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Biomedical subjects

Gerald S Berenson

Publications and source records attributed to Gerald S Berenson.

At least 19 recordsLinked to original sources

Cardiovascular risk factors and excess adiposity among overweight children and adolescents: the Bogalusa Heart Study.

OBJECTIVE: To explore the accuracy of various body mass index (BMI) cutpoints in identifying children who have excess adiposity (based on skinfold thicknesses), adverse levels of lipids, insulin, and blood pressures, and a high risk for severe adult obesity. STUDY DESIGN: Cross-sectional (n = 10,099) and longitudinal (n = 2392) analyses were performed among subjects who participated in the Bogalusa Heart Study. RESULTS: Of children with a BMI > or =95th percentile (P) of the Centers for Disease Control (CDC) growth charts, 39% had at least two risk factors, 65% had excess adiposity, and 65% had an adult BMI of > or =35 kg/m(2). Of those with a BMI > or =99th P, 59% had at least two risk factors, 94% had excess adiposity, and 88% had an adult BMI of > or =35 kg/m(2). About 4% of children in the US now have a BMI > or =99th P. CONCLUSIONS: The 99th P of BMI-for-age may be appropriate for identifying children who are at very high risk for biochemical abnormalities and severe adult obesity. More aggressive weight control strategies may be warranted for this subgroup.

Adolescent↗

Race (black-white) and gender divergences in the relationship of childhood cardiovascular risk factors to carotid artery intima-media thickness in adulthood: the Bogalusa Heart Study.

It has been established that childhood cardiovascular (CV) risk factors are predictive of adulthood vascular changes as measured by carotid intima-media thickness (IMT). However, whether this relationship is race- and gender-specific is not known. This aspect was examined in a black-white cohort of 868 adults (29% blacks, 42% males) aged 25-44 years who were examined at least twice in childhood for traditional CV risk factors with an average follow-up period of 26.4 years. The average value of the two earliest childhood measurements was used as the childhood value, standardized to age, race, and gender-specific z-score. Carotid IMT was measured by B-mode ultrasonography. The mean of the maximum carotid IMT readings of three right and three left far walls for common, bulb and internal segments was used. In univariate analysis, significant correlates of adulthood carotid IMT (standardized to age-, race- and gender-specific z-score) were, in the order of decreasing magnitude, triglyceride and LDL cholesterol in white males; systolic blood pressure, LDL cholesterol, and body mass index (BMI) in white females; systolic blood pressure in black males; BMI and systolic blood pressure in black females. In multivariate regression analysis, significant predictors of carotid IMT were triglycerides and LDL cholesterol in white males; systolic blood pressure and LDL cholesterol in white females; systolic blood pressure in black males; and BMI and LDL cholesterol in black females. In conclusion, the predictability of childhood CV risk factors for increased carotid IMT in adulthood varies by race and gender. The prevention implications of these findings need further investigation.

Adolescent↗

Predictors of left ventricular dilatation in young adults (from the Bogalusa Heart Study).

Left ventricular (LV) dilatation may be an early sign of cardiac decompensation progressing to LV dysfunction. Determinants of LV dilatation in young asymptomatic adults are unknown. Five hundred six asymptomatic subjects (mean age 32 +/- 3 years) enrolled in the Bogalusa Heart Study underwent echocardiographic examination. LV dilatation (LV end-diastolic diameter >5.5 cm) as measured by M-mode echocardiography was found in 31 subjects (6%). Subjects with LV dilatation had greater body mass indexes (32 +/- 9 vs 27 +/- 6 kg/m2, p <0.0001), systolic (119 +/- 15 vs 112 +/- 12 mm Hg, p = 0.007) and diastolic (79 +/- 12 vs 75 +/- 9 mm Hg, p = 0.04) blood pressures, and LV mass (230 +/- 50 vs 123 +/- 39 g, p <0.0001). Age, gender, race, and metabolic parameters (glucose, insulin, and lipoprotein levels) did not differ significantly between the subjects with and without LV dilatation. After correction for age, gender, and race differences, adulthood obesity (body mass index >30 kg/m2) was associated with a threefold odds ratio (2.9, 95% confidence interval 1.4 to 6.1), and hypertension (defined as per the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure) was also associated with a threefold odds ratio (3.0, 95% confidence interval 1.2 to 7.1) for an increased incidence of LV dilatation. There was an incremental increase in LV end-diastolic dimension depending on the presence of hypertension or obesity, and subjects with obesity and hypertension in adulthood had the greatest degree of LV end-diastolic dimensions. In multiple regression analyses, body mass index in childhood was the only significant predictor of LV dilatation in adulthood (odds ratio 1.47, 95% confidence interval 1.03 to 2.09). In conclusion, obesity beginning in childhood and obesity and hypertension in young adulthood are predictors of LV dilatation in an otherwise healthy young adult population.

Adult↗

Changes in metabolic syndrome variables since childhood in prehypertensive and hypertensive subjects: the Bogalusa Heart Study.

That essential hypertension is associated with metabolic syndrome is known. However, information is scant regarding the course of development of adverse levels of blood pressure and other risk variables of metabolic syndrome in youth at risk for developing hypertension. This aspect was studied, retrospectively, in a community-based cohort of normotensive (n=2206), prehypertensive (n=721), and hypertensive (n=328) subjects examined serially during childhood (4 to 11 years), adolescence (12 to 18 years), and adulthood (19 to 42 years). Prehypertensive subjects versus normotensive subjects had significantly higher body mass index and subscapular skinfold, systolic (SBP) and diastolic (DBP) blood pressures, and triglycerides beginning in childhood; higher glucose in adolescence; and higher low-density lipoprotein cholesterol, fasting insulin, and insulin resistance index in adulthood. Hypertensive subjects versus normotensive subjects had higher adiposity measures, SBP and DBP, glucose, and triglycerides beginning in childhood; higher insulin and insulin resistant index in childhood and adulthood; and lower high-density lipoprotein, cholesterol in adulthood. Most of these variables progressed adversely at an increased rate in prehypertensive and hypertensive subjects. In a multivariate analysis, adverse changes in adiposity, SBP, and DBP were independently associated with prehypertensive status; and adverse changes in adiposity, SBP and DBP, insulin resistant index, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides with hypertension status. As young adults, prehypertensive and hypertensive subjects showed significantly higher prevalence of obesity, hyperinsulinemia, hyperglycemia, and dyslipidemias. Thus, excess adiposity and blood pressure beginning in childhood and accelerated adverse longitudinal changes in risk variables of metabolic syndrome through young adulthood characterize the early natural history of hypertension.

Adiposity↗

A genome scan for loci influencing levels and trends of lipoprotein lipid-related traits since childhood: The Bogalusa Heart Study.

Coronary heart disease is the result of life-long processes. Previous genetic linkage analyses of lipid and lipoprotein variables that can be measured throughout life have focused on a single measure at one point in time. Genome-wide linkage analyses were performed in the present study to identify loci influencing the long-term levels and trends of high-density lipoprotein cholesterol (HDLC) and low-density lipoprotein cholesterol (LDLC) and triglycerides in a longitudinal cohort. Microsatellite markers (n=357) were typed on 779 white and 444 black siblings, ages 14-43 years. Subjects had been examined serially 2-13 times with 6963 serial observations over an average of 22 years from childhood to adulthood. Total and incremental area under the growth curves of lipid traits was calculated and used as measures for long-term levels and trends. After adjusting for age, sex and body mass index, heritability estimates of total area values for all lipid variables were higher than those of a single measurement in either childhood or adulthood. In blacks, significant linkage to LDLC incremental area (peak LOD=3.6 at 50 cM) was observed on chromosome 1; and suggestive linkage for total area of LDLC (LOD=2.9 at 21 cM) on chromosome 19. Only one suggestive linkage (LOD=2.2 at 161 cM) on chromosome 2 was identified in whites for LDLC incremental area. Other suggestive linkage (LOD> or =2.0) was noted for LDLC and HDLC in terms of either total or incremental area on chromosomes 2, 5, 7 and 15 for blacks and whites. Several lipid-related candidate genes such as low-density lipoprotein receptor (LDLR), LDL receptor-related proteins 3 and 8, ApoE, ApoAII and ApoCII are located in these regions. Linkage evidence found in this community-based study indicates that regions on these chromosomes harbor genetic loci that affect the propensity to develop dyslipidemia from childhood.

Adolescent↗

Correlates of vascular structure and function measures in asymptomatic young adults: the Bogalusa Heart Study.

BACKGROUND: Adverse changes in arterial structure and function, independent predictors of cardiovascular (CV) disease morbidity and mortality, are known to be associated with CV risk factors, especially in middle-aged and older adults. Although non-invasive studies in this regard are beginning to emerge in a younger age population, information is lacking on the correlates of measures of vascular structure and function obtained simultaneously by different non-invasive methods. METHODS: In 518 black and white subjects (72% white, 44% male) aged 27-43 years, vascular structure and function were measured in terms of (1) carotid artery intima-media thickness (IMT), (2) aorta-femoral pulse wave velocity (af-PWV), and (3) pulsatile arterial function in terms of large (C1) and small (C2) artery compliances. RESULTS: Blacks versus whites and males versus females had higher carotid IMT; blacks versus whites higher af-PWV; and blacks versus whites and females versus males lower C1 and C2. In a multivariate regression model, significant predictors in the order of entry into the model were systolic blood pressure, male gender, age, cigarette smoking, and LDL cholesterol for carotid IMT (R(2)=0.189); systolic blood pressure, homeostasis model assessment of insulin resistance (HOMA-IR), cigarette smoking, and age for af-PWV (R(2)=0.200); systolic blood pressure, female gender, and HOMA-IR for C1 (R(2)=0.258); and systolic blood pressure, female gender, age, diastolic blood pressure, cigarette smoking, triglycerides, and black race for C2 (R(2)=0.394). CONCLUSION: In asymptomatic young adults, CV risk factors influence adversely measures of both structure and function of the vasculature to varying degrees, with small artery compliance showing maximum variance. As part of preventive cardiology, assessment of structure/function measures of the vasculature by simple non-invasive methods may be helpful in identifying early vascular damage in a high-risk young population group.

Adult↗

Comparison of the measures of pulsatile arterial function between asymptomatic younger adult smokers and former smokers: the Bogalusa Heart Study.

Cigarette smoking, an established cardiovascular (CV) disease risk factor, is known to impair pulsatile arterial function. However, information is scant in this regard on asymptomatic younger adult former smokers. As part of the Bogalusa Heart Study, the pulsatile arterial function was examined noninvasively in 278 nonsmokers, 277 current smokers, and 104 former smokers, aged 18 to 44 years, mean 36.4 years by radial artery pressure pulse contour analysis. Compared to current smokers, former smokers had higher body mass index (BMI, 29.6 v 27.7 kg/m2, P=.02), after adjusting for age, ethnicity, and sex, and higher levels of glucose (94.8 v 85.3 mg/dL, P=.008) and insulin (15.0 v 10.9 microU/mL, P=.01), after adjusting for age, ethnicity, sex, and BMI. Compared to nonsmokers, former smokers had similar BMI, but marginally high glucose (P=.08) and insulin (P=.11). With respect to measures of pulsatile arterial function, nonsmokers versus current smokers versus former smokers had similar large artery compliance (15.2 v 15.1 v 15.1 mL/mmHgx10) but increased (P=.01) small artery compliance after smoking cessation (6.6 v 5.8 v 6.5 mL/mmHgx100), and decreased (P=.03) systemic vascular resistance after smoking cessation (1300.5 v 1376.9 v 1292.2 dynes.sec.cm-5), and increases in small artery compliance (P=.0003) and decreases in systemic vascular resistance (P=.01) were found among those who quit smoking 10 years or more, after adjusting for ethnicity, sex, age, glucose, insulin, and alcohol use. These findings, although cross-sectional in nature, indicate the potential for improving arterial wall dynamics after smoking cessation in younger adults.

Adolescent↗

Distribution and metabolic syndrome correlates of plasma C-reactive protein in biracial (black-white) younger adults: the Bogalusa Heart Study.

The association between plasma C-reactive protein (CRP), a marker of systemic inflammation, and the metabolic syndrome is well recognized. However, information is scant regarding the component of metabolic syndrome that is critical in modulating CRP levels in younger adults. This aspect was examined in a biracial (black-white) community-based sample of 1083 younger adults (mean age, 36.1 years; 71% white, 45% male) enrolled in the Bogalusa Heart Study. Plasma CRP along with metabolic syndrome variables were measured. CRP levels showed a significant race (black>white, P=.01) and sex (female>male, P=.0001) differences, and related to measures of obesity (body mass index [BMI], waist circumference, and sagittal diameter), blood pressure (systolic, diastolic, and mean arterial blood pressure), lipoproteins (low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, total cholesterol-high-density lipoprotein cholesterol ratio), glucose homeostasis (insulin, glucose, homeostasis model assessment of insulin resistance), and uric acid, after adjusting for age, race, sex, and cigarette smoking. Furthermore, CRP levels increased with increasing number of metabolic syndrome risk factors, as defined by the National Cholesterol Education Program Adult Treatment Panel III, regardless of race and sex (P for trend<0001). In multivariate analysis, using 3 separate models for different obesity measures, obesity was the major contributor to the explained variance in each model with BMI, waist, and sagittal diameter contributing 17.0%, 13.4%, and 17.1% of the variance, respectively. In contrast, homeostasis model assessment of insulin resistance contributed 1.2%, 0.3%, and 0% to the explained variance in the models with BMI, waist, and sagittal diameter, respectively. In conclusion, CRP levels differ among race and sex groups and correlate to metabolic syndrome variables in younger adults. In addition, these findings strongly suggest that although obesity and insulin resistance are the main underlying features of the metabolic syndrome, the former appears to be the major mediator of CRP levels, which has important health implications.

Adult↗

Adiponectin and its correlates of cardiovascular risk in young adults: the Bogalusa Heart Study.

Adiponectin, a novel adipocytokine produced exclusively in the adipose tissue, plays a major role in the development of metabolic syndrome, type 2 diabetes mellitus, and related cardiovascular (CV) diseases. However, information is scant regarding the association of adiponectin with measures of CV risk in young adults. This aspect was examined in a biracial (black-white) community-based sample of 1153 individuals (mean age, 36.2 years; 70% white, 43% male) who participated in the Bogalusa Heart Study. Adiponectin levels showed race (white > black, P < .0001) and sex (female > male, P < .0001) differences, and correlated significantly in a beneficial manner to measures of obesity (body mass index, waist circumference, and abdominal height), mean arterial blood pressure, lipoprotein variables (low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides), measures of glucose homeostasis (insulin, glucose, homeostasis model assessment of insulin resistance [HOMA-IR]), and uric acid, after adjusting for age, race, sex, and cigarette smoking. In multivariate analysis that used either body mass index or abdominal height as a measure of general and visceral adiposity in 2 separate models, HOMA-IR was the major contributor explaining 18.4% and 18.1% of the variance, respectively. There was a significant interaction between abdominal height and HOMA-IR on adiponectin level in that the inverse association between adiponectin and insulin resistance was pronounced at higher level of visceral adiposity. Furthermore, adiponectin levels decreased with increasing number of metabolic syndrome risk factors defined by the National Cholesterol Education Program Adult Treatment Panel III (P for trend <.0001). Moreover, adiponectin levels were low among those with positive parental histories of coronary heart disease (P = .03), hypertension (P = .04), and type 2 diabetes mellitus (P = .01), considered as surrogate measures of risk. These findings, by showing an inverse association of adiponectin with insulin resistance, visceral adiposity, and related metabolic syndrome, and also with positive parental histories of coronary heart disease, hypertension, and type 2 diabetes mellitus, underscore the value of adiponectin in CV and type 2 diabetes mellitus risk assessments in young adults.

Adiponectin↗

Longitudinal analysis of haplotypes and polymorphisms of the APOA5 and APOC3 genes associated with variation in serum triglyceride levels: the Bogalusa Heart Study.

Polymorphisms in the APOC3 and APOA5 genes, from the APOA1/APOC3/APOA4/APOA5 gene cluster on chromosome 11q23, have been associated with interindividual variation in plasma triglycerides. APOA5 polymorphisms implicated include 2 in the promoter region (-1131 T/C and -3 A/G) and 1 in exon 2 (+56 C/G). APOC3 polymorphisms implicated include 1 (SstI) in the 3' untranslated region and 1 (-2854 G/T) in the APOC3-APOA4 intergenic region. We analyzed the associations of haplotypes and multilocus genotypes of these polymorphisms on longitudinal serum triglyceride profiles in 360 African American and 823 white subjects from the Bogalusa Heart Study. Subjects were examined from 2 to 8 times (mean +/- SD, 5.4 +/- 1.3) between 1973 and 1996, at ages ranging from 4 to 38 years, with 1978 observations in African Americans and 4465 in whites. Serum triglycerides were significantly higher among whites across all ages. Allele frequencies differed significantly between African Americans and whites at all but the APOA5 +56 C/G locus. Linkage disequilibrium among the loci was higher in whites and haplotype diversity lower: 6 haplotypes had estimated frequencies of more than 1% in African Americans, 5 in whites. Individually, all polymorphisms except APOC3 -2854 G/T showed significant associations with triglyceride levels in the full sample. However, genotype models including all 5 loci showed significant triglyceride associations for only 3 (APOC3 SstI, APOA5 -1131 T/C, and APOA5 +56 C/G); significant interactions among them indicated their effects were not independent. Neither APOC3 -2854 G/T nor APOA5 -3 A/G had significant effects when the other 3 loci were in the models. The EM algorithm was used to estimate haplotype frequencies and assign haplotype probabilities to individuals, which is conditional on their genotypes; individuals' haplotype probability vectors were then used as predictors in multilevel mixed models of longitudinal triglyceride profiles. Of haplotypes comprising, in order, APOC3 SstI and -2854 G/T and APOA5 -1131 T/C, -3 A/G, and +56 C/G, 3 were significantly associated with higher triglycerides, even after adjusting for multiple tests: GGTAG (P = .002), GTTAG (P < .0001), and CGCGC (P = .0002). Each GGTAG haplotype carried would be expected to raise triglyceride levels (relative to those of GTTAC homozygotes) by approximately 19 mg/dL, each GTTAG haplotype by approximately 15 mg/dL, and each CGCGC haplotype by approximately 7 mg/dL. Haplotypes comprising the 3 loci implicated by genotype analyses (SstI, -1131 T/C, and +56 C/G) were also tested: haplotypes C_C_C and G_T_G significantly raised triglycerides, even after adjustment for multiple comparisons (P < .002 for both), with each copy of C_C_C expected to raise triglycerides by approximately 7 mg/dL and each copy of G_T_G by approximately 15 mg/dL. Overall, our findings support those of others in associating specific polymorphisms and haplotypes in the APOA1/C3/A4/A5 gene cluster with higher serum triglyceride levels. However, the degree to which polymorphisms in the APOC3 and APOA5 genes may be independently associated with triglyceride levels remains to be determined.

Adolescent↗

Association of calcium intake, dairy product consumption with overweight status in young adults (1995-1996): the Bogalusa Heart Study.

OBJECTIVE: To examine the association between calcium intake and dairy product consumption with overweight and obesity in young adults. METHODS: The sample used in this study consisted of 1306 young adults, ages 19-38 years, who participated in the 1995-1996 young adult survey. Analysis was performed with analysis of covariance (ANCOVA) for ethnicity-gender groups separately. RESULTS: No significant association was found between dairy product consumption, calcium intake and overweight, defined by body mass index or waist circumference. However, there was a significant inverse association between calcium intake, low-fat dairy product consumption and waist-to-hip ratio in white males. CONCLUSION: Increasing intake of calcium and low-fat dairy products may be associated with lower abdominal adiposity, particularly in young adult white males.

Adult↗

Different effects of atherogenic lipoproteins and blood pressure on arterial structure and function: the Bogalusa Heart Study.

Differential impact of non-high-density lipoprotein cholesterol (total cholesterol minus high-density lipoprotein cholesterol) and blood pressure on arterial wall thickness and stiffness was examined in 900 black and white adults aged 24-43 years. Blacks compared with whites had greater values of pulse wave velocity (5.4 m/sec vs. 5.2 m/sec; p<0.01) and carotid artery intima-media thickness (0.83 mm vs. 0.80 mm; p<0.01). Non-high-density lipoprotein cholesterol was significantly associated with carotid intima-media thickness (standardized regression coefficient [b]=0.21; p<0.01), but not with pulse wave velocity (b=0.03; p=0.37), after adjusting for race, sex, age, body mass index, insulin, glucose, and smoking. Systolic blood pressure was associated significantly stronger with pulse wave velocity (b=0.36; p<0.01) than with carotid intima-media thickness (b=0.15; p<0.01). No race difference in these relationships was found. The results of this study indicate that atherogenic lipoproteins and blood pressure may play different roles in the development of arterial wall stiffness and atherosclerosis.

Adult↗

Utility of childhood non-high-density lipoprotein cholesterol levels in predicting adult dyslipidemia and other cardiovascular risks: the Bogalusa Heart Study.

OBJECTIVE: This study sought to examine the usefulness of non-high-density lipoprotein cholesterol levels in predicting future dyslipidemia and other cardiovascular risk in adulthood. METHODS: The study sample consisted of a longitudinal cohort of subjects (n = 1163; 30.1% black and 55.4% female) who participated in the Bogalusa Heart Study both as children at 5 to 14 years of age and as adults 27 years later. RESULTS: The childhood level of non-high-density lipoprotein cholesterol, like low-density lipoprotein cholesterol, was the best predictor of the adulthood level; the next best predictor for both variables was the change in BMI from childhood to adulthood. Furthermore, those in the age-, race-, and gender-specific top quartile, compared with those in the bottom quartile, of non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol levels in childhood were 4.5 and 3.5 times more likely, respectively, to develop adult dyslipidemia, independent of baseline BMI and BMI change after 27 years. Although, at equivalent cutoff points, childhood high-risk versus acceptable-risk status for both lipid measures was associated significantly with increased prevalence of obesity and adverse levels of low-density lipoprotein cholesterol and triglycerides in adulthood, only childhood non-high-density lipoprotein cholesterol high-risk status was associated with increased prevalence of low high-density lipoprotein cholesterol levels, hyperinsulinemia, and hyperglycemia (marginal). CONCLUSIONS: Adverse levels of non-high-density lipoprotein cholesterol versus low-density lipoprotein cholesterol in childhood not only equally persist over time and better predict adult dyslipidemia but also are related to nonlipid cardiovascular risk factors in adulthood.

Body Mass Index↗

Body mass index and lipid levels in children from Ankara, Turkey versus Bogalusa, Louisiana.

BACKGROUND: Turkish Heart Study demonstrated that low high density lipoprotein cholesterol levels are prevalent among Turkish adults. METHODS: We compared body mass index and lipid levels of Turkish children (n = 1525, ages 10-17) with the bi-racial community of Bogalusa Heart Study. RESULTS: Turkish children have lower body mass index than American children (19.0 +/- 3 kg/m(2) for Turkish girls, 20.2 +/- 4 for White American girls, 20.9 +/- 5 for African American girls; and 18.9 +/- 3 kg/m(2) for Turkish boys, 20.2 +/- 4 for White American boys, 20.0 +/- 4 for African American boys, P < 0.01). Turkish children have higher triglyceride and lower high density lipoprotein cholesterol levels despite their lower body mass index. High density lipoprotein cholesterol levels (mmol/L) are 1.3 +/- 0.3 for Turkish girls and boys versus 1.4 +/- 0.5 for White American girls and boys, versus 1.6 +/- 0.5 and 1.7 +/- 0.5 for African American girls and boys, respectively (P < 0.01). Triglyceride levels (mmol/L) are 1.0 +/- 0.6 and 1.0 +/- 0.5 for Turkish girls and boys versus 0.9 +/- 0.5 and 0.8 +/- 0.5 for White American; and 0.7 +/- 0.3 for African American girls and boys, respectively (P < 0.01). CONCLUSIONS: Our observation of a lower HDL-C and a higher TG level in Turkish children (despite their lower BMI) is of interest and may indicate that unique characteristics in lipoprotein levels of Turkish adults start early in life.

Adolescent↗

Increased subclinical atherosclerosis in young adults with metabolic syndrome: the Bogalusa Heart Study.

OBJECTIVES: The purpose of this study was to investigate the association of metabolic syndrome (MetS) with subclinical atherosclerosis, determined by ultrasound carotid intima-media thickness (CIMT) measurements, in young adults. BACKGROUND: Metabolic syndrome is associated with subclinical atherosclerosis and increased cardiovascular risk in older and middle-aged adults; however, these associations have not been studied among young adults. METHODS: Non-diabetic subjects from Bogalusa Heart Study, a longitudinal study of atherosclerosis in young adults, underwent B-mode ultrasonography of the carotid arteries. Metabolic syndrome was defined with the National Cholesterol Education Program Adult Treatment Panel III (MetSNCEP) and World Health Organization (MetSWHO) definitions. CIMT and MetS associations were evaluated with multivariable regression and area under receiver-operator characteristic curve (AUC) analyses. RESULTS: Of 507 subjects (29% black, 39% male, mean [SD] age 32 [3] years), 67 (13%) had MetSNCEP and 65 (13%) had MetSWHO. Common (mean = 0.70 [0.11] mm vs. 0.66 [0.08] mm, p = 0.002) and internal CIMT (0.72 [0.21] mm vs. 0.68 [0.12] mm, p = 0.020) were higher among those with MetS(NCEP) than those without MetS(NCEP). Common (0.69 [0.11] mm vs. 0.66 [0.08] mm, p = 0.020) and internal CIMT (0.73 [0.23] mm vs. 0.68 [0.12] mm, p = 0.012) also were higher among those with MetSWHO than those without MetSWHO. Composite CIMT increased with the number of MetS components present (MetSNCEP r = 0.997, p < 0.001; MetSWHO r = 0.946, p = 0.053). Metabolic syndromeNCEP (AUC = 0.557, 95% confidence interval [CI] 0.513 to 0.601) and MetSWHO (AUC = 0.539, 95% CI 0.495 to 0.584) both predicted composite CIMT > or =75th percentile. CONCLUSIONS: In young adults, MetS is associated with increased atherosclerotic burden, and therefore, increased cardiovascular risk. These results support the importance of screening and early intervention in this population.

Adult↗

Rise in insulin resistance is associated with escalated telomere attrition.

BACKGROUND: Insulin resistance predisposes to cardiovascular disease and shortens human lifespan. We therefore tested the hypothesis that a rise in insulin resistance in concert with gain in body mass is associated with accelerated white blood cell telomere attrition. METHODS AND RESULTS: We measured white blood cell telomere dynamics and age-related changes in insulin resistance and body mass index in young adults of the Bogalusa Heart Study. Over 10.1 to 12.8 years, the relative changes in telomere length were correlated with the homeostasis model assessment of insulin resistance (r=-0.531, P<0.001) and changes in the body mass index (r=-0.423, P<0.001). CONCLUSIONS: These findings provide the first tangible nexus of telomere biology with insulin resistance and adiposity in humans.

Adiposity↗

Autosomal genome scan for loci linked to blood pressure levels and trends since childhood: the Bogalusa Heart Study.

Genetic loci influencing the long-term levels and trends of blood pressure over time were investigated using 775 white siblings, ages 13 to 43 years, enrolled in the Bogalusa Heart Study, and 357 microsatellite markers on the 22 autosomal chromosomes. Subjects had been examined serially 2 to 12 times with 4365 serial observations over an average of 22 years from childhood to adulthood. Total and incremental area under the curve was calculated based on a cubic growth curve and used as long-term levels and trends, respectively. After adjusting for age, sex, and body mass index, heritability estimates of total area were 0.66 for systolic and 0.68 for diastolic blood pressure. Heritability of incremental area was 0.38 for systolic and 0.46 for diastolic blood pressure. Significant linkage to the total area of diastolic blood pressure (peak logarithm of odds [LOD]=3.9 at 73 cM) was observed on chromosome 2, with a region spanning from 44 cM to 103 cM showing supporting linkage evidence of LOD >3.0. In addition, suggestive linkage for total area of systolic (LOD=1.6 at 182 cM) and diastolic blood pressure (LOD=2.0 at 36 cM) on chromosome 4 and diastolic blood pressure incremental area (LOD=2.2 at 28 cM) on chromosome 18 was noted. Several hypertension candidate genes such as alpha-adducin, beta-adducin, sodium bicarbonate co-transporter, and G protein-coupled receptor kinase 4 are located in these regions. Linkage evidence found in this community-based study indicates that regions on these chromosomes harbor genetic loci that affect the propensity for development of hypertension from childhood.

Adolescent↗