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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.

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 sexspecific 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 ~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. Diabetes 49:1042-1048, 2000 D yslipidemia, hypertension, hyperinsulinemia, and obesity have been recognized as potent risk factors for coronary heart disease in adults (1-3). These risk factors have also been found to be associated with early atherosclerotic lesions in youth (4,5). Further, the extent of coronary atherosclerosis in youth increased markedly with the number of multiple risk factors (6). Coexistence of the above cardiovascular risk variables often occurs in both children (7-10) and adults (7,8,(11)(12)(13). Such a condition has been termed Syndrome X (14), deadly quartet (15), insulin resistance syndrome (11,16), and multiple metabolic syndrome (17).Although the clustering of cardiovascular risk factors related to Syndrome X has been found to occur at a very early age (7-10) and persist from childhood into adulthood (8), very little is known about the age-related trend in clustering of risk variables during this period. The Bogalusa Heart Study, a long-term community-based investigation of cardiovascular disease risk factors in black and white children and young adults (18)(19)(20), provided a unique opportunity to examine the age-related trend in clustering of risk variables during this period. The objective of the present study was to determine the age-related patterns in the magnitude of clus...

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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.

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BACKGROUND:The b2-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 weightrelated 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 b2-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 b2-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.