RESUMO
The pandemic of overweight and obesity continues to rise in an alarming rate in western countries and around the globe representing a major public health challenge in desperate need for new strategies tackling obesity. In the United States nearly two thirds of the population is overweight or obese. Worldwide the number of persons who are overweight or obese exceeded 1.6 billion. These rising figures have been clearly associated with increased morbidity and mortality. For example, in the Framingham study, the risk of death increases with each additional pound of weight gain even in the relatively younger population between 30 and 42 years of age. Overweight and obesity are also associated with increased co-morbid conditions such as diabetes, hypertension and cardiovascular disease as well as certain types of cancer. In this review we discuss the epidemic of obesity, highlighting the pathophysiologic mechanisms of weight gain. We also provide an overview of the assessment of overweight and obese individuals discussing possible secondary causes of obesity. In a detailed section we discuss the currently approved therapeutic interventions for obesity highlighting their mechanisms of action and evidence of their efficacy and safety as provided in clinical trials. Finally, we discuss novel therapeutic interventions that are in various stages of development with a special section on the weight loss effects of anti-diabetic medications. These agents are particularly attractive options for our growing population of obese diabetic individuals.
RESUMO
A body of epidemiologic and clinical evidence dating back to the early 1960s establishes the relationships between sleep apnea and cardiovascular disease (CVD). Individuals with obstructive sleep apnea, the most common type of sleep-disordered breathing, are at increased risk for coronary artery disease, congestive heart failure, and stroke. Evidence that treatment of sleep apnea with continuous positive airway pressure reduces blood pressure, improves left ventricular systolic function, and diminishes platelet activation further supports linkage between obstructive sleep apnea and CVD. Notwithstanding, complex associations between these two conditions remain largely unexplained due to dearth of systematic experimental studies. Arguably, several intermediary mechanisms including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress might be involved. Other abnormalities such as dysfunctions in coagulation factors, endothelial damage, platelet activation, and increased systemic inflammation might also play a fundamental role. This review examines evidence for the associations between obstructive sleep apnea and CVD and suggested underlying anatomical and physiological mechanisms. Specific issues pertaining to definition, prevalence, diagnosis, and treatment of sleep apnea are also discussed. Consistent with rising interest in the potential role of the metabolic syndrome, this review explores the hypothesized mediating effects of each of the components of the metabolic syndrome.