Background-Secular trend data on hypertension in children and adolescents are scarce and inconsistent. In the face of growing obesity, we sought to assess high blood pressure (HBP) secular trends in children and adolescents enrolled in national surveys and to determine whether the HBP trend reversed its course with the rise in obesity. Methods and Results-National survey data obtained from multistage probability sampling of the US noninstitutionalized population from 1963 to 2002 were examined; 8-to 17-year-old non-Hispanic blacks and whites and Mexican Americans were included. HBP ascertainment was based on age-, gender-, and height percentile-specific systolic and diastolic BPs. Weighted analyses were performed to account for the complex design. The BP, pre-HBP, and HBP trends were downward from 1963 to 1988 and upward thereafter. Pre-HBP and HBP increased 2.3% (Pϭ0.0003) and 1% (Pϭ0.17), respectively, between 1988 and 1999. Obesity increase, more so abdominal than general obesity, partially explained the rise in HBP and pre-HBP from 1988 to 1999. BP and HBP reversed their downward trends 10 years after the increase in the prevalence of obesity. Additionally, an ethnic and gender gap appeared in 1988 for pre-HBP and in 1999 for HBP; non-Hispanic blacks and Mexican Americans had a greater prevalence of HBP and pre-HBP than non-Hispanic whites, and males had a greater prevalence than females. Conclusions-HBP and pre-HBP in children and adolescents are on the rise. These new findings have implications for the cardiovascular disease public health burden, particularly the risk of a new cardiovascular disease transition. They reinforce the urgent call for early prevention of obesity and HBP and illustrate racial/ethnic disparities in this age group.

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BackgroundCompared with whites, black Americans suffer from a disproportionate burden of cardiovascular disease (CVD). We hypothesized that racial differences in the prevalence of CVD could be attributed, in part, to impaired vascular function in blacks after adjustment for differences in risk factor burden.Methods and ResultsWe assessed vascular function in 385 black and 470 white subjects (mean age, 48±11 years; 45% male). Using digital pulse amplitude tonometry (EndoPAT) we estimated the reactive hyperemia index (RHI), a measure of microvascular endothelial function, and peripheral augmentation index (PAT‐AIx). Central augmentation index (C‐AIx) and pulse‐wave velocity (PWV) were measured as indices of wave reflections and arterial stiffness, respectively, using applanation tonometry (Sphygmocor). Compared with whites, blacks had lower RHI (2.1±0.6 versus 2.3±0.6, P<0.001), greater arterial wave reflections assessed as both PAT‐AIx (20.4±21.5 versus 17.0±22.4, P=0.01) and CAIx (20.8±12.3 versus 17.5±13.3, P=0.001), and greater arterial stiffness, measured as PWV (7.4±1.6 versus 7.1±1.6 m/s, P=0.001). After adjustment for traditional CVD risk factors, black race remained a significant predictor of lower RHI and higher PAT‐AIx and CAIx (all P<0.001) in all subjects and of higher PWV in men (P=0.01). Furthermore, these associations persisted in a subgroup analysis of “healthy” individuals free of CVD risk factors.ConclusionBlack race is associated with impaired microvascular vasodilatory function, and greater large arterial wave reflections and stiffness. Because impairment in these vascular indices may be associated with worse long‐term outcomes, they may represent underlying mechanisms for the increased CVD risk in blacks.

BackgroundCompared with whites, sleep disturbance and sleep deprivation appear more prevalent in African Americans (AA). Long-term sleep deprivation may increase the risk of obesity through multiple metabolic and endocrine alterations. Previous studies have reported contradictory results on the association between habitual sleep duration and obesity. Accordingly, we aimed to assess whether sleep quality and duration are inversely associated with body mass index (BMI) and obesity and test whether these associations are modified by psychosocial stress, known to influence sleep quality.MethodsA sample of 1,515 AA residents of metropolitan Atlanta, aged 30-65 years, was recruited by a random-digit-dialing method in 2007-08. The outcome obesity was defined by BMI (kg/m2) continuously and categorically (BMI ≥ 30 versus BMI < 30). Global sleep quality (GSQ) score was computed as the sum of response values for the seven components of the Pittsburgh Sleep Quality Index (PSQI) scale. GSQ score was defined as a continuous variable (range 0-21) and as tertiles. The general perceived stress (GPS), derived from the validated Cohen scale, was categorized into tertiles to test the interaction. Chi-square tests, correlation coefficients and weighted multiple linear and logistic regression were used to assess the associations of GSQ, GPS and obesity.ResultsThe mean (standard deviation) age was 47.5 (17.0) years, and 1,096 (72%) were women. GSQ score categorized into tertiles was associated with BMI. Among women, after multivariable adjustment that included age, gender, physical activity, smoking status, education, total family income, financial stress and history of hypertension, hypercholesterolemia, diabetes and myocardial infarction, obesity was associated with sleep quality as assessed by GSQ continuous score, [odds ratio, OR (95% C.I.): 1.08 (1.03 - 1.12)], and with a worse sleep disturbance subcomponent score [OR (95% C.I.): 1.48 (1.16 - 1.89)]. Among all participants, stress modified the association between obesity and sleep quality; there was an increased likelihood of obesity in the medium stress category, OR (95% C.I.): 1.09 (1.02 - 1.17).ConclusionSleep quality was associated with obesity in women. The association of sleep quality with obesity was modified by perceived stress. Our results indicate the need for simultaneous assessment of sleep and stress.

This report on arterial mechanics in African Americans suggests that large artery stiffening either occurs earlier, or is more accelerated in African Americans than in whites in our sample, perhaps as a result of earlier exposure to multiple risk factors. This finding may have implications for hypertension prevention, as arterial stiffness is associated with the development of hypertension.