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This study examined the association between depression symptoms and metabolic syndrome (MetS) or its components prospectively. It assessed the mediator role of high-sensitivity C-reactive protein (hs-CRP) and intracellular adhesion molecule-1 (ICAM-1). Self-reported depression symptoms were assessed using the Center for Epidemiologic Studies-Depression scale. MetS was defined as having at least three of the following five criteria: (1) waist circumference &gt, 102 centimeters (cm) in men or &gt, 88 cm in women, (2) triglycerides ≥ 50 milligrams per deciliter (mg/dL), (3) high-density lipoprotein cholesterol &lt, 40 mg/dL in men or &lt, 50 mg/dL in women, (4) blood pressure: systolic ≥ 30 and diastolic ≥85 mm of mercury or on antihypertensive medication, and (5) fasting glucose ≥110 mg/dL. The risk ratios (RR) with 95% confidence interval (CI) were estimated using multivariate Poisson regression models. A total of 419 White and 180 Black individuals with a mean age of 36 years were followed for 6.9 years. The findings demonstrated that hs-CRP mediated the influence of depression symptoms on central obesity in White young adults. The adjusted RR for central obesity was 1.08 with 95% CI of 0.88–1.32, and the value for hs-CRP was 1.12 with 95% CI of 1.02–1.23. Although depression did not influence MetS in this study cohort, the complete mediator role of hs-CRP was established for central obesity, a component of MetS in White young adults.

The early onset of menarche is related to the adulthood risk of cardiovascular (CV) disease. This study examines the relation of early onset of menarche to carotid artery intima-media thickness (IMT), which is a surrogate marker of CV disease, among asymptomatic young adult women in a black-white community.A cohort of 461 women (31% black, 69% white) aged 24 to 43 years (mean of 35.6 years) were participants in the Bogalusa Heart Study. The age at menarche was retrospectively collected. In addition to CV risk factor variable measurements B-mode ultrasound images of the far walls of carotid artery segments were obtained. The multivariate linear regression model along with mediating effect by Sobel test was applied to analyze menarcheal age effect on carotid artery IMT, adjusting for covariates.Waist to height ratio was significantly greater (P = .01) in early menarcheal age (11 years) versus menarcheal age (≥11 years) in both black and white women. Homeostasis model assessment of insulin resistance (HOMA-IR) was significantly greater (P = .01) in early menarcheal age (11 years) versus menarcheal age (≥11 years) in white women and also similar direction in black women. Internal carotid artery IMT was the same in early menarcheal age (11 years) versus menarcheal age (≥11 years) in white women but higher (P = .02) in black women. Given as previously mentioned these different associations, the mediation analysis by race was performed. The effect of early menarcheal age (11 years) versus menarcheal age (≥11 years) was mediated by waist to height ratio and HOMA-IR in white women after adjusting for parental education and age. The mediating effect of waist to height ratio (Sobel test = -2.26 and P = .02) and HOMA-IR (Sobel test = -1.85 and P = .06) on internal carotid artery IMT was noted in white women. The direct effect of early menarcheal age (11 years) versus menarcheal age (≥11 years) on internal carotid artery IMT (β = -0.150, P = .01) was observed in black women.The observed deleterious effect of early onset of menarche on carotid artery IMT in asymptomatic black and white younger adult women has biological, social, and public health implications.

The association between birth weight and long-term within-individual variability of blood pressure (BP) was examined in a longitudinal cohort of 1,454 adults (939 whites and 515 blacks; adulthood age = 19–50 years) enrolled in the Bogalusa Heart Study in Bogalusa, Louisiana, in 1973–2010. BP variability was depicted as standard deviation, coefficient of variation, and deviation from age-predicted values using 6–15 serial BP measurements from childhood to adulthood over an average of 25.7 years. Birth weight was significantly and negatively associated with adulthood BP levels, long-term BP levels, and rate of change. Importantly, low birth weight was significantly associated with increased BP variability in terms of standard deviation, coefficient of variation, and deviation. As evaluated using the regression coefficients, a 1-kg lower birth weight was associated with increases in systolic BP variability measures (−0.38 mm Hg, P = 0.04 for standard deviation; −0.004 mm Hg, P = 0.01 for coefficient of variation; and −0.16 mm Hg, P = 0.04 for deviation) after adjustment for race, age, sex, mean BP levels, and gestational age; similar trends in the associations were noted for diastolic BP variability measures. In conclusion, these findings suggest that birth weight affects not only BP levels but also the magnitude of within-individual BP fluctuations over time through fetal programming in BP regulation mechanisms.

OBJECTIVE The risk factors for middle-age onset of type 2 diabetes are well known. However, information is scant regarding the age onset of type 2 diabetes and its correlates in community-based black and white relatively young adults. RESEARCH DESIGN AND METHODS This prospective cohort study consisted of normoglycemic (n = 2,459) and type 2 diabetic (n = 144) adults aged 18–50 years who were followed for an average of 16 years. RESULTS The incidence rate of the onset of type 2 diabetes was 1.6, 4.3, 3.9, and 3.4 per 1,000 person-years for age-groups 18–29, 30–39, and 40–50 and total sample, respectively. Incidences of diabetes increased with age by race and sex groups (P for trend ≤0.01); higher in black females versus white females and blacks versus whites in total sample (P < 0.05). In a multivariable Cox model, baseline parental diabetes (hazard ratio [HR] 5.24) and plasma insulin were significantly associated with diabetes incidence at the youngest age (18–29 years); black race, BMI, and glucose at age 30–39 years; female sex, parental diabetes (HR 2.44), BMI, ratio of triglycerides and HDL cholesterol (TG/HDL-C ratio), and glucose at age 40–50 years; and black race, parental diabetes (HR 2.44), BMI, TG/HDL-C ratio, and glucose in whole cohort. Further, patients with diabetes, regardless of age onset, displayed a significantly higher prevalence of maternal history of diabetes at baseline (P < 0.01). CONCLUSIONS In relatively young adults, predictability of baseline cardiometabolic risk factors along with race, sex, and parental history of diabetes for the onset of type 2 diabetes varied by age-group. These findings have implications for early prevention and intervention in relatively young adults.

Blood pressure (BP) is a highly variable physiologic trait with short-term and long-term fluctuations within the same individual at different time points. The burden of BP on the cardiovascular (CV) system has been studied in terms of multiple cross-sectional BP measurements at rest, response of BP to stresses, and long-term longitudinal variability of BP. Observations from childhood are available extending into early middle age in the biracial (black-white) population of Bogalusa, Louisiana. Left ventricular mass index was used to illustrate damaging effects on the CV system by both resting BP levels and fluctuations. Long-term BP variability reflecting intermittent and repeated variability was shown to have a greater effect in blacks. The childhood BP response to several stressors was found to be greater in blacks. These observations suggest that, although at rest a greater vagal effect occurs in blacks, they show a greater response when reacting to a stimulus. This, along with aspects such as carbohydrate-insulin metabolism or other biochemical/physiological differences, may account for the greater acceleration of CV atherosclerosis in blacks. The racial contrasts suggest, in part, that effects of lipoproteins may be greater in whites, whereas the effects of excess BP levels and variability of BP and Na(+)-K(+) intake and diet as well as other environmental effects result in more CV damage in blacks. The strong association of hemodynamic measures with anatomic, metabolic, and environmental factors emphasizes the need to begin prevention of risk factors at an early age. Taken together, understanding racial (black-white) contrasts to stress contribute to both prevention and treatment of hypertension, especially for black males.

Carotid intima-media thickness (CIMT) progression is predictive of future cardiovascular events in middle-age and older adults. However, information is scant on segment-specific CIMT progression by race (black vs white) and gender and its predictors during short-term follow-up in asymptomatic young adults. B-mode ultrasound images of the far walls of both carotid arteries were obtained in 842 subjects aged 24 to 43 years and enrolled in the Bogalusa Heart Study (70% whites and 42% men). The CIMT and cardiometabolic risk variables were measured at baseline and after an average of 2.4 years. The mean CIMT progression rates/year adjusted for age, race, and gender were greatest at the bulb, followed by the internal and common carotid segments (p

That circulating soluble form of intercellular adhesion molecule-1 (sICAM-1) is associated with an increased risk for coronary artery disease is well recognized. However, information is scant regarding the distribution and cardiovascular (CV) risk correlates of sICAM-1 in asymptomatic young adults.Plasma sICAM-1 was measured in 1,184 black and white persons in the Bogalusa Heart Study cohort (70% white, 43% male), aged 24 to 44 years. CV risk was assessed in terms of CV risk factors, status of parental CV disease, and composite carotid intima-media thickness (IMT).sICAM-1 levels displayed race difference (whitesblacks, p0.0001), but no sex difference. In multivariate analysis including age, race, sex, smoking status, waist circumference, mean arterial pressure, low- and high-density lipoprotein (LDL and HDL) cholesterols, triglycerides, insulin resistance index, C-reactive protein (CRP), and adiponectin, the significant predictors of sICAM-1, in order of entry, were race (whiteblack), smoking, CRP, and waist circumference. Furthermore, there was a smoking by waist circumference interaction in that smoking attenuated the magnitude of correlation between waist circumference and sICAM-1. Levels of sICAM-1 adjusted for age, race, sex, and smoking increased with number of metabolic syndrome components (p for trend0.01); positive family history of CV disease (p0.05); and increased in composite carotid IMT specific for age, race, and sex (p for trend0.05).These findings underscore the potential value of plasma sICAM-1 as an additional biomarker for CV risk among asymptomatic young adults.

Data on the utility of the waist-to-height ratio in detecting central obesity and related cardiovascular risk among normal weight younger adults are scant. This aspect was examined in 639 normal weight (body mass index 18.5 to 24.9 kg/m(2)) black and white adults (75% white and 36% men) 20 to 44 years old. The subjects with a waist-to-height ratio > or =0.5 were grouped as having central obesity normal weight, with the rest considered the control group. The subjects with central obesity, compared to the controls, after adjusting for age, race, and gender, had significantly greater diastolic blood pressure, mean arterial pressure, low-density lipoprotein cholesterol level, triglycerides, triglycerides/high-density lipoprotein cholesterol ratio, insulin, homeostasis model assessment of insulin resistance, uric acid, C-reactive protein, and liver function enzymes (alanine aminotransferase and gamma-glutamyl transferase). On multivariate analysis, the central obesity group compared to the control group was 1.9, 2.2, 2.9, and 2.5 times more likely to have significantly adverse levels (top tertile vs the rest) of mean arterial pressure, triglycerides/high-density lipoprotein cholesterol ratio, homeostasis model assessment of insulin resistance, and C-reactive protein, respectively. The central obesity group also had a greater prevalence of dyslipidemia, hypertension, insulin resistance, hyperuricemia, and elevated C-reactive protein. The age-, race-, and gender-adjusted mean value of the common carotid intima-media thickness, a measure of subclinical atherosclerosis, was greater in the central obesity group compared to the control group (0.76 vs 0.71 mm, p = 0.009). In conclusion, these findings underscore the utility of the waist-to-height ratio in detecting central obesity and related adverse cardiovascular risk among normal weight younger adults.

The aim of this study was to determine the association between homocysteine and arterial wall stiffness in a biracial (black and white) community-based cohort of asymptomatic young adults. That increased plasma homocysteine was adversely associated with atherothrombosis was well recognized. However, findings about the association of homocysteine and arterial wall stiffness, an indicator of vascular damage, were conflicting. Plasma homocysteine and other cardiovascular disease risk-factor variables were measured in 735 white and 294 black subjects aged 24 to 44 years enrolled in the Bogalusa Heart Study. Large-artery stiffness was assessed in terms of aorta-femoral pulse wave velocity (af-PWV) using echocardiography Doppler. Men versus women had higher fasting homocysteine (8.85 vs 7.32 micromol/L; p0.01), and blacks versus whites had higher af-PWV (5.47 vs 5.24 m/s; p0.01). In bivariate analyses, log-transformed homocysteine significantly correlated with af-PWV (p = 0.0004). In multivariate stepwise regression analyses, systolic blood pressure, age, heart rate, log-homocysteine, log-Homeostasis Model Assessment of Insulin Resistance, and smoking, in that order, were independently and positively associated with af-PWV. In conclusion, plasma homocysteine was an independent correlate of arterial stiffness in asymptomatic black and white young adults and may be a potential marker for cardiovascular disease risk in this age group.

Genetic susceptibility is considered an important predictor of coronary artery disease (CAD) and its risk factors. This study was conducted to assess the hypothesis that parental CAD, a surrogate measure of genetic susceptibility, increases the vulnerability of the arterial wall to adverse effects of the metabolic syndrome and the aging process in asymptomatic young adults. The study cohort consisted of 1,073 black and white subjects (29.1% black, 43.7% male) aged 25 to 44 years. Carotid intima-media thickness (IMT) of the common carotid, carotid bulb, and internal carotid segments was measured using B-mode ultrasound. Subjects with parental CAD had greater composite (average of 3 segments) carotid IMT (0.839 vs 0.802 mm, p = 0.04) and a higher prevalence of the metabolic syndrome (20.7% vs 13.3%, p0.01) compared with those without such a history. Furthermore, the association of the metabolic syndrome with composite, carotid bulb, and internal carotid IMT was significantly stronger in subjects with parental CAD than those without such a history (p = 0.022, p = 0.032, and p = 0.035 for comparison of slopes, respectively). After adjusting for race, gender, and the metabolic syndrome components, only internal carotid IMT showed significantly more increase with age in subjects with parental CAD compared with those without such a history (regression coefficient: beta = 0.014 vs beta = 0.006, p = 0.010 for comparison of slopes). In conclusion, parental CAD amplifies the adverse effects of the metabolic syndrome and aging on carotid artery IMT, especially internal carotid IMT, in asymptomatic young adults. These findings reinforce the value of using family history of CAD in risk assessment algorithm.

Direct comparative data on the utility of non-high-density lipoprotein (HDL) cholesterol versus low-density lipoprotein cholesterol, HDL cholesterol, triglycerides, apolipoprotein (apo) B, apo A-I, ratio to total cholesterol to HDL cholesterol, and ratio of apo B to apo A-I in detecting increased carotid intima-media thickness (IMT), a validated measurement of subclinical atherosclerosis, in asymptomatic younger adults are scant. This aspect was examined in 1,203 black and white subjects (71% white, 43% men) 24 to 43 years of age. In multivariate logistic regression analysis of each lipoprotein measurement (top quartile vs lower 3 quartiles specific for age, race, and gender) for detecting increased carotid IMT (top decile vs lower 9 deciles specific for age, race, and gender), only non-HDL cholesterol, total cholesterol/HDL cholesterol, and apo B emerged as significant correlates with respective odds ratios of 1.75 (95% confidence interval [CI] 1.10 to 2.78), 2.02 (95% CI 1.27 to 3.19), and 2.13 (95% CI 1.38 3.29), after adjusting for body mass index, systolic blood pressure, and other lipoprotein measurements. Regarding discriminating values of different lipoprotein measurements in detecting increased carotid IMT, area (c-value) under the receiver operating characteristic curve analysis for each lipoprotein measurement adjusted for age, race, gender, body mass index, and systolic blood pressure indicated that the c-value for non-HDL cholesterol (0.73) was similar to those for low-density lipoprotein cholesterol (0.76), total cholesterol/HDL cholesterol (0.72), apo B/apo A-I (0.71), and HDL cholesterol (0.70), but significantly (p

Elevations in alanine aminotransferase (ALT) and gamma-glutamyl transferase (GGT), markers of liver dysfunction and nonalcoholic fatty liver, are considered as part of the metabolic syndrome and related diseases. However, information is limited regarding the persistence (tracking) in levels of these enzymes over time and their influence on cardiovascular (CV) risk in young adults. The study sample consisted of white and black subjects (N = 489, 40% male, 73% white; baseline age, 18-32 years) followed over a period of 12 years as part of the Bogalusa Heart Study, with repeat measurements of CV risk factor variables and liver enzymes. Both at baseline and follow-up, males vs females had higher ALT (P < .01 to .0001) and GGT (P < .0001); blacks vs whites had higher GGT (P < .0001). With respect to persistence in enzyme levels over time, of those individuals who had ALT and GGT at the top quintile specific for age, race, and sex at baseline, about 50% of them continued to remain so with high values after 12 years. Individuals with levels persistently in the highest quintile vs those in the lowest quintile showed higher (P < .0001) body mass index, waist circumference, triglycerides, low-density lipoprotein cholesterol, glucose, insulin, insulin resistance index, and systolic and diastolic blood pressures; lower (P < .0001) high-density lipoprotein cholesterol; and higher (P < .05 to .001) prevalence of obesity, hypertension, dyslipidemia, metabolic syndrome as defined by the National Cholesterol Education Program Adult Treatment Panel III, positive parental history of type 2 diabetes, and coronary heart disease. In addition, based on a multivariate analysis using 2 separate models for ALT and GGT, baseline levels of both enzymes were independent predictors of follow-up; insulin resistance index and baseline GGT were also predictive of follow-up systolic blood pressure. Elevations in liver enzymes ALT and GGT, within "reference" range, persist over time and relate to clinically relevant adverse CV risk profile in young adults.

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 (whiteblack, P.0001) and sex (femalemale, 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.

A sensitive, specific and rapid high performance liquid chromatography - tandem mass spectrometric (LC/MS/MS) method for the determination of cyclovirobuxine D in human plasma was developed and validated. The triple-quadrupole tandem mass spectrometric detector with an electrospray interface (ESI) was operated under the selected reaction monitoring (SRM) mode. After the addition of citalopram as an internal standard (IS), plasma samples were extracted with ethyl acetate. Chromatographic separation of the analytes was performed on a Kromasil CN column with a mobile phase of methanol/water (88/12, v/v) containing 0.4% formic acid. Linearity was established for the range of concentration 0.2-40ng/ml. Under optimized conditions, the mean recovery was 86.6%. The intra-day precision ranged from 4.56% to 7.81%, while the intra-day accuracy ranged from 2.75% to 11.0%. The inter-day precision was in the range 3.87-10.7%, and the inter-day accuracy was in the range -4.00% to 2.50%. The cyclovirobuxine D was stable in human plasma after three freeze-thaw cycles, under storage at room temperature for 12h, in a freezer at -20 degrees C for 15 days and during processing (in autosampler) at 10 degrees C for 24h. The validated method is suitable for quantitative determination of cyclovirobuxine D in human plasma in pharmacokinetics study and has been successfully applied to the analysis of clinical samples.

OBJECTIVE To examine the association between white blood cell (WBC) count and metabolic syndrome (MetS) by growth periods in black versus white individuals in the general population. RESEARCH DESIGN AND METHODS The study cohort consisted of 4,184 black and white preadolescents, adolescents, and adults. In this cohort, 743 adults were followed for 8.1–20.8 years longitudinally. RESULTS White versus black subjects had a significantly higher WBC count in all age-groups. WBC count was associated with more MetS components in whites than in blacks. Mean values of WBC increased significantly with increasing number of MetS components with adverse levels in adolescents and adults, with a stronger trend in whites. WBC count was longitudinally associated with MetS in whites only (P < 0.001). CONCLUSIONS The findings on the association between higher WBC count and MetS beginning in childhood, particularly in whites, underscore a potentially mechanistic link between systemic inflammation, MetS, and cardiovascular risk.

To assess the association of childhood parental history of type 2 diabetes and the risk of diabetes in adulthood. Observations were made on a community-based cohort of normoglycemic (n = 1619), pre-diabetic (n = 78), and type 2 diabetic (n = 50) adult subjects followed serially for cardiovascular risk factors over 22 years from childhood and noting their relation to a parental history of diabetes. In a longitudinal multivariate model including parental diabetes observed in the offspring's childhood, BMI, MAP, HDL cholesterol, LDL cholesterol, triglycerides, insulin, and glucose, adjusted for age, age(2), race, sex, and race by sex interaction, parental diabetes and adverse changes in LDL cholesterol and glucose were independently associated with pre-diabetic status in adulthood (regression coefficient [beta] = 0.74 (95% CI: 0.04-1.45), 0.44 (95% CI: 0.24-0.64), and 1.99 (95% CI: 1.73-2.25), respectively), while parental diabetes and adverse changes in BMI, HDL cholesterol, and glucose were associated with the diabetic status (beta = 1.14 (95% CI: 0.35-1.92), 0.08 (95% CI: 0.05-0.11), -0.51 (95% CI: -1.03 to -0.003), and 1.79 (95% CI: 1.48-2.09), respectively). Childhood parental history of diabetes along with adverse changes in adiposity, glucose, and lipoprotein variables of metabolic syndrome since childhood are associated with the increased risk of pre-diabetic and diabetic status in adulthood.

Background —Elevated homocysteine is associated with increased risk for coronary artery disease (CAD) in adults, but its distribution in children is not well documented. We examined the distribution of homocysteine in children and its relation to parental history of CAD. Methods and Results —A subsample of 1137 children (53% white, 47% black) aged 5 to 17 years in 1992 to 1994 examined in the Bogalusa Heart Study (n=3135), including all with a positive parental history of CAD (n=154), had plasma homocysteine levels measured. Homocysteine correlated positively with age ( r =0.16, P =0.001). No race or sex differences in homocysteine levels were observed; geometric mean (GM) levels were 5.8 μmol/L (95% CI, 5.6 to 6.1) among white males, 5.8 μmol/L (95% CI, 5.5 to 6.0) among white females, 5.6 μmol/L (95% CI, 5.4 to 5.8) among black males, and 5.6 μmol/L (95% CI, 5.4 to 5.9) among black females. Children with a positive parental history of CAD had a significantly greater age-adjusted GM homocysteine level (GM, 6.7 μmol/L; 95% CI, 6.4 to 7.1) than those without a positive history (GM, 5.6 μmol/L; 95% CI, 5.4 to 5.7); this relation was observed in each race-sex group. Conclusions —Higher homocysteine levels were observed among children with a positive family history of CAD. Additional studies should elucidate the contribution of genetic, dietary, and other factors to homocysteine levels in children.

Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white malesblack males P-value0.0001; malesfemales P-value 0.04), C2 (whitesblacks P-value 0.0004; malesfemales P-value0.0001) and hsCRP (blackswhites P-value 0.03; femalesmales P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (3 mg l(-1)) were significantly lower than those with average (1-3 mg l(-1)) and low levels (1 mg l(-1)) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P=0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (β=-0.35, P=0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.

Not all obese adults have cardiometabolic abnormalities. It is unknown whether this is true in children and, if true, whether children who have metabolically healthy overweight/obesity (MHO) will also have favorable cardiometabolic profiles in adulthood. These aspects were examined in 1,098 individuals who participated as both children (aged 5–17 years) and adults (aged 24–43 years) in the Bogalusa Heart Study between 1997 and 2002 in Bogalusa, Louisiana. MHO was defined as being in the top body mass index quartile, while low density lipoprotein cholesterol, triglycerides, mean arterial pressure, and glucose were in the bottom 3 quartiles, and high density lipoprotein cholesterol was in the top 3 quartiles. Forty-six children (4.2%) had MHO, and they were more likely to retain MHO status in adulthood compared with children in other categories (P < 0.0001). Despite markedly increased obesity in childhood and in adulthood, these same MHO children and adults showed a cardiometabolic profile generally comparable to that of nonoverweight/obese children (P > 0.05 in most cases). Moreover, there was no difference in carotid intima-media thickness in adulthood between MHO children and nonoverweight/obese children. Further, carotid intima-media thickness in adulthood was lower in MHO children than in metabolically abnormal, overweight/obese children (P = 0.003). In conclusion, the MHO phenotype starts in childhood and continues into adulthood.

To investigate the short-term effectiveness of Swanson artificial joint replacement in treating post-traumatic metacarpophalangeal joint stiffness.Between August 2007 and May 2010, 11 cases (13 fingers) of metacarpophalangeal joint stiffness with soft tissue defects underwent Swanson artificial joint replacement. There were 7 males (9 fingers) and 4 females (4 fingers), aged 43 to 65 years with an average of 49 years. The involved fingers included 4 thumbs, 4 index fingers, 3 middle fingers, and 2 ring fingers. The types of injury included open and crush injury in 8 fingers, fracture of the metacarpophalangeal joint in 3 fingers, metacarpophalangeal joint severing in 2 fingers. The time from joint stiffness to hospitalization was 12 to 48 weeks (mean, 24 weeks). The joint activity was (136.82 +/- 28.96) degrees. According to total active motion (TAM) assessment, included good in 1 finger, fair in 6 fingers, and poor in 6 fingers before operation. The activities of daily living were assessed by Sollerman score, which was 45.64 +/- 11.04. The X-ray films and CT scan showed traumatic arthritis of the metacarpophalangeal joint.The incision healed by first intention. All patients were followed up 12 to 34 months (mean, 24.1 months). At last follow-up, the joint activity was (194.64 +/- 28.86) degrees, showing significant difference when compared with preoperative value (t = 25.214, P = 0.000). According to TAM assessment, including excellent in 1 finger, good in 4 fingers, fair in 7 fingers, and poor in 1 finger. The Sollerman score was 67.45 +/- 8.20 postoperatively, showing significant difference when compared with the preoperative score (t = -10.470, P = 0.000). X-ray examination showed no prosthesis fracture, periprosthetic fracture, or joint dislocation occurred at last follow-up.Swanson artificial joint replacement can be applied to treat post-traumatic metacarpophalangeal joint stiffness, which can improve the joint activity and has satisfactory short-term effectiveness.

OBJECTIVES: To determine the prevalence of carotid and femoral artery atherosclerotic plaque in a community-based population of asymptomatic African American and white men and women, with an age range of 29 to 51 years, and the potential relations with cardiovascular risk factors. METHODS: Between 2007 and 2010, 914 subjects, 58% women and 69% white, who were part of the Bogalusa Heart Study, an ongoing study of a southern biracial community in Bogalusa, Louisiana, were followed up from childhood through adulthood and assessed for plaque formation using ultrasound. Of the total number of subjects, those with a history of cardiovascular/cerebrovascular events were excluded. RESULTS: Plaque prevalence ranged from 8% to 14%, with greater frequency in white men. Plaque formation was also associated with smoking, hypertension, diabetes mellitus, age, and white race, in descending order. CONCLUSIONS: In this population, studied sequentially since 1973, the presence of plaque correlated with widely recognized cardiovascular risk factors, although we did not detect significant contributions from either obesity or elevated lipids, including low-density lipoprotein cholesterol. It is possible that interventions, such as diet alteration and statin therapy, may have a positive impact on these potential contributors to plaque formation, and hypertension, diabetes mellitus and smoking remain of great importance.

Elevated serum phosphorus has been associated with increased mortality from cardiovascular (CV) disease. However, information is scant regarding the influence of serum phosphorus within the normal range on vascular risk in terms of subclinical atherosclerosis in asymptomatic young adults. Serum phosphorus along with other CV risk factor variables were measured in 856 white and 354 black subjects without known CV disease or renal disease. Carotid intima-media thickness (IMT) was measured by B-mode ultrasonography. Significant race and sex differences were noted for serum phosphorus (blacks>whites) and carotid IMT (black females>white females; males>females). In bivariate analyses, serum phosphorus was correlated with carotid IMT (p

To determine whether childhood elevated fasting plasma glucose (FPG) levels within the normoglycemic range predict diabetes in adulthood.Retrospective cohort study.Community of Bogalusa, Louisiana.Normoglycemic (n = 1723), prediabetic (n = 79), and type 2 diabetic (n = 47) adults aged 19 to 44 years followed up serially for an average of 21 years since childhood. Main Exposures Association of elevated baseline childhood FPG levels with the prediabetic or diabetic status at the last survey in adulthood.Receiver operating characteristic analysis and longitudinal logistic regression odds ratios.The prevalent rate of adult diabetes status by quartiles of baseline childhood FPG levels showed an adverse trend for prediabetes (P.001) and diabetes (P = .03), with an apparent threshold occurring at or above the 50th percentile (86 mg/dL). Regarding the predictive value of the above threshold, the area under the receiver operating curve analysis yielded a C value of 0.855 for prediabetes and 0.789 for diabetes models, with sensitivity and specificity, respectively, of 76.9% and 85.2% for prediabetes and 75.0% and 76.0% for diabetes. In a multivariate analysis that included anthropometric, hemodynamic, and metabolic variables from childhood to adulthood and baseline childhood FPG status (or = vs50th percentile), individuals with elevated childhood FPG levels were 3.40 times more likely to develop prediabetes (P.001) and 2.06 times more likely to develop diabetes (P = .05) as adults.The fact that elevated FPG level in childhood, even within the normoglycemic range, is a predictor of type 2 diabetes in younger adulthood has implications for health care policy.

OBJECTIVE This study examines the usefulness of childhood glucose homeostasis variables (glucose, insulin, and insulin resistance index [homeostasis model assessment of insulin resistance {HOMA-IR}]) in predicting pre-diabetes and type 2 diabetes and related cardiometabolic risk factors in adulthood. RESEARCH DESIGN AND METHODS This retrospective cohort study consisted of normoglycemic (n = 1,058), pre-diabetic (n = 37), and type 2 diabetic (n = 25) adults aged 19–39 years who were followed on average for 17 years since childhood. RESULTS At least 50% of the individuals who ranked highest (top quintile) in childhood for glucose homeostasis variables maintained their high rank by being above the 60th percentile in adulthood. In a multivariate model, the best predictors of adulthood glucose homeostasis variables were the change in BMI Z score from childhood to adulthood and childhood BMI Z score, followed by the corresponding childhood levels of glucose, insulin, and HOMA-IR. Further, children in the top decile versus the rest for insulin and HOMA-IR were 2.85 and 2.55 times, respectively, more likely to develop pre-diabetes; children in the top decile versus the rest for glucose, insulin, and HOMA-IR were 3.28, 5.54, and 5.84 times, respectively, more likely to develop diabetes, independent of change in BMI Z score, baseline BMI Z score, and total-to-HDL cholesterol ratio. In addition, children with adverse levels (top quintile versus the rest) of glucose homeostasis variables displayed significantly higher prevalences of, among others, hyperglycemia, hypertriglyceridemia, and metabolic syndrome. CONCLUSIONS Adverse levels of glucose homeostasis variables in childhood not only persist into adulthood but also predict adult pre-diabetes and type 2 diabetes and relate to cardiometabolic risk factors.

That plasma homocysteine is elevated markedly in renal dysfunction is well recognized. But whether the increased homocysteine is an independent correlate of glomerular filtration rate, a marker of renal function, in asymptomatic younger individuals is not clear. The aim of this study was to determine the association between plasma homocysteine and renal function in a biracial (black-white) community-based cohort of asymptomatic young adults. Plasma homocysteine along with cardiovascular disease risk factor variables were measured in 805 white and 330 black subjects, ages 24-44 years, enrolled in the Bogalusa Heart Study. Modification of Diet in Renal Disease Study equation was used to calculate the estimated glomerular filtration rate (eGFR) from serum creatinine level. Males versus females showed higher homocysteine levels (8.83 +/- 3.16 vs. 7.35 +/- 2.84 micromol/L, p0.0001) and lower eGFR (99.1 +/- 17.6 vs. 102.5 +/- 21.0 mL/min/1.73 m(2), p = 0.024). Whites versus blacks had lower eGFR (97.3 +/- 18.0 vs. 110.0 +/- 20.6 mL/min/1.73 m(2), p0.0001). In a multivariate regression analysis that included age, race, sex, body mass index, blood pressure, lipoprotein variables, insulin resistance index and homocysteine, white race, age and homocysteine, in that order, were independently and negatively associated with eGFR. The odds ratio (95% confidence interval) of individuals in the homocysteine quintiles II, III, IV and V vs. I for having the risk of impaired eGFR defined as10th percentile was 2.28 (0.95-5.50, p = 0.065), 2.97 (1.24-7.12, p = 0.015), 3.32 (1.45-7.60, p = 0.005) and 6.99 (3.06-15.94, p0.0001), respectively. Homocysteine is an independent correlate of renal function in asymptomatic black and white young adults.

OBJECTIVE. This study sought to examine the usefulness of childhood non–high-density lipoprotein cholesterol level versus low-density lipoprotein cholesterol level, high-density lipoprotein cholesterol level, triglyceride level, apolipoprotein B level, apolipoprotein A-I level, total cholesterol/high-density lipoprotein cholesterol ratio, and apolipoprotein B/apolipoprotein A-I ratio in predicting adult excess carotid intima-media thickness, an indicator of subclinical atherosclerosis.METHODS. This retrospective cohort study included 437 black and white subjects (70% white and 40% male) who participated in the Bogalusa Heart Study as children 5 to 17 years of age and as adults 16 to 19 years later.RESULTS. In analyses of each lipoprotein measure as a risk factor for predicting excess carotid intima-media thickness in adulthood, non–high-density lipoprotein cholesterol level, low-density lipoprotein cholesterol level, total cholesterol/high-density lipoprotein cholesterol ratio, apolipoprotein B level, and apolipoprotein B/apolipoprotein A-I ratio emerged as significant predictors, with respective odds ratios of 2.60, 2.95, 1.78, 1.44, and 1.69, after adjustment for childhood BMI, systolic blood pressure, other lipoprotein measures, and follow-up years; the odds ratios for high-density lipoprotein cholesterol, triglyceride, and apolipoprotein A-I levels were not significant. Regarding the discriminating value of different childhood lipoprotein measures in predicting excess carotid intima-media thickness in adulthood, analyses of the area under the receiver operating characteristic curve for each lipoprotein measure, adjusted for the aforementioned nonlipoprotein covariates, indicated that the value of 0.65 for the non–high-density lipoprotein cholesterol level was similar in magnitude to those for other lipoprotein measures, with values ranging from 0.62 to 0.66.CONCLUSIONS. Childhood non–high-density lipoprotein cholesterol levels are as good as other lipoprotein measures in predicting subclinical atherosclerosis in adulthood, which has practical implications for coronary artery disease risk assessment and intervention in pediatric populations.

Excess glycated hemoglobin (HbA(1c)), an indicator of long-term glucose homeostasis, is recognized as a risk factor for cardiovascular (CV) disease and mortality even among persons without diabetes. However, information is scant regarding its distribution and correlates of CV risk in nondiabetic younger adults. This aspect was examined in a biracial (black-white) community-based sample of 1111 younger adults (mean age: 36.2 years; 71% white, 43% male) enrolled in the Bogalusa Heart Study. Blacks vs whites and women vs men had higher HbA(1c) values (P < .0001). In bivariate analysis adjusted for age, race, sex, and smoking status, significant adverse trends were noted for body mass index, waist circumference, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), total cholesterol to HDL-C ratio, insulin, glucose, and homeostasis model assessment of insulin resistance across HbA(1c) quartiles; trends were not significant for mean arterial blood pressure, triglycerides, C-reactive protein, adiponectin, and estimated glomerular filtration rate. In multivariate analysis, besides race and sex, total cholesterol to HDL-C ratio and waist circumference were independent correlates of HbA(1c). Furthermore, the prevalence of excess (top decile) HbA(1c) was 1.6-fold (P < .05) higher among those with metabolic syndrome defined by the National Cholesterol Education Program Adult Treatment Panel III and 2.1-fold (P < .01) and 1.5-fold (P < .05) higher, respectively, among those with positive parental history of CV disease and type 2 diabetes mellitus. These findings underscore the potential value of HbA(1c) in risk assessments of CV disease and type 2 diabetes mellitus in nondiabetic, apparently "healthy" younger adults.

Clustering of long-term rates of change in metabolic syndrome variables (body mass index, homeostasis model assessment of insulin resistance, ratio of triglycerides to high-density lipoprotein cholesterol, and mean arterial pressure) from childhood to adulthood was evaluated longitudinally (1982-2003) in a cohort of 389 Blacks and 631 Whites who were examined 3-6 times both as children (ages 4-17 years) and as adults (ages 18-38 years) over an average of 16 years (3,874 observations). The incremental area under the growth curve was used as a measure of long-term rates of change in risk variables since childhood. Intraclass correlations, a measure of the degree of clustering, among the four variables were significant (p < 0.001) for childhood, adulthood, and incremental area values and were higher in adulthood than in childhood. Blacks showed a higher degree of clustering of long-term rates of change in risk variables than did Whites. Adjustment for body mass index reduced the degree of clustering by approximately 50%. These results show that metabolic syndrome variables coexist in terms not only of their levels in childhood and adulthood but also of long-term rates of change. Obesity is of critical importance in the development of metabolic syndrome, and its prevention beginning in childhood needs to be addressed.

Most epidemiologic studies have focused on the adverse impact of the metabolic syndrome on cardiovascular (CV) disease. However, information on the relationship between the clustering of metabolic syndrome variables at favorable levels in childhood and the measures of CV risk in adulthood is not known.The study cohort included 1,474 individuals (552 blacks and 922 whites) who were examined for CV risk factors in childhood (aged 4-17 years) and again in adulthood (aged 19-41 years) in Bogalusa, Louisiana, during 1982-2003, with an average follow-up period of 15.8 years.In childhood, 9.0% of the cohort displayed clustering of three- or four-criterion risk variables at the bottom quartiles of BMI, homeostasis model assessment of insulin resistance, systolic blood pressure, and total-to-HDL cholesterol ratio. The clustering was significantly higher than expected by chance alone (P0.01). These children, compared with those having clustering of less than three risk variables at the bottom quartiles, had a lower prevalence of metabolic syndrome in adulthood (clustering at top quartiles) (3.8 vs. 14.6%, P0.001). A higher prevalence of clustering of risk variables at low levels in childhood was associated with negative parental histories of coronary heart disease (9.4 vs. 5.0%, P = 0.024) and hypertension (10.5 vs. 6.6%, P = 0.012). Mean values of carotid intima-media thickness in adulthood decreased with an increasing number of risk variables clustering at the bottom quartiles in childhood (P for trend = 0.013).The constellation of metabolic syndrome variables at low levels in childhood is associated with lower measures of CV risk in adulthood.

Cigarette smoking, an established cardiovascular (CV) disease risk factor, is known to impair pulsatile arterial function in middle-aged and older adults. However, information is scant in healthy young adults for whom smoking is the only CV risk factor, at current guidelines. Nonsmokers (n = 145) and smokers (n = 142) aged on average 36 years were selected for not having obesity, hypertension, dyslipidemia, diabetes, or clinically manifest CV disease. Pulsatile arterial function was measured in terms of large artery compliance (C1), small artery compliance (C2), and systemic vascular resistance (SVR) by noninvasively recorded radial artery waveforms. Smokers versus nonsmokers had significantly lower measures of adiposity and LDL-cholesterol; and higher systolic blood pressure and triglycerides. In addition, smokers versus nonsmokers had lower C2 (5.09 v 6.63 mL/mm Hg x 100, P = .0009) and higher SVR (1399.0 v 1325.5 dyn . sec . cm(-5), P = .006), after adjustment for race, sex, and age. Decreases in C2 (P for trend = .001) and increases in SVR (P for trend = .01) were noted with increasing years of smoking. Multivariate analysis revealed that duration of smoking was associated adversely with C2 (P = .004), independent of race, sex, age, systolic and diastolic blood pressures, HDL-cholesterol, triglycerides, glucose, and insulin. The odds of having adverse C2 (bottom 10 percentile) and SVR (top 10 percentile) were, respectively, 2.9 (P = .01) and 2.6 (P = .07) times higher in smokers versus nonsmokers. The observed deleterious effects of cigarette smoking on arterial wall dynamics in otherwise healthy young adults underscore the need for aggressive early prevention and intervention strategies to control smoking behavior.

Age and metabolic syndrome are major risk factors for atherosclerosis. However, limited information is available regarding whether cigarette smoking, another major, modifiable risk factor, has synergistic effects with age and metabolic syndrome on subclinical atherosclerosis, particularly in young adults. This aspect was examined in 1,051 adults (747 whites and 304 blacks; aged 24-43 years) from the Bogalusa Heart Study. General linear models were used to examine the effects of cigarette smoking and its interactive effects with age and metabolic syndrome on carotid intima-media thickness (CIMT). After adjusting for age, race, and sex, current smokers had lower BMI (mean ± SE: 27.4 ± 0.4, 29.3 ± 0.5, and 29.9 ± 0.3 kg/m2 in current, former, and never smokers, respectively; p