Obesity From Wikipedia, the free encyclopedia Obesity Classification and external resources Silhouettes and waist circumferences

representing normal, overweight, and obese ICD-10 E66. ICD-9 278 OMIM 601665 DiseasesDB 9099 MedlinePlus 003101 eMedicine med/1653 MeSH C23.888.144.699.500 Obesity is a medical condition in which excess body fat has accumulated to the e xtent that it may have an adverse effect on health, leading to reduced life expe ctancy and/or increased health problems.[1][2] Body mass index (BMI), a measurem ent which compares weight and height, defines people as overweight (pre-obese) i f their BMI is between 25 and 30 kg/m2, and obese when it is greater than 30 kg/ m2.[3] Obesity increases the likelihood of various diseases, particularly heart disease , type 2 diabetes, breathing difficulties during sleep, certain types of cancer, and osteoarthritis.[2] Obesity is most commonly caused by a combination of exce ssive food energy intake, lack of physical activity, and genetic susceptibility, although a few cases are caused primarily by genes, endocrine disorders, medica tions or psychiatric illness. Evidence to support the view that some obese peopl e eat little yet gain weight due to a slow metabolism is limited; on average obe se people have a greater energy expenditure than their thin counterparts due to the energy required to maintain an increased body mass.[4][5] Dieting and physical exercise are the mainstays of treatment for obesity. Moreov er, it is important to improve diet quality by reducing the consumption of energ y-dense foods such as those high in fat and sugars, and by increasing the intake of dietary fiber. To supplement this, or in case of failure, anti-obesity drugs may be taken to reduce appetite or inhibit fat absorption. In severe cases, sur gery is performed or an intragastric balloon is placed to reduce stomach volume and/or bowel length, leading to earlier satiation and reduced ability to absorb nutrients from food.[6][7] Obesity is a leading preventable cause of death worldwide, with increasing preva lence in adults and children, and authorities view it as one of the most serious public health problems of the 21st century.[8] Obesity is stigmatized in much o f the modern world (particularly in the Western world), though it was widely per ceived as a symbol of wealth and fertility at other times in history, and still is in some parts of the world.[2][9] Contents [hide] 1 Classification 2 Effects on health 2.1 Mortality 2.2 Morbidity 2.3 Survival paradox 3 Causes 3.1 Diet 3.2 Sedentary lifestyle 3.3 Genetics 3.4 Medical and psychiatric illness 3.5 Social determinants 3.6 Infectious agents 4 Pathophysiology 5 Management 6 Epidemiology

7 Public health 8 Economic impact 9 History and culture 9.1 Etymology 9.2 Historical trends 9.3 The arts 9.4 Size acceptance 10 Childhood obesity 11 In other animals 12 See also 13 Notes 14 References 15 Further reading 16 External links Classification Main article: Classification of obesity Obesity is a medical condition in which excess body fat has accumulated to the e xtent that it may have an adverse effect on health.[1] It is defined by body mas s index (BMI) and further evaluated in terms of fat distribution via the waist hip ratio and total cardiovascular risk factors.[10][11] BMI is closely related to both percentage body fat and total body fat.[12] A "super obese" male with a BMI of 47 kg/m2: weight 146 kg (322 lb), height 177 cm (5 ft 10 in) In children, a healthy weight varies with age and sex. Obesity in children and a dolescents is defined not as an absolute number, but in relation to a historical normal group, such that obesity is a BMI greater than the 95th percentile.[13] The reference data on which these percentiles are based are from 1963 to 1994, a nd thus have not been affected by the recent increases in weight.[14] BMI Classification < 18.5 underweight 18.5 24.9 normal weight 25.0 29.9 overweight 30.0 34.9 class I obesity 35.0 39.9 class II obesity = 40.0 class III obesity BMI is calculated by dividing the subject's mass by the square of his or her hei ght, typically expressed either in metric or US "customary" units: Metric: BMI = kilograms / meters2 US customary and imperial: BMI = lb * 703 / in2 where lb is the subject's weight in pounds and in is the subject's height in inc hes. The most commonly used definitions, established by the World Health Organization (WHO) in 1997 and published in 2000, provide the values listed in the table at right.[3] Some modifications to the WHO definitions have been made by particular bodies. T he surgical literature breaks down "class III" obesity into further categories w hose exact values are still disputed.[15] Any BMI = 35 or 40 is severe obesity A BMI of = 35 or 40 44.9 or 49.9 is morbid obesity A BMI of = 45 or 50 is super obesity As Asian populations develop negative health consequences at a lower BMI than Ca ucasians, some nations have redefined obesity; the Japanese have defined obesity as any BMI greater than 25[16] while China uses a BMI of greater than 28.[17] Effects on health Excessive body weight is associated with various diseases, particularly cardiova scular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain type

s of cancer, and osteoarthritis.[2] As a result, obesity has been found to reduc e life expectancy.[2] Mortality Relative risk of death over 10 years for White men (left) and women (right) who have never smoked in the United States by BMI.[18] Obesity is one of the leading preventable causes of death worldwide.[8][19][20] Large-scale American and European studies have found that mortality risk is lowe st at a BMI of 20 25 kg/m2[18][21] in non-smokers and at 24 27 kg/m2 in current smok ers, with risk increasing along with changes in either direction.[22][23] A BMI above 32 has been associated with a doubled mortality rate among women over a 16 -year period.[24] In the United States obesity is estimated to cause an excess 1 11,909 to 365,000 deaths per year,[2][20] while 1 million (7.7%) of deaths in th e European Union are attributed to excess weight.[25][26] On average, obesity re duces life expectancy by six to seven years:[2][27] a BMI of 30 35 reduces life ex pectancy by two to four years,[21] while severe obesity (BMI > 40) reduces life expectancy by 10 years.[21] Morbidity Main article: Obesity-associated morbidity Obesity increases the risk of many physical and mental conditions. These comorbi dities are most commonly shown in metabolic syndrome,[2] a combination of medica l disorders which includes: diabetes mellitus type 2, high blood pressure, high blood cholesterol, and high triglyceride levels.[28] Complications are either directly caused by obesity or indirectly related throug h mechanisms sharing a common cause such as a poor diet or a sedentary lifestyle . The strength of the link between obesity and specific conditions varies. One o f the strongest is the link with type 2 diabetes. Excess body fat underlies 64% of cases of diabetes in men and 77% of cases in women.[29] Health consequences fall into two broad categories: those attributable to the ef fects of increased fat mass (such as osteoarthritis, obstructive sleep apnea, so cial stigmatization) and those due to the increased number of fat cells (diabete s, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[2][30] In creases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state,[31][32] and a prothrombotic state.[30][33] Medical field Condition Medical field Condition Cardiology ischemic heart disease:[34] angina and myocardial infarction congestive heart failure[2] high blood pressure[2] abnormal cholesterol levels[2] deep vein thrombosis and pulmonary embolism[35] Dermatology stretch marks[36] acanthosis nigricans[36] lymphedema[36] cellulitis[36] hirsutism[36] intertrigo[37] Endocrinology and Reproductive medicine diabetes mellitus[2] polycystic ovarian syndrome[2] menstrual disorders[2] infertility[2][38] complications during pregnancy[2][38] birth defects[2] intrauterine fetal death[38] Gastrointestinal gastroesophageal reflux disease[2][39] fatty liver disease[2]

cholelithiasis (gallstones)[2] Neurology stroke[2] meralgia paresthetica[40] migraines[41] carpal tunnel syndrome[42] dementia[43] idiopathic intracranial hypertension[44] multiple sclerosis[45] Oncology[46] breast, ovarian esophageal, colorectal liver, pancreatic gallbladder, stomach endometrial, cervical prostate, kidney non-Hodgkin's lymphoma, multiple myeloma Psychiatry depression in women[2] social stigmatization[2] Respirology obstructive sleep apnea[2][47] obesity hypoventilation syndrome[2][47] asthma[2][47] increased complications during general anaesthesia[2][5] Rheumatology and Orthopedics gout[48] poor mobility[49] osteoarthritis[2] low back pain[50] Urology and Nephrology erectile dysfunction[51] urinary incontinence[52] chronic renal failure[53] hypogonadism[54] Survival paradox See also: Obesity paradox Although the negative health consequences of obesity in the general population a re well supported by the available evidence, health outcomes in certain subgroup s seem to be improved at an increased BMI, a phenomenon known as the obesity sur vival paradox.[55] The paradox was first described in 1999 in overweight and obe se people undergoing hemodialysis,[55] and has subsequently been found in those with heart failure and peripheral artery disease (PAD).[56] In people with heart failure, those with a BMI between 30.0 34.9 had lower mortali ty than those with a normal weight. This has been attributed to the fact that pe ople often lose weight as they become progressively more ill.[57] Similar findin gs have been made in other types of heart disease. People with class I obesity a nd heart disease do not have greater rates of further heart problems than people of normal weight who also have heart disease. In people with greater degrees of obesity, however, risk of further events is increased.[58][59] Even after cardi ac bypass surgery, no increase in mortality is seen in the overweight and obese. [60] One study found that the improved survival could be explained by the more a ggressive treatment obese people receive after a cardiac event.[61] Another foun d that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD the benefit of obesity no longer exists.[56] Causes At an individual level, a combination of excessive food energy intake and a lack of physical activity is thought to explain most cases of obesity.[62] A limited number of cases are due primarily to genetics, medical reasons, or psychiatric

illness.[63] In contrast, increasing rates of obesity at a societal level are fe lt to be due to an easily accessible and palatable diet,[64] increased reliance on cars, and mechanized manufacturing.[65][66] A 2006 review identified ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) endocrine disruptors (environmental poll utants that interfere with lipid metabolism), (3) decreased variability in ambie nt temperature, (4) decreased rates of smoking, because smoking suppresses appet ite, (5) increased use of medications that can cause weight gain (e.g., atypical antipsychotics), (6) proportional increases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may cause susceptibility to o besity in children), (8) epigenetic risk factors passed on generationally, (9) n atural selection for higher BMI, and (10) assortative mating leading to increase d concentration of obesity risk factors (this would not necessarily increase the number of obese people, but would increase the average population weight).[67] While there is substantial evidence supporting the influence of these mechanisms on the increased prevalence of obesity, the evidence is still inconclusive, and the authors state that these are probably less influential than the ones discus sed in the previous paragraph. Diet Main article: Diet and obesity Map of dietary energy availability per person per day in 1961 (left) and 2001 2003 (right) in kcal/person/day.[68] no data <1600 1600 1800 1800 2000 2000 2200 2200 2400 2400 2600 2600 2800 2800 3000 3000 3200 3200 3400 3400 3600 >3600 Average per capita energy consumption of the world from 1961 to 2002[68] The per capita dietary energy supply varies markedly between different regions a nd countries. It has also changed significantly over time.[68] From the early 19 70s to the late 1990s the average calories available per person per day (the amo unt of food bought) increased in all parts of the world except Eastern Europe. T he United States had the highest availability with 3,654 calories per person in 1996.[68] This increased further in 2003 to 3,754.[68] During the late 1990s Eur opeans had 3,394 calories per person, in the developing areas of Asia there were 2,648 calories per person, and in sub-Saharan Africa people had 2,176 calories per person.[68][69] Total calorie consumption has been found to be related to ob esity.[70] The widespread availability of nutritional guidelines[71] has done little to add ress the problems of overeating and poor dietary choice.[72] From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%.[73] During the same period, an increase occurred in the average amount of food energy consumed . For women, the average increase was 335 calories per day (1,542 calories in 19 71 and 1,877 calories in 2004), while for men the average increase was 168 calor ies per day (2,450 calories in 1971 and 2,618 calories in 2004). Most of this ex tra food energy came from an increase in carbohydrate consumption rather than fa t consumption.[74] The primary sources of these extra carbohydrates are sweetene d beverages, which now account for almost 25 percent of daily food energy in you ng adults in America.[75] Consumption of sweetened drinks is believed to be cont

ributing to the rising rates of obesity.[76][77] As societies become increasingly reliant on energy-dense, big-portions, and fast -food meals, the association between fast-food consumption and obesity becomes m ore concerning.[78] In the United States consumption of fast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.[79] Agricultural policy and techniques in the United States and Europe have led to l ower food prices. In the United States, subsidization of corn, soy, wheat, and r ice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables.[80] Obese people consistently under-report their food consumption as compared to peo ple of normal weight.[81] This is supported both by tests of people carried out in a calorimeter room[82] and by direct observation. Sedentary lifestyle See also: Sedentary lifestyle and Exercise trends A sedentary lifestyle plays a significant role in obesity.[83] Worldwide there h as been a large shift towards less physically demanding work,[84][85][86] and cu rrently at least 60% of the world's population gets insufficient exercise.[85] T his is primarily due to increasing use of mechanized transportation and a greate r prevalence of labor-saving technology in the home.[84][85][86] In children, th ere appear to be declines in levels of physical activity due to less walking and physical education.[87] World trends in active leisure time physical activity a re less clear. The World Health Organization indicates people worldwide are taki ng up less active recreational pursuits, while a study from Finland[88] found an increase and a study from the United States found leisure-time physical activit y has not changed significantly.[89] In both children and adults, there is an association between television viewing time and the risk of obesity.[90][91][92] A 2008 meta-analysis found 63 of 73 st udies (86%) showed an increased rate of childhood obesity with increased media e xposure, with rates increasing proportionally to time spent watching television. [93] Genetics Main article: Genetics of obesity A 1680 painting by Juan Carreno de Miranda of a girl presumed to have Prader-Wil li syndrome[94] Like many other medical conditions, obesity is the result of an interplay betwee n genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when sufficient food energy presen t. As of 2006 more than 41 of these sites have been linked to the development of obesity when a favorable environment is present.[95] People with two copies of the FTO gene (fat mass and obesity associated gene) has been found on average to weigh 3 4 kg more and have a 1.67-fold greater risk of obesity compared to those without the risk allele.[96] The percentage of obesity that can be attributed to genetics varies, depending on the population examined, from 6% to 85%.[97] Obesity is a major feature in several syndromes, such as Prader-Willi syndrome, Bardet-Biedl syndrome, Cohen syndrome, and MOMO syndrome. (The term "non-syndrom ic obesity" is sometimes used to exclude these conditions.)[98] In people with e arly-onset severe obesity (defined by an onset before 10 years of age and body m ass index over three standard deviations above normal), 7% harbor a single point DNA mutation.[99] Studies that have focused upon inheritance patterns rather than upon specific ge nes have found that 80% of the offspring of two obese parents were obese, in con trast to less than 10% of the offspring of two parents who were of normal weight .[100] The thrifty gene hypothesis postulates that certain ethnic groups may be more pr one to obesity in an equivalent environment. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserve s would be more likely survive famine. This tendency to store fat, however, woul

d be maladaptive in societies with stable food supplies.[101] This is the presum ed reason that Pima Indians, who evolved in a desert ecosystem, developed some o f the highest rates of obesity when exposed to a Western lifestyle.[102] Medical and psychiatric illness Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some cong enital or acquired conditions: hypothyroidism, Cushing's syndrome, growth hormon e deficiency,[103] and the eating disorders: binge eating disorder and night eat ing syndrome.[2] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.[104] The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.[105] Certain medications may cause weight gain or changes in body composition; these include insulin, sulfonylureas, thiazolidinediones, atypical antipsychotics, ant idepressants, steroids, certain anticonvulsants (phenytoin and valproate), pizot ifen, and some forms of hormonal contraception.[2] Social determinants Main article: Social determinants of obesity While genetic influences are important to understanding obesity, they cannot exp lain the current dramatic increase seen within specific countries or globally.[1 06] Though it is accepted that energy consumption in excess of energy expenditur e leads to obesity on an individual basis, the cause of the shifts in these two factors on the societal scale is much debated. There are a number of theories as to the cause but most believe it is a combination of various factors. The correlation between social class and BMI varies globally. A review in 1989 f ound that in developed countries women of a high social class were less likely t o be obese. No significant differences were seen among men of different social c lasses. In the developing world, women, men, and children from high social class es had greater rates of obesity.[107] An update of this review carried out in 20 07 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization.[108] Among de veloped countries, levels of adult obesity, and percentage of teenage children w ho are overweight, are correlated with income inequality. A similar relationship is seen between US states: more adults, even in higher social classes, are obes e in more unequal states.[109] Many explanations have been put forth for associations between BMI and social cl ass. It is thought that in developed countries, the wealthy are able to afford m ore nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness. In undeveloped countries the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns.[108] Attitudes toward body mass held by peo ple in one's life may also play a role in obesity. A correlation in BMI changes over time has been found between friends, siblings, and spouses.[110] Stress and perceived low social status appear to increase risk of obesity.[109][111][112] Smoking has a significant effect on an individual's weight. Those who quit smoki ng gain an average of 4.4 kilograms (9.7 lb) for men and 5.0 kilograms (11.0 lb) for women over ten years.[113] However, changing rates of smoking have had litt le effect on the overall rates of obesity.[114] In the United States the number of children a person has is related to their ris k of obesity. A woman's risk increases by 7% per child, while a man's risk incre ases by 4% per child.[115] This could be partly explained by the fact that havin g dependent children decreases physical activity in Western parents.[116] In the developing world urbanization is playing a role in increasing rate of obe sity. In China overall rates of obesity are below 5%; however, in some cities ra tes of obesity are greater than 20%.[117] Malnutrition in early life is believed to play a role in the rising rates of obe sity in the developing world.[118] Endocrine changes that occur during periods o f malnutrition may promote the storage of fat once more food energy becomes avai

lable.[118] Infectious agents See also: Infectobesity The study of the effect of infectious agents on metabolism is still in its early stages. Gut flora has been shown to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the me tabolic potential. This apparent alteration of the metabolic potential is believ ed to confer a greater capacity to harvest energy contributing to obesity. Wheth er these differences are the direct cause or the result of obesity has yet to be determined unequivocally.[119] An association between viruses and obesity has been found in humans and several different animal species. The amount that these associations may have contribute d to the rising rate of obesity is yet to be determined.[120] Pathophysiology

A comparison of a mouse unable to produce leptin thus resulting in obesity (left ) and a normal mouse (right) Flier summarizes the many possible pathophysiological mechanisms involved in the development and maintenance of obesity.[121] This field of research had been al most unapproached until leptin was discovered in 1994. Since this discovery, man y other hormonal mechanisms have been elucidated that participate in the regulat ion of appetite and food intake, storage patterns of adipose tissue, and develop ment of insulin resistance. Since leptin's discovery, ghrelin, insulin, orexin, PYY 3-36, cholecystokinin, adiponectin, as well as many other mediators have bee n studied. The adipokines are mediators produced by adipose tissue; their action is thought to modify many obesity-related diseases. Leptin and ghrelin are considered to be complementary in their influence on appe tite, with ghrelin produced by the stomach modulating short-term appetitive cont rol (i.e. to eat when the stomach is empty and to stop when the stomach is stret ched). Leptin is produced by adipose tissue to signal fat storage reserves in th e body, and mediates long-term appetitive controls (i.e. to eat more when fat st orages are low and less when fat storages are high). Although administration of leptin may be effective in a small subset of obese individuals who are leptin de ficient, most obese individuals are thought to be leptin resistant and have been found to have high levels of leptin.[122] This resistance is thought to explain in part why administration of leptin has not been shown to be effective in supp ressing appetite in most obese people.[121] A graphic depiction of a leptin molecule While leptin and ghrelin are produced peripherally, they control appetite throug h their actions on the central nervous system. In particular, they and other app etite-related hormones act on the hypothalamus, a region of the brain central to the regulation of food intake and energy expenditure. There are several circuit s within the hypothalamus that contribute to its role in integrating appetite, t he melanocortin pathway being the most well understood.[121] The circuit begins with an area of the hypothalamus, the arcuate nucleus, that has outputs to the l ateral hypothalamus (LH) and ventromedial hypothalamus (VMH), the brain's feedin g and satiety centers, respectively.[123] The arcuate nucleus contains two distinct groups of neurons.[121] The first grou p coexpresses neuropeptide Y (NPY) and agouti-related peptide (AgRP) and has sti mulatory inputs to the LH and inhibitory inputs to the VMH. The second group coe xpresses pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated tran script (CART) and has stimulatory inputs to the VMH and inhibitory inputs to the LH. Consequently, NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding. Both groups of arcuate nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP g roup while stimulating the POMC/CART group. Thus a deficiency in leptin signalin

g, either via leptin deficiency or leptin resistance, leads to overfeeding and m ay account for some genetic and acquired forms of obesity.[121] Management Main article: Management of obesity Orlistat (Xenical) the most commonly used medication to treat obesity and sibutr amine (Meridia) a recently withdrawn medication due to cardiovascular side effec ts The main treatment for obesity consists of dieting and physical exercise.[62] Di et programs may produce weight loss over the short term,[124] but maintaining th is weight loss is frequently difficult and often requires making exercise and a lower food energy diet a permanent part of a person's lifestyle.[125][126] Succe ss rates of long-term weight loss maintenance with lifestyle changes are low ran ging from 2 20%.[127] One medication, orlistat (Xenical), is current widely available and approved for long term use. Weight loss however is modest with an average of 2.9 kg (6.4 lb) at 1 to 4 years and there is little information on how these drugs affect longe r-term complications of obesity.[128] It use is associated with high rates of ga strointestinal side effects[128] and concerns have been raised about negative ef fects on the kidneys.[129] The most effective treatment for obesity is bariatric surgery. Surgery for sever e obesity is associated with long-term weight loss and decreased overall mortali ty. One study found a weight loss of between 14% and 25% (depending on the type of procedure performed) at 10 years, and a 29% reduction in all cause mortality when compared to standard weight loss measures.[130] However, due to its cost an d the risk of complications, researchers are searching for other effective yet l ess invasive treatments. Epidemiology Main article: Epidemiology of obesity World obesity prevalence among males (left) and females (right).[131] <5% 5 10% 10 15% 15 20% 20 25% 25 30% 30 35% 35 40% 40 45% 45 50% 50 55% >55% Before the 20th century, obesity was rare;[132] in 1997 the WHO formally recogni zed obesity as a global epidemic.[75] As of 2005 the WHO estimates that at least 400 million adults (9.8%) are obese, with higher rates among women than men.[13 3] The rate of obesity also increases with age at least up to 50 or 60 years old [134] and severe obesity in the United States, Australia, and Canada is increasi ng faster than the overall rate of obesity.[15][135][136] Once considered a problem only of high-income countries, obesity rates are risin g worldwide and affecting both the developed and developing world.[25] These inc reases have been felt most dramatically in urban settings.[133] The only remaini ng region of the world where obesity is not common is sub-Saharan Africa.[2] Public health The World Health Organization (WHO) predicts that overweight and obesity may soo n replace more traditional public health concerns such as undernutrition and inf

ectious diseases as the most significant cause of poor health.[137] Obesity is a public health and policy problem because of its prevalence, costs, and health e ffects.[138] Public health efforts seek to understand and correct the environmen tal factors responsible for the increasing prevalence of obesity in the populati on. Solutions look at changing the factors that cause excess food energy consump tion and inhibit physical activity. Efforts include federally reimbursed meal pr ograms in schools, limiting direct junk food marketing to children,[139] and dec reasing access to sugar-sweetened beverages in schools.[140] When constructing u rban environments, efforts have been made to increase access to parks and to dev elop pedestrian routes.[141] Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelines were published, titled "Clinical Guidelines on t he Identification, Evaluation, and Treatment of Overweight and Obesity in Adults : The Evidence Report".[142] In 2006 the Canadian Obesity Network published the "Canadian Clinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children". This is a comprehensive evidence-based guideli ne to address the management and prevention of overweight and obesity in adults and children.[143] In 2004, the United Kingdom Royal College of Physicians, the Faculty of Public H ealth and the Royal College of Paediatrics and Child Health released the report "Storing up Problems", which highlighted the growing problem of obesity in the U K.[144] The same year, the House of Commons Health Select Committee published it s "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in the UK and possible approaches to the problem.[145] In 2006, the National Institute for Health and Clinical Excellence (NICE) issued a guideline on the diagnosis and management of obesity, as well as policy implicat ions for non-healthcare organizations such as local councils.[146] A 2007 report produced by Sir Derek Wanless for the King's Fund warned that unle ss further action was taken, obesity had the capacity to cripple the National He alth Service financially.[147] In the United States organizations such as the Bi ll Clinton Foundation's Alliance for a Healthier Generation and Action for Healt hy Kids are working to combat childhood obesity. Additionally, the Centers for D isease Control and Prevention co-hosted the first-ever Weight of the Nation Conf erence in 2009 with the goal of focusing national attention on the obesity epide mic.[148] Comprehensive approaches are being looked at to address the rising rates of obes ity. The Obesity Policy Action (OPA) framework divides measure into 'upstream' p olicies, 'midstream' policies, 'downstream' policies. 'Upstream' policies look a t changing society, 'midstream' policies try to alter individuals' behavior to p revent obesity, and 'downstream' policies try to treat currently afflicted peopl e.[149] Economic impact

Services must accommodate obese people with specialist equipment such as much wi der chairs.[150] In addition to its health impacts, obesity leads to many problems including disa dvantages in employment[151][152] and increased business costs. These effects ar e felt by all levels of society from individuals, to corporations, to government s. The estimate range for annual expenditures on diet products is $40 billion to $1 00 billion in the US alone.[153] In 1998, the medical costs attributable to obes ity in the US were $78.5 billion or 9.1% of all medical expenditures,[154][155] while the cost of obesity in Canada was estimated at CA$2 billion in 1997 (2.4% of total health costs).[62] Obesity prevention programs have been found to reduce the cost of treating obesi ty-related disease. However, the longer people live, the more medical costs they incur. Researchers therefore conclude that reducing obesity may improve the pub lic's health, but it is unlikely to reduce overall health spending.[156]

Obesity can lead to social stigmatization and disadvantages in employment.[151] When compared to their normal weight counterparts, obese workers on average have higher rates of absenteeism from work and take more disability leave, thus incr easing costs for employers and decreasing productivity.[157] A study examining D uke University employees found that people with a BMI over 40 filed twice as man y workers' compensation claims as those whose BMI was 18.5 24.9. They also had mor e than 12 times as many lost work days. The most common injuries in this group w ere due to falls and lifting, thus affecting the lower extremities, wrists or ha nds, and backs.[158] The US state of Alabama Employees' Insurance Board approved a controversial plan to charge obese workers $25 per month if they do not take measures to reduce their weight and improve their health. These measures started in January 2010 and apply to those with a BMI of greater than 35 kg/m2 who fail to make improvements in their health after one year.[159] Some research shows that obese people are less likely to be hired for a job and are less likely to be promoted.[160] Obese people are also paid less than their non-obese counterparts for an equivalent job. Obese women on average make 6% les s and obese men make 3% less.[161] Specific industries, such as the airline and food industries, have special conce rns. Due to rising rates of obesity, airlines face higher fuel costs and pressur es to increase seating width.[162] In 2000, the extra weight of obese passengers cost airlines US$275 million.[163] Costs for restaurants are increased by litig ation accusing them of causing obesity.[164] In 2005 the US Congress discussed l egislation to prevent civil law suits against the food industry in relation to o besity; however, it did not become law.[164] History and culture Etymology Obesity is from the Latin obesitas, which means "stout, fat, or plump." Esus is the past participle of edere (to eat), with ob (over) added to it.[165] The Oxfo rd English Dictionary documents its first usage in 1611 by Randle Cotgrave.[166] Historical trends During the Middle Ages and the Renaissance obesity was often seen as a sign of w ealth, and was relatively common among the elite: The Tuscan General Alessandro del Borro, attributed to Charles Mellin, 1645[167] The Greeks were the first to recognize obesity as a medical disorder.[132] Hippo crates wrote that "Corpulence is not only a disease itself, but the harbinger of others".[2] The Indian surgeon Sushruta (6th century BCE) related obesity to di abetes and heart disorders.[168] He recommended physical work to help cure it an d its side effects.[168] For most of human history mankind struggled with food s carcity.[169] Obesity has thus historically been viewed as a sign of wealth and prosperity. It was common among high officials in Europe in the Middle Ages and the Renaissance[167] as well as in Ancient East Asian civilizations.[170] With the onset of the industrial revolution it was realized that the military an d economic might of nations were dependent on both the body size and strength of their soldiers and workers.[75] Increasing the average body mass index from wha t is now considered underweight to what is now the normal range played a signifi cant role in the development of industrialized societies.[75] Height and weight thus both increased through the 19th century in the developed world. During the 20th century, as populations reached their genetic potential for height, weight began increasing much more than height, resulting in obesity.[75] In the 1950s i ncreasing wealth in the developed world decreased child mortality, but as body w eight increased heart and kidney disease became more common.[75][171] During thi s time period insurance companies realized the connection between weight and lif e expectancy and increased premiums for the obese.[2] Many cultures throughout history have viewed obesity as the result of a characte r flaw. The obesus or fat character in Greek comedy was a glutton and figure of mockery. During Christian times food was viewed as a gateway to the sins of slot h and lust.[9] In modern Western culture, excess weight is often regarded as una

ttractive, and obesity is commonly associated with various negative stereotypes. People of all ages can face social stigmatization, and may be targeted by bulli es or shunned by their peers. Obesity is once again a reason for discrimination. [160] Venus of Willendorf created 24,000 22,000 BC Public perceptions in Western society regarding healthy body weight differ from those regarding the weight that is considered ideal and both have changed since the beginning of the 20th century. The weight that is viewed as an ideal has be come lower since the 1920s. This is illustrated by the fact that the average hei ght of Miss America pageant winners increased by 2% from 1922 to 1999, while the ir average weight decreased by 12%.[172] On the other hand, people's views conce rning healthy weight have changed in the opposite direction. In Britain the weig ht at which people considered themselves to be overweight was significantly high er in 2007 than in 1999.[173] These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being n ormal.[173] Obesity is still seen as a sign of wealth and well-being in many parts of Africa . This has become particularly common since the HIV epidemic began.[2] The arts The first sculptural representations of the human body 20,000 35,000 years ago dep ict obese females. Some attribute the Venus figurines to the tendency to emphasi ze fertility while others feel they represent "fatness" in the people of the tim e.[9] Corpulence is, however, absent in both Greek and Roman art, probably in ke eping with their ideals regarding moderation. This continued through much of Chr istian European history, with only those of low socioeconomic status being depic ted as obese[citation needed]. During the Renaissance some of the upper class began flaunting their large size, as can be seen in portraits of Henry the VIII and Alessandro del Borro.[9] Rube ns (1577 1640) regularly depicted full-bodied women in his pictures, from which de rives the term Rubenesque. These women, however, still maintained the "hourglass " shape with its relationship to fertility.[174] During the 19th century, views on obesity changed in the Western world. After centuries of obesity being synony mous with wealth and social status, slimness began to be seen as the desirable s tandard.[9] Size acceptance United States President William Howard Taft was often ridiculed for being overwe ight See also: Fat acceptance movement The principal goal of the fat acceptance movement is to decrease discrimination against people who are overweight and obese.[175][176] However, some in the move ment are also attempting to challenge the established relationship between obesi ty and negative health outcomes.[177] A number of organizations exist that promote the acceptance of obesity. They hav e increased in prominence in the latter half of the 20th century.[178] The US-ba sed National Association to Advance Fat Acceptance (NAAFA) was formed in 1969 an d describes itself as a civil rights organization dedicated to ending size discr imination.[179] However, fat activism remains a marginal movement.[180] The International Size Acceptance Association (ISAA) is a non-governmental organ ization (NGO) which was founded in 1997. It has more of a global orientation and describes its mission as promoting size acceptance and helping to end weight-ba sed discrimination.[181] These groups often argue for the recognition of obesity as a disability under the US Americans With Disabilities Act (ADA). The America n legal system, however, has decided that the potential public health costs exce ed the benefits of extending this anti-discrimination law to cover obesity.[177] Childhood obesity

Main article: Childhood obesity The healthy BMI range varies with the age and sex of the child. Obesity in child ren and adolescents is defined as a BMI greater than the 95th percentile.[13] Th e reference data that these percentiles are based on is from 1963 to 1994 and th us has not been affected by the recent increases in rates of obesity.[14] Childh ood obesity has reached epidemic proportions in 21st century, with rising rates in both the developed and developing world. Rates of obesity in Canadian boys ha ve increased from 11% in 1980s to over 30% in 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children.[182] As with obesity in adults, many different factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believ ed to be the two most important in causing the recent increase in the rates.[183 ] Because childhood obesity often persists into adulthood and is associated with numerous chronic illnesses, children who are obese are often tested for hyperte nsion, diabetes, hyperlipidemia, and fatty liver.[62] Treatments used in childre n are primarily lifestyle interventions and behavioral techniques. In the United States, medications are not FDA approved for use in this age group.[182] In other animals Main article: Obesity in pets Obesity in pets is common in many countries. Rates of overweight and obesity in dogs in the United States range from 23% to 41% with about 5.1% obese.[184] Rate s of obesity in cats was slightly higher at 6.4%.[184] In Australia the rate of obesity among dogs in a veterinary setting has been found to be 7.6%.[185] The r isk of obesity in dogs is related to whether or not their owners are obese; howe ver, there is no similar correlation between cats and their owners.[186] See also Maternal obesity Notes ^ a b WHO 2000 p.6 ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai Haslam DW, James WP (2005). "Obesity". Lancet 366 (9492): 1197 209. doi:10.1016/S 0140-6736(05)67483-1. PMID 16198769. ^ a b WHO 2000 p.9 ^ Kushner, Robert (2007). Treatment of the Obese Patient (Contemporary Endocrino logy). Totowa, NJ: Humana Press. pp. 158. ISBN 1-59745-400-1. Retrieved April 5, 2009. ^ a b Adams JP, Murphy PG (July 2000). "Obesity in anaesthesia and intensive car e". Br J Anaesth 85 (1): 91 108. doi:10.1093/bja/85.1.91. PMID 10927998. ^ NICE 2006 p.10 11 ^ Imaz I, Martnez-Cervell C, Garca-Alvarez EE, Sendra-Gutirrez JM, Gonzlez-Enrquez J (July 2008). "Safety and effectiveness of the intragastric balloon for obesity. A meta-analysis". Obes Surg 18 (7): 841 6. doi:10.1007/s11695-007-9331-8. PMID 184 59025. ^ a b Barness LA, Opitz JM, Gilbert-Barness E (December 2007). "Obesity: genetic , molecular, and environmental aspects". Am. J. Med. Genet. A 143A (24): 3016 34. doi:10.1002/ajmg.a.32035. PMID 18000969. ^ a b c d e Woodhouse R (2008). "Obesity in art: A brief overview". Front Horm R es 36: 271 86. doi:10.1159/000115370. ISBN 9783805584296. PMID 18230908. ^ Sweeting HN (2007). "Measurement and definitions of obesity in childhood and a dolescence: A field guide for the uninitiated". Nutr J 6: 32. doi:10.1186/1475-2 891-6-32. PMC 2164947. PMID 17963490. ^ NHLBI p.xiv ^ Gray DS, Fujioka K (1991). "Use of relative weight and Body Mass Index for the determination of adiposity". J Clin Epidemiol 44 (6): 545 50. doi:10.1016/0895-43 56(91)90218-X. PMID 2037859. ^ a b "Healthy Weight: Assessing Your Weight: BMI: About BMI for Children and Te ens". Center for disease control and prevention. Retrieved April 6, 2009.

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Pool, Robert (2001). Fat: Fighting the Obesity Epidemic. Oxford, UK: Oxford Univ ersity Press. ISBN 0-19-511853-7. External links

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