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Obesity has reached epidemic proportions in the U.S. and more developed countries, particularly so among adolescents. A substantial impact on public health could be achieved if other factors causing obesity besides the conventional ones of diet and physical activity could be identified and acted upon. The present study investigates whether there is a link between low sleep quality and obesity in a tri-ethnic, cross-sectional sample (n = 383) of male and female adolescents ages 11-16 years old (Heartfelt Study). Sleep quality was expressed as two variables, total sleep time and sleep disturbance time obtained by 24-hour wrist actigraphy. Percent body fat and body mass index (BMI) were used together to define obesity. The potential influence of demographic and behavioral confounders were considered in models that described the relation of sleep to obesity occurrence. Obese adolescents experienced less sleep than nonobese adolescents (P < 0.01). For each hour of lost sleep, the odds of obesity increased by 80%. Sleep disturbance was not directly related to obesity in the sample, but influenced physical activity level (P < 0.01). Daytime physical activity diminished by 3% for every hour increase in sleep disturbance. The above observations were independent of potential confounding variables. Inadequate and poor sleep quality in adolescents may be important factors to consider in the prevention of childhood obesity.

Background-This study was planned at a time when important questions were being raised about the adequacy of using one hormone to treat hypothyroidism instead of two.

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C ardiovascular disease (CVD) is a leading cause of morbidity and premature mortality in women and men in the United States, most of the industrialized world, and many developing countries. 1 Data accumulated over the past 3 decades indicate that atherosclerotic-CVD processes begin early in childhood and are influenced over the life course by genetic and potentially modifiable risk factors and environmental exposures. Taken together, these data provide compelling evidence for primary prevention of CVD beginning early in childhood. Within the pediatric healthcare community, this evidence has prompted and informed the development of science-based guidelines with recommendations for individual/high-risk and population-based approaches to primary prevention of CVD in children and youth. The purpose of this statement is to provide an overview of the evidence and current science-based recommendations and to emphasize the role of advanced practice nurses in the implementation of strategies consistent with population-based and individual/high-risk approaches to CVD prevention in children and youth. Evidence for CVD Prevention in ChildhoodEvidence-based guidelines for primary and secondary prevention of CVD in adults are informed by the results of randomized controlled trials. The existing evidence (discussed below) argues convincingly for prevention of CVD beginning early in childhood. It is noteworthy that data from randomized controlled trials documenting the effect of risk reduction in childhood on the development of CVD in adulthood are nonexistent. Similarly, no long-term longitudinal studies have been conducted to determine the absolute levels of risk factors measured in childhood that predict CVD in adult life. However, evidence from laboratory, clinical, and epidemiological studies supports the need for primary prevention of CVD beginning early in life and has prompted and informed existing guidelines for children and adolescents. Laboratory/Pathology and In Vivo/Clinical StudiesAutopsy studies conducted as part of the Bogalusa Heart Study 2,3 and the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Study 4,5 demonstrate significant positive associations between potentially modifiable CVD risk factors and the presence and extent of atherosclerotic lesions in the aorta and coronary arteries. [2][3][4][5] In the pathology component of the Bogalusa Heart Study, a long-term epidemiological study of risk factors for CVD in a biracial (black-white) population, risk factors were measured in free-living, healthy children and adolescents before death from non-CVD causes. 2,3 The PDAY study quantified risk factors by analyses of postmortem blood samples obtained at autopsy from Ϸ3000 persons 15 to 34 years of age who died from external causes, including accidents and homicides. 4,5 The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the w...