Influence of the beta2-adrenergic receptor Arg16Gly polymorphism on longitudinal changes in obesity from childhood through young adulthood in a biracial cohort: the Bogalusa Heart Study.

BACKGROUND: The beta2-adrenergic receptor (ADRB2) plays a major role in regulating energy expenditure by stimulating lipid metabolism in human adipose tissue. Polymorphisms in the ADRB2 gene have been associated with obesity and various weight-related traits in cross-sectional studies of adults, but little is known about the effects of the ADRB2 gene on childhood obesity or the propensity to gain weight over time. OBJECTIVE: To assess the effects of a polymorphism in codon 16 (Arg16-->Gly) of the ADRB2 gene, which has been associated with a decrease in beta2-receptor density and efficiency, on longitudinal changes in obesity from childhood to young adulthood in a biracial cohort. DESIGN: Seven cross-sectional screenings of children and five cross-sectional screenings of young adults who were previously examined as children produced longitudinal data from childhood to young adulthood. METHODS: Height, weight and subscapular and triceps skinfolds were measured by trained examiners following identical protocols over the course of the study. Gender- and age-stratified analyses using random coefficients models were used to examine longitudinal genetic effects on obesity in 1151 African-American and Caucasian males and females who attended an average of six examinations over a 24 y period from childhood to young adulthood. RESULTS: Age-stratified analyses showed no clear genetic relationships with changes in obesity measures over time in females, but an age-dependent association was observed in males, where the relationship between the Arg16Gly polymorphism and obesity became stronger with age. In males who were 4-9 y of age at the beginning of the study in 1973, body mass index (BMI) was 4% higher in Gly/Gly and Arg/Gly males compared to those with Arg/Arg by 26 y of age. Subscapular skinfold measurements in Gly/Gly males became significantly different from Arg/Arg males (20% higher) by age 20. In the oldest male cohort (10-14 y of age in 1973), BMI increased at a significantly greater rate (0.4%/y) in males carrying the Gly16 form of the receptor relative to Arg/Arg males. BMI was significantly different between homozygous genotypes by approximately 26 y of age, and reached 8% higher in Gly/Gly males by age 32. Subscapular skinfolds also increased at a significantly greater rate (2%/y) in Gly/Gly males compared to Arg/Arg males, becoming significantly different (27%) by approximately 22 y of age and reaching a maximum difference of 50% by age 32. CONCLUSIONS: Our data suggest that the beta2-adrenergic receptor is associated with the propensity to gain weight from childhood to young adulthood in males. An increased understanding of genetic influences on the development of obesity may improve the effectiveness of interventions designed to reduce excess body weight and help define the role of genetic factors in diabetes and cardiovascular disease.

Trends of lipoprotein variables from childhood to adulthood in offspring of parents with coronary heart disease: the Bogalusa Heart Study.

Although dyslipidemia among offspring of parents with coronary heart disease (CHD) has been known, the development of this adverse relationship with respect to specific lipoprotein variables from childhood to young adulthood has not been elucidated. This aspect was examined in a young adult cohort with (n = 271) and without (n = 805) a parental history of CHD followed longitudinally since childhood by repeated surveys from 1973 to 1991. Trends in fasting lipoprotein variables by parental CHD status were assessed by Lowess smoothing curve and Generalized Estimating Equations (GEE). In multivariate analyses adjusted for race and sex, parental CHD associated positively with low-density lipoprotein cholesterol (LDL-C, P <.01) and triglycerides (P <.05) mainly at the young adulthood age, whereas a positive association was noted with very-low-density lipoprotein cholesterol (VLDL-C) during both childhood and young adulthood (P <.05). The positive association between parental CHD and LDL-C in young adulthood persisted independently of body mass index (BMI) and fasting insulin, but disappeared when fasting glucose was added to the model. With respect to triglycerides and VLDL-C, inclusion of BMI, insulin, and/or glucose eliminated the adverse association with parental CHD. These observations suggest that parental CHD is just one more explanatory variable that loses its partial contribution to lipoprotein profiles in their offspring when other strongly interrelated contributory variables such as age, body fatness, and measures of glucose homeostasis are taken into account. Information on these risk variables in conjunction with parental or family history of CHD may enhance the potential of CHD risk assessment in youth.

Influence of lipoprotein lipase serine 447 stop polymorphism on tracking of triglycerides and HDL cholesterol from childhood to adulthood and familial risk of coronary artery disease: the Bogalusa heart study.

The effects of the lipoprotein lipase (LPL) Serine 447 Stop (S447X) polymorphism on high-density lipoprotein cholesterol (HDLC) and triglycerides (TG) have been demonstrated. However, little is known about its effect on the tracking of HDLC and TG over time and familial risk of coronary artery disease (CAD). This aspect was examined in black and white individuals (n=829) aged 5-18 year at baseline, followed on average 18.8 yr. The frequency of the X447 allele was lower in Blacks than Whites (0.043 vs. 0.087, P=0.002). Carriers vs. noncarriers of the X447 allele had lower TG (99.3 vs 122.1 mg/dl, P<0.01) and higher HDLC (51.1 vs. 49.7 mg/dl, P<0.05) in adulthood, but not in childhood. The trends in genotype-specific means of childhood and adulthood levels of HDLC and TG in sex or race subgroups were similar to those in the total sample. With respect to tracking over time, of those in the bottom quartile of HDLC in childhood, 46.1% of the noncarriers vs. 23.1% of the carriers remained in this lowest quartile into adulthood (P=0.03); corresponding values for the top quartile of HDLC were 37.5% for the noncarriers vs. 57.1% for the carriers (P=0.03). Although TG tended to track better among the carriers in the bottom quartile and among the noncarriers in the top quartile, this trend was not significant. Carriers showed lower prevalence of parental history of CAD than noncarriers (6.9% vs. 14.1%, P=0.02) independently of lipoprotein variables, adiposity, blood pressure, age, sex and race. Thus, the X447 allele of the LPL gene is associated with an increase in HDLC and a decrease in TG in adults, tracking of HDLC since childhood, and a lower family history of CAD.

Distribution and correlates of lipoproteins and their subclasses in black and white young adults. The Bogalusa Heart Study.

Lipoprotein subclasses vary in CAD risk potential, but their distribution and correlates are not well documented in black and white young adults. A subsample of 449 (32%) young adults (67% white, 58% female) aged 20-37 years examined in the Bogalusa Heart Study had lipoprotein subclasses measured in terms of cholesterol by vertical spin density-gradient ultracentrifugation. LDL subclass pattern was characterized as either predominantly LDL(1) (large, buoyant), LDL(2) (intermediate) or LDL(3) (small, dense). Whites had significantly higher levels of VLDL, VLDL(3), and LDL and lower levels of HDL(2) and HDL(3) than blacks. White females had significantly higher levels of HDL(2) than white males. Visceral fatness, measured as waist circumference, and race were the major contributors to the explained variance (6-22%) of these lipoproteins, with adverse trends seen among whites and persons with large waist circumferences. Sex (males>females), waist circumference (positive), HDL(2) (negative), and HDL(3) (positive) were the predictor variables for the likelihood of having the LDL(3) pattern. When glucose and insulin were included in the multivariate analysis, insulin (positive), sex (males>females), HDL(2) (negative) and HDL(3) (positive) became significant predictors of LDL(3) pattern. Positive parental history of CAD was associated with LDL (P=0.009) in white males, and HDL(2) (P=0.008) and LDL(3) subclass pattern (P=0.038) in white females; whereas none in blacks. The observed correlates of lipoprotein subclasses and patterns need to be considered in estimating CAD risk in young adults.

Combined effects of endothelial nitric oxide synthase gene polymorphism (G894T) and insulin resistance status on blood pressure and familial risk of hypertension in young adults: the Bogalusa Heart Study.

Impaired endothelial function with decreased nitric oxide production is shared by insulin resistance and essential hypertension. Although there are limited data on the association between the endothelial nitric oxide synthase (eNOS) G894T polymorphism and hypertension, information is absent on the combined effects of eNOS G894T genotype and insulin resistance status on blood pressure (BP) levels and the familial risk of hypertension. This aspect was examined in a community-based sample of 1021 unrelated African American and white young adults aged 19 to 38 years. African Americans displayed a lower frequency of the T894 allele than whites (0.105 v 0.324, P < .001). After adjusting for sex, age, and body mass index (BMI), noncarriers versus carriers of the T894 allele had significantly higher systolic (SBP), diastolic (DBP) BP and mean arterial pressure (MAP) levels (111.7 v 109.2 mm Hg for SBP; 73.6 v 72.3 mm Hg for DBP; 86.3 v 84.6 mm Hg for MAP), with both African Americans and whites showing similar trends. This association was modulated by insulin resistance status, measured by the homeostasis model assessment of insulin resistance (HOMA IR) using fasting insulin and glucose. Subjects with high insulin resistance (above the median HOMA IR) showed significantly greater differences in BP levels between noncarriers and carriers of the T894 allele. Furthermore, the G894T genotype and insulin resistance also showed a combined effect on the prevalence of parental hypertension, a measure of familial risk, with noncarriers versus carriers in the high insulin resistance group showing higher prevalence (70.5% v 51.3%, P = .006, adjusted for race). Thus, the allelic variation (G894T) in the eNOS gene locus in conjunction with insulin resistance may be one factor contributing to the predisposition to hypertension.

The Ser(447)-Stop polymorphism of lipoprotein lipase is associated with variation in longitudinal serum high-density lipoprotein-cholesterol profiles: the Bogalusa Heart Study.

The Ser(447)-Stop polymorphism of lipoprotein lipase (LPL) has been associated with altered high-density lipoprotein-cholesterol (HDL-C) and triglyceride (TG) levels at individual measurements, but nothing is known of its associations with lipid profiles derived from serial measurements. We used multilevel statistical models to study effects of this polymorphism on longitudinal lipid profiles in 1,006 Bogalusa Heart Study subjects examined 4 to 9 times between the ages of 4 and 38 years. Stop(447) allele frequencies in African Americans (0.053 +/- 0.011) and whites (0.091 +/- 0.009) differed significantly (chi(2) = 7.595, 1 df, P =.006; Stop(447) homozygotes and heterozygotes combined). Overall, TG levels were lower and HDL-C levels higher in blacks than in whites of the same age and sex. Longitudinal TG profiles were lower in Stop(447) carriers at all ages. However, longitudinal HDL-C profiles differed among genotype groups with age: the Stop(447) allele was associated with higher HDL-C only in subjects above approximately 10 years of age. Genotype-specific HDL-C profiles also differed significantly among race/sex groups. Thus, we found evidence of LPL genotype effects that vary within individuals with age. Possible mechanisms, which could account for age-related changes in the effects of LPL variants, are discussed.

Comparison of weight-for-height indices as a measure of adiposity and cardiovascular risk from childhood to young adulthood: the Bogalusa heart study.

The development of obesity in childhood is considered a major determinant of cardiovascular risk. Currently the body mass index (BMI = weight/height(2)) is widely used as a measure of obesity. However, since BMI is associated with height during childhood, a weight for height index (weight/height(p)) that is independent of height is thought to be more appropriate. Therefore, to compare the utility of such weight/height(p) index with BMI in assessing adiposity and its relation to cardiovascular risk variable data from the Bogalusa Heart Study participants aged 6 months to 21 years were examined. A total of 31,796 observations on 12,827 subjects was used in the data analysis. Study variables include height, weight, subscapular and triceps skinfolds, blood pressure, serum lipids and lipoproteins, and plasma glucose and insulin. The optimal exponential for the weight/height(p) index started from 2.42 in the 6 month olds, decreased to 1.86 in 2 to 3 year olds, increased to 3.29 among 10 to 11 year olds, and then decreased to 2.15 in the 20 to 21 year olds. The BMI showed slightly higher correlations than weight/height(p) index with subscapular skinfold in children. Both in children and young adults BMI also showed a slightly higher correlation with other cardiovascular risk factor variables regardless of age-race-sex groups. These results indicate that weight/height(p) index is not superior to BMI as an indicator of adiposity and related cardiovascular risk factors during childhood.

Trends in nutrient intake of 10-year-old children over two decades (1973-1994) : the Bogalusa Heart Study.

Dietary intakes of 10-year-old children were examined in seven cross-sectional surveys to observe secular trends in nutrient intake and food consumption patterns over 2 decades (1973-1994). Total energy intake remained unchanged from 1973 to 1994. However, when expressed as energy per kilogram body weight, intake decreased from 65.5 kcal in 1973 to 55.4 kcal in 1994 because children's weight increased. A significant trend was noted in ponderal index, which increased from 12.31 (1973-1974) to 13.71 (1992-1994), with an actual weight gain of 1.45 kg from 1973 to 1979 and 2.71 kg from 1981 to 1994. Linear trends also were noted for total fat (negative), saturated fat (negative), dietary cholesterol (negative), polyunsaturated fat (positive), and total carbohydrate (positive). There was a significant increase in percent energy from protein and carbohydrate and a significant decrease in percent energy from fat, primarily saturated and monounsaturated fat. Trends in nutrient intakes of children reflected trends in food consumption. The percentage of total fat from fats/oils, mixed meats, eggs, milk, pork, and desserts decreased, while that from poultry, cheese, and snacks increased. Although more children met dietary recommendations for total fat, saturated fat, and dietary cholesterol, the vast majority continued to exceed prudent diet recommendations.

Apolipoprotein E polymorphism modulates the association between obesity and dyslipidemias during young adulthood: The Bogalusa Heart Study.

To elucidate to what extent apolipoprotein (apo) E polymorphism modulates obesity-induced dyslipidemias during young adulthood, longitudinal data on 759 individuals (72% white/28% black; initial and follow-up mean age, 25.9 and 32.7 years) were examined. Among both races and the total sample, the apo E2 group (with E2/2 or E2/3 phenotype) had significantly lower and the apo E4 (with E4/4 or E3/4 phenotype) group higher low-density lipoprotein (LDL) cholesterol than the apo E3 (with E3/3 phenotype) group at both examinations. In addition, the apo E2 group displayed higher high-density lipoprotein (HDL) cholesterol in the total sample. No allele-specific effect was noted for the longitudinal changes (Delta). An increase in Delta adiposity, measured as Delta body mass index (BMI), was accompanied by higher increase in Delta LDL cholesterol in the e4 carriers than the e2 carriers among the whites (P <.05) and the total sample (P <.01); an increase in Delta triglycerides and decrease in Delta HDL cholesterol in the e2 carriers than the e4 carriers among all the groups (P <.05 to.001). Among the apo E phenotype groups, the incidence of high (>75th percentile specific for race and sex) LDL cholesterol at follow-up was in the order E4 > E3 > E2 both in the obese (BMI > 30; P for trend =.033) and the nonobese (BMI < 25; P for trend =.035) groups. Although the increase of low (<25th percentile specific for race and sex) HDL cholesterol or high triglycerides showed no apo E phenotype-specific trend, the incidence of high triglycerides without high LDL cholesterol was in the order E2 > E3 > E4 only in the obese group (P for trend =.025). The prevalence trend for dyslipidemias at follow-up among the persistently obese and nonobese groups also gave similar results. Thus, apo E gene locus influences not only the levels of certain lipoprotein variables during young adulthood, but also modulates the association between obesity and dyslipidemias.

Distribution and cardiovascular risk correlates of serum triglycerides in young adults from a biracial community: the Bogalusa Heart Study.

Elevated serum triglyceride level is increasingly being recognized as an important indicator of cardiovascular risk. The distribution and correlates of serum triglycerides were examined in a biracial (black-white) community-based sample of 1342 young adults (30% black) aged 20-37 years. Triglyceride levels showed significant race (white>black) and sex (male>female) differences. Black females, despite their relatively increased body fatness, had lowest triglyceride levels. In terms of conjoint trait of dyslipidemia based on the National Cholesterol Education Program cutpoints, 9% of white males displayed high triglyceride (> or =200 mg/dl) in combination with low high-density lipoprotein (HDL)-cholesterol (<35 mg/dl). In comparison, none of the black females fell into this category. Serum triglycerides even at levels between 100 and 150 mg/dl were significantly adversely associated with risk variables of insulin resistance syndrome such as adiposity and visceral fatness measures, HDL-cholesterol, insulin, and systolic blood pressure, especially among whites. Visceral fatness as measured by waist circumference (except black males) and insulin were the major predictors of triglyceride levels. Overall, triglyceride levels above 150 mg/dl were associated with increased risk of hypertension (odds ratio (OR)=1.8, 95% confidence interval (CI)=1.8-3.0), type 2 diabetes (OR=3.1, CI=1.4-6.9), parental history of hypertension (OR=1.3, CI=1.0-1.8) and parental history of type 2 diabetes (OR=1.7, CI=1.2-2.3). Thus, serum triglyceride levels may be valuable in the assessment of cardiovascular risk during young adulthood.

Temporal relation between blood pressure and serum creatinine in young adults from a biracial community: the Bogalusa Heart Study.

It is well recognized that end-stage renal disease (ESRD) is associated with accelerated and malignant hypertension. The association of renal disease and what is considered as normal blood pressure is still not clear. The present study examined the temporal relation between blood pressure and renal function reflected by serum creatinine in a biracial (black-white) community-based population enrolled in the Bogalusa Heart Study. The study included 662 young adults aged 19 to 32 years, (white men, n = 188; white women, n = 289; black men, n = 67; and black women, n = 118) who were followed for an average of 7.4 years. In black men, partial correlation adjusted for age, body mass index, serum glucose, uric acid, and cigarette smoking showed that baseline systolic and diastolic blood pressure are not significantly related to baseline serum creatinine, but significantly related to serum creatinine at follow-up (r = 0.38, P = .008 and r = 0.42, P = .003, respectively). Multivariate regression analysis further showed a significant prediction of serum creatinine at follow-up by baseline systolic and diastolic blood pressure (0.031 mg/dL and 0.037 mg/dL rise in follow-up serum creatinine for every 10 mm Hg increase in systolic (P = .000) and diastolic (P = .001) blood pressure at baseline, but not the other way around. Other race and sex groups did not show such significant temporal relations. We conclude that in young black men, higher blood pressure levels within normal range precede and explain part of the increase in serum creatinine, a measure of decline in renal function. Thus, our results underscore the beneficial effect of maintaining blood pressure levels lower than what is considered as the upper normal limit, particularly in black men.

Age-related patterns of the clustering of cardiovascular risk variables of syndrome X from childhood to young adulthood in a population made up of black and white subjects: the Bogalusa Heart Study.

The age-related patterns of clustering of cardiovascular risk variables of Syndrome X from childhood to adulthood were examined in a community-based sample of black and white children (aged 5-10 years, n = 2,389), adolescents (aged 11-17 years, n = 3,371), and young adults (aged 18-37 years, n = 2,115). In the analysis of clustering, insulin resistance index, BMI, triglycerides/ HDL cholesterol ratio, and mean arterial pressure were used either as categorical variables (age-, race- and sex-specific values >75th percentiles) to calculate risk ratios (observed frequency/expected frequency) or as continuous variables (normal scores based on ranks) to compute intraclass correlations. In the total sample, the risk ratio for clustering of adverse levels of all 4 variables was 9.8 for whites (P < 0.01) versus 7.4 for blacks (P < 0.01); the intraclass correlation was 0.33 for whites (P < 0.001) versus 0.26 for blacks (P < 0.001). Both the risk ratio and intraclass correlation were significantly higher in whites than in blacks in the total sample. The intraclass correlations of the 4 variables were significant (P < 0.001) in all race and age-groups, and they were higher during preadolescence and adulthood than during adolescence. Furthermore, unlike risk ratios, intraclass correlations showed a continuous increase with age during adulthood. When BMI was adjusted, the intraclass correlations involving the other 3 variables were reduced by approximately 50%, and the age-related pattern was no longer evident. These results suggest that the degree of clustering of risk variables of Syndrome X varies with age from childhood to adulthood and is likely influenced by the age-related changes in obesity and the attendant insulin resistance.

Relation of abdominal height to cardiovascular risk factors in young adults: the Bogalusa heart study.

Obesity and fat patterns are important predictors of coronary heart disease risk. The relations of abdominal height (sagittal diameter) and various obesity measures to coronary heart disease risk factors were examined in a community-based sample of 409 Blacks and 1,011 Whites aged 20-38 years in Bogalusa, Louisiana (1995-1996). Obesity measures used included weight, waist circumference, waist:hip ratio, waist:height ratio, abdominal height, triceps and subscapular skinfold thicknesses, body mass index, and conicity index. Abdominal height was highly correlated with other obesity measures, especially waist circumference (0.937-0.944, p < 0.001), and was least correlated with height. In multivariate analysis, abdominal height was an independent predictor of levels of total cholesterol, triglycerides, very low density lipoprotein cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol, glucose, and insulin and of systolic and diastolic blood pressures (p < 0.05 to p < 0.001), with total R2 values ranging from 0.13 to 0.52. Abdominal height contributed more to the prediction of blood pressure than did other measures of central obesity. In canonical analysis, abdominal height was correlated more strongly with the coronary disease risk factor variables as a group than were other obesity measures. These results suggest that abdominal height adds another dimension to measures of obesity in that it may help to assess a component of visceral fat that other measures miss.

Cardiovascular risk factors clustering features of insulin resistance syndrome (Syndrome X) in a biracial (Black-White) population of children, adolescents, and young adults: the Bogalusa Heart Study.

Recently, independent factors representing different features of insulin resistance syndrome (Syndrome X) have been identified by factor analysis in middle-aged and elderly adult populations. In this study, factor analysis was applied to the clustering characteristics of Syndrome X in a biracial (Black-White) community-based population of 4,522 children (ages 5-11 years), adolescents (ages 12-17 years), and young adults (ages 18-38 years) from the Bogalusa Heart Study who were screened during 1988-1996. Ponderal index (weight (kg)/height (m)3), levels of insulin, glucose, triglycerides, and high density lipoprotein cholesterol, and systolic and diastolic blood pressure were used as measures of components of Syndrome X. No evidence was found to support a one-factor hypothesis for this syndrome, but factor analysis yielded two uncorrelated factors (factor 1: insulin/lipids/glucose/ponderal index; factor 2: insulin/blood pressure). These two factors explained 54.6% of the total variance in the entire sample. The factor loading patterns were very similar in all race and age groups, based on high values of coefficients of congruence (0.89-1.0). These results suggest that Syndrome X is characterized by the linking of a metabolic entity (hyperinsulinemia/insulin resistance, dyslipidemia, and obesity) to a hemodynamic factor (hypertension) through shared correlation with hyperinsulinemia/insulin resistance, and that the clustering features are independent of sex and age in both Black and White populations.

Association of fasting blood sugar level, insulin level, and obesity with left ventricular mass in healthy children and adolescents: The Bogalusa Heart Study.

BACKGROUND: Insulin resistance, often associated with obesity, is hypothesized to be involved in the pathogenesis of essential hypertension and may relate to increased left ventricular mass (LVM). METHODS: We examined correlations between echocardiographic LVM and fasting blood glucose and insulin levels in a cross-section of 216 black and white healthy children and young adults aged 13 to 27 years in Bogalusa, Louisiana. Anthropometric measurements and blood pressure readings were also obtained. RESULTS: Positive bivariate correlation was found between fasting blood glucose level and LVM corrected for growth (LVMC) (LVMC = LVM/Height2.7) with all race/sex groups combined (r = 0.17, P

The association of cardiovascular risk factor clustering related to insulin resistance syndrome (Syndrome X) between young parents and their offspring: the Bogalusa Heart Study.

Cardiovascular risk factor clustering related to insulin resistance syndrome (Syndrome X) was examined in a community-based sample of 599 genetically unrelated school-aged children (5-17 years) and their parents. Risk factors used as components of Syndrome X included hyperinsulinemia, obesity, dyslipidemia and high blood pressure defined by values above the age-, sex- and race-specific 75th percentiles of fasting insulin, body mass index, triglycerides/high-density lipoprotein cholesterol ratio and mean arterial pressure, respectively. Based on observed to expected ratio there was an excess of parents (father and/or mother) and their offspring with clusters of three or four disorders (P < 0.05-0.001). In contrast, the number of parents and offspring with two disorders was significantly lower than expected by chance alone (P < 0.05-0.01). Based on paternal, maternal, and parental Syndrome X, the odds ratios (95% confidence interval) for offspring having the same cluster were 7.2 (1.9-27.2), 8.6 (3.1-23.6) and 7.9 (3.5-18.1), respectively. In terms of individual risk factors of parents used as predictors, adverse levels of their insulin and BMI significantly increased the risk of offspring having Syndrome X (P < 0.01-0.001), whereas the effect of parental insulin was considerably reduced after parental BMI was adjusted for. In contrast, parental dyslipidemia and high blood pressure were not associated with the occurrence of Syndrome X in their offspring. These results confirm the familial nature of Syndrome X and suggest that conditions of obesity and the attendant hyperinsulinemia in parents may underlie this familial association.

Black-white differences in postprandial triglyceride response and postheparin lipoprotein lipase and hepatic triglyceride lipase among young men.

Black-white differences in serum triglycerides and high-density lipoprotein (HDL) cholesterol concentrations are known. However, the metabolic basis for these differences is not clear. This study determined the magnitude of postprandial triglyceride concentrations, lipoprotein lipase and hepatic triglyceride lipase activities in postheparin plasma, and serum lipid and lipoprotein cholesterol concentrations in healthy young adult black men (n = 22) and white men (n = 28). Postprandial triglyceride concentrations were measured at 2, 3, 4, 5, 6, and 8 hours after a standardized test meal. Serum lipid and lipoprotein cholesterol concentrations were similar between the races in this study sample. However, incremental (above basal) increases in triglycerides were significantly greater in white men versus black men at 2 hours (P = .01) and tended to be greater at 3 hours (P = .12) and 4 hours (P = .06) after the fat load. In a multivariate analysis that included age, race, apolipoprotein E (apoE) genotype, fasting triglycerides, obesity measures, alcohol intake, and cigarette use, fasting triglycerides (P = .04) and, to a lesser extent, race (P = .07) were associated independently with the 2-hour incremental increase in triglycerides. The incremental triglyceride response correlated inversely with HDL cholesterol in both whites (r = -.38, P = .04) and blacks (r = -.59, P = .004). Lipoprotein lipase activity was higher (P = .049) and hepatic triglyceride lipase activity lower (P = .0001) in black men compared with white men; racial differences persisted after adjusting for the covariates. While lipoprotein lipase activity tended to associate inversely with the postprandial triglyceride concentration in both races, hepatic triglyceride lipase activity tended to correlate positively in whites and inversely in blacks. These results suggest that compared with whites, blacks may have an efficient lipid-clearing mechanism that could explain the black-white differences in lipoproteins found in the population at large.

Are some children and adolescents in Louisiana addicted to tobacco? The Bogalusa Heart Study.

The US Surgeon General concluded that nicotine in tobacco is addictive. Few studies actually explore the nature of nicotine addiction in youth. In Bogalusa, Louisiana, surveys to assess tobacco usage were administered to 11-18 year olds according to a standardized protocol developed in 1976. In 1991-92, a special substudy explored the nature of nicotine addiction in youth. Overall, 14.7% were current cigarette smokers; however, as many as 44.3% of white females, ages 15-16, indicated they were current smokers. Twelve percent of the surveyed population purchased single cigarettes. Thirty-two percent of current smokers reported they smoke a cigarette within 30 minutes after waking up. Thirty-one percent said they would find it difficult to refrain from smoking in places where it is forbidden. And 23% said they continue to smoke cigarettes when they are ill. From the findings in this study, it is clear there are young people who are addicted to tobacco. It is important to develop prevention of tobacco usage in childhood. Those who are addicted require a carefully developed intervention program to assist them with their cessation efforts.

Influence of apolipoprotein E polymorphism on serum lipids and lipoprotein changes from childhood to adulthood: the Bogalusa Heart Study.

The influence of apolipoprotein (apo) E polymorphism on serum lipoproteins from childhood to adulthood was examined in 1520 individuals, aged 5-14 years at baseline, followed over a 16-year period. At both times, the e2 allele associated with lower LDL cholesterol (P < 0.001) and higher HDL cholesterol (P < 0.05-0.01), the e4 allele with higher LDL cholesterol (P < 0.001). The e2 allele lowered the adulthood LDL cholesterol level to a greater extent than the childhood level (P < 0.05). With respect to tracking, at the lowest quartile of LDL cholesterol distribution, the persistence in ranks over time was higher in the apoE2 group with E2/3 and E2/2 phenotypes compared with the apoE3 group with E3/3 phenotype and the apoE4 group with E3/4 and E4/4 phenotypes (P = 0.001). Longitudinal increases in the ponderal index (weight/height3) lowered the adulthood HDL cholesterol to a larger extent in e2 carriers (P = 0.017). The interindividual variability in LDL cholesterol due to childhood and adulthood ponderal index was 1.8- to 2.3-fold greater in the apoE2 group versus the apoE3 group. Likewise, cigarette smoking, alcohol use and oral contraceptive use in adulthood explained greater variability in triglycerides (5.3-fold), VLDL cholesterol (7.8-fold) and HDL cholesterol (2.9-fold) in the apoE2 group versus the apoE3 group. Thus, the apoE locus influences not only the levels and tracking of certain lipoproteins from childhood to adulthood but also modulates the association between lifestyle-related factors and lipoproteins.

Distribution and correlates of serum high-density lipoprotein subclasses (LpA-I and LpA-I:A-II) in children from a biracial community. The Bogalusa Heart Study.

High-density lipoprotein (HDL) subclasses are considered to differ in terms of antiatherogenic potential. Therefore, the distribution and correlates of serum lipoprotein A-I (LpA-I) and LpA-I:A-II were examined in a random community-based subsample of black (n = 1,021) and white (n = 1,087) children aged 5 to 17 years. Black children had significantly higher LpA-I levels than white children. With respect to LpA-I:A-II, prepubertal (age 5 to 10 years) black males and pubertal (age 11 to 17 years) white children showed significantly higher values than their counterparts. With the exception of the LpA-I:A-II difference among prepubertal males, the observed black-white difference was independent of the racial differential in serum triglycerides, a metabolic correlate of HDL. A significant sex differential (males > females) was noted among blacks and whites for both HDL subclasses, with the exception of LpA-I levels at the pubertal age. Among the pubertal age group, a male-female crossover trend (females > males) in LpA-I levels was apparent after age 14. Sexual maturation and age were the major factors (negative) contributing to the variability in the levels of HDL subclasses among race-sex groups; adiposity (negative), insulin (negative), alcohol intake (positive), and oral contraceptive use (positive) emerged as minor but significant predictor variables. In terms of a relation to other lipoprotein variables, LpA-I compared with LpA-I:A-II correlated much more strongly with HDL cholesterol. Unlike LpA-I, LpA-I:A-II was associated significantly (positively) with low-density lipoprotein (LDL) cholesterol. These findings are indicative of intrinsic metabolic differences among the race-sex groups early in life, resulting in variability in the HDL subclass pattern and attendant antiatherogenic potential.