Blood pressure in children has consistently been related to adult blood pressure, with implications for long-term prevention of cardiovascular disease. The epidemic of obesity in children has resulted in corresponding increases in childhood blood pressure. In this paper, the authors develop norms for childhood blood pressure among normal-weight children (body mass index <85th percentile based on Centers for Disease Control and Prevention guidelines) as a function of age, sex, and height, using data from 49,967 children included in the database of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents (the Pediatric Task Force). The authors considered three types of models for pediatric blood pressure data, including polynomial regression, restricted cubic splines, and quantile regression, with the latter providing the best fit. The sex-specific norms presented here are a nonlinear function of both age and height and are generally slightly lower than previously developed norms based on Pediatric Task Force data including both normal-weight and overweight children.

The obesity epidemic in children makes it plausible that prevalence rates of elevated blood pressure (BP) are increasing over time. Yet, previous literature is inconsistent because of small sample sizes. Also, it is unclear whether adjusting for risk factors can explain longitudinal trends in prevalence of elevated BP. Thus, we analyzed a population-based sample of 3248 children in National Health and Nutrition Examination Survey (NHANES) III (1988–1994) and 8388 children in continuous NHANES (1999–2008), aged 8 to 17 years. Our main outcome measure was elevated BP (systolic BP or diastolic BP ≥90th percentile or systolic BP/diastolic BP ≥120/80 mm Hg). We found that the prevalence of elevated BP increased from NHANES III to NHANES 1999–2008 (Boys: 15.8% to 19.2%, P =0.057; Girls: 8.2% to 12.6%, P =0.007). Body mass index (Q4 versus Q1; odds ratio=2.00; P <0.001), waist circumference (Q4 versus Q1; odds ratio=2.14; P <0.001), and sodium (Na) intake (≥3450 mg versus <2300 mg/2000 calories; odds ratio=1.36; P =0.024) were independently associated with prevalence of elevated BP. Also, mean systolic BP, but not diastolic BP, was associated with increased Na intake in children (quintile 5 [Q5] versus quintile 1 [Q1] of Na intake; β=1.25±0.58; P =0.034). In conclusion, we demonstrate an association between high Na intake and elevated BP in children. After adjustment for age, sex, race/ethnicity, body mass index, waist circumference, and sodium intake, odds ratio for elevated BP in NHANES 1999–2008 versus NHANES III=1.27, P =0.069.

Breast cancer (BC) is the most common cancer to affect women worldwide.¹ The annual incidence ranges from 11.8 per 100 000 women in Eastern China to 86.3 per 100 000 in North America,² suggesting the influence of environmental or lifestyle factors in the etiology of BC. Tobacco smoking is one of the leading preventable risk factors of cancer in respiratory and nonrespiratory sites.^3,4 Tobacco smoke contains potential human breast carcinogens, including polycyclic aromatic hydrocarbons, aromatic amines, and N -nitrosamines.^3,5-7 Carcinogens in tobacco pass through the alveolar membrane and enter the bloodstream⁸ and are transported to mammary tissue through plasma lipoproteins.^9,10 Metabolites of cigarette smoke have been detected in nonlactating cigarette smokers in breast fluid obtained through standard nipple aspiration techniques.^11,12 Furthermore, because these breast carcinogens are lipophilic, they may be stored in breast adipose tissue and metabolized and activated by mammary epithelial cells.^13,14 Conversely, smoking has been postulated to have an antiestrogenic effect,¹⁵ which may be associated with a lower risk of BC. The antiestrogenic effect of smoking has been supported by an increased risk of osteoporosis,^16,17 an early age at natural menopause,¹⁸ and attenuated effects of hormone therapy (HT) among smokers.¹⁶

Introduction: Body mass index (BMI) during adulthood is inversely related to the incidence of premenopausal breast cancer, but the role of body fatness earlier in life is less clear. We examined prospectively the relation between body fatness during childhood and adolescence and the incidence of breast cancer in premenopausal women. Methods: Participants were 109,267 premenopausal women in the Nurses' Health Study II who recalled their body fatness at ages 5, 10 and 20 years using a validated 9-level figure drawing. Over 12 years of follow up, 1318 incident cases of breast cancer were identified. Cox proportional hazards regression was used to compute relative risks (RRs) and 95% confidence intervals (CIs) for body fatness at each age and for average childhood (ages 5–10 years) and adolescent (ages 10–20 years) fatness. Results: Body fatness at each age was inversely associated with premenopausal breast cancer incidence; the multivariate RRs were 0.48 (95% CI 0.35–0.55) and 0.57 (95% CI 0.39–0.83) for the most overweight compared with the most lean in childhood and adolescence, respectively (P for trend < 0.0001). The association for childhood body fatness was only slightly attenuated after adjustment for later BMI, with a multivariate RR of 0.52 (95% CI 0.38–0.71) for the most overweight compared with the most lean (P for trend = 0.001). Adjustment for menstrual cycle characteristics had little impact on the association. Conclusion: Greater body fatness during childhood and adolescence is associated with reduced incidence of premenopausal breast cancer, independent of adult BMI and menstrual cycle characteristics.