Introduction
Background
Obesity is a substantial public-health crisis in the United States and in the rest of the developed world. The prevalence is increasing rapidly in numerous developing nations worldwide. This growing rate represents a pandemic that needs urgent attention if its potential morbidity, mortality, and economic tolls are to be avoided. (See image below and Image 1.)
The annual cost of managing obesity in the United States alone amounts to approximately $100 billion, of which approximately $52 billion are direct costs of healthcare. These costs amount to approximately 5.7% of all US health expenditure. The cost of lost productivity due to obesity is approximately $3.9 billion, and another $33 billion is spent annually on weight-loss products and services.
Central nervous system neurocircuitry for satiety and feeding cycles.
Body fat percentage, body mass index, skin thicknesses, and anthropomorphic measures
Obesity represents a state of excess storage of body fat. Although similar, the term overweight is puristically defined as an excess body weight for height. Although men have a body fat percentage of 15-20%, women have approximately 25-30%.1 Because differences in weight among individuals are only partly due to variations in body fat, body weight is a limited, though easily obtained, index of obesity.
The body mass index (BMI), also known as the Quetelet index, is used far more commonly than body fat percentage to define obesity. BMI is closely correlated with the degree of body fat in most settings. BMI = weight/height2, where weight is in kilograms and height is in meters.
The body fat percentage can be estimated by using the Deurenberg equation, as follows: body fat percentage = 1.2(BMI) + 0.23(age) - 10.8(sex) - 5.4, where age is in years and sex is 1 for male and 0 for female. This equation has a standard error of 4% and accounts for approximately 80% of the variation in body fat.
Although the BMI is typically closely correlated with percentage body fat in a curvilinear fashion, some important caveats to its interpretation apply. In mesomorphic (muscular) persons, BMIs that usually indicate overweight or mild obesity may be spurious, whereas in some persons with sarcopenia (especially among persons of Asian descent), a typically normal BMI may conceal underlying excess adiposity characterized by increased percentage fat mass and reduced muscle mass.
In view of these limitations, some authorities advocate a definition of obesity based on percentage body fat. For men, percentage body fat greater than 25% defines obesity, and 21-25% is borderline. For women, over 33% defines obesity, and 31-33% is borderline.
Other indices used to estimate the degree and distribution of obesity include the 4 standard skin thicknesses (ie, subscapular, triceps, biceps, suprailiac) and various anthropometric measures, of which waist and hip circumferences are the most important.
Classifications and definitions of obesity
Although several classifications and definitions for degrees of obesity are accepted, the most widely accepted is the World Health Organization (WHO) criteria based on BMI. Under this convention for adults, grade 1 overweight (commonly and simply called overweight) is a BMI of 25-29.9 kg/m2. Grade 2 overweight (commonly called obesity) is a BMI of 30-39.9 kg/m2. Grade 3 overweight (commonly called severe or morbid obesity) is a BMI greater than or equal to 40 kg/m2.
The surgical literature often uses a different classification to recognize particularly severe obesity. In this setting, a BMI greater than 40 kg/m2 is described as severe obesity, a BMI of 40-50 kg/m2 is termed morbid obesity, and a BMI greater than 50 kg/m2 is termed super obese.
The definition of obesity in children involves BMIs greater than the 85th (commonly used to define overweight) or the 95th (commonly used to define obesity) percentile, respectively, for age-matched and sex-matched control subjects.
Comorbidities associated with obesity
Apart from total body fat mass, accumulating data suggest that regional fat distribution substantially affects the incidence of comorbidities associated with obesity. High abdominal fat content (including visceral and, to a lesser extent, subcutaneous abdominal fat) is strongly correlated with worsened metabolic and clinical consequences of obesity. As a result, android obesity, which is predominantly abdominal, is more predictive of adipose-related comorbidities than gynecoid obesity, which has a relatively peripheral (gluteal) distribution. (See image below and Image 2.)
Comorbidities of obesity.
Waist circumferences greater than 94 cm in men and greater than 80 cm in women and waist-to-hip ratios greater than 0.95 in men and greater than 0.8 in women are the thresholds for significantly increased potential cardiovascular risk. Circumferences of 102 cm in men and 88 cm in women indicate a markedly increased potential risk requiring urgent therapeutic intervention; these are the thresholds used in the Adult Treatment Panel III (ATPIII) definition of the metabolic syndrome.
Obesity is associated with a host of potential comorbidities that significantly increase the potential morbidity and mortality associated with the condition. Although no cause-and-effect relationship is exhaustively demonstrated for all these comorbidities, amelioration of these conditions after substantial weight loss suggests that obesity probably plays an important role in their development.
Relevant anatomy and areas of research
The adipocyte, which is the cellular basis for obesity, is increasingly found to be a complex and metabolically active cell. At present, the adipocyte is being perceived as an endocrine gland with several peptides and metabolites that may be relevant to the control of body weight, and these are being studied intensively. Among the products of the adipocyte involved in complex intermediary metabolism are cytokines, tumor necrosis factor-alpha, interleukin-6, lipotransin, adipocyte lipid-binding protein, acyl-stimulation protein, prostaglandins, adipsin, perilipins, lactate, adiponectin, monobutyrin, and phospholipid transfer protein.
Among critical enzymes involved in adipocyte metabolism are endothelial derived lipoprotein lipase (lipid storage), hormone-sensitive lipase (lipid elaboration and release from adipocyte depots), acyl-coenzyme A (acyl-CoA) synthetases (fatty acid synthesis), and a cascade of enzymes (beta oxidation and fatty acid metabolism). The ongoing flurry of investigation into the intricacies of adipocyte metabolism in the last 5 years not only improved our understanding of the pathogenesis of obesity but also offered several potential targets for therapy.
Another area of active research is investigation of the cues for the differentiation of preadipocytes to adipocytes. With the recognition that this process occurs in white and brown adipose tissue, even in adults, its potential role in the development of obesity and the relapse to obesity after weight loss has become more important than before. Among the identified factors in this process are transcription factors peroxisome proliferator-activated receptors-gamma (PPAR-gamma); retinoid-X receptor ligands; perilipin; adipocyte differentiation-related protein (ADRP); and CCAAT enhancer-binding proteins (C/EBP) alpha, beta, and delta.
Pathophysiology
The pathogenesis of obesity is far more complex than the simple paradigm of an imbalance between energy intake and energy output. Although this concept allows easy conceptualization of the various mechanisms involved in the development of obesity, obesity is far more than the mere result of too much eating and/or too little exercise. However, the prevalence of inactivity in developed countries is considerable and relevant. In the United States, only approximately 22% of adults and 25% of adolescents report notable regular physical activity. Approximately 25% of adults in the United States report no remarkable physical activity during leisure, while approximately 14% of adolescents have similar reports of inactivity. (See image below and Image 3.)
Energy balance equation.
Two major groups of factors with a balance that variably intertwines in the development of obesity are genetics, which is presumed to explain 40-70% of the variance in obesity, and environmental factors. Although the high prevalence of obesity in the children of parents who are obese and the high concordance of obesity in identical twins suggest a substantial genetic component to the pathogenesis of obesity, the secular trends of the last few decades, which have been coincident with changes in dietary habits and activity, also suggest an important role for environmental factors.
Leptin
Friedman and colleagues discovered leptin (from the Greek word leptos, meaning thin) in 1994 and ushered in an explosion of research and a great increase in knowledge about regulation of the human feeding and satiation cycle. Since this discovery, neuromodulation of satiety and hunger with feeding has been found to be far more complex than the old, simplistic model of the ventromedial hypothalamic nucleus and limbic centers of satiety and the feeding centers of the lateral hypothalamus. Leptin is a 16-kD protein produced predominantly in white adipose tissue and, to a lesser extent, in the placenta, skeletal muscle, and stomach fundus in rats. Leptin has a myriad of functions in carbohydrate, bone, and reproductive metabolism that are still being unraveled, but its role in body weight regulation is the main reason it came to prominence.
The major role of leptin in body-weight regulation is to signal satiety to the hypothalamus and, thus, reduce dietary intake and fat storage while modulating energy expenditure and carbohydrate metabolism to prevent further weight gain. Unlike the Ob/Ob mouse model in which this peptide was first characterized, most humans who are obese are not leptin deficient but rather leptin resistant. Therefore, they have elevated circulating levels of leptin.
Lieb et al assayed plasma leptin in 818 elderly participants in the Framingham Heart Study.2 Leptin levels, which were higher in women, were strongly correlated with BMI. On follow-up (mean, 8 y), it was found that congestive heart failure had developed in 129 participants (out of 775 individuals who had been free of congestive heart failure), a first cardiovascular disease event had occurred in 187 participants (out of 532 individuals who had been free of cardiovascular disease), and 391 persons had died. The authors' data indicated that higher circulating leptin levels were associated with a greater risk of congestive heart failure and cardiovascular disease but that leptin did not offer incremental prognostic information beyond BMI.
Although more than 90% of human cases of obesity are polygenic, the recognition of monogenic variants has greatly enhanced our knowledge about the etiopathogenesis of obesity.3
Monogenic models for obesity in humans and experimental animals
Various monogenic models have greatly increased our knowledge about mechanisms of obesity, and they have provided several potential targets for future antiobesity medications.
Proopiomelanocortin (POMC) and alpha–melanocyte-stimulating hormone (alpha-MSH) both act centrally on the melanocortin receptor 4 (MC 4) to reduce dietary intake.4 Genetic defects in POMC production and mutations in the MC4 gene are described as monogenic causes of obesity in humans.5 Of particular interest is that patients with POMC mutations tend to have red hair because of the resultant deficiency in MSH production. Also, because of their diminished levels of adrenocorticotropic hormone (ACTH), they tend to have central adrenal insufficiency. Data suggest that as many as 5% of children who are obese have MC4 or POMC mutations. If confirmed, these would be the most common identifiable genetic defects associated with obesity in humans (band 2p23 for POMC and band 18q21.3 for MC4).
Ob/Ob mice were the prototypical mice that enabled the discovery of leptin. These mice lack the leptin gene and are overweight and hyperphagic. A few humans with a similar genetic defect and similar phenotypic consequences have been identified. This variant of obesity, though minor in the grand scheme of human obesity, is exquisitely sensitive to leptin injection, with reduced dietary intake and profound weight loss. (The involved band is at 7q31.)
Db/Db mice have mutations of the leptin receptor in the hypothalamus. Fa/Fa mice also have leptin-receptor mutations. These mice have early-onset obesity and hyperphagia like the Ob/Ob mice, but they also have normal or elevated leptin levels. Human counterparts of this model are rare; their conditions are associated with hyperphagia, hypogonadotropic hypogonadism, and defective thyrotropin secretion but not associated with hypercortisolism, hyperglycemia, and hypothermia, as occurs in Db/Db mice (involvement at band 1p31). The leptin receptor is one of the cytokine receptor families of receptors and is activated through the Janus kinases/signal transducers and activators of transcription (JAK/STAT) mechanisms.
Prohormone convertase is an enzyme that is critical in protein processing, and it appears to be involved in the conversion of POMC to alpha-MSH. Rare patients identified to have alterations in this enzyme have clinically significant obesity, hypogonadotropic hypogonadism, and central adrenal insufficiency. This is one of the few models of obesity not associated with insulin resistance. (The involved band is 5q15-21.)
PPAR-gamma is a transcription factor that is involved in adipocyte differentiation. All humans with mutations of the receptor (at band 3p25) described so far have severe obesity.
In addition to the monogenic models of obesity mentioned above, genome-wide linkage analyses and microarray technology have revealed a rapidly growing list of potential susceptibility obesity genes. Among those identified that are being actively studied are genes on chromosome arms 2p, 10p, 5p, 11q, and 20q.
In the same line as the evidence that proved Helicobacter pylori as the cause for peptic ulcer disease, evolving data suggest that a notable inflammatory and possibly infective etiology may exist for obesity. Adipose tissue is known to be a repository of various cytokines, especially interleukin-6 and tumor necrosis factor-alpha.
Data have shown that adenovirus 36 infection is associated with obesity in chickens and mice. Other data suggest that, though humans who are not obese have a 5% prevalence of adenovirus 36 infection, humans who are obese have a prevalence of 20-30%.
Frequency
United States
Approximately 100 million adults in the United States are at least overweight or obese. Approximately 35% of women and 31% of men older than 19 years are obese or overweight. The numbers among children are even more imposing than these. The prevalence of obesity in children in the United States has increased markedly between the time of the National Health and Nutrition Examination Survey (NHANES) 2 and 3 trials. Approximately 20-25% of children are either overweight or obese, and the prevalence is even greater than this in some minority groups, including Pima Indians, Mexican Americans, and African Americans. Conservative estimates suggest that the management of obesity costs approximately $100 billion yearly, not including the costs of various commercial dietary and weight-loss programs.
International
The prevalence of obesity worldwide is increasing, particularly in the developed nations of the Northern hemisphere, such as the United States, Canada, and most countries of Europe. Available data from the Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) project suggest that at least 15% of men and 22% of women in Europe are obese.
Similar data now are being reported from many developing countries, particularly in those in Asia and, to a lesser extent, those in Africa. Reports from countries such as Malaysia, Japan, Australia, New Zealand, and China detail an epidemic of obesity in the past 2-3 decades. Data from the Middle Eastern countries of Bahrain, Saudi Arabia, Egypt, Jordan, Tunisia, and Lebanon, among others, indicate this same disturbing trend, with alarming levels of obesity often exceeding 40% and particularly worse in women than in men.
Data from the Caribbean and from South America also highlight similar trends. Although data from Africa on this issue are scant, a clear and distinct secular trend of profoundly increased BMIs is clearly observed when people from Africa immigrate to northwestern hemispheric countries. Comparisons of these indices among Nigerians and Ghanaians residing in their native countries with indices in recent immigrants to the United States show this trend poignantly.
Conservative estimates suggest that as many as 250 million people (approximately 7% of the estimated current world population) are obese. Two- to three-times more people than this are probably overweight. Although socioeconomic class and the prevalence of obesity are negatively correlated in most developed countries, including the United States, this correlation is distinctly reversed in many relatively undeveloped areas, including China, Malaysia, parts of South America, and sub-Saharan Africa.
Mortality/Morbidity
- Data from insurance databases and large prospective cohorts such as findings from the Framingham and NHANES studies clearly indicate that obesity is associated with a substantial increase in morbidity and mortality rates. Although the exact magnitude of the attributable excess in mortality associated with obesity (about 112,000-365,000 excess deaths annually) has been disputed, obesity is indisputably the greatest preventable health-related cause of mortality after cigarette smoking.6
- Some evidence suggests that, if unchecked, trends in obesity in the United States may be associated with overall reduced longevity of the population in the next few years. Data also show that obesity is associated with an increased risk and duration of lifetime disability. Furthermore, obesity in middle age is associated with poor indices of quality of life at old age.
- The mortality data appear to have a U - or J -shaped conformation in relation to weight distribution.7 However, the degree of obesity (generally indicated by the BMI) at which mortality discernibly increases in African Americans and Hispanic Americans than in white Americans; this observation suggests a notable racial spectrum and difference in this effect. The optimal BMI in terms of life expectancy is about 23-25 for whites and 23-30 for blacks. Emerging data suggest that the ideal BMI for Asians is substantially lower than that for Caucasians. For subjects with severe obesity (BMIs >40), life expectancy is reduced by as much as 20 years in men and by about 5 years in women. Coexisting obesity and smoking are associated with even greater risks than these for premature mortality.
- Several factors modulate the morbidity and mortality associated with obesity. They include age of onset and duration of obesity, severity of obesity, amount of central adiposity, other comorbidities, sex, and level of cardiorespiratory fitness.
Race
- Obesity is a cosmopolitan disease that affects all races worldwide. However, certain ethnic and racial groups appear to be particularly predisposed. The Pima Indians of Arizona and other ethnic groups native to North America have a particularly high prevalence of obesity. In addition, Polynesians, Micronesians, Anurans, Maoris of the West and East Indies, African Americans in North America, and the Hispanic populations (both Mexican and Puerto Rican in origin) in North America also have particularly high predispositions to developing obesity.
- Secular trends clearly emphasize the importance of environmental factors (particularly dietary issues) in the development of obesity. In many genetically similar cohorts of the high-risk ethnic and racial groups mentioned above, the prevalence for obesity in their countries of origin might be low, but this rate considerably changes when such groups emigrate to the affluent countries of the Northern hemisphere, where they alter their dietary and activity habits. These findings form the core concept of the thrifty gene hypothesis that Neal and colleagues espoused.
- See also Mortality/Morbidity above.
Sex
- No significant sex difference is reported in the prevalence of obesity.
Age
- The prevalence and age distribution of obesity has substantially changed in the last 2-3 decades.
- Although the prevalence has remained at 30-50% of the adult population in the United States, the prevalence in children has increased to 15-25%.
- As evidenced in secular trends, children and particularly adolescents who are obese have a high probability of growing to be adults who are obese; hence, the bimodal distribution of obesity portends a large-scale obesity epidemic in the next few decades.
Clinical
History
In most patients, the presentation is straightforward, with the patient indicating problems with weight or repeated failure in achieving sustained weight loss. However, in other cases, the subject may present with complications and/or associations of obesity.
- A full history must include a dietary inventory and an analysis of the subject's activity level.
- Screening questions to exclude depression are vital because this may be a consequence or a cause of excessive dietary intake and reduced activity.
- Because almost 30% of patients who are obese have eating disorders, screen for these in the history. The possibility of binging, purging, lack of satiety, food-seeking behavior, and other abnormal feeding habits must be identified because management of these habits is crucial to the success of any weight-management program.
- Also, determine if any of the previously mentioned comorbidities have occurred, and include questions to exclude the possible and rare secondary causes of obesity (see image below and Image 4).
Secondary causes of obesity.
- When asking patients about their history, investigate whether the rest of the patient's family has weight problems, inquire about the patient's expectations, and estimate the patient's level of motivation.
- Comorbidities related to obesity include the following (see also Image 2):
- Cardiovascular - Essential hypertension, coronary artery disease, left ventricular hypertrophy, cor pulmonale, obesity-associated cardiomyopathy, accelerated atherosclerosis, pulmonary hypertension of obesity
- CNS - Stroke, idiopathic intracranial hypertension, meralgia paresthetica
- GI - Gall bladder disease (cholecystitis, cholelithiasis), nonalcoholic steatohepatitis (NASH), fatty liver infiltration, reflux esophagitis
- Respiratory - Obstructive sleep apnea, obesity hypoventilation syndrome (Pickwickian syndrome), increased predisposition to respiratory infections, increased incidence of bronchial asthma
- Malignant - Association with endometrial, prostate, gall bladder, breast, colon, and, possibly, lung cancer
- Psychologic - Social stigmatization, depression
- Orthopedic - Osteoarthritis, coxa vera, slipped capital femoral epiphyses, Blount disease and Legg-Calvé-Perthes disease, chronic lumbago
- Metabolic - Insulin resistance, hyperinsulinemia, type 2 diabetes mellitus, dyslipidemia (characterized by high total cholesterol, high triglycerides, normal or elevated low-density lipoprotein, and low high-density lipoprotein) (See image below and Image 5.)
- Reproductive - Anovulation, early puberty, infertility, hyperandrogenism and polycystic ovaries in women, hypogonadotropic hypogonadism in men
- Obstetric and perinatal - Pregnancy-related hypertension, fetal macrosomia, pelvic dystocia8
- Surgical - Increased surgical risk and postoperative complications, including wound infection, deep venous thrombosis, pulmonary embolism, and postoperative pneumonia
- Pelvic - Stress incontinence
- Cutaneous - Intertrigo (bacterial and/or fungal), acanthosis nigricans, hirsutism, increased risk for cellulitis and carbuncles
- Extremity - Venous varicosities, lower extremity venous and/or lymphatic edema
- Miscellaneous - Reduced mobility, difficulty maintaining personal hygiene
Simplified scheme for the pathophysiology of type 2 diabetes mellitus.
Physical
- In the clinical examination, measure anthropometric parameters and perform the standard, detailed examination required in evaluating people with any chronic multisystemic disorder, such as obesity.
- Waist and hip circumference are useful surrogates in estimating visceral fat. Serial tracking of these measurements helps in estimating the clinical risk over time.
- Neck circumference is predictive of a risk of sleep apnea, and its serial measurement in the individual patient is clinically useful for risk stratification.
- In the skin examination, include a search for hirsutism in women, intertriginous rashes, acanthosis nigricans, and possible contact dermatoses.
- A detailed cardiac and respiratory evaluation is crucial to exclude cardiomegaly and respiratory insufficiency.
- In the abdominal examination, attempt to exclude tender hepatomegaly (which may suggest nonalcoholic steatohepatitis [NASH]) and distinguishing the striae distensae from the pink and broad striae that suggest cortisol excess.
- When examining the extremities, search for joint deformities (eg, coxa vara), evidence of osteoarthrosis, and any pressure ulcerations.
Causes
The etiology of obesity is multifactorial.
- Among the facets to be considered in the development of obesity are the following:
- Metabolic factors
- Genetic factors
- Level of activity
- Behavior
- Endocrine factors
- Race, sex, and age factors
- Ethnic and cultural factors
- Socioeconomic status
- Dietary habits
- Smoking cessation
- Pregnancy and menopause
- Psychologic factors
- History of gestational diabetes
- Lactational history in mothers
- Secondary causes of obesity may include the following (also see Image 4):
- Hypothyroidism
- Cushing syndrome
- Insulinoma
- Hypothalamic obesity
- Polycystic ovarian syndrome
- Genetic syndromes (eg, Prader-Willi syndrome, Alström syndrome, Bardet-Biedl syndrome, Cohen syndrome, Börjeson-Forssman-Lehmann syndrome, Fröhlich syndrome)
- Growth hormone deficiency
- Oral contraceptive use
- Medication-related (eg, phenothiazines, sodium valproate, carbamazepine, tricyclic antidepressants, lithium, glucocorticoids, megestrol acetate, thiazolidinediones, sulphonylureas, insulin, adrenergic antagonists, serotonin antagonists [especially cyproheptadine])
- Eating disorders (especially binge-eating disorder, bulimia nervosa, night-eating disorder)
- Hypogonadism
- Pseudohypoparathyroidism
- Obesity related to tube feeding
More on Obesity |
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References
Gallagher D, Heymsfield SB, Heo M, et al. Healthy percentage body fat ranges: an approach for developing guidelines based on body mass index. Am J Clin Nutr. Sep 2000;72(3):694-701.
[Best Evidence] Lieb W, Sullivan LM, Harris TB, et al. Plasma leptin levels and incidence of heart failure, cardiovascular disease, and total mortality in elderly individuals. Diabetes Care. Apr 2009;32(4):612-6. [Medline].
Reinehr T, Kleber M, de Sousa G, et al. Leptin concentrations are a predictor of overweight reduction in a lifestyle intervention. Int J Pediatr Obes. May 13 2009;1-9. [Medline].
Cummings DE, Schwartz MW. Melanocortins and body weight: a tale of two receptors. Nat Genet. Sep 2000;26(1):8-9. [Medline].
Vaisse C, Clement K, Durand E. Melanocortin-4 receptor mutations are a frequent and heterogeneous cause of morbid obesity. J Clin Invest. Jul 2000;106(2):253-62. [Medline].
Allison DB, Fontaine KR, Manson JE. Annual deaths attributable to obesity in the United States. JAMA. Oct 27 1999;282(16):1530-8. [Medline].
Flegal KM, Graubard BI, Williamson DF, et al. Excess deaths associated with underweight, overweight, and obesity. JAMA. Apr 20 2005;293(15):1861-7. [Medline].
Galtier-Dereure F, Boegner C, Bringer J. Obesity and pregnancy: complications and cost. Am J Clin Nutr. May 2000;71(5 Suppl):1242S-8S. [Medline].
[Best Evidence] Stolley MR, Fitzgibbon ML, Schiffer L, et al. Obesity reduction black intervention trial (ORBIT): six-month results. Obesity (Silver Spring). Jan 2009;17(1):100-6. [Medline].
Maffeis C. Childhood obesity: the genetic-environmental interface. Baillieres Best Pract Res Clin Endocrinol Metab. Apr 1999;13(1):31-46. [Medline].
Proimos J, Sawyer S. Obesity in childhood and adolescence. Aust Fam Physician. Apr 2000;29(4):321-7. [Medline].
Harsha DW, Bray GA. Body composition and childhood obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):871-85. [Medline].
Dansinger ML, Gleason JA, Griffith JL, et al. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA. Jan 5 2005;293(1):43-53.
Goldfield GS, Lorello C, Doucet E. Methylphenidate reduces energy intake and dietary fat intake in adults: a mechanism of reduced reinforcing value of food?. Am J Clin Nutr. Aug 2007;86(2):308-15. [Medline].
Grudell AB, Sweetser S, Camilleri M, et al. A controlled pharmacogenetic trial of sibutramine on weight loss and body composition in obese or overweight adults. Gastroenterology. Oct 2008;135(4):1142-54. [Medline].
Heck AM, Yanovski JA, Calis KA. Orlistat, a new lipase inhibitor for the management of obesity. Pharmacotherapy. Mar 2000;20(3):270-9. [Medline].
Gadde KM, Xiong GL. Bupropion for weight reduction. Expert Rev Neurother. Jan 2007;7(1):17-24. [Medline].
Rosenstock J, Hollander P, Gadde KM, et al. A randomized, double-blind, placebo-controlled, multicenter study to assess the efficacy and safety of topiramate controlled release in the treatment of obese type 2 diabetic patients. Diabetes Care. Jun 2007;30(6):1480-6. [Medline].
Black SC. Cannabinoid receptor antagonists and obesity. Curr Opin Investig Drugs. Apr 2004;5(4):389-94.
Van Gaal LF, Rissanen AM, Scheen AJ, et al. Effects of the cannabinoid-1 receptor blocker rimonabant on weight reduction and cardiovascular risk factors in overweight patients: 1-year experience from the RIO-Europe study. Lancet. Apr 16-22 2005;365(9468):1389-97.
Cox SL. Rimonabant hydrochloride: an investigational agent for the management of cardiovascular risk factors. Drugs Today (Barc). Aug 2005;41(8):499-508.
Fernandez JR, Allison DB. Rimonabant Sanofi-Synthelabo. Curr Opin Investig Drugs. Apr 2004;5(4):430-5.
Desilets AR, Dhakal-Karki S, Dunican KC. Role of metformin for weight management in patients without type 2 diabetes. Ann Pharmacother. Jun 2008;42(6):817-26. [Medline].
Gadde KM, Franciscy DM, Wagner HR 2nd, Krishnan KR. Zonisamide for weight loss in obese adults: a randomized controlled trial. JAMA. Apr 9 2003;289(14):1820-5.
Lustig RH, Hinds PS, Ringwald-Smith K, et al. Octreotide therapy of pediatric hypothalamic obesity: a double-blind, placebo-controlled trial. J Clin Endocrinol Metab. Jun 2003;88(6):2586-92.
Batterham RL, Cohen MA, Ellis SM, et al. Inhibition of food intake in obese subjects by peptide YY3-36. N Engl J Med. Sep 4 2003;349(10):941-8.
Boggiano MM, Chandler PC, Oswald KD, et al. PYY3-36 as an anti-obesity drug target. Obes Rev. Nov 2005;6(4):307-22.
Roth CL, Enriori PJ, Harz K, et al. Peptide YY is a regulator of energy homeostasis in obese children before and after weight loss. J Clin Endocrinol Metab. Dec 2005;90(12):6386-91.
Ashley S, Bird DL, Sugden G. Vertical banded gastroplasty for the treatment of morbid obesity. Br J Surg. Nov 1993;80(11):1421-3. [Medline].
Flickinger EG, Pories WJ, Meelheim HD. The Greenville gastric bypass. Progress report at 3 years. Ann Surg. May 1984;199(5):555-62. [Medline].
Sugerman HJ, Kellum JM, Engle KM. Gastric bypass for treating severe obesity. Am J Clin Nutr. Feb 1992;55(2 Suppl):560S-566S. [Medline].
Klein S, Fontana L, Young VL, et al. Absence of an effect of liposuction on insulin action and risk factors for coronary heart disease. N Engl J Med. Jun 17 2004;350(25):2549-57.
Cigaina V. Gastric pacing as therapy for morbid obesity: preliminary results. Obes Surg. 2002/04;12 Suppl 1:12S-16S.
[Best Evidence] Nagao T, Meguro S, Hase T, et al. A catechin-rich beverage improves obesity and blood glucose control in patients with type 2 diabetes. Obesity (Silver Spring). Feb 2009;17(2):310-7. [Medline].
Adelman RD, Restaino IG, Alon US, Blowey DL. Proteinuria and focal segmental glomerulosclerosis in severely obese adolescents. J Pediatr. 138(4):481-5. [Medline].
Kasiske BL, Napier J. Glomerular sclerosis in patients with massive obesity. Am J Nephrol. 1985;5(1):45-50. [Medline].
Jennette JC, Charles L, Grubb W. Glomerulomegaly and focal segmental glomerulosclerosis associated with obesity and sleep-apnea syndrome. Am J Kidney Dis. Dec 1987;10(6):470-2. [Medline].
AHA Nutrition Committee. American Heart Association guidelines for weight management programs for healthy adults. AHA Nutrition Committee. Heart Dis Stroke. Jul-Aug 1994;3(4):221-8. [Medline].
Ahima RS, Flier JS. Leptin. Annu Rev Physiol. 2000;62:413-37. [Medline].
Albrecht RJ, Pories WJ. Surgical intervention for the severely obese. Baillieres Best Pract Res Clin Endocrinol Metab. Apr 1999;13(1):149-72. [Medline].
Alvarez Bartolome M, Borque M, Martinez-Sarmiento J, et al. Peptide YY secretion in morbidly obese patients before and after vertical banded gastroplasty. Obes Surg. Jun 2002;12(3):324-7.
Arner P. Obesity--a genetic disease of adipose tissue?. Br J Nutr. Mar 2000;83 Suppl 1:S9-16. [Medline].
Astrup A. Dietary approaches to reducing body weight. Baillieres Best Pract Res Clin Endocrinol Metab. Apr 1999;13(1):109-20. [Medline].
Atkinson RL. Role of nutrition planning in the treatment for obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):955-64. [Medline].
Atkinson RL, Uwaifo G. In: Goldstein DJ, ed. Combination therapies for obesity. 2nd ed. Totowa, NJ: Humana; 2005:277-91.
Balsiger BM, Kennedy FP, Abu-Lebdeh HS. Prospective evaluation of Roux-en-Y gastric bypass as primary operation for medically complicated obesity. Mayo Clin Proc. Jul 2000;75(7):673-80. [Medline].
Barsh GS, Farooqi IS, O''Rahilly S. Genetics of body-weight regulation. Nature. Apr 6 2000;404(6778):644-51. [Medline].
Bays HE. Current and investigational antiobesity agents and obesity therapeutic treatment targets. Obes Res. Aug 2004;12(8):1197-211.
Blundell JE, Cooling J. Routes to obesity: phenotypes, food choices and activity. Br J Nutr. Mar 2000;83 Suppl 1:S33-8. [Medline].
Bray GA. Clinical evaluation of the obese patient. Baillieres Best Pract Res Clin Endocrinol Metab. Apr 1999;13(1):71-92. [Medline].
Bray GA. Drug therapy of Obesity. UpToDate [serial on CD-ROM]. [Full Text].
Bray GA. Etiology and pathogenesis of obesity. Clin Cornerstone. 1999;2(3):1-15. [Medline].
Bray GA. Etiology of obesity. UpToDate [serial on CD-ROM].
Bray GA. Health hazards of obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):907-19. [Medline].
Bray GA. Surgical therapy of obesity. UpToDate [serial on CD-ROM]. [Full Text].
Bray GA, Greenway FL. Current and potential drugs for treatment of obesity. Endocr Rev. Dec 1999;20(6):805-75. [Medline].
Bray GA, Ryan DH. Clinical evaluation of the overweight patient. Endocrine. Oct 2000;13(2):167-86.
Bray GA, Tartaglia LA. Medicinal strategies in the treatment of obesity. Nature. Apr 6 2000;404(6778):672-7. [Medline].
Campfield LA, Smith FJ. The pathogenesis of obesity. Baillieres Best Pract Res Clin Endocrinol Metab. Apr 1999;13(1):13-30. [Medline].
Chagnon YC, Perusse L, Weisnagel SJ. The human obesity gene map: the 1999 update. Obes Res. Jan 2000;8(1):89-117. [Medline].
Chicurel M. Whatever happened to leptin?. Nature. Apr 6 2000;404(6778):538-40. [Medline].
Crepaldi G, Belfiore F, Bosello O. Italian Consensus Conference--overweight, obesity and health. Int J Obes. Nov 1991;15(11):781-90. [Medline].
Cruz JA. Dietary habits and nutritional status in adolescents over Europe-- Southern Europe. Eur J Clin Nutr. Mar 2000;54 Suppl 1:S29-35. [Medline].
D'Argent J. Gastric electrical stimulation as therapy of morbid obesity: preliminary results from the French study. Obes Surg. Apr 2002;12 Suppl 1:21S-25S.
Daviglus ML, Liu K, Yan LL, et al. Body mass index in middle age and health-related quality of life in older age: the Chicago heart association detection project in industry study. Arch Intern Med. Nov 10 2003;163(20):2448-55.
Deitel M, Shikora SA. Introduction. Gastric pacing for obesity. Obes Surg. Apr 2002;12 Suppl 1:2S.
DeLany JP, Lovejoy JC. Energy expenditure. Endocrinol Metab Clin North Am. Dec 1996;25(4):831-46. [Medline].
Despres JP. The insulin resistance-dyslipidemic syndrome of visceral obesity: effect on patients'' risk. Obes Res. Apr 1998;6 Suppl 1:8S-17S. [Medline].
Egger G, Cameron-Smith D, Stanton R. The effectiveness of popular, non-prescription weight loss supplements. Med J Aust. Dec 6-20 1999;171(11-12):604-8. [Medline].
Expert Panel on the Identification, Evaluation, and Treatment of Overweight Adults. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: executive summary. Expert Panel on the Identification, Evaluation, and Treatment of Overweight in Adults. Am J Clin Nutr. Oct 1998;68(4):899-917. [Medline].
Faloia E, Giacchetti G, Mantero F. Obesity and hypertension. J Endocrinol Invest. Jan 2000;23(1):54-62. [Medline].
Flier JS. Insulin resistance: Definition and clinical spectrum. UpToDate [serial on CD-ROM]. 2000. Available at http://www.uptodate.com.
Fontaine KR, Redden DT, Wang C, et al. Years of life lost due to obesity. JAMA. Jan 8 2003;289(2):187-93.
Foreyt JP, Poston WS 2nd. What is the role of cognitive-behavior therapy in patient management?. Obes Res. Apr 1998;6 Suppl 1:18S-22S. [Medline].
Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med. May 22 2003;348(21):2082-90.
Frayn KN. Visceral fat and insulin resistance--causative or correlative?. Br J Nutr. Mar 2000;83 Suppl 1:S71-7. [Medline].
Friedman JM. Obesity in the new millennium. Nature. Apr 6 2000;404(6778):632-4. [Medline].
Geiselman PJ. Control of food intake. A physiologically complex, motivated behavioral system. Endocrinol Metab Clin North Am. Dec 1996;25(4):815-29. [Medline].
Gidding SS, Leibel RL, Daniels S. Understanding obesity in youth. A statement for healthcare professionals from the Committee on Atherosclerosis and Hypertension in the Young of the Council on Cardiovascular Disease in the Young and the Nutrition Committee, American Heart Association. Circulation. Dec 15 1996;94(12):3383-7. [Medline].
Greenway FL. Surgery for obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):1005-27. [Medline].
Halford JC, Blundell JE. Pharmacology of appetite suppression. Prog Drug Res. 2000;54:25-58. [Medline].
Hill JO. Dealing with obesity as a chronic disease. Obes Res. Apr 1998;6 Suppl 1:34S-38S. [Medline].
Himes JH, Dietz WH. Guidelines for overweight in adolescent preventive services: recommendations from an expert committee. The Expert Committee on Clinical Guidelines for Overweight in Adolescent Preventive Services. Am J Clin Nutr. Feb 1994;59(2):307-16. [Medline].
Institute of Medicine, National Academy. Summary: weighing the options--criteria for evaluating weight- management programs. Committee to Develop Criteria for Evaluating the Outcomes of Approaches to Prevent and Treat Obesity Food and Nutrition Board, Institute of Medicine, National Academy. J Am Diet Assoc. Jan 1995;95(1):96-105. [Medline].
Internation Federation for the Surgery of Obesity. Statement on morbid obesity and its treatment. Obes Surg. Feb 1997;7(1):40-1. [Medline].
Ioannides-Demos LL, Proietto J, McNeil JJ. Pharmacotherapy for obesity. Drugs. 2005;65(10):1391-418.
Jeffery RW, Drewnowski A, Epstein LH. Long-term maintenance of weight loss: current status. Health Psychol. Jan 2000;19(1 Suppl):5-16. [Medline].
Johnston CS, Tjonn SL, Swan PD. High-protein, low-fat diets are effective for weight loss and favorably alter biomarkers in healthy adults. J Nutr. Mar 2004;134(3):586-91.
Kambham N, Markowitz GS, Valeri AM. Obesity-related glomerulopathy: an emerging epidemic. Kidney Int. Apr 2001;59(4):1498-509. [Medline].
Kasiske BL, Crosson JT. Renal disease in patients with massive obesity. Arch Intern Med. Jun 1986;146(6):1105-9. [Medline].
Khaodhiar L, McCowen KC, Blackburn GL. Obesity and its comorbid conditions. Clin Cornerstone. 1999;2(3):17-31. [Medline].
Kopelman PG. Obesity as a medical problem. Nature. Apr 6 2000;404(6778):635-43. [Medline].
Kushner R. Managing the obese patient after bariatric surgery: a case report of severe malnutrition and review of the literature. JPEN J Parenter Enteral Nutr. Mar-Apr 2000;24(2):126-32. [Medline].
Lean ME. Is long-term weight loss possible?. Br J Nutr. Mar 2000;83 Suppl 1:S103-11. [Medline].
Lean ME, Han TS, Seidell JC. Impairment of health and quality of life using new US federal guidelines for the identification of obesity. Arch Intern Med. Apr 26 1999;159(8):837-43. [Medline].
Leiter LA, Abbott D, Campbell NR, et al. Lifestyle modifications to prevent and control hypertension. 2. Recommendations on obesity and weight loss. Canadian Hypertension Society, Canadian Coalition for High Blood Pressure Prevention and Control, Laboratory Centre for Disease Control at Health Canada, Heart and Stroke Foundation of Canada. CMAJ. May 4 1999;160(9 Suppl):S7-12.
Ludwig DS. Dietary glycemic index and obesity. J Nutr. Feb 2000;130(2S Suppl):280S-283S. [Medline].
Madani KA, al-Amoudi NS, Kumosani TA. The state of nutrition in Saudi Arabia. Nutr Health. 2000;14(1):17-31. [Medline].
Maggio CA. Obesity Drug Development Summit. 21-22 July, 2005, Arlington, VA, USA. IDrugs. Sep 2005;8(9):701-3.
Miller-Kovach K, Hermann M, Winick M. The psychological ramifications of weight management. J Womens Health Gend Based Med. May 1999;8(4):477-82. [Medline].
Molarius A, Seidell JC, Sans S. Varying sensitivity of waist action levels to identify subjects with overweight or obesity in 19 populations of the WHO MONICA Project. J Clin Epidemiol. Dec 1999;52(12):1213-24. [Medline].
Molarius A, Seidell JC, Sans S. Waist and hip circumferences, and waist-hip ratio in 19 populations of the WHO MONICA Project. Int J Obes Relat Metab Disord. Feb 1999;23(2):116-25. [Medline].
Montague CT, O''Rahilly S. The perils of portliness: causes and consequences of visceral adiposity. Diabetes. Jun 2000;49(6):883-8. [Medline].
Musaiger AO. The state of nutrition in Bahrain. Nutr Health. 2000;14(1):63-74. [Medline].
Musaiger AO, Miladi SS. Nutrition situation in the Near East Region. Nutr Health. 2000;14(1):3-16. [Medline].
National Institutes of Health. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults--The Evidence Report. National Institutes of Health. Obes Res. Sep 1998;6 Suppl 2:51S-209S. [Medline].
National Institutes of Health. Very low-calorie diets. National Task Force on the Prevention and Treatment of Obesity, National Institutes of Health. JAMA. Aug 25 1993;270(8):967-74. [Medline].
National task force on the prevention and treatment of obesity. Dieting and the development of eating disorders in overweight and obese adults. Arch Intern Med. Sep 25 2000;160(17):2581-9. [Medline].
Nonogaki K. Obesity: autonomic circuits versus feeding. Nat Med. Jul 1999;5(7):742-3. [Medline].
North American Association for the Study of Obesity. Guidelines for the approval and use of drugs to treat obesity. A position paper of The North American Association for the Study of Obesity. Obes Res. Sep 1995;3(5):473-8. [Medline].
Olshansky SJ, Passaro DJ, Hershow RC, et al. A potential decline in life expectancy in the United States in the 21st century. N Engl J Med. Mar 17 2005;352(11):1138-45.
Parizkova J. Dietary habits and nutritional status in adolescents in Central and Eastern Europe. Eur J Clin Nutr. Mar 2000;54 Suppl 1:S36-40. [Medline].
Pastorek JG 2nd. Addressing obesity in medical practice: is weight loss medically beneficial?. Medscape Womens Health. May-Jun 2000;5(3):E3. [Medline].
Peeters A, Bonneux L, Nusselder WJ, et al. Adult obesity and the burden of disability throughout life. Obes Res. Jul 2004;12(7):1145-51.
Pirozzo S, Glasziou P. Weight loss. The role of low fat diets. Aust Fam Physician. Jun 2000;29(6):566-9. [Medline].
Preston SH. Deadweight?--The influence of obesity on longevity. N Engl J Med. Mar 17 2005;352(11):1135-7.
Ramsay TG. Fat cells. Endocrinol Metab Clin North Am. Dec 1996;25(4):847-70. [Medline].
Rippe JM. The case for medical management of obesity: a call for increased physician involvement. Obes Res. Apr 1998;6 Suppl 1:23S-33S. [Medline].
Rolland-Cachera MF, Bellisle F, Deheeger M. Nutritional status and food intake in adolescents living in Western Europe. Eur J Clin Nutr. Mar 2000;54 Suppl 1:S41-6. [Medline].
Samuelson G. Dietary habits and nutritional status in adolescents over Europe. An overview of current studies in the Nordic countries. Eur J Clin Nutr. Mar 2000;54 Suppl 1:S21-8. [Medline].
Sarwer DB, Wadden TA. The treatment of obesity: what''s new, what''s recommended. J Womens Health Gend Based Med. May 1999;8(4):483-93. [Medline].
Schirmer BD. Laparoscopic bariatric surgery. Surg Clin North Am. Aug 2000;80(4):1253-67, vii. [Medline].
Schmitz MK, Jeffery RW. Public health interventions for the prevention and treatment of obesity. Med Clin North Am. Mar 2000;84(2):491-512, viii. [Medline].
Schwartz MW, Woods SC, Porte D Jr. Central nervous system control of food intake. Nature. Apr 6 2000;404(6778):661-71. [Medline].
Seidell JC. Epidemiology: definition and classification of obesity. In: Kopelman PG, Stock M, eds. Clinical Obesity. Oxford, England: Blackwell Science;: 1998:1-17.
Seidell JC. Obesity, insulin resistance and diabetes--a worldwide epidemic. Br J Nutr. Mar 2000;83 Suppl 1:S5-8. [Medline].
Seidell JC. Prevention of obesity: the role of the food industry. Nutr Metab Cardiovasc Dis. Feb 1999;9(1):45-50. [Medline].
Smith SR. The endocrinology of obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):921-42. [Medline].
Stern JS, Hirsch J, Blair SN. Weighing the options: criteria for evaluating weight-management programs. The Committee to Develop Criteria for Evaluating the Outcomes of Approaches to Prevent and Treat Obesity. Obes Res. Nov 1995;3(6):591-604. [Medline].
Sugerman HJ. The epidemic of severe obesity: the value of surgical treatment. Mayo Clin Proc. Jul 2000;75(7):669-72. [Medline].
Summary. Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med. Sep 28 1998;158(17):1855-67. [Medline].
The Atkins diet. Med Lett Drugs Ther. Jun 12 2000;42(1080):52.
Tremblay A. Physical activity and obesity. Baillieres Best Pract Res Clin Endocrinol Metab. Apr 1999;13(1):121-9. [Medline].
Van der Ploeg LH. Obesity: an epidemic in need of therapeutics. Curr Opin Chem Biol. Aug 2000;4(4):452-60. [Medline].
VanItallie TB. Prevalence of obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):887-905. [Medline].
Wadden TA, Sarwer DB, Berkowitz RI. Behavioural treatment of the overweight patient. Baillieres Best Pract Res Clin Endocrinol Metab. Apr 1999;13(1):93-107. [Medline].
West DB. Genetics of obesity in humans and animal models. Endocrinol Metab Clin North Am. Dec 1996;25(4):801-13. [Medline].
Wilding J. Clinical evaluation of anti-obesity drugs. Curr Drug Targets. Apr 2004;5(3):325-32.
Williamson DA, Perrin LA. Behavioral therapy for obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):943-54. [Medline].
Wolf AM. What is the economic case for treating obesity?. Obes Res. Apr 1998;6 Suppl 1:2S-7S. [Medline].
Zachwieja JJ. Exercise as treatment for obesity. Endocrinol Metab Clin North Am. Dec 1996;25(4):965-88. [Medline].
Further Reading
Related eMedicine topics:
Bariatric Surgery
Body Contouring, Abdominoplasty
Laparoscopic Gastric Bypass
Laparoscopic Lap Band Placement
Obesity [Pediatrics: General Medicine]
Obesity-Hypoventilation Syndrome and Pulmonary Consequences of Obesity
Prader-Willi Syndrome
Clinical guidelines:
Adult weight management evidence-based nutrition practice guideline. American Dietetic Association - Professional Association. 2006 May. Various pagings. NGC:006622
American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery medical guidelines for clinical practice for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient. American Association of Clinical Endocrinologists - Medical Specialty Society
American Society for Metabolic and Bariatric Surgery - Professional Association
The Obesity Society - Disease Specific Society. 2008 Jul-Aug. 83 pages. NGC:006716
Pediatric weight management evidence-based nutrition practice guideline. American Dietetic Association - Professional Association. 2007 Jun. Various pagings. NGC:006623
Prevention and treatment of pediatric obesity: an Endocrine Society clinical practice guideline. The Endocrine Society - Disease Specific Society. 2008 Dec. 38 pages. NGC:006944
SAGES guideline for clinical application of laparoscopic bariatric surgery. Society of American Gastrointestinal and Endoscopic Surgeons - Medical Specialty Society. 2003 Jul (revised 2008 Oct). 20 pages. NGC:006413
Screening for obesity in adults: recommendations and rationale. United States Preventive Services Task Force - Independent Expert Panel. 1996 (revised 2003 Dec 2). 13 pages. NGC:003163
Clinical trials:
Evaluating the Transferability of a Successful, Hospital-Based, Childhood Obesity Clinic to Primary Care: a Pilot Study
Investigating the Use of Quercetin on Glucose Absorption in Obesity, and Obesity With Type 2 Diabetes
Mitochondrial Function in Pediatric Obesity
Observational Study of Early Metabolic and Vascular Changes in Obesity (STYJOBS)
Keywords
obesity, weight loss, diet, BMI, overweight, type 2 diabetes, obese, gastric bypass, body mass index, weight loss surgery, weight control, childhood obesity, bariatric surgery, insulin resistance, leptin, over weight, overeating, child obesity, gastric bypass surgery, hypertension, obesity children, obesity in children, obesity America, obesity surgery, adipose tissue, causes of obesity, obesity treatment, adipocyte, adiponectin, increased BMI, excess body fat, excess adiposity, increased body mass index, Quetelet index, POMC, MC4, satiety, weight loss, weight gain, severe obesity, morbid obesity, super obese, body weight, percentage body fat, fat distribution, android obesity, gynecoid obesity, waist circumference, Atkinsdiet, South Beach diet
