degree of tracking at either extreme of the distribution and for the group as a whole appears to have cohesiveness and may be useful for prediction of future lipid and lipoprotein levels, individual children at the extremes of the distributions will need to be followed over longer periods of time, to identify the continuity of childhood and adult values, and eventual CHD risk.Speculation: Children who tend to track in the lowest and highest deciles for cholesterol and C-LDL may mature to become adults respectively at reduced and increased coronary heart disease (CHD) risk. Children who tend to track in the lovest and highest deciles for C-HDL may also mature to become adults respectively at increased and reduced CHD risk.

Blood pressure determinants in progeny of parents taking or not taking antihypertensive drugs

Parent-child associations of blood pressure determinants were studied in 163 kindreds randomly recalled in the Princeton School Family Study, comparing 132 kindreds (337 children) with neither parents nor parental siblings on hypotensive agents (H-), and 31 kindreds (64 children) with at least one parent on hypotensives (H+). The following mean (SE) blood pressure determinants, covariance adjusted for age, race, and sex, differed in children from H+ and H- kindreds (∗P ⩽ 0.04, ∗∗P < 0.01): Weight (kg) Quetelet (wt/ht2) Hematocrit (%) Bilirubin (mg/dl) H+ 53 ± 1.5 2.1 ± 0.04 44 ± 0.4 0.68 ± 0.04 H- 49 ± 0.7∗ 1.9 ± 0.2∗∗ 43 ± 0.2∗∗ 0.52 ± 0.02∗∗ Mean covariance-adjusted total cholesterol, high- and low-density lipoprotein cholesterol, and triglyceride did not differ in children from H+ and H- kindreds, P > 0.1. Children of H+ parents have blood pressure determinants which, in aggregate, may facilitate their later expression of high blood pressure, and reflect familial sharing of high blood pressure. Since obesity is a major determinant of blood pressure, we speculate that in children from H+ kindreds, potentially predisposed to high blood pressure, control of obesity might be explored as one way to prevent the eventual development of high blood pressure or reduce its severity.

742 LIPOPROTEIN CORRELATIONS IN PARENTS AND THEIR ADULT AND PEDIATRIC PROGENY

Parent-adult progeny(>20yrs old)(P-AP), and and parent-pediatric progeny (6-19 yrs old)(P-PP) correlations for plasma low and high density lipoprotein cholesterols(C-LDL,C-HDL) were assessed in randomly recalled white subjects in the LRC Princeton school family study to compare intrafamilial lipoprotein associations among family members still sharing and no longer sharing a common household environment. Father(F)-son(S), F-daughter(D),mother(M)-S, M-D C-LDL and C-HDL correlations in the 75 P-AP pairs and 245 P-PP pairs, (*p<.05, **p<01), were as follows:For C-LDL, F-S and F-D relationships were significant and comparable for both P-AP and P-PP pairs; M-S and M-D C-LDL correlations were less consistent than for F-S or F-D, and were significant only for M-S in the P-PP pairs. For C-HDL, in contrast to C-LDL, there were no significant P-AP relationships. For C-HDL, in P-PP pairs, the M-S, M-D, and F-D relationships were significant. The general similarities in C-LDL relationships in P-AP and P-PP pairs, particularly in F-S and F-D, suggest a lasting genetic influence on C-LDL. The loss of significant P-AP C-HDL relationships, when compared to those in P-PP suggests a substantial differential environmental effect when common households are no longer shared.

1166 LIPID AND LIPOPROTEIN CORRELATIONS IN BLACK AND WHITE ADULT AND CHILD SIB PAIRS

To compare intrafamilial associations among siblings(S) who still share and no longer share a common household environment, S-S correlations for total cholesterol(TC), high and low density lipoprotein cholesterol(C-HDL, C-LDL), and triglyceride(TG) were calculated.For the 54 black(B) and 230 white(W) adult(>20yrs old) (A) S-S pairs, and for the 97 B and 274 W child (6-19 yrs old)(C) S-S pairs, the correlations (*p<.02,**<.01,†<001) were:There were no consistent B-W differences in lipid-lipoprotein correlations in A or C S-S pairs. S-S correlations for C-LDL, TC, and TG were either comparable or stronger in A S-S than in C S-S pairs, despite the loss of shared households in the A S-S pairs. This suggests a lasting and persistent influence of genetic factors on C-LDL and TG, or, speculatively, persistence into adulthood of shared environmental effects. In contrast, S-S correlations for C-HDL were stronger in C than in A S-S pairs, suggesting a substantial influence of environmental factors on C-HDL, revealed when common households are no longer shared. Explication of environmental factors which affect C-HDL might be realized by longitudinal studies of lipoproteins from childhood to adulthood.

Cross-Cultural, Ethnic, Demographic, and Environmental Factors Affecting High Density Lipoprotein Cholesterol and Their Mutual Interrelationships with Coronary Heart Disease

Population studies in diverse geographical areas including the United States (Gordon et al. 1977), Norway (Miller et al. 1977), Hawaii (Rhoads et al. 1976), and Israel (Goldbourt et al. 1979) have revealed that C-HDL is an independent risk factor inversely associated with coronary heart disease (CHD) risk. Detailed kindred studies have shown that familial elevations of high density lipoprotein cholesterol are associated with reduced CHD morbidity and mortality and with decreased longevity (Glueck et al. 1975, 1976). Studies of cohorts selected by extraordinary age (octo- and nonagenarians [Glueck et al. 1977; Nicholson et al. 1979]) identify many subjects having relatively high levels of C-HDL, some with familial hyperalpha-lipoproteinemia, and many having relatively low levels of the major atherogenic lipoprotein cholesterol, low density lipoprotein cholesterol, C-LDL. Because of the uniformity and consistency of these findings both in populations and in kindred studies, attention has been focused upon factors which may affect high density lipoprotein cholesterol levels, with the ultimate aim of better understanding HDL physiology, and pathophysiology, and ultimately to devise methods to consistently, safely, and effectively raise C-HDL levels.

Nutrient Intake, Lipids, and Lipoproteins in 6–19-Year-Old Schoolchildren

Dietary intake of cholesterol, saturated and polyunsaturated fats, and (perhaps) carbohydrates and total calories may relate to lipid and lipoprotein levels and to the ultimate development of coronary heart disease (CHD) (InterSociety Commision, 1970; National Diet Heart Study 1968; Connor and Connor 1972). However, the strength, consistency, and predictability of nutrient-CHD risk associations remains controversial (Mann 1977; Glueck et al. 1978).