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INTRODUCTION

Obesity is a state of excess adipose tissue mass. Obesity should not be defined by body weight alone, as muscular individuals may be overweight by arbitrary standards without having increased adiposity. The most widely used method to classify weight status and risk of disease is the body mass index (BMI), which is equal to weight/height2 in kg/m2 (Table 183-1). At a similar BMI, women have more body fat than men. Furthermore, regional fat distribution may influence the risks associated with obesity. Central (primarily visceral) obesity [high ratio of the circumference of the waist to the circumference of the hips (waist-to-hip ratio), >0.9 in women and 1.0 in men] is independently associated with a higher risk for metabolic syndrome, diabetes mellitus, hyperandrogenism in women, and cardiovascular disease. The prevalence of obesity has increased dramatically over the past 3 decades. In the United States in 2008, 34% of adults age >20 were obese (BMI >30), and another 34% were overweight (BMI 25–30). Most alarming is the same trend among children, where 17% between ages 2 and 19 were obese, and another 18% were overweight. This has led to an epidemic of type 2 diabetes in children, a condition almost never seen until recently. These trends to increased obesity are not limited to Western societies but are occurring worldwide.

TABLE 183-1CLASSIFICATION OF WEIGHT STATUS AND RISK OF DISEASE

ETIOLOGY

Obesity can result from increased energy intake, decreased energy expenditure, or a combination of the two. Excess accumulation of body fat is the consequence of environmental and genetic factors; social factors and economic conditions also represent important influences. The recent increase in obesity can be attributed to a combination of excess caloric intake and decreasing physical activity. Poorly understood reasons for increased food assimilation due to dietary composition have also been postulated, as have sleep deprivation and an unfavorable gut flora. The susceptibility to obesity is polygenic in nature, and 30–50% of the variability in total fat stores is believed to be genetically determined. Among monogenic causes, mutations in the melanocortin receptor 4 are most common and account for ~1% of obesity in the general population and ~6% in severe, early-onset obesity. Syndromic obesity forms include Prader-Willi syndrome and Laurence-Moon-Biedl syndrome. Other monogenetic or syndromic causes are extremely rare. Secondary causes of obesity include hypothalamic injury, hypothyroidism, Cushing's syndrome, and ...

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