ABSTRACT
As the major causes of death and health-care expenditures in the United States and most other countries are cardiovascular disease (CVD) and cancer, the approach to obesity should be designed primarily to reduce the risks and costs of these medical conditions. This chapter will discuss a classication of obesity that is based on anatomic, etiologic, and functional considerations. We will then use the natural history of the development of obesity to identify the factors associated with its progression and to suggest a stepped approach to evaluate the overweight and obese patient. This discussion is done in the context of obesity as a disease of energy storage [1] whose etiology is a cumulatively greater energy intake than is needed for daily activities. The pathology is enlarged fat cells. The extent to which these enlarged cells produce detrimental health consequences depends on two major factors. The rst is the mass of fat, which leads to changes in body conguration and resulting reactions (e.g., stigma, osteoarthritis, or obstructive sleep apnea [OSA]). The second is the location of fat cells. The principal detrimental metabolic consequences of adiposity occur when fat cells enlarge or are unable to adequately expand to accommodate excessive caloric storage. Increased intra-abdominal, visceral, or ectopic fat deposition may result in and accentuate this problem [2]. Production of adipocytokines, inammatory markers, vascular factors, and leptin from enlarged visceral fat cells or ectopic overow sites causes the primary metabolic derangements, such as diabetes, atherogenic dyslipidemia (decreased high-density lipoprotein [HDL]-cholesterol and increased triglycerides), and release of inammatory markers such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) or procoagulant factors such as plasminogen activator inhibitor-1 [3,4].
