Camilo Fernandez

Utility of waist-to-height ratio in assessing the status of central obesity and related cardiometabolic risk profile among normal weight and overweight/obese children: The Bogalusa Heart Study

BackgroundBody Mass Index (BMI) is widely used to assess the impact of obesity on cardiometabolic risk in children but it does not always relate to central obesity and varies with growth and maturation. Waist-to-Height Ratio (WHtR) is a relatively constant anthropometric index of abdominal obesity across different age, sex or racial groups. However, information is scant on the utility of WHtR in assessing the status of abdominal obesity and related cardiometabolic risk profile among normal weight and overweight/obese children, categorized according to the accepted BMI threshold values.MethodsCross-sectional cardiometabolic risk factor variables on 3091 black and white children (56% white, 50% male), 4-18 years of age were used. Based on the age-, race- and sex-specific percentiles of BMI, the children were classified as normal weight (5th - 85th percentiles) and overweight/obese (≥ 85th percentile). The risk profiles of each group based on the WHtR (<0.5, no central obesity versus ≥ 0.5, central obesity) were compared.Results9.2% of the children in the normal weight group were centrally obese (WHtR ≥0.5) and 19.8% among the overweight/obese were not (WHtR < 0.5). On multivariate analysis the normal weight centrally obese children were 1.66, 2.01, 1.47 and 2.05 times more likely to have significant adverse levels of LDL cholesterol, HDL cholesterol, triglycerides and insulin, respectively. In addition to having a higher prevalence of parental history of type 2 diabetes mellitus, the normal weight central obesity group showed a significantly higher prevalence of metabolic syndrome (p < 0.0001). In the overweight/obese group, those without central obesity were 0.53 and 0.27 times less likely to have significant adverse levels of HDL cholesterol and HOMA-IR, respectively (p < 0.05), as compared to those with central obesity. These overweight/obese children without central obesity also showed significantly lower prevalence of parental history of hypertension (p = 0.002), type 2 diabetes mellitus (p = 0.03) and metabolic syndrome (p < 0.0001).ConclusionWHtR not only detects central obesity and related adverse cardiometabolic risk among normal weight children, but also identifies those without such conditions among the overweight/obese children, which has implications for pediatric primary care practice.

Low birth weight is associated with higher blood pressure variability from childhood to young adulthood: the Bogalusa Heart Study.

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.

Temporal Relationship Between Elevated Blood Pressure and Arterial Stiffening Among Middle-Aged Black and White Adults The Bogalusa Heart Study

This study assessed the temporal relationship between elevated blood pressure (BP) and arterial stiffness in a biracial (black-white) cohort of middle-aged adults aged 32-51 years from the semirural community of Bogalusa, Louisiana. Measurements of aortic-femoral pulse wave velocity (afPWV; n = 446) and large- and small-arterial compliance (n = 381) were obtained at 2 time points between 2000 and 2010, with an average follow-up period of 7 years. A cross-lagged path analysis model was used to examine the temporal relationship of elevated BP to arterial stiffness and elasticity. The cross-lagged path coefficients did not differ significantly between blacks and whites. The path coefficient (ρ2) from baseline BP to follow-up afPWV was significantly greater than the path coefficient (ρ1) from baseline afPWV to follow-up BP (ρ2 = 0.20 vs. ρ1 = 0.07 (P = 0.048) for systolic BP; ρ2 = 0.19 vs. ρ1 = 0.05 (P = 0.034) for diastolic BP). The results for this 1-directional path from baseline BP to follow-up afPWV were confirmed, although marginally significant, by using large- and small-artery elasticity measurements. These findings provide strong evidence that elevated BP precedes large-artery stiffening in middle-aged adults. Unlike the case in older adults, the large-arterial wall is not stiff enough in youth to alter BP levels during young adulthood.

Uric Acid Is Associated with Metabolic Syndrome in Children and Adults in a Community: The Bogalusa Heart Study

Background Elevated serum uric acid (UA) is commonly found in subjects with metabolic syndrome (MetS). This study examined the association of UA with levels of individual MetS components and the degree of their clustering patterns in both children and adults. Methods The study sample consisted of 2614 children aged 4–18 years and 2447 adults aged 19–54 years. MetS components included body mass index (BMI), mean arterial pressure (MAP), triglycerides to high-density lipoprotein cholesterol ratio (TG/HDLC), and homeostasis model assessment of insulin resistance (HOMA). Observed/expected (O/E) ratio and intra-class correlation coefficient (ICC) were used as a measure of the degree of clustering of categorical and continuous MetS variables, respectively. Results UA was positively and significantly associated only with BMI in children but with all four components in adults. The odds ratio for MetS associated with 1 mg/dL increase of UA was 1.74 (p<0.001) in children and 1.92 (p<0.001) in adults. O/E ratios showed a significant, increasing trend with increasing UA quartiles in both children and adults for 3- and 4-variable clusters with p-values for trend <0.001, except for BMI-MAP-TG/HDLC and MAP-TG/HDLC-HOMA clusters in children and MAP-TG/HDLC-HOMA cluster in adults. ICCs of 3 and 4 components increased with increasing UA quartiles in children and adults. Conclusions These results indicate that UA may play a role in the development of MetS in both pediatric and adult populations alike, which may aid in the identification and treatment of high risk individuals for MetS and related clinical disorders in early life.

Tobacco smoking strengthens the association of elevated blood pressure with arterial stiffness: the Bogalusa Heart Study.

Objectives: The study assessed the hypothesis that smoking strengthens the association of adult arterial stiffness with long-term cumulative burden of blood pressure (BP) from childhood to adulthood. Backgrounds: Tobacco smoking and elevated BPs are important risk factors of vascular stiffness. However, the synergistic effect of these two risk factors is not well established, especially for the long-term burden of elevated BP since childhood. Methods: The study cohort consisted of 945 adults (661 whites and 284 blacks, aged 24–43 years) who have BP measured 4–15 times since childhood (aged 4–17 years) in Bogalusa, Louisiana. The adult arterial stiffness was measured as aorta–femoral pulse wave velocity (afPWV); the total area under the curve (AUC) and incremental AUC were used as a measure of long-term burden and trends of BP, respectively. Results: Increased adult afPWV was significantly associated with higher adulthood (P < 0.001), total AUC (P < 0.001) and incremental AUC (P < 0.001) values of SBP and DBP, but not with childhood BP, after adjusting for age, race, sex, BMI and heart rate. Furthermore, smoking was a significant predictor of increased adult afPWV and BP levels. In the interaction analyses, the increasing trend of afPWV with increasing adult SBP (P = 0.009) and its incremental AUC (P = 0.007) were significantly greater among the current smokers than among the nonsmokers. DBP showed a similar pattern regarding the smoking–BP interaction on afPWV. Conclusion: These results, by showing the synergistic effect of tobacco smoking and long-term BP measures from childhood to adulthood on arterial stiffening process, underscore the importance of undertaking preventive strategies early in life and smoking behavior control.

Cigarette smoking exacerbates the adverse effects of age and metabolic syndrome on subclinical atherosclerosis: the Bogalusa Heart Study.

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<0.0001) and lower levels of fasting glucose (82.8±0.9, 89.5±2.3, and 87.1±1.1 mg/dL, respectively; p = 0.001) and insulin (10.6±0.4, 14.2±1.0, 13.6±0. 6 µU/ml, respectively; p<0.0001). Despite being lean and having favorable levels of glucose and insulin, current smokers had greater CIMT (0.850±0.012, 0.808±0.011, and 0.801±0.006 mm, respectively; p = 0.0004). Importantly, cigarette smoking showed significant interactions with age and metabolic syndrome on CIMT: Age-related change in CIMT in current smokers was significantly greater (0.013±0.002 mm/year) than in nonsmokers (former and never smokers combined) (0.008±0.001 mm/year) (p for interaction = 0.005); the difference in CIMT between those with and without metabolic syndrome was significantly greater in current smokers (0.154±0.030 mm, p<0.0001) than in nonsmokers (0.031±0.014 mm, p = 0.03) (p for interaction<0.0001). In conclusion, cigarette smoking significantly exacerbates the adverse effects of age and metabolic syndrome on subclinical atherosclerosis in young adults, which underscores the importance of prevention and cessation of cigarette smoking behavior in the young.

Long-term Impact of Childhood Adiposity on Adult Metabolic Syndrome Is Modified by Insulin Resistance: The Bogalusa Heart Study.

Childhood adiposity and insulin resistance are well-known risk factors for adult metabolic syndrome (MetS). This study aims to examine whether the association between childhood adiposity and adult MetS is modified by insulin resistance. The cohort consisted of 1,593 black and white subjects, aged 19–50 years at follow-up, who were examined 19 years apart on average as children and adults for MetS variables. The prevalence of adult MetS was compared between the insulin-sensitive obesity and insulin-resistant obesity groups in childhood. Adult MetS prevalence was higher in the insulin-resistant obesity group than in the insulin-sensitive obesity group (34.9% vs. 24.3%, p = 0.008). In multivariable logistic regression analyses adjusted for age, race, gender, and follow-up years, individuals with insulin-resistant obesity in childhood were 1.7 times (p = 0.011) more likely to have MetS 19 years later on average than those with insulin-sensitive obesity in childhood. Odds ratio did not differ significantly between blacks and whites (p = 0.724). ORs for the association of childhood BMI with adult MetS significantly increased with increasing tertiles of childhood HOMA (p < 0.001 for trend). These findings suggest that insulin resistance amplifies the association between childhood adiposity and adult MetS and underscore the importance of preventing both adiposity and insulin resistance in early life.

Impact of Adiposity on Incident Hypertension Is Modified by Insulin Resistance in Adults: Longitudinal Observation From the Bogalusa Heart Study

Adiposity and insulin resistance are closely associated with hypertension. This study aims to investigate whether the association between adiposity and hypertension is modified by insulin resistance. The cohort consisted of 1624 middle-aged normotensive black and white adults aged 18 to 43 years at baseline who followed for 16 years on average. Overweight/obesity at baseline was defined as body mass index (BMI) ≥25, and insulin resistance was measured using homeostasis model assessment of insulin resistance. Prevalence of incident hypertension was compared between the insulin-sensitive adiposity and insulin-resistant adiposity groups. The prevalence of incident hypertension was higher in the insulin-resistant adiposity than in the insulin-sensitive adiposity group (32.1% versus 22.1%, P<0.001). In multivariable logistic analyses, adjusted for baseline age, race, sex, follow-up years, and smoking, baseline insulin-resistant obesity was associated with incident hypertension (odds ratio, 1.9; P=0.008). Odds ratios did not differ between blacks and whites (P=0.238). Of note, the odds ratios of BMI associated with hypertension significantly increased with increasing quartiles of baseline homeostasis model assessment (odds ratio, 1.3, 1.1, 1.5, and 2.5 in quartiles I, II, III, and IV, respectively; P=0.006 for trend). Slopes of increasing follow-up blood pressure with baseline BMI, measured as regression coefficients (&bgr;), were significantly greater in insulin-resistant than in insulin-sensitive individuals (&bgr;=0.74 versus &bgr;=0.35 for systolic blood pressure, P=0.004 for difference; &bgr;=0.51 versus &bgr;=0.23 for diastolic blood pressure, P=0.001 for difference). These findings suggest that insulin resistance has a synergistic effect on the obesity–hypertension association in young adults, indicating that the role of adiposity in the development of hypertension is modified by insulin resistance.Adiposity and insulin resistance are closely associated with hypertension. This study aims to investigate whether the association between adiposity and hypertension is modified by insulin resistance. The cohort consisted of 1624 middle-aged normotensive black and white adults aged 18 to 43 years at baseline who followed for 16 years on average. Overweight/obesity at baseline was defined as body mass index (BMI) ≥25, and insulin resistance was measured using homeostasis model assessment of insulin resistance. Prevalence of incident hypertension was compared between the insulin-sensitive adiposity and insulin-resistant adiposity groups. The prevalence of incident hypertension was higher in the insulin-resistant adiposity than in the insulin-sensitive adiposity group (32.1% versus 22.1%, P <0.001). In multivariable logistic analyses, adjusted for baseline age, race, sex, follow-up years, and smoking, baseline insulin-resistant obesity was associated with incident hypertension (odds ratio, 1.9; P =0.008). Odds ratios did not differ between blacks and whites ( P =0.238). Of note, the odds ratios of BMI associated with hypertension significantly increased with increasing quartiles of baseline homeostasis model assessment (odds ratio, 1.3, 1.1, 1.5, and 2.5 in quartiles I, II, III, and IV, respectively; P =0.006 for trend). Slopes of increasing follow-up blood pressure with baseline BMI, measured as regression coefficients (β), were significantly greater in insulin-resistant than in insulin-sensitive individuals (β=0.74 versus β=0.35 for systolic blood pressure, P =0.004 for difference; β=0.51 versus β=0.23 for diastolic blood pressure, P =0.001 for difference). These findings suggest that insulin resistance has a synergistic effect on the obesity–hypertension association in young adults, indicating that the role of adiposity in the development of hypertension is modified by insulin resistance. # Novelty and Significance {#article-title-47}

Stimulus response of blood pressure in black and white young individuals helps explain racial divergence in adult cardiovascular disease: the Bogalusa Heart Study.

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.

Sex and Race (Black-White) Differences in the Relationship of Childhood Risk Factors to Adulthood Arterial Stiffness: The Bogalusa Heart Study

Background:Cardiovascular risk factors in childhood are predictive of adulthood arterial stiffness. However, it is unknown whether this relationship varies by race or sex. Methods:Six hundred and eighty adults aged 24 to 43 had been followed for an average of 26.3 years, from the Bogalusa Heart Study. Brachial to ankle pulse wave velocity (baPWV) measured by an automatic oscillometric technique was used as the outcome variable for arterial stiffness during adulthood. Body mass index (BMI), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), glucose, and systolic blood pressure (SBP), all measured in childhood, were used as predictors. The average values of childhood measurements at multiple time points were used, standardized to age, race, and sex-specific z-scores. Results:In the total sample, childhood SBP was the only significant predictor (P < 0.001) for adult baPWV. Significant interactions between sex and BMI (P = 0.001), between sex and LDL-C (P = 0.035), and between race and HDL-C (P = 0.002) on adult baPWV were identified. Childhood predictors of adult baPWV were BMI (30.9 cm/s reduction in baPWV per standard deviation increase, 95% confidence interval [CI]: −55.0, −6.9 cm/s), LDL-C (30.8 cm/s increase, 95% CI: 2.9, 59.5 cm/s), and HDL-C (46.8 cm/s reduction, 95% CI: −76.2, −17.4 cm/s) in white males; SBP (38.2 cm/s increase, 95% CI: 11.0, 65.4 cm/s) in white females; BMI (71.3 cm/s reduction, 95% CI: −119.9, −22.7 cm/s) in black males; and none in black females. Conclusions:The associations of childhood cardiovascular risk factors with adult arterial stiffness varied by race and sex.