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15/05/15 21:19 Obesity - Wikipedia, the free encyclopedia Página 1 de 33 http://en.wikipedia.org/wiki/Obesity Obesity Silhouettes and waist circumferences representing normal, overweight, and obese Classification and external resources ICD-10 E66 (http://apps.who.int/classifications/icd10/browse/2015/en#/E66) ICD-9 278 (http://www.icd9data.com/getICD9Code.ashx?icd9=278) OMIM 601665 (http://omim.org/entry/601665) DiseasesDB 9099 (http://www.diseasesdatabase.com/ddb9099.htm) MedlinePlus 007297 (http://www.nlm.nih.gov/medlineplus/ency/article/007297.htm) eMedicine med/1653 (http://www.emedicine.com/med/topic1653.htm) MeSH C23.888.144.699.500 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi? mode=&term=Obesity&field=entry#TreeC23.888.144.699.500) Obesity From Wikipedia, the free encyclopedia Obesity is a medical condition in which excess body fat has accumulated to the extent that it may have a negative effect on health, leading to reduced life expectancy and/or increased health problems. [1][2] In Western countries, people are considered obese when their body mass index (BMI), [3] a measurement obtained by dividing a person's weight by the square of the person's height, exceeds 30 kg/m 2 , with the range 25-30 kg/m 2 defined as overweight. Some East Asian countries use stricter criteria. Obesity increases the likelihood of various diseases, particularly heart disease, type 2 diabetes, obstructive sleep apnea, certain types of cancer, and osteoarthritis. [2] Obesity is most commonly caused by a combination of excessive food energy intake, lack of physical activity, and genetic susceptibility, although a few cases are caused primarily by genes, endocrine disorders, medications, or psychiatric illness. Evidence to support the view that some obese people eat little yet gain weight due to a slow metabolism is limited. On average, obese 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 exercising are the main treatments for obesity. Diet quality can be improved by reducing the consumption of energy-dense foods, such as those high in fat and sugars, and by increasing the intake of dietary fiber. With a suitable diet, anti-obesity drugs may be taken to reduce appetite or decrease fat absorption. If diet, exercise, and medication are not effective, a gastric balloon may assist with weight loss, or surgery may be performed to reduce stomach volume and/or bowel length, leading to feeling full earlier and a reduced ability to absorb nutrients from food. [6][7]

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Página 1 de 33http://en.wikipedia.org/wiki/Obesity

Obesity

Silhouettes and waist circumferences representing normal, overweight, andobese

Classification and external resources

ICD-10 E66(http://apps.who.int/classifications/icd10/browse/2015/en#/E66)

ICD-9 278 (http://www.icd9data.com/getICD9Code.ashx?icd9=278)

OMIM 601665 (http://omim.org/entry/601665)

DiseasesDB 9099 (http://www.diseasesdatabase.com/ddb9099.htm)

MedlinePlus 007297(http://www.nlm.nih.gov/medlineplus/ency/article/007297.htm)

eMedicine med/1653 (http://www.emedicine.com/med/topic1653.htm)

MeSH C23.888.144.699.500(https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?mode=&term=Obesity&field=entry#TreeC23.888.144.699.500)

ObesityFrom Wikipedia, the free encyclopedia

Obesity is a medical condition inwhich excess body fat has accumulatedto the extent that it may have anegative effect on health, leading toreduced life expectancy and/orincreased health problems.[1][2] InWestern countries, people areconsidered obese when their bodymass index (BMI),[3] a measurementobtained by dividing a person's weightby the square of the person's height,exceeds 30 kg/m2, with the range25-30 kg/m2 defined as overweight.Some East Asian countries use strictercriteria.

Obesity increases the likelihood ofvarious diseases, particularly heartdisease, type 2 diabetes, obstructivesleep apnea, certain types of cancer,and osteoarthritis.[2] Obesity is mostcommonly caused by a combination ofexcessive food energy intake, lack ofphysical activity, and geneticsusceptibility, although a few cases arecaused primarily by genes, endocrinedisorders, medications, or psychiatricillness. Evidence to support the viewthat some obese people eat little yetgain weight due to a slow metabolismis limited. On average, obese people have a greater energy expenditure than their thin counterparts due to theenergy required to maintain an increased body mass.[4][5]

Dieting and exercising are the main treatments for obesity. Diet quality can be improved by reducing theconsumption of energy-dense foods, such as those high in fat and sugars, and by increasing the intake of dietaryfiber. With a suitable diet, anti-obesity drugs may be taken to reduce appetite or decrease fat absorption. If diet,exercise, and medication are not effective, a gastric balloon may assist with weight loss, or surgery may beperformed to reduce stomach volume and/or bowel length, leading to feeling full earlier and a reduced ability toabsorb nutrients from food.[6][7]

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Obesity is a leading preventable cause of death worldwide, with increasing rates in adults and children.Authorities view it as one of the most serious public health problems of the 21st century.[8] Obesity isstigmatized in much of the modern world (particularly in the Western world), though it was widely seen as asymbol of wealth and fertility at other times in history and still is in some parts of the world.[2][9] In 2013, theAmerican Medical Association classified obesity as a disease.[10][11]

Contents1 Classification2 Effects on health

2.1 Mortality2.2 Morbidity2.3 Survival paradox

3 Causes3.1 Diet3.2 Sedentary lifestyle3.3 Genetics3.4 Other illnesses3.5 Social determinants3.6 Infectious agents

4 Pathophysiology5 Public health6 Management7 Epidemiology8 History

8.1 Etymology8.2 Historical attitudes8.3 The arts

9 Society and culture9.1 Economic impact9.2 Size acceptance

10 Childhood obesity11 Other animals12 Notes13 Further reading

ClassificationObesity is a medical condition in which excess body fat has accumulated to the extent that it may have anadverse effect on health.[1] It is defined by body mass index (BMI) and further evaluated in terms of fatdistribution via the waist–hip ratio and total cardiovascular risk factors.[12][13] BMI is closely related to bothpercentage body fat and total body fat.[14]

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A "super obese" male with a BMI of47 kg/m2: weight 146 kg (322 lb),height 177 cm (5 ft 10 in)

BMI (kg/m2) Classification[17]

from up to18.5 underweight

18.5 25.0 normal weight25.0 30.0 overweight30.0 35.0 class I obesity35.0 40.0 class II obesity40.0 class III obesity

In children, a healthy weight varies with age and sex. Obesity in children and adolescents is defined not as anabsolute number but in relation to a historical normal group, such that obesity is a BMI greater than the95th percentile.[15] The reference data on which these percentiles were based date from 1963 to 1994, and thushave not been affected by the recent increases in weight.[16]

BMI is defined as the subject'sweight divided by the square oftheir height and is calculated asfollows.

,

where m and h are thesubject's weight and heightrespectively.

BMI is usually expressed inkilograms per square metre,resulting when weight is measured in kilograms and height in metres. To convert from pounds per square inchmultiply by 703 (kg/m2)/(lb/sq in).[18]

The most commonly used definitions, established by the World Health Organization (WHO) in 1997 andpublished in 2000, provide the values listed in the table at right.[3]

Some modifications to the WHO definitions have been made by particular bodies. The surgical literature breaksdown "class III" obesity into further categories whose exact values are still disputed.[19]

Any BMI ≥ 35 or 40 kg/m2 is severe obesity.A BMI of ≥ 35 kg/m2 and experiencing obesity-related health conditions or ≥40–44.9 kg/m2 is morbidobesity.A BMI of ≥ 45 or 50 kg/m2 is super obesity.

As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nationshave redefined obesity; the Japanese have defined obesity as any BMI greater than 25 kg/m2[20] while Chinauses a BMI of greater than 28 kg/m2.[21]

Effects on healthExcessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetesmellitus type 2, obstructive sleep apnea, certain types of cancer, osteoarthritis[2] and asthma.[2][22] As a result,obesity has been found to reduce life expectancy.[2]

Mortality

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Relative risk of death over 10 years for white men (left) and women(right) who have never smoked in the United States by BMI.[23]

Obesity is one of the leading preventablecauses of death worldwide.[8][24][25] Large-scale American and European studies havefound that mortality risk is lowest at a BMIof 20–25 kg/m2[23][26] in non-smokers andat 24–27 kg/m2 in current smokers, withrisk increasing along with changes in eitherdirection.[27][28] In Asians risk begins toincrease between 22–25 kg/m2.[29] A BMIabove 32 kg/m2 has been associated with adoubled mortality rate among women overa 16-year period.[30] In the United States obesity is estimated to cause 111,909 to 365,000 deaths per year,[2][25]

while 1 million (7.7%) of deaths in Europe are attributed to excess weight.[31][32] On average, obesity reduceslife expectancy by six to seven years,[2][33] a BMI of 30–35 kg/m2 reduces life expectancy by two tofour years,[26] while severe obesity (BMI > 40 kg/m2) reduces life expectancy by ten years.[26]

Morbidity

Obesity increases the risk of many physical and mental conditions. These comorbidities are most commonlyshown in metabolic syndrome,[2] a combination of medical disorders which includes: diabetes mellitus type 2,high blood pressure, high blood cholesterol, and high triglyceride levels.[34]

Complications are either directly caused by obesity or indirectly related through mechanisms sharing a commoncause such as a poor diet or a sedentary lifestyle. The strength of the link between obesity and specificconditions varies. One of the strongest is the link with type 2 diabetes. Excess body fat underlies 64% of casesof diabetes in men and 77% of cases in women.[35]

Health consequences fall into two broad categories: those attributable to the effects of increased fat mass (suchas osteoarthritis, obstructive sleep apnea, social stigmatization) and those due to the increased number of fatcells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[2][36] Increases in body fatalter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates aproinflammatory state,[37][38] and a prothrombotic state.[36][39]

Medical field Condition Medical field Condition

Cardiology

ischemic heart disease:[40] anginaand myocardial infarctioncongestive heart failure[2]

high blood pressure[2]

abnormal cholesterol levels[2]

deep vein thrombosis and pulmonary

Dermatology

stretch marks[42]

acanthosis nigricans[42]

lymphedema[42]

cellulitis[42]

hirsutism[42]

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embolism[41] intertrigo[43]

EndocrinologyandReproductivemedicine

diabetes mellitus[2]

polycystic ovarian syndrome[2]

menstrual disorders[2]

infertility[2][44]

complications duringpregnancy[2][44]

birth defects[2]

intrauterine fetal death[44]

Gastrointestinal

gastroesophageal refluxdisease[2][45]

fatty liver disease[2]

cholelithiasis(gallstones)[2]

Neurology

stroke[2]

meralgia paresthetica[46]

migraines[47]

carpal tunnel syndrome[48]

dementia[49]

idiopathic intracranialhypertension[50]

multiple sclerosis[51]

Oncology[52]

esophagealcolorectalpancreaticgallbladder,endometrialkidneyLeukemiamalignant melanoma

Psychiatry depression in women[2]

social stigmatization[2] Respirology

obstructive sleepapnea[2][22]

obesity hypoventilationsyndrome[2][22]

asthma[2][22]

increased complicationsduring generalanaesthesia[2][5]

RheumatologyandOrthopedics

gout[53]

poor mobility[54]

osteoarthritis[2]

low back pain[55]

Urology andNephrology

erectile dysfunction[56]

urinary incontinence[57]

chronic renal failure[58]

hypogonadism[59]

buried penis[60]

Survival paradox

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Although the negative health consequences of obesity in the general population are well supported by theavailable evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, aphenomenon known as the obesity survival paradox.[61] The paradox was first described in 1999 in overweightand obese people undergoing hemodialysis,[61] and has subsequently been found in those with heart failure andperipheral artery disease (PAD).[62]

In people with heart failure, those with a BMI between 30.0 and 34.9 had lower mortality than those with anormal weight. This has been attributed to the fact that people often lose weight as they become progressivelymore ill.[63] Similar findings have been made in other types of heart disease. People with class I obesity andheart disease do not have greater rates of further heart problems than people of normal weight who also haveheart disease. In people with greater degrees of obesity, however, the risk of further cardiovascular events isincreased.[64][65] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight andobese.[66] One study found that the improved survival could be explained by the more aggressive treatmentobese people receive after a cardiac event.[67] Another found that if one takes into account chronic obstructivepulmonary disease (COPD) in those with PAD, the benefit of obesity no longer exists.[62]

CausesAt an individual level, a combination of excessive food energy intake and a lack of physical activity is thoughtto explain most cases of obesity.[68] A limited number of cases are due primarily to genetics, medical reasons, orpsychiatric illness.[69] In contrast, increasing rates of obesity at a societal level are felt to be due to an easilyaccessible and palatable diet,[70] increased reliance on cars, and mechanized manufacturing.[71][72]

A 2006 review identified ten other possible contributors to the recent increase of obesity: (1) insufficient sleep,(2) endocrine disruptors (environmental pollutants that interfere with lipid metabolism), (3) decreasedvariability in ambient temperature, (4) decreased rates of smoking, because smoking suppresses appetite, (5)increased use of medications that can cause weight gain (e.g., atypical antipsychotics), (6) proportionalincreases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may causesusceptibility to obesity in children), (8) epigenetic risk factors passed on generationally, (9) natural selectionfor higher BMI, and (10) assortative mating leading to increased concentration of obesity risk factors (thiswould increase the number of obese people by increasing population variance in weight).[73] While there issubstantial evidence supporting the influence of these mechanisms on the increased prevalence of obesity, theevidence is still inconclusive, and the authors state that these are probably less influential than the onesdiscussed in the previous paragraph.

Diet

Dietary energy supply per capita varies markedly between different regions and countries. It has also changedsignificantly over time.[74] From the early 1970s to the late 1990s the average food energy available per personper day (the amount of food bought) increased in all parts of the world except Eastern Europe. The UnitedStates had the highest availability with 3,654 calories (15,290 kJ) per person in 1996.[74] This increased further

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1961 2001–03

Map of dietary energy availability per person per day in 1961 (left) and2001–2003 (right)[74] Calories per person per day (kilojoules perperson per day)

no data

<1,600 (<6,700)

1,600–1,800 (6,700–7,500)

1,800–2,000 (7,500–8,400)

2,000–2,200 (8,400–9,200)

2,200–2,400 (9,200–10,000)

2,400–2,600 (10,000–10,900)

2,600–2,800 (10,900–11,700)

2,800–3,000 (11,700–12,600)

3,000–3,200 (12,600–13,400)

3,200–3,400 (13,400–14,200)

3,400–3,600 (14,200–15,100)

>3,600 (>15,100)

Average per capita energyconsumption of the world from 1961to 2002[74]

in 2003 to 3,754 calories (15,710 kJ).[74]

During the late 1990s Europeans had 3,394calories (14,200 kJ) per person, in thedeveloping areas of Asia there were 2,648calories (11,080 kJ) per person, and in sub-Saharan Africa people had 2,176 calories(9,100 kJ) per person.[74][75] Total foodenergy consumption has been found to berelated to obesity.[76]

The widespread availability of nutritionalguidelines[77] has done little to address theproblems of overeating and poor dietarychoice.[78] From 1971 to 2000, obesityrates in the United States increased from14.5% to 30.9%.[79] During the sameperiod, an increase occurred in the averageamount of food energy consumed. Forwomen, the average increase was 335calories (1,400 kJ) per day (1,542 calories (6,450 kJ) in 1971 and 1,877calories (7,850 kJ) in 2004), while for men the average increase was 168calories (700 kJ) per day (2,450 calories (10,300 kJ) in 1971 and 2,618calories (10,950 kJ) in 2004). Most of this extra food energy came froman increase in carbohydrate consumption rather than fatconsumption.[80] The primary sources of these extra carbohydrates aresweetened beverages, which now account for almost 25 percent of dailyfood energy in young adults in America,[81] and potato chips.[82]

Consumption of sweetened drinks such as soft drinks, fruit drinks, icedtea, and energy and vitamin water drinks is believed to be contributing tothe rising rates of obesity[83][84] and to an increased risk of metabolicsyndrome and type 2 diabetes.[85]

As societies become increasingly reliant on energy-dense, big-portions, and fast-food meals, the associationbetween fast-food consumption and obesity becomes more concerning.[86] In the United States consumption offast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.[87]

Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the UnitedStates, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources ofprocessed food cheap compared to fruits and vegetables.[88] Calorie count laws and nutrition facts labelsattempt to steer people toward making healthier food choices, including awareness of how much food energy isbeing consumed.

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A 1680 painting by JuanCarreno de Miranda of a girlpresumed to have Prader–Willi syndrome[102]

Obese people consistently under-report their food consumption as compared to people of normal weight.[89]

This is supported both by tests of people carried out in a calorimeter room[90] and by direct observation.

Sedentary lifestyle

A sedentary lifestyle plays a significant role in obesity.[91] Worldwide there has been a large shift towards lessphysically demanding work,[92][93][94] and currently at least 30% of the world's population gets insufficientexercise.[93] This is primarily due to increasing use of mechanized transportation and a greater prevalence oflabor-saving technology in the home.[92][93][94] In children, there appear to be declines in levels of physicalactivity due to less walking and physical education.[95] World trends in active leisure time physical activity areless clear. The World Health Organization indicates people worldwide are taking up less active recreationalpursuits, while a study from Finland[96] found an increase and a study from the United States found leisure-timephysical activity has not changed significantly.[97]

In both children and adults, there is an association between television viewing time and the risk ofobesity.[98][99][100] A review found 63 of 73 studies (86%) showed an increased rate of childhood obesity withincreased media exposure, with rates increasing proportionally to time spent watching television.[101]

Genetics

Like many other medical conditions, obesity is the result of an interplaybetween genetic and environmental factors. Polymorphisms in various genescontrolling appetite and metabolism predispose to obesity when sufficient foodenergy is present. As of 2006, more than 41 of these sites on the human genomehave been linked to the development of obesity when a favorable environment ispresent.[103] People with two copies of the FTO gene (fat mass and obesityassociated gene) have been found on average to weigh 3–4 kg more and have a1.67-fold greater risk of obesity compared with those without the risk allele.[104]

The differences in BMI between people that are due to genetics variesdepending on the population examined from 6% to 85%.[105]

Obesity is a major feature in several syndromes, such as Prader–Willi syndrome,Bardet–Biedl syndrome, Cohen syndrome, and MOMO syndrome. (The term"non-syndromic obesity" is sometimes used to exclude these conditions.)[106] Inpeople with early-onset severe obesity (defined by an onset before 10 years ofage and body mass index over three standard deviations above normal), 7%harbor a single point DNA mutation.[107]

Studies that have focused on inheritance patterns rather than on specific geneshave found that 80% of the offspring of two obese parents were also obese, in contrast to less than 10% of theoffspring of two parents who were of normal weight.[108] Different people exposed to the same environment

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The disease scroll (Yamai no soshi,late 12th century) depicts a womanmoneylender with obesity, considereda disease of the rich.

have different risks of obesity due to their underlying genetics.[109]

The thrifty gene hypothesis postulates that, due to dietary scarcity during human evolution, people are prone toobesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would beadvantageous during times of varying food availability, and individuals with greater adipose reserves would bemore likely to survive famine. This tendency to store fat, however, would be maladaptive in societies withstable food supplies.[110] This theory has received various criticisms, and other evolutionarily-based theoriessuch as the drifty gene hypothesis and the thrifty phenotype hypothesis have also been proposed.[111][112]

Other illnesses

Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk ofobesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as wellas some congenital or acquired conditions: hypothyroidism, Cushing's syndrome, growth hormonedeficiency,[113] and the eating disorders: binge eating disorder and night eating syndrome.[2] However, obesityis not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.[114]

The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons withoutpsychiatric disorders.[115]

Certain medications may cause weight gain or changes in body composition; these include insulin,sulfonylureas, thiazolidinediones, atypical antipsychotics, antidepressants, steroids, certain anticonvulsants(phenytoin and valproate), pizotifen, and some forms of hormonal contraception.[2]

Social determinants

While genetic influences are important to understanding obesity, theycannot explain the current dramatic increase seen within specificcountries or globally.[116] Though it is accepted that energy consumptionin excess of energy expenditure leads to obesity on an individual basis,the cause of the shifts in these two factors on the societal scale is muchdebated. There are a number of theories as to the cause but most believeit is a combination of various factors.

The correlation between social class and BMI varies globally. A reviewin 1989 found that in developed countries women of a high social classwere less likely to be obese. No significant differences were seen amongmen of different social classes. In the developing world, women, men,and children from high social classes had greater rates of obesity.[117]

An update of this review carried out in 2007 found the samerelationships, but they were weaker. The decrease in strength ofcorrelation was felt to be due to the effects of globalization.[118] Amongdeveloped countries, levels of adult obesity, and percentage of teenage

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children who are overweight, are correlated with income inequality. A similar relationship is seen among USstates: more adults, even in higher social classes, are obese in more unequal states.[119]

Many explanations have been put forth for associations between BMI and social class. It is thought that indeveloped countries, the wealthy are able to afford more nutritious food, they are under greater social pressureto remain slim, and have more opportunities along with greater expectations for physical fitness. In undevelopedcountries the ability to afford food, high energy expenditure with physical labor, and cultural values favoring alarger body size are believed to contribute to the observed patterns.[118] Attitudes toward body weight held bypeople in one's life may also play a role in obesity. A correlation in BMI changes over time has been foundamong friends, siblings, and spouses.[120] Stress and perceived low social status appear to increase risk ofobesity.[119][121][122]

Smoking has a significant effect on an individual's weight. Those who quit smoking gain an average of4.4 kilograms (9.7 lb) for men and 5.0 kilograms (11.0 lb) for women over ten years.[123] However, changingrates of smoking have had little effect on the overall rates of obesity.[124]

In the United States the number of children a person has is related to their risk of obesity. A woman's riskincreases by 7% per child, while a man's risk increases by 4% per child.[125] This could be partly explained bythe fact that having dependent children decreases physical activity in Western parents.[126]

In the developing world urbanization is playing a role in increasing rate of obesity. In China overall rates ofobesity are below 5%; however, in some cities rates of obesity are greater than 20%.[127]

Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world.[128]

Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more foodenergy becomes available.[128]

Consistent with cognitive epidemiological data, numerous studies confirm that obesity is associated withcognitive deficits.[129] Whether obesity causes cognitive deficits, or vice versa is unclear at present.

Infectious agents

The study of the effect of infectious agents on metabolism is still in its early stages. Gut flora has been shown todiffer between lean and obese humans. There is an indication that gut flora in obese and lean individuals canaffect the metabolic potential. This apparent alteration of the metabolic potential is believed to confer a greatercapacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result ofobesity has yet to be determined unequivocally.[130]

An association between viruses and obesity has been found in humans and several different animal species. Theamount that these associations may have contributed to the rising rate of obesity is yet to be determined.[131]

Pathophysiology

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A comparison of a mouse unable toproduce leptin thus resulting inobesity (left) and a normal mouse(right)

A graphic depiction of a leptinmolecule

There are many possible pathophysiological mechanisms involved in thedevelopment and maintenance of obesity.[132] This field of research hadbeen almost unapproached until the leptin gene was discovered in 1994by J. M. Friedman's laboratory.[133] These investigators postulated thatleptin was a satiety factor. In the ob/ob mouse, mutations in the leptingene resulted in the obese phenotype opening the possibility of leptintherapy for human obesity. However, soon thereafter J. F. Caro'slaboratory could not detect any mutations in the leptin gene in humanswith obesity. On the contrary Leptin expression was increased proposingthe possibility of Leptin-resistance in human obesity.[134] Since thisdiscovery, many other hormonal mechanisms have been elucidated thatparticipate in the regulation of appetite and food intake, storage patternsof adipose tissue, and development of insulin resistance. Since leptin'sdiscovery, ghrelin, insulin, orexin, PYY 3-36, cholecystokinin, adiponectin, as well as many other mediatorshave been studied. The adipokines are mediators produced by adipose tissue; their action is thought to modifymany obesity-related diseases.

Leptin and ghrelin are considered to be complementary in their influence on appetite, with ghrelin produced bythe stomach modulating short-term appetitive control (i.e. to eat when the stomach is empty and to stop whenthe stomach is stretched). Leptin is produced by adipose tissue to signal fat storage reserves in the body, andmediates long-term appetitive controls (i.e. to eat more when fat storages are low and less when fat storages arehigh). Although administration of leptin may be effective in a small subset of obese individuals who are leptindeficient, most obese individuals are thought to be leptin resistant and have been found to have high levels ofleptin.[135] This resistance is thought to explain in part why administration of leptin has not been shown to beeffective in suppressing appetite in most obese people.[132]

While leptin and ghrelin are produced peripherally, they control appetitethrough their actions on the central nervous system. In particular, theyand other appetite-related hormones act on the hypothalamus, a regionof the brain central to the regulation of food intake and energyexpenditure. There are several circuits within the hypothalamus thatcontribute to its role in integrating appetite, the melanocortin pathwaybeing the most well understood.[132] The circuit begins with an area ofthe hypothalamus, the arcuate nucleus, that has outputs to the lateralhypothalamus (LH) and ventromedial hypothalamus (VMH), the brain'sfeeding and satiety centers, respectively.[136]

The arcuate nucleus contains two distinct groups of neurons.[132] Thefirst group coexpresses neuropeptide Y (NPY) and agouti-related peptide

(AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH. The second group coexpressespro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) and has stimulatoryinputs to the VMH and inhibitory inputs to the LH. Consequently, NPY/AgRP neurons stimulate feeding andinhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding. Both groups of arcuate

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nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP group while stimulating thePOMC/CART group. Thus a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leadsto overfeeding and may account for some genetic and acquired forms of obesity.[132]

Public healthThe World Health Organization (WHO) predicts that overweight and obesity may soon replace more traditionalpublic health concerns such as undernutrition and infectious diseases as the most significant cause of poorhealth.[137] Obesity is a public health and policy problem because of its prevalence, costs, and healtheffects.[138] The United States Preventive Services Task Force recommends screening for all adults followed bybehavioral interventions in those who are obese.[139] Public health efforts seek to understand and correct theenvironmental factors responsible for the increasing prevalence of obesity in the population. Solutions look atchanging the factors that cause excess food energy consumption and inhibit physical activity. Efforts includefederally reimbursed meal programs in schools, limiting direct junk food marketing to children,[140] anddecreasing access to sugar-sweetened beverages in schools.[141] When constructing urban environments, effortshave been made to increase access to parks and to develop pedestrian routes.[142]

Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelineswere published, titled "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight andObesity in Adults: The Evidence Report".[143] In 2006 the Canadian Obesity Network published the "CanadianClinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children".This is a comprehensive evidence-based guideline to address the management and prevention of overweight andobesity in adults and children.[68]

In 2004, the United Kingdom Royal College of Physicians, the Faculty of Public Health and the Royal Collegeof Paediatrics and Child Health released the report "Storing up Problems", which highlighted the growingproblem of obesity in the UK.[144] The same year, the House of Commons Health Select Committee publishedits "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in theUK and possible approaches to the problem.[145] In 2006, the National Institute for Health and ClinicalExcellence (NICE) issued a guideline on the diagnosis and management of obesity, as well as policyimplications for non-healthcare organizations such as local councils.[146] A 2007 report produced by Sir DerekWanless for the King's Fund warned that unless further action was taken, obesity had the capacity to cripple theNational Health Service financially.[147]

Comprehensive approaches are being looked at to address the rising rates of obesity. The Obesity Policy Action(OPA) framework divides measure into 'upstream' policies, 'midstream' policies, 'downstream' policies.'Upstream' policies look at changing society, 'midstream' policies try to alter individuals' behavior to preventobesity, and 'downstream' policies try to treat currently afflicted people.[148]

Management

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The main treatment for obesity consists of dieting and physical exercise.[68] Diet programs may produce weightloss over the short term,[149] but maintaining this weight loss is frequently difficult and often requires makingexercise and a lower food energy diet a permanent part of a person's lifestyle.[150][151] All types of low-carbohydrate and low-fat diets appear equally beneficial.[152] The heart disease and diabetes risks associatedwith different diets also appear to be similar.[153] Success rates of long-term weight loss maintenance withlifestyle changes are low, ranging from 2–20%.[154] Dietary and lifestyle changes are effective in limitingexcessive weight gain in pregnancy and improve outcomes for both the mother and the child.[155] Intensivebehavioral counseling is recommended in those who are both obese and have other risk factors for heartdisease.[156]

Three medications, orlistat (Xenical), lorcaserin (Belviq) and a combination of phentermine and topiramate(Qsymia) are currently available and have evidence for long term use.[157] Weight loss with orlistat is modest,an average of 2.9 kg (6.4 lb) at 1 to 4 years.[158] Its use is associated with high rates of gastrointestinal sideeffects[158] and concerns have been raised about negative effects on the kidneys.[159] The other two medicationsare available in the United States but not Europe.[160] Lorcaserin results in an average 3.1 kg weight loss (3% ofbody weight) greater than placebo over a year;[161] however, it may increase heart valve problems.[160] Acombination of phentermine and topiramate is also somewhat effective;[162] however, it may be associated withheart problems.[160] There is no information on how these drugs affect longer-term complications of obesitysuch as cardiovascular disease or death.[157]

The most effective treatment for obesity is bariatric surgery.[163] Surgery for severe obesity is associated withlong-term weight loss, improvement in obesity related conditions,[164] and decreased overall mortality. Onestudy found a weight loss of between 14% and 25% (depending on the type of procedure performed) at10 years, and a 29% reduction in all cause mortality when compared to standard weight loss measures.[165]

Complications occur in about 17% of cases and reoperation is needed in 7% of cases.[164] Due to its cost andrisks, researchers are searching for other effective yet less invasive treatments including devices that occupyspace in the stomach.[166]

EpidemiologyIn earlier historical periods obesity was rare, and achievable only by a small elite, although already recognisedas a problem for health. But as prosperity increased in the Early Modern period, it affected increasingly largergroups of the population.[168] In 1997 the WHO formally recognized obesity as a global epidemic.[81] As of2008 the WHO estimates that at least 500 million adults (greater than 10%) are obese, with higher rates amongwomen than men.[169] The rate of obesity also increases with age at least up to 50 or 60 years old[170] andsevere obesity in the United States, Australia, and Canada is increasing faster than the overall rate ofobesity.[19][171][172]

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World obesity prevalence among males (left) and females (right).[167]

<5%

5–10%

10–15%

15–20%

20–25%

25–30%

30–35%

35–40%

40–45%

45–50%

50–55%

>55%

Once considered a problem only of high-income countries, obesity rates are risingworldwide and affecting both thedeveloped and developing world.[31] Theseincreases have been felt most dramaticallyin urban settings.[169] The only remainingregion of the world where obesity is notcommon is sub-Saharan Africa.[2]

History

Etymology

Obesity is from the Latin obesitas, which means "stout, fat, or plump". Ēsus is the past participle of edere (toeat), with ob (over) added to it.[173] The Oxford English Dictionary documents its first usage in 1611 by RandleCotgrave.[174]

Historical attitudes

Ancient Greek medicine recognizes obesity as a medical disorder, and records that the Ancient Egyptians saw itin the same way.[168] Hippocrates wrote that "Corpulence is not only a disease itself, but the harbinger ofothers".[2] The Indian surgeon Sushruta (6th century BCE) related obesity to diabetes and heart disorders.[176]

He recommended physical work to help cure it and its side effects.[176] For most of human history mankindstruggled with food scarcity.[177] Obesity has thus historically been viewed as a sign of wealth and prosperity. Itwas common among high officials in Europe in the Middle Ages and the Renaissance[175] as well as in AncientEast Asian civilizations.[178]

With the onset of the industrial revolution it was realized that the military and economic might of nations weredependent on both the body size and strength of their soldiers and workers.[81] Increasing the average bodymass index from what is now considered underweight to what is now the normal range played a significant rolein the development of industrialized societies.[81] Height and weight thus both increased through the19th century in the developed world. During the 20th century, as populations reached their genetic potential forheight, weight began increasing much more than height, resulting in obesity.[81] In the 1950s increasing wealthin the developed world decreased child mortality, but as body weight increased heart and kidney disease becamemore common.[81][179] During this time period insurance companies realized the connection between weightand life expectancy and increased premiums for the obese.[2]

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During the Middle Ages andthe Renaissance obesity wasoften seen as a sign ofwealth, and was relativelycommon among the elite:The Tuscan GeneralAlessandro del Borro,attributed to Charles Mellin,1645[175]

Venus of Willendorf created24,000–22,000 BC

Many cultures throughout history have viewed obesity as the result of acharacter flaw. The obesus or fat character in Greek comedy was a glutton andfigure of mockery. During Christian times food was viewed as a gateway to thesins of sloth and lust.[9] In modern Western culture, excess weight is oftenregarded as unattractive, and obesity is commonly associated with variousnegative stereotypes. People of all ages can face social stigmatization, and maybe targeted by bullies or shunned by their peers.[180]

Public perceptions in Western society regarding healthy body weight differ fromthose regarding the weight that is considered ideal – and both have changedsince the beginning of the 20th century. The weight that is viewed as an idealhas become lower since the 1920s. This is illustrated by the fact that the averageheight of Miss America pageant winners increased by 2% from 1922 to 1999,while their average weight decreased by 12%.[181] On the other hand, people'sviews concerning healthy weight have changed in the opposite direction. InBritain the weight at which people considered themselves to be overweight wassignificantly higher in 2007 than in 1999.[182] These changes are believed to bedue to increasing rates of adiposity leading to increased acceptance of extrabody fat as being normal.[182]

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 agodepict obese females. Some attribute the Venus figurines to the tendency toemphasize fertility while others feel they represent "fatness" in the people of thetime.[9] Corpulence is, however, absent in both Greek and Roman art, probablyin keeping with their ideals regarding moderation. This continued through muchof Christian European history, with only those of low socioeconomic statusbeing depicted as obese.[9]

During the Renaissance some of the upper class began flaunting their large size,as can be seen in portraits of Henry VIII of England and Alessandro delBorro.[9] Rubens (1577–1640) regularly depicted full-bodied women in hispictures, from which derives the term Rubenesque. These women, however, stillmaintained the "hourglass" shape with its relationship to fertility.[183] During the19th century, views on obesity changed in the Western world. After centuries ofobesity being synonymous with wealth and social status, slimness began to beseen as the desirable standard.[9]

Society and culture

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Services must accommodate obesepeople with specialist equipment suchas much wider chairs.[192]

Economic impact

In addition to its health impacts, obesity leads to many problems including disadvantages inemployment[184][185] and increased business costs. These effects are felt by all levels of society fromindividuals, to corporations, to governments.

In 2005, the medical costs attributable to obesity in the US were an estimated $190.2 billion or 20.6% of allmedical expenditures,[186][187][188] while the cost of obesity in Canada was estimated at CA$2 billion in 1997(2.4% of total health costs).[68] The total annual direct cost of overweight and obesity in Australia in 2005 wasA$21 billion. Overweight and obese Australians also received A$35.6 billion in government subsidies.[189] Theestimate range for annual expenditures on diet products is $40 billion to $100 billion in the US alone.[190]

Obesity prevention programs have been found to reduce the cost of treating obesity-related disease. However,the longer people live, the more medical costs they incur. Researchers therefore conclude that reducing obesitymay improve the public's health, but it is unlikely to reduce overall health spending.[191]

Obesity can lead to social stigmatization and disadvantages inemployment.[184] When compared to their normal weight counterparts,obese workers on average have higher rates of absenteeism from workand take more disability leave, thus increasing costs for employers anddecreasing productivity.[193] A study examining Duke Universityemployees found that people with a BMI over 40 kg/m2 filed twice asmany workers' compensation claims as those whose BMI was 18.5–24.9 kg/m2. They also had more than 12 times as many lost work days.The most common injuries in this group were due to falls and lifting,thus affecting the lower extremities, wrists or hands, and backs.[194] TheAlabama State Employees' Insurance Board approved a controversialplan to charge obese workers $25 a month for health insurance thatwould otherwise be free unless they take steps to lose weight andimprove their health. These measures started in January 2010 and apply

to those state workers whose BMI exceeds 35 kg/m2 and who fail to make improvements in their health afterone year.[195]

Some research shows that obese people are less likely to be hired for a job and are less likely to bepromoted.[180] Obese people are also paid less than their non-obese counterparts for an equivalent job; obesewomen on average make 6% less and obese men make 3% less.[196]

Specific industries, such as the airline, healthcare and food industries, have special concerns. Due to rising ratesof obesity, airlines face higher fuel costs and pressures to increase seating width.[197] In 2000, the extra weightof obese passengers cost airlines US$275 million.[198] The healthcare industry has had to invest in specialfacilities for handling severely obese patients, including special lifting equipment and bariatric ambulances.[199]

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United States PresidentWilliam Howard Taft wasoften ridiculed for beingoverweight

Costs for restaurants are increased by litigation accusing them of causing obesity.[200] In 2005 the US Congressdiscussed legislation to prevent civil lawsuits against the food industry in relation to obesity; however, it did notbecome law.[200]

With the American Medical Association's 2013 classification of obesity as a chronic disease,[10] it is thoughtthat health insurance companies will more likely pay for obesity treatment, counseling and surgery, and the costof research and development of fat treatment pills or gene therapy treatments should be more affordable ifinsurers help to subsidize their cost.[201] The AMA classification is not legally binding, however, so healthinsurers still have the right to reject coverage for a treatment or procedure.[201]

In 2014, The European Court of Justice ruled that morbid obesity is a disability. The Court argued that if anemployee's obesity prevents him from "full and effective participation of that person in professional life on anequal basis with other workers", then it shall be considered a disability and that firing someone on such groundsis discriminatory.[202]

Size acceptance

The principal goal of the fat acceptance movement is to decrease discriminationagainst people who are overweight and obese.[203][204] However, some in themovement are also attempting to challenge the established relationship betweenobesity and negative health outcomes.[205]

A number of organizations exist that promote the acceptance of obesity. They haveincreased in prominence in the latter half of the 20th century.[206] The US-basedNational Association to Advance Fat Acceptance (NAAFA) was formed in 1969and describes itself as a civil rights organization dedicated to ending sizediscrimination.[207]

The International Size Acceptance Association (ISAA) is a non-governmentalorganization (NGO) which was founded in 1997. It has more of a global orientationand describes its mission as promoting size acceptance and helping to end weight-based discrimination.[208] These groups often argue for the recognition of obesityas a disability under the US Americans With Disabilities Act (ADA). TheAmerican legal system, however, has decided that the potential public health costsexceed the benefits of extending this anti-discrimination law to cover obesity.[205]

Childhood obesityThe healthy BMI range varies with the age and sex of the child. Obesity in children and adolescents is definedas a BMI greater than the 95th percentile.[15] The reference data that these percentiles are based on is from 1963to 1994 and thus has not been affected by the recent increases in rates of obesity.[16] Childhood obesity has

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reached epidemic proportions in the 21st century, with rising rates in both the developed and developing world.Rates of obesity in Canadian boys have increased from 11% in the 1980s to over 30% in the 1990s, whileduring this same time period rates increased from 4 to 14% in Brazilian children.[209]

As with obesity in adults, many factors contribute to the rising rates of childhood obesity. Changing diet anddecreasing physical activity are believed to be the two most important causes for the recent increase in theincidence of child obesity.[210] Because childhood obesity often persists into adulthood and is associated withnumerous chronic illnesses, children who are obese are often tested for hypertension, diabetes, hyperlipidemia,and fatty liver.[68] Treatments used in children are primarily lifestyle interventions and behavioral techniques,although efforts to increase activity in children have had little success.[211] In the United States, medications arenot FDA approved for use in this age group.[209]

Other animalsObesity in pets is common in many countries. In the United States, 23–41% of dogs are overweight, and about5.1% are obese.[212] The rate of obesity in cats was slightly higher at 6.4%.[212] In Australia the rate of obesityamong dogs in a veterinary setting has been found to be 7.6%.[213] The risk of obesity in dogs is related towhether or not their owners are obese; however, there is no similar correlation between cats and theirowners.[214]

Notes1. WHO 2000 p.62. Haslam DW, James WP (2005). "Obesity". Lancet (Review) 366 (9492): 1197–209. doi:10.1016/S0140-6736(05)67483-

1 (https://dx.doi.org/10.1016%2FS0140-6736%2805%2967483-1). PMID 16198769(https://www.ncbi.nlm.nih.gov/pubmed/16198769).

3. WHO 2000 p.94. Kushner, Robert (2007). Treatment of the Obese Patient (Contemporary Endocrinology) (http://books.google.com/?

id=vWjK5etS7PMC). Totowa, NJ: Humana Press. p. 158. ISBN 1-59745-400-1. Retrieved April 5, 2009.5. Adams JP, Murphy PG (July 2000). "Obesity in anaesthesia and intensive care"

(http://bja.oxfordjournals.org/cgi/content/full/85/1/91). Br J Anaesth 85 (1): 91–108. doi:10.1093/bja/85.1.91(https://dx.doi.org/10.1093%2Fbja%2F85.1.91). PMID 10927998 (https://www.ncbi.nlm.nih.gov/pubmed/10927998).

6. NICE 2006 p.10–117. Imaz I, Martínez-Cervell C, García-Alvarez EE, Sendra-Gutiérrez JM, González-Enríquez 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 (https://dx.doi.org/10.1007%2Fs11695-007-9331-8). PMID 18459025(https://www.ncbi.nlm.nih.gov/pubmed/18459025).

8. Barness LA, Opitz JM, Gilbert-Barness E (December 2007). "Obesity: genetic, molecular, and environmental aspects".American Journal of Medical Genetics 143A (24): 3016–34. doi:10.1002/ajmg.a.32035(https://dx.doi.org/10.1002%2Fajmg.a.32035). PMID 18000969 (https://www.ncbi.nlm.nih.gov/pubmed/18000969).

9. Woodhouse R (2008). "Obesity in art: A brief overview" (http://books.google.com/?id=nXRU4Ea1aMkC&pg=PA271&lpg=PA271). Front Horm Res. Frontiers of Hormone Research 36: 271–86.doi:10.1159/000115370 (https://dx.doi.org/10.1159%2F000115370). ISBN 978-3-8055-8429-6. PMID 18230908(https://www.ncbi.nlm.nih.gov/pubmed/18230908).

10. Pollack, Andrew (June 18, 2013). "A.M.A. Recognizes Obesity as a Disease" (http://www.webcitation.org/6Hav05TK0).New York Times. Archived from the original (http://www.nytimes.com/2013/06/19/business/ama-recognizes-obesity-as-a-disease.html?_r=0) on June 18, 2013.

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a-disease.html?_r=0) on June 18, 2013.11. Weinstock, Matthew (June 21, 2013). "The Facts About Obesity"

(http://www.hhnmag.com/hhnmag/HHNDaily/HHNDailyDisplay.dhtml?id=5870001020). H&HN. American HospitalAssociation. Retrieved June 24, 2013.

12. Sweeting HN (2007). "Measurement and Definitions of Obesity In Childhood and Adolescence: A field guide for theuninitiated" (http://www.nutritionj.com/content/6/1/32). Nutr J 6 (1): 32. doi:10.1186/1475-2891-6-32(https://dx.doi.org/10.1186%2F1475-2891-6-32). PMC 2164947(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2164947). PMID 17963490(https://www.ncbi.nlm.nih.gov/pubmed/17963490).

13. NHLBI p.xiv14. 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:10.1016/0895-4356(91)90218-X (https://dx.doi.org/10.1016%2F0895-4356%2891%2990218-X). PMID 2037859 (https://www.ncbi.nlm.nih.gov/pubmed/2037859).

15. "Healthy Weight: Assessing Your Weight: BMI: About BMI for Children and Teens"(http://www.cdc.gov/nccdphp/dnpa/healthyweight/assessing/bmi/childrens_BMI/about_childrens_BMI.htm). Center fordisease control and prevention. Retrieved April 6, 2009.

16. Flegal KM, Ogden CL, Wei R, Kuczmarski RL, Johnson CL (June 2001). "Prevalence of overweight in US children:comparison of US growth charts from the Centers for Disease Control and Prevention with other reference values forbody mass index" (http://www.ajcn.org/cgi/content/full/73/6/1086). Am. J. Clin. Nutr. 73 (6): 1086–93. PMID 11382664(https://www.ncbi.nlm.nih.gov/pubmed/11382664).

17. "BMI classification" (http://apps.who.int/bmi/index.jsp?introPage=intro_3.html). World Health Organization. Retrieved15 February 2014.

18. 1 (lb/sq in) is more precisely 703.06957964 (kg/m2).19. Sturm R (July 2007). "Increases in morbid obesity in the USA: 2000–2005"

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15/05/15 21:19Obesity - Wikipedia, the free encyclopedia

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Many authors (2015). "Obesity 2015" (http://www.thelancet.com/series/obesity-2015). The Lancet.Fumento, Michael (1997). The Fat of the Land: Our Health Crises and How Overweight Americans can HelpThemselves (http://books.google.com/books?id=Qr8hAQAAMAAJ). New York: Penguin Books. ISBN 0-14-026144-3.Keller, Kathleen (2008). Encyclopedia of Obesity (http://books.google.com/?id=aRp2rJrEqZsC). Thousand Oaks, Calif:Sage Publications, Inc. ISBN 1-4129-5238-7.Kolata, Gina (2007). Rethinking Thin: The New Science of Weight Loss – and the Myths and Realities of Dieting.Picador. ISBN 0-312-42785-9.Kopelman, Peter G.; Caterson, Ian D.; Dietz, William H., eds. (2009). Clinical obesity in Adults and Children(http://books.google.com/books?id=1W2M1lnHeccC) (3rd ed.). John Wiley & Sons. ISBN 978-1-4443-0763-4.Levy-Navarro, Elena (2008). The Culture of Obesity in Early and Late Modernity. Palgrave Macmillan. ISBN 0-230-60123-5.Pool, Robert (2001). Fat: Fighting the Obesity Epidemic. Oxford, UK: Oxford University Press. ISBN 0-19-511853-7.

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