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There is a growing consensus on the importance of addressing obesity in clinical practice. This consensus is the product of clear evidence that obesity has become an extremely common condition, that it is associated with adverse health consequences, and that treatment modalities are available that can not only reduce weight, but improve some of the associated comorbidities. In this chapter, some of the evidence that obesity, as defined by body mass index and waist circumference, is associated with adverse health consequences will be reviewed. An approach to the assessment of the obese patient that involves a focused weight history, evaluating diet and physical activity habits, and determining the patient's goals and readiness for treatment will be discussed. Assessing for secondary causes of weight gain and risk stratification based on a history, physical exam, and laboratory evaluation are also discussed. The role of other health professionals in a multidisciplinary approach to assessment is proposed. Later chapters in this volume will discuss a variety of treatment approaches that can be used with obese patients. [ABSTRACT FROM AUTHOR]

Child obesity has increased dramatically in prevalence and severity over the past 40 yr. The tendency for obesity in childhood and adolescence to persist into adult life ties it to other risk factors for cardiovascular disease. This chapter will cover the epidemiology, evaluation, and management of child and adolescent obesity, with an emphasis on the impact of obesity as a life-span condition. The relationship between childhood obesity and other medical conditions will be reviewed. The impact of obesity psychologically, socially, and economically on the individual, family, and society will also be discussed. The bulk of the chapter will include information to assist the clinician in the evaluation of children and adolescents who are overweight and a description of the variety of medical, behavioral, and surgical approaches currently used in the management of this condition. [ABSTRACT FROM AUTHOR]

The National Weight Control Registry (NWCR) is a registry of more than 6000 individual s who have succeeded in long-term weight loss. This is the largest group of successful weight loss maintainers that has ever been studied. Over the past decade, we have identified many similarities in how these individuals are managing their body weight. We think this information can be useful in helping more people succeed at long-term weight management. We have eight recommendations for weight management based on our research: (1) treat weight-loss maintenance differently from weight loss; (2) make sure you are physically active during weight loss; (3) low-fat diets are best for preventing weight regain; (4) eat breakfast every day; (5) weigh yourself regularly and periodically keep diet and physical activity diaries; (6) get at least 1 h each day of physical activity; (7) maintain a consistent eating pattern; and (8) limit television viewing. [ABSTRACT FROM AUTHOR]

Bariatric surgery is associated with development of several micronutrient deficiencies that are predictable based on the surgically altered anatomy and the imposed dietary changes. The three restrictive malabsorptive procedures—Roux-en-Y gastric bypass (RYGB), biliopancreatic diversion (BPD), and biliopancreatic diversion with duodenal switch (BPD/DS) — pose a greater risk for micronutrient malabsorption and deficiency than the purely restrictive laparoscopic adjustable silicone gastric banding (LASGB). Metabolic and clinical deficiencies of two minerals (iron and calcium) and four vitamins (thiamine, folate, vitamin B12, vitamin D) have been well described in the literature. This chapter reviews the pathophysiology, clinical presentation, screening tests, and treatment for each micronutrient deficiency. With careful monitoring and adequate supplementation, these deficiencies are largely avoidable and treatable. [ABSTRACT FROM AUTHOR]

Weight-loss surgery is the only effective treatment for severe, medically complicated, and refractory obesity. It reverses, eliminates, or significantly ameliorates numerous life-threatening medical comorbidities that occur as part of the pathophysiology of obesity. Rapid changes in surgical technology and in demand for weight-loss surgery have made the field one of medicine's most dynamic. This chapter reviews available surgical procedures, their possible mechanisms of action through the enterohypothalamic endocrine axis, and their risks and outcomes. [ABSTRACT FROM AUTHOR]

Obesity is increasing in prevalence and its medical liabilities are largely related to central adiposity and the associated insulin resistance. The present drugs available for the treatment of obesity and metabolic syndrome are few in number and limited in efficacy. This chapter reviews the drugs approved by the US Food and Drug Administration (FDA) to treat obesity, drugs approved by the FDA for other indications than weight loss, drugs in the late development process that have not been approved by the FDA, drugs in earlier stages of drug development for which clinical information is limited, drugs that have been dropped from development, and new potential drug targets for which essentially no clinical data yet exist. We also review the nonprescription products sold for the treatment of obesity and metabolic syndrome. The developmental pipeline of drugs for the treatment of obesity and the metabolic syndrome is rich. Because drugs to treat obesity are being developed in an era characterized by more sophisticated tools for drug development than existed when hypertension drugs were being developed, much faster progress in developing safe and effective drugs for obesity and metabolic syndrome is anticipated. With safe and effective drugs available, we anticipate that the chronic treatment of obesity with weight loss medication will become as well-accepted and prevalent as is the chronic drug treatment of hypertension and diabetes in the medical practice of today. [ABSTRACT FROM AUTHOR]

Counseling by health care professionals represents a potentially important component of the public health response to rising rates of obesity in the United States. One promising approach to weight control counseling is motivational interviewing (MI). This manuscript explores conceptual issues related to the application of MI for the prevention and treatment of obesity in medical practice. Given the paucity of studies on MI and obesity, we examine what is known about the application of MI to adult diet and physical activity behaviors, as well as the use of MI to modify weight, diet, and activity in children and adolescents. We begin with a brief overview of MI and describe some nuances of applying this approach to obesity counseling. Recommendations for future research and clinical practice are also presented. [ABSTRACT FROM AUTHOR]

There is an increasing prevalence of overweight and obesity in the United States and other developed countries. This can have significant public health implications because of the association of excess body weight with increased risk of chronic diseases. It has been suggested that the increasing prevalence of excess body weight (overweight and obesity) and related diseases also has a significant impact on health care costs. Physical activity can significantly affect weight control and can also have an independent effect on associated chronic disease risk factors. However, physical activity participation is less than optimal. Thus, it is important for health care professionals to understand the role of physical activity in weight loss, the prevention of weight gain, and the prevention of weight regain, and to understand how to provide accurate and meaningful information to their patients. [ABSTRACT FROM AUTHOR]

Traditionally, the gold standard for obesity treatment has been the combination of a low-fat, low-calorie diet with regular physical activity and behavior therapy. This combination has been shown to be safe and effective; however, the best dietary approach to weight loss continues to be a matter of debate among professionals and the public alike. Preliminary short-term findings suggesting that low-carbohydrate diets are effective in reducing body weight and do not appear to increase the risk of cardiovascular disease have generated interest in the low-carbohydrate approach and have spawned further research. This chapter reviews the most recent findings from short- and long-term studies evaluating the effects of low-carbohydrate diets on weight, lipids, lipoprotein subfractions, inflammatory biomarkers, blood pressure, and insulin sensitivity. [ABSTRACT FROM AUTHOR]

Prescribing diets to treat obese patients and to prevent type 2 diabetes poses a challenge to clinicians. Overemphasis on carbohydrate-to-fat ratio, with insufficient attention directed toward diet quality, may partially explain disappointing outcomes with available approaches. The glycemic index (GI) is an alternative system for classifying carbohydrate-containing foods according to postprandial blood glucose responses to portions containing a standard amount of available carbohydrate, thereby providing a measure of carbohydrate quality. Because (31 is based on standardized portions, glycemic load (GL; product of GI and carbohydrate amount) values are used to describe how portions differing in both quality and quantity of carbohydrate affect postprandial glycemia. Plausible physiologic mechanisms link high-GI or -GL meals with disease processes. Selecting carbohydrate sources to reduce dietary GI— either without altering the contribution of carbohydrate to total energy intake or in combination with a moderate decrease in carbohydrate consumption— is a promising weight management strategy that can be implemented using a pragmatic approach. [ABSTRACT FROM AUTHOR]

Reducing caloric intake is the cornerstone of dietary therapy for long-term healthy weight management. Strategies individuals have typically used include limiting portion sizes, food groups, or certain macronutrients. Although such restrictive approaches can lead to weight loss in the short term, they can result in feelings of hunger or dissatisfaction, which can limit their acceptability, sustainability, and long-term effectiveness. An alternative positive strategy to manage energy intake is for individuals to eat more foods that are low in calories for a given measure of food—that is, they are low in energy density (kcal/g). Data have shown that people eat a fairly consistent amount of food on a day-to-day basis; therefore, the energy density of the foods an individual consumes influences energy intake. Encouraging patients to eat more foods low in energy density and to substitute these foods for those higher in energy density allows them to decrease their energy intake while eating sati sfying portions, thereby controlling hunger and lowering energy intake. This type of diet fi ts with the current Dietary Guidelines for Americans in that it incorporates high quantities of fruits, vegetables, and fiber, which are often suboptimal in typical low-calorie diets, and it provides ample intakes of numerous micronutrients. Moreover, studies have found that individuals who consume lower-energy-dense diets consume more food by weight and have lower body weights compared with individuals who consume higher-energy-dense diets. This chapter reviews the evidence supporting the use of diets rich in low-energy-dense foods for weight management and provides practical approaches to lowering the energy density of the diet. [ABSTRACT FROM AUTHOR]

Obesity and impaired glucose tolerance (IGT) are associated with a greater health risk for a number of conditions, including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, coagulation abnormalities, inflammatory markers, and coronary heart disease. Lifestyle changes can delay or prevent the development of type 2 diabetes in patients with obesity and IGT. The risks improve with weight loss and increased physical activity. A decrease of 7 to 10% or more from baseline weight can have a significant effect. This has now been documented in a number of randomized controlled studies. This essay is directed on how the Diabetes Prevention Program approach to lifestyle change can be translated in a meaningful way to routine clinical care practice settings. [ABSTRACT FROM AUTHOR]

Polycystic ovary syndrome (PCOS) is a common but poorly understood endocrinopathy diagnosed by the combination of oligomenorrhea, hyperandrogenism, and polycystic ovaries. Many of the women with PCOS are also uniquely and variably insulin-resistant. This can manifest as hyperinsulinemia, glucose intolerance, and frank diabetes. Affected women are plagued by infertility, menstrual disorders, dysfunctional uterine bleeding, and peripheral skin disorders including acne and hirsutism. The etiology of the syndrome is poorly understood. Many, if not most, US women with PCOS are also obese, which exacerbates many of the symptoms of the syndrome. This suggests that lifestyle interventions should be the first line treatment for these obese women. Treatment tends to be symptom-based, although some treatments can address multiple presenting complaints. The two most commonly used medications for chronic treatment, oral contraceptives and insulin sensitizing, do appear to improve multiple aspects of the syndrome simultaneously. Unfortunately, clinical trials have focused primarily on surrogate measures rather than clinical outcomes. [ABSTRACT FROM AUTHOR]

The past two decades have seen a dramatic increase in the prevalence of obesity in the US population. Although increasing obesity was observed in every sociodemographic group, at every point in time groups with lower education, African Americans and Native Americans, and women in lower income households had higher rates of obesity and related chronic conditions such as diabetes. Also noteworthy is the much faster increase of severe obesity compared with moderate obesity, which added further strain to the health care system and proved especially challenging to health care providers. We provide data on the populationwide trends in weight gain, economic consequences of health care cost growth and the socioeconomic disparities in obesity and diabetes. We further di scuss the socioeconomic and environmental changes that are likely underlying mechanisms for the obesity epidemic and related disparities. We conclude the chapter by discussing implications of these trends for the prevention and treatment of diabetes and challenges and opportunities faced by the health care system and providers. [ABSTRACT FROM AUTHOR]

Body weight is dependent on an intricate balance between energy intake and energy expenditure. When energy intake exceeds energy expenditure weight is gained, and the majority of this excess energy is stored as body fat. Whether the culprit of weight gain is increased food intake or reduced energy expenditure is generally unknown but it is most likely to be both, with proportions varying from case to case. An accurate assessment of dietary energy intake is difficult and precise only under laboratory conditions, but then the dietary intake tends not to accurately represent everyday life. Measurements of food intake in free-living conditions are, however, weakened by poor accuracy and precision. Scientists, therefore, have concentrated on the energy expenditure side of the energy balance equation. This chapter will review the methods by which energy expenditure can be measured in humans, the components of daily energy expenditure, their inherent interindividual variability, and their contribution to weight gain in adults and children. Finally, recent advances in our understanding of some of the molecular mechanisms underlying the regulation of energy expenditure will be discussed. [ABSTRACT FROM AUTHOR]

This chapter examines common methods for measuring body composition in obesity. These methods range from simple anthropometric measures that indirectly assess adiposity to more complex measures such as magnetic resonance imaging (MRI) and computed tomography (CT) that are able to directly measure numerous tissues in vivo. Anthropometric measurements are inexpensive, and are readily used in clinical settings and epidemiological studies, but lack precision to accurately quantify specific fat depots. On the other hand, imaging techniques such as MRI and CT are associated with high accuracy, but are limited by their availability and high cost. Application of other body composition measurement techniques such as dual-energy X-ray absorptiometry and magnetic resonance spectroscopy will also be considered. The focus of this review is on strengths and limitations of these body composition measurement techniques, and how they advance our understanding of how body composition influences the associations between obesity, morbidity, and mortality. [ABSTRACT FROM AUTHOR]

The development of obesity induces resistance to the effect of insulin to stimulate uptake of glucose and suppress release of fatty acids. These metabolic impairments are inter-related and competition between glucose and fatty acids i s a key aspect of the pathogenesis of insulin resistance. Another important factor is that fat calories accumulate within muscle and liver and the presence of an increased fat content in these organs correlates with severity of insulin resistance. This chapter reviews recent findings and background concepts regarding "ectopic fat" and substrate competition and how these contribute to obesity induced insulin resistance. [ABSTRACT FROM AUTHOR]

Epidemiological studies suggest that maternal undernutrition, obesity, and diabetes during gestation and lactation can all produce obesity in offspring. Animal models provide a means of assessing the independent consequences of altering the preversus postnatal environments on a variety of metabolic, physiologic, and neuroendocrine functions that lead to the development of offspring obesity, diabetes, hypertension, and hyperlipidemia. During the gestational period, maternal malnutrition, obesity, type 1 and type 2 diabetes, and psychological, immunological, and pharmacological Stressors can all promote offspring obesity. Normal postnatal nutrition can sometimes reduce the adverse impact of some of these prenatal factors but may also exacerbate the development of obesity and diabetes in offspring of dams that were malnourished during gestation. The genetic background of the individual is also an important determinant of outcome when the perinatal environment is perturbed. Individuals with an obesity-prone genotype are more likely to be adversely affected by factors such as maternal obesity and high-fat diets. Many perinatal manipulations are associated with reorganization of the central neural pathways that regulate food intake, energy expenditure, and storage in ways that enhance the development of obesity and diabetes in offspring. Both leptin and insuli n have strong neurotrophi c properties so that either an excess or an absence of either during the perinatal period may underlie some of these adverse developmental changes. Because perinatal manipulations can permanently and adversely alter the systems that regulate energy homeostasis, it behooves us to gain a better understanding of the factors during this period that promote the development of offspring obesity as a means of stemming the tide of the emerging worldwide obesity epidemic. [ABSTRACT FROM AUTHOR]

Adipose tissue (AT) is composed of adipocytes and a diverse population of nonadipocytes that are commonly referred to as stronial-vascular cells. Adipose tissue has traditionally been considered a passive storage energy depot that, indeed, does serve as a long-term reservoir for fuel stored as triglyceride. However, laboratory, clinical, and epidemiological studies over the past decade have redefined and greatly expanded our understanding of the physiological role of AT. We now appreciate that AT is an endocrine organ with important roles in maintaining whole-body energy homeostasis and systemic metabolism. This appreciation derives in large part from the identification of multiple AT-secreted factors that modulate central and peripheral processes. These include free fatty acids, which have significant effects on glucose and insulin homeostasis, as well as bioactive peptides termed adipokines. Adipokines act in an autocrine, paracrine, and/or endocrine fashion to promote metabolic homeostasis, and integrate adipose tissue, liver, muscle, and CNS physiology. There are currently more than 50 known adipokines, as well as locally generated hormones and metabolites that, together, affect multiple physiological functions including food intake, glucose homeostasis, lipid metabolism, inflammation, vascular tone, and angiogenesis. Because they affect such diverse and important processes, regulation of adipokine secretion from AT is critically important to regulating systemic metabolism. Notably, increased AT mass (as in obesity) induces characteristic qualitative and quantitative changes in adipose tissue metabolism and adipokine secretion. These changes are now implicated in the development of metabolic syndrome and its progression to more severe obesity-associated pathologies, including type 2 diabetes and cardiovascular disease. [ABSTRACT FROM AUTHOR]

Obesity occurs as a result of excessive energy intake and /or reduced energy expenditure. The hypothalamus is the principal region in the central nervous system that regulates appetite and energy homeostasis by incorporating neural and hormonal signals from the periphery. A large number of such hormones (gut peptides) are synthesized and secreted by cells in the gastrointestinal tract in addition to its function as a digestive system. Increasing evidence supports the role of gut peptides as short-term satiety signals regulating appetite and food intake. The anorexigenic gut peptides include PYY, PP, oxyntomodulin (OXM), GLP-1, and CCK. They are secreted mainly from the intestine, inhibit appetite, and promote satiety, whereas ghrelin, the only orexigenic peptide produced by the stomach, increases food intake. In this chapter we discuss the pathophysiology of gut peptides in health and disease. [ABSTRACT FROM AUTHOR]

The body's endogenous endocannabinoid system includes two endogenous agoni sts for cannabinoid-(CB)-l receptors, anadamide and 2-arachidonoyl-glycerol (2-AG). Both of these endocannabinoids (ECs) are fatty acid signals derived from cell membranes. They exert a coordinated action at multiple tissues to promote increased food intake, lipogenesis, and storage of fat. Endocannabinoids interact with multiple hypothalamic circuits and transmitter systems to stimulate food intake in general, and they also act in reward areas of the brain to selectively enhance intake of palatable foods. Activation of CB1 receptors increases enzyme activity that causes de novo fatty acids to be formed in the liver and circulating lipids to be taken up by fat cells. All these actions are reversed in animals lacking CB1 receptors, and there is growing evidence that activity of the endocannabinoid system is tonically increased in animal and human obesity. Acute or chronic administration of selective synthetic CB1 antagonists to overweight or obese individuals causes weight loss, reduced waist circumference, and an improved lipid and glycemic profile. Developing ligands for endocannabinoid receptors is an important novel therapeutic strategy for the treatment of metabolic dysregulation. [ABSTRACT FROM AUTHOR]

This chapter reviews current literature on hormonal and neural signals critical for the regulation of individual meals and body fat. Body weight is regulated via an ongoing process called energy homeostasis, or the long-term matching of food intake to energy expenditure. Reductions from an individual's "normal" weight owing to a lack of sufficient food lowers levels of adiposity signals (leptin and insulin) reaching the brain from the blood, activates anabolic hormones that stimulate food intake, and decreases the efficacy of meal-generated signals (such as cholecystokinin) that normally reduce meal size. A converse sequence of events happens when individuals gain weight, adiposity signals are increased, catabolic hormones are stimulated, and the consequence is a reduction in food intake and a normalization of body weight. The brain also functions as a "fuel sensor" and thereby senses nutrients and generates signals and activation of neuronal systems and circuits that regulate energy homeostasis. This chapter focuses on how these signals are received and integrated by the central nervous system. [ABSTRACT FROM AUTHOR]