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Cardiovascular disease risk factors were studied in Hispanic children in Brooks County, Texas, and in white and black children in Bogalusa, Louisiana, in 1984-1985. The same protocols were used at both sites; examiners in Brooks County were trained by Bogalusa Heart Study staff. All blood samples were analyzed in a single laboratory standardized by the Centers for Disease Control. Hispanic children were about 4 cm shorter and were about the same weight as white and black children. Subscapular skinfolds were thickest in Hispanic children. Little difference was noted for blood pressure levels in the three ethnic groups. Total cholesterol levels were highest in black children, with a drop during puberty being noted in all of the ethnic groups. This drop with puberty appeared somewhat earlier in the Hispanic children. Lipoprotein levels for Hispanic children were, in general, similar to those noted for white children. Some of the Hispanic-black differences in lipid and lipoprotein levels could be explained by differences in body size. Because Hispanics are at increased risk for specific diseases, such as diabetes, increased study of this population is warranted. Intervention and education programs aimed at altering this risk must address the unique cultural heritage of this population.

Serum lipids (total cholesterol and triglycerides) and lipoprotein cholesterol fractions (low density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and high density lipoprotein (HDL) cholesterol) have been measured approximately every 3 years on children and young adults since 1973-1974 in Bogalusa, Louisiana, a community of approximately 22,000 individuals, one-third of whom are black and two-thirds of whom are white. A total of 1,586 children were examined both at baseline (1973-1974) and at the most recent survey (1984-1986), providing 12 years of follow-up. The decreases in levels noted during puberty for total cholesterol and LDL cholesterol, primarily for boys, were followed by a rise until age 26 years. HDL cholesterol levels, particularly for white boys, continued to drop after age 14 years, yielding increasingly high LDL cholesterol/HDL cholesterol ratios. Tracking, as measured by both correlation coefficients and persistence at extreme quartiles, was evident for all of the lipids and lipoproteins. The 12-year correlation coefficients were greatest for LDL cholesterol and no trend in the magnitude of the correlation coefficients with age was noted. Tracking for HDL cholesterol was better after age 9 years, particularly for white males. Approximately 50% of those children who had total cholesterol levels or LDL cholesterol levels above the 75th percentile at baseline remained elevated 12 years later. For HDL cholesterol, a trend with age was noted for white boys: 42% of those aged 9-14 years in the lower most quartile persisted in this rank 12 years later. The best predictor of follow-up lipid or lipoprotein level was baseline level. The next best predictor was increase in weight as defined by weight/height, an index of obesity. That serum lipid and lipoprotein levels continue to track from childhood into young adulthood points to the necessity of measurement early in life and, where indicated, the introduction of preventive and interventional programs aimed at developing healthy lifestyles.

There is increasing interest in identifying children at risk for later development of cardiovascular disease. The authors studied 1,457 children who were first examined as part of the Bogalusa Heart Study in 1973 and again 15 years later as young adults. Age-, race-, and sex-specific quartiles were defined for each of three risk factor variables-ponderal index (weight/height3), systolic blood pressure, and cholesterol--for both the child and adult measures. Adults were classified as clustered if they were in the top quartile for each of the variables. Clustered adults had higher levels of several risk factor variables, in addition to the criteria variables, than did nonclustered individuals. Of children who placed in the top quartile on three factors, 21.8% were clustered as adults. Only 1.1% of those with no risk factor levels in the top quartile were clustered as adults (p < 0.0001). Logistic regression was used to predict adult cluster status from childhood variables levels. All three factors were significant predictors, with blood pressure being the most powerful. This well-fitting model is easily interpretable in terms of standard deviations and can be a useful model for identifying at-risk children.

The relationship between parental history of vascular disease (heart attack, stroke, diabetes mellitus, and hypertension) and risk factor variables for cardiovascular disease was assessed in 3,312 offspring aged 5-17 years during the 1981-1982 school year in the biracial community of Bogalusa, Louisiana. Risk factors studied included systolic blood pressure, diastolic blood pressure, serum total cholesterol, triglycerides, and individual lipoprotein cholesterol (beta-, low density lipoprotein (LDL) cholesterol; pre-beta, very low density lipoprotein (VLDL) cholesterol; and alpha-, high density lipoprotein (HDL) cholesterol). Risk factors were adjusted for age, race, sex, and height (blood pressure only) prior to testing parental history effects. Univariate comparisons between risk factors in children and vascular disease in parents resulted in statistically significant increases in systolic and diastolic pressures associated with the presence of maternal or paternal hypertension (p less than 0.001). Paternal heart attack was also associated with elevations in diastolic pressure (p less than 0.01) of children. Maternal diabetes mellitus was associated with an increase in serum total cholesterol (p less than 0.05). Paternal diabetes mellitus and maternal heart attack (for female progeny only) were associated with increases in mean triglyceride levels of children. VLDL cholesterol results were similar to those for triglycerides. For HDL cholesterol, paternal diabetes mellitus was associated with a small decrease in mean levels (p less than 0.05). Dramatic increases to the highest decile of risk were found in association with the following parental disease combinations: paternal heart attack-paternal diabetes for serum total cholesterol (p less than 0.0001), maternal heart attack-paternal diabetes (p less than 0.001) and paternal stroke-maternal diabetes (p less than 0.0001) for LDL cholesterol. Multivariate analysis detected no significant effects of single parental vascular disease. However, paternal heart attack in combination with either diabetes mellitus or hypertension was statistically significant in their relationship to the risk factors overall.

The interrelationships of serum lipids and lipoproteins with measures of body habitus and maturation stages were analyzed in a biracial population of 3151 children, ages 5--14 years. In general, triglycerides, pre-beta-lipoprotein, and beta-lipoprotein were positively correlated with body habitus and maturation while alpha-lipoprotein was negatively correlated. The relationships in most instances were more apparent in whites than in blacks, with the highest correlations observed in white boys. No significant correlations were observed between serum cholesterol and the anthropometric variables except in white boys. The most obese children tended to have higher levels of triglycerides, pre-beta-lipoprotein, and beta-lipoprotein, and lower levels of alpha-lipoprotein than the remaining population. In the total population, the multiple correlation coefficients with the children's age, race, sex weight-height index, triceps skinfold and maturation stage as the independent variables and the concentrations of the different serum variables as the dependent variables ranged from 0.04 to 0.11.

Risk factors for cardiovascular disease were measured in 990 young adults, aged 17-24 years, in a 1982-1983 survey of the biracial (black-white) community of Bogalusa, Louisiana. Even after controlling for age and obesity, several lifestyle factors (cigarette smoking, alcohol consumption, and oral contraceptive use) were independently related (p less than 0.05) to levels of serum lipids, lipoprotein cholesterol fractions, and blood pressure. Oral contraceptive use was associated with increased levels of both serum triglycerides (20 mg/dl, blacks; 25 mg/dl, whites) and low density lipoprotein (LDL) cholesterol (19 mg/dl, whites), and decreased levels of high density lipoprotein (HDL) cholesterol (-6 mg/dl, whites). Linear regression analyses also showed that cigarette smoking was associated with elevated levels of serum triglycerides (ranging from 15 to 26 mg/dl) and decreased levels of HDL cholesterol (ranging from -9 to -11 mg/dl) in white males and females. Although persons who smoked cigarettes were also likely to consume alcohol, alcohol intake in nonsmokers was positively associated with levels of serum triglycerides, LDL cholesterol, and very low density lipoprotein cholesterol in white males, and with blood pressure levels in black males. A statistically significant association between alcohol intake and HDL cholesterol levels (r = 0.24) was observed only in white females who did not smoke. These adverse influences of lifestyle factors on cardiovascular disease risk may provide a rational basis for intervention during adolescence and early adulthood.

The relation of obesity to clustering of systolic blood pressure, fasting insulin, and ratio of low and very low density lipoprotein cholesterol to high density lipoprotein cholesterol [LDL-C + VLDL-C)/HDL-C) was investigated in 3,503 subjects aged 5-24 years in Bogalusa, Louisiana, from September 1981 to September 1983. Risk ratios (RR) were calculated as the number of subjects with risk factor variables in the upper tertile divided by the expected number. The variables showed strong clustering (RR = 3.1); however, after adjusting for obesity, clustering of systolic pressure, (LDL-C + VLDL-C)/HDL-C, and insulin was reduced (RR = 1.3). Lean subjects (lower tertile of obesity) showed less clustering than expected (RR = 0.4), while more obese subjects (upper tertile of obesity) had greater clustering than expected (RR = 3.1). Furthermore, trunk fat deposition (subscapular skinfold) had a greater impact on clustering at high levels than limb fat deposition (triceps skinfold). Since obesity is related to clustering of risk factor variables in children and young adults, the prevention of the onset of obesity in early life may be important to reducing the risk of coronary heart disease in later life.

To examine the influence of cigarette smoking initiation on serum lipid and lipoprotein changes in early life, 747 nonsmoking 9- to 17-year-olds from the biracial community of Bogalusa, Louisiana were reexamined five to six years following an initial screening. Upon reexamination in 1981-1983, 147 reported smoking cigarettes (mean duration, 3.5 years; median number of weekly cigarettes, 20). Compared with nonsmokers, persons who began smoking had more unfavorable changes in serum triglycerides and lipoprotein cholesterol levels during follow-up, independently of age, sexual maturation, obesity, alcohol consumption, and oral contraceptive use in females. Smoking initiation was not associated with increases in serum total cholesterol levels, but compared with nonsmokers, white males and white females smoking three or more packs weekly showed additional mean increases of 13.2 and 11.6 mg/dl in low density lipoprotein cholesterol, additional 5.9 and 2.4 mg/dl increases in very low density lipoprotein cholesterol (VLDL-C), and additional decreases of 15.6 and 9.2 mg/dl in high density lipoprotein cholesterol levels, respectively. Black smokers showed larger increases in serum triglycerides and VLDL-C levels than did black nonsmokers. These findings indicate that the start of even modest cigarette smoking may have potentially long-term atherogenic effects. Prevention of smoking in early life should therefore be an important aspect of cardiovascular disease intervention.

A cross-sectional study of 4074 children, ages 5--17 years, in Bogalusa, Louisiana indicated significant changes of serum lipids and lipoproteins occurring during puberty. These changes could be related to both age and maturation and likely reflect the influence of sex hormones on serum lipoprotein metabolism. Considerable differences were observed in the race/sex groups, with boys showing a more marked decrease of serum total cholesterol, reflecting decreases of beta- and alpha- lipoproteins. While the ratio of mean beta-lipoprotein cholesterol/mean alpha-lipoprotein cholesterol for the white girls and black children remained relatively constant over the age span, the ratio beginning around age 11 years rose dramatically in white boys, reflecting an inordinate decrease of alpha-lipoprotein and an earlier beginning rise of beta-lipoprotein. The observations have important implications for earlier coronary artery disease in white men.