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__NOTOC__
{{DiseaseDisorder infobox |
{{DiseaseDisorder infobox |
   Name        = Obesity |
   Name        = Obesity |
   Image      = Obesity-waist circumference.PNG |
   Image      = Obesity-waist circumference.PNG |
   Caption    = Silhouettes representing healthy, overweight, and obese. |
   Caption    = Silhouettes representing healthy, overweight, and obese. |
  DiseasesDB  = 9099 |
 
  ICD10      = {{ICD10|E|66| |e|65}} |
  ICD9        = {{ICD9|278}} |
  MedlinePlus = 003101 |
  eMedicineSubj  = med |
  eMedicineTopic =1653 |
  MeshName    = Obesity |
  MeshNumber  = C23.888.144.699.500 |
}}
}}
{{SI}}
'''For patient information click [[Obesity (patient information)|here]]'''
{{CMG}}
{{Obesity}}
__NOTOC__
{{CMG}}; {{AE}} {{CZ}}  [[User:Raviteja Reddy Guddeti|Raviteja Guddeti, M.B.B.S.]] [mailto:ravitheja.g@gmail.com]
'''Associate Editor-In-Chief:'''  {{CZ}}
 
{{Editor Join}}
 
==Overview==
 
'''Obesity'''  is a condition in which the natural energy reserve, stored in the [[adipose tissue|fatty tissue]] of [[human]]s and other [[mammal]]s, is increased to a point where it is associated with certain [[health]] conditions or increased [[death|mortality]].
 
Although obesity is an individual clinical condition, it is increasingly viewed as a serious and growing [[public health]] problem: excessive body weight has been shown to predispose to various [[diseases]], particularly [[cardiovascular diseases]], [[diabetes  mellitus type 2]], [[sleep apnea]] and [[osteoarthritis]].<ref name=NHLBI>{{cite book |author=National Heart, Lung, and Blood Institute |title=Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults |publisher=International Medical Publishing, Inc |location= |year= |pages= |isbn=1-58808-002-1 |oclc= |url=http://www.nhlbi.nih.gov/guidelines/obesity/ob_gdlns.pdf}}</ref><ref name=HaslamJames>{{cite journal |author=Haslam DW, James WP |title=Obesity |journal=Lancet |volume=366 |issue=9492 |pages=1197–209 |year=2005 |pmid=16198769 |doi=10.1016/S0140-6736(05)67483-1}}</ref>
 
Obesity is characterized as a state of excess adipose mass with abnormal increase of fat on the subcutaneous connective tissue. Obesity is generally gauged by the Body Mass Index(BMI). A high BMI is associated with a higher risk for potentially lethal medical problems.
{| style="background:silver; color:black"
| '''BMI (kg/m2)'''
|- style="background:silver; color:black"
| '''Appropriate Weight'''
| 18.5-25
|- style="background:silver; color:black"
| '''Overweight'''
| >25
|- style="background:silver; color:black"
| '''Obesity'''
| >30
|}
 
==Classification==
Obesity can be defined in absolute or relative terms. In practical settings, obesity is typically evaluated in absolute terms by measuring BMI ([[body mass index]]), but also in terms of its distribution through waist circumference or waist-hip circumference ratio measurements.<ref>{{cite journal |journal= Nutr J |date=2007 |volume=6 |pages=32 |title= Measurement and definitions of obesity in childhood and adolescence: a field guide for the uninitiated |author= Sweeting HN |doi=10.1186/1475-2891-6-32 |pmid=17963490 |url=http://www.nutritionj.com/content/6/1/32}}</ref> In addition, the presence of obesity needs to be regarded in the context of other [[risk factor]]s and [[comorbidities]] (other medical conditions that could influence risk of complications).<ref name=NHLBI/>
 
===BMI===
BMI, or [[body mass index]], is a simple and widely used method for estimating body fat.<ref>Mei Z, Grummer-Strawn LM, Pietrobelli A, Goulding A, Goran MI, Dietz WH. Validity of body mass index compared with other body-composition screening indexes for the assessment of body fatness in children and adolescents. ''Am J Clin Nutr'' 2002;75:978-85. PMID 12036802.</ref> BMI was developed by the Belgian statistician and [[anthropometry|anthropometrist]] [[Adolphe Quetelet]].<ref>Quetelet LAJ. (1871). ''Antropométrie ou Mesure des Différences Facultés de l'Homme.'' Brussels: Musquardt.</ref>  It is calculated by dividing the subject's weight by the square of his/her height, typically expressed either in [[Metric system|metric]] or [[US customary units|US "Customary"]] units:
 
:Metric:  <math>BMI = kg/m^2</math>
 
Where <math>kg</math> is the subject's weight in [[kilograms]] and <math>m</math> is the subject's height in [[metres]].
 
:US/Customary: <math>BMI=lb*703/in^2</math>
 
Where <math>lb</math> is the subject's weight in [[pound (mass)|pounds]] and <math>in</math> is the subject's height in [[inches]].
 
The current definitions commonly in use establish the following values, agreed in 1997 and published in 2000:<ref>World Health Organization Technical report series 894: "Obesity: preventing and managing the global epidemic.". Geneva: [[World Health Organization]], 2000. [http://whqlibdoc.who.int/trs/WHO_TRS_894_(part1).pdf PDF]. ISBN 92-4-120894-5.</ref>
* A BMI less than 18.5 is ''underweight''
* A BMI of 18.5–24.9 is ''normal weight''
* A BMI of 25.0–29.9 is ''overweight''
* A BMI of 30.0–39.9 is ''obese''
* A BMI of 40.0 or higher is ''severely (or morbidly) obese''
* A BMI of 35.0 or higher ''in the presence of at least one other significant comorbidity'' is also classified by some bodies as ''morbid obesity''.<ref>{{cite web|url=http://www.nice.org.uk/page.aspx?o=34790 |title=NICE issues guidance on surgery for morbid obesity |accessdate=2007-03-08 |date=19th July 2002 |publisher=National Institute for Health and Clinical Excellence }}</ref><ref>{{cite web| url=http://www.surgery.usc.edu/divisions/cr/bariatricsurgery.html |title=Bariatric Surgery |accessdate=2007-03-08 |date=2006 |work=USC Center for Colorectal and Pelvic Floor Disorders |publisher=University of Southern California }}</ref>
 
In a ''clinical'' setting, physicians take into account race, ethnicity, lean mass (muscularity), age, sex, and other factors which can affect the interpretation of BMI. BMI overestimates body fat in persons who are very muscular, and it can underestimate body fat in persons who have lost body mass (e.g. many elderly).<ref name=NHLBI/> Mild obesity as defined by BMI alone is not a cardiac risk factor, and hence BMI cannot be used as a sole clinical and epidemiological predictor of cardiovascular health.<ref>{{cite journal |author=Romero-Corral A, Montori VM, Somers VK, ''et al'' |title=Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: a systematic review of cohort studies |journal=Lancet |volume=368 |issue=9536 |pages=666–78 |year=2006 |pmid=16920472 |doi=10.1016/S0140-6736(06)69251-9}}</ref>
 
===Waist circumference===
BMI does not take into account differing ratios of [[adipose]] to lean tissue; nor does it distinguish between differing forms of adiposity, some of which may correlate more closely with [[cardiovascular]] risk. Increasing understanding of the biology of different forms of adipose tissue has shown that ''visceral'' fat or ''[[central obesity]]'' (male-type or apple-type obesity) has a much stronger correlation, particularly with [[cardiovascular disease]], than the BMI alone.<ref name=Yusuf2004>{{cite journal | author=Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L, INTERHEART Study Investigators. | title=Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study.|journal=[[The Lancet|Lancet]] | year=2004 | pages=937-52 | volume=364 | id=PMID 15364185}}</ref>
 
The absolute waist circumference (>102 cm in men and >88 cm in women) or [[waist-hip ratio]] (>0.9 for men and >0.85 for women)<ref name=Yusuf2004/> are both used as measures of central obesity.
 
In a cohort of almost 15,000 subjects from the [[National Health and Nutrition Examination Survey]] (NHANES) III study, waist circumference explained obesity-related health risk significantly better than BMI when [[metabolic syndrome]] was taken as an outcome measure.<ref>{{cite journal |author=Janssen I, Katzmarzyk PT, Ross R |title=Waist circumference and not body mass index explains obesity-related health risk |journal=Am. J. Clin. Nutr. |volume=79 |issue=3 |pages=379–84 |year=2004 |pmid=14985210 |url=http://www.ajcn.org/cgi/content/abstract/79/3/379}}</ref>
 
===Body fat measurement===
An alternative way to determine obesity is to assess percent [[body fat]]. Doctors and scientists generally agree that men with more than 25% body fat and women with more than 30% body fat are obese. However, it is difficult to measure body fat precisely. The most accepted method has been to weigh a person underwater, but underwater weighing is a procedure limited to laboratories with special equipment. Two simpler methods for measuring body fat are the ''skinfold test'', in which a pinch of skin is precisely measured to determine the thickness of the [[subcutaneous]] fat layer; or bioelectrical impedance analysis, usually only carried out at specialist clinics. Their routine use is discouraged.<ref name=NICECG043>[[National Institute for Health and Clinical Excellence]]. ''[http://guidance.nice.org.uk/CG43 Clinical guideline 43: Obesity: the prevention, identification, assessment and management of overweight and obesity in adults and children].'' London, 2006.</ref>
 
Other measurements of body fat include [[computed tomography]] (CT/CAT scan), [[magnetic resonance imaging]] (MRI/NMR), and [[dual energy X-ray absorptiometry]] (DXA).<ref>Vanhecke TE, Franklin BA, Lillystone MA, Sandberg KR, deJong AT, Krause KR, Chengelis DL, McCullough PA. Caloric expenditure in the morbidly obese using dual energy X-ray absorptiometry. ''J Clin Densitomet'' 2006;9:438-444. PMID 17097530.</ref>
 
===Risk factors and comorbidities===
The presence of risk factors and diseases associated with obesity are also used to establish a clinical diagnosis. [[Coronary heart disease]], [[Diabetes mellitus type 2|type 2 diabetes]], and [[sleep apnea]] are possible life-threatening risk factors that would indicate clinical treatment of obesity.<ref name=NHLBI/> Smoking, hypertension, age and family history are other risk factors that may indicate treatment.<ref name=NHLBI/>
 
== Differential Diagnosis ==
=== Contributory Factors ===
*[[Anxiety]] - related obesity
*Cultural - ethnic factors
*[[Depression]] - related obesity
*[[Diet]]ary factors
*[[Drugs]]
*Familial influences
*Infant feeding practices
*Maternal [[nutrition]]al factors
*Physical inactivity
*[[Pregnancy]]
*Socioeconomic
 
=== Genetic factors ===
*[[Alstrom's Syndrome]]
*[[Frohlich's Syndrome]]
*[[Klinefelter's Syndrome]]
*Inherited predisposition
*[[Laurence-Moon-Bardet-Biedl Syndrome]]
*[[Prader-Willi Syndrome]]
*[[Pseudohypoparathyroidism]]
*[[Stewart-Morel-Morgagni Syndrome]]
 
=== Hypothalamic Dysfunction ===
*[[Increased intracranial pressure]]
*Inflammation
*Surgery
*[[Trauma]]
*[[Tumor]]
 
=== Endocrine ===
*[[Cushing's Syndrome]]
*[[Hyperinsulinism]]
*[[Hypopituitaryism]]
*[[Hypothyroidism]]
*[[Menopause]]
*Pubertal obesity
*[[Stein-Leventhal syndrome]]
 
=== Lipomatosis ===
*Andler's Disease
*Launois-Bensaude Syndrome
*Madelung's Disease
*Multiple [[lipomas]]
 
==Effects on health==
Excessive body [[Human weight|weight]] is associated with various [[diseases]], particularly [[cardiovascular diseases]], [[diabetes mellitus type 2]], [[obstructive sleep apnea]], certain types of [[cancer]], and [[osteoarthritis]].<ref name=HaslamJames/> As a result, obesity has been found to reduce [[life expectancy]].<ref name=HaslamJames/>
 
===Mortality===
Obesity is one of the leading preventable causes of death worldwide.<ref name=Barn1999>{{cite journal |author=Barness LA, Opitz JM, Gilbert-Barness E |title=Obesity: genetic, molecular, and environmental aspects |journal=Am. J. Med. Genet. A |volume=143A |issue=24 |pages=3016–34 |year=2007 |month=December |pmid=18000969 |doi=10.1002/ajmg.a.32035 |url=}}</ref>{{cite journal |author=Mokdad AH, Marks JS, Stroup DF, Gerberding JL |title=Actual causes of death in the United States, 2000 |journal=JAMA |volume=291 |issue=10 |pages=1238–45 |year=2004 |month=March |pmid=15010446 |doi=10.1001/jama.291.10.1238 |url=http://www.csdp.org/research/1238.pdf|format=PDF}}</ref><ref name=Allison>{{cite journal |author=Allison DB, Fontaine KR, Manson JE, Stevens J, VanItallie TB |title=Annual deaths attributable to obesity in the United States |journal=JAMA |volume=282 |issue=16 |pages=1530–8 |year=1999 |month=October |pmid=10546692 |doi= 10.1001/jama.282.16.1530|url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=10546692}}</ref> Large scale American and European studies have found that mortality risk varies with BMI; the lowest risk is found at a BMI of 22.5–25&nbsp;kg/m<sup>2</sup><ref name=Lancet2009>{{cite journal |author=Whitlock G, Lewington S, Sherliker P, ''et al'' |title=Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies |journal=Lancet |volume=373 |issue=9669 |pages=1083–96 |year=2009 |month=March |pmid=19299006 |doi=10.1016/S0140-6736(09)60318-4 |url=}}</ref> in non smokers and at a BMI of 24–27&nbsp;kg/m<sup>2</sup> in current smokers and increases with changes in either direction.<ref>{{cite journal |author=Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW |title=Body-mass index and mortality in a prospective cohort of U.S. adults |journal=N. Engl. J. Med. |volume=341 |issue=15 |pages=1097–105 |year=1999 |month=October |pmid=10511607 |doi= 10.1056/NEJM199910073411501|url=http://content.nejm.org/cgi/content/full/341/15/1097}}</ref><ref name=Euro2008>{{cite journal |author=Pischon T, Boeing H, Hoffmann K, ''et al'' |title=General and abdominal adiposity and risk of death in Europe |journal=N. Engl. J. Med. |volume=359 |issue=20 |pages=2105–20 |year=2008 |month=November |pmid=19005195 |doi=10.1056/NEJMoa0801891 |url=}}</ref> Obesity increases the risk of death in current and former smokers as well as in those who have never smoked.<ref name=Euro2008/>  A BMI of over 32 has been associated with a doubled [[mortality rate]] among women over a 16-year period<ref>{{cite journal |author=Manson JE, Willett WC, Stampfer MJ, ''et al.'' |title=Body weight and mortality among women |journal=N. Engl. J. Med. |volume=333 |issue=11 |pages=677–85 |year=1995 |pmid=7637744| doi = 10.1056/NEJM199509143331101 }}</ref> and obesity is estimated to cause an excess 111,909 to 365,000 death per year in the United States.<ref name=Allison/><ref name=HaslamJames>{{cite journal |author=Haslam DW, James WP |title=Obesity |journal=Lancet |volume=366 |issue=9492 |pages=1197–209 |year=2005 |pmid=16198769 |doi=10.1016/S0140-6736(05)67483-1}}</ref> Obesity on average reduces life expectancy by six to seven&nbsp;years.<ref>{{cite journal |author=Peeters A, Barendregt JJ, Willekens F, Mackenbach JP, Al Mamun A, Bonneux L |title=Obesity in adulthood and its consequences for life expectancy: A life-table analysis |journal=Ann. Intern. Med. |volume=138 |issue=1 |pages=24–32 |year=2003 |month=January |pmid=12513041 |doi= |url=http://www.annals.org/cgi/reprint/138/1/24 | format=PDF}}</ref><ref name=HaslamJames/>  A BMI of 30–35 reduces life expectancy by two to four&nbsp;years<ref name=Lancet2009/> while severe obesity (BMI&nbsp;>&nbsp;40) reduces life expectancy by 20&nbsp;years for men and five&nbsp;years for women.<ref name=emedicine>
{{cite web |url=http://www.emedicine.com/med/TOPIC1653.HTM |author=Schwarz, Steven| title=Obesity |accessdate=2008-09-30 |work= |publisher=emedicine |date=November 1, 2007 }}</ref>
 
===Morbidity===
 
Obesity increases the risk of many physical and mental conditions. These comorbidities are reflected predominantly in [[metabolic syndrome]].<ref name=HaslamJames/>  Metabolic syndrome being a combination of medical disorders, which includes [[diabetes mellitus type 2]], [[hypertension|high blood pressure]], [[hypercholesterolemia|high blood cholesterol]], and [[hypertriglyceridemia|high triglyceride levels]].<ref>{{cite journal |author=Grundy SM |title=Obesity, metabolic syndrome, and cardiovascular disease |journal=J. Clin. Endocrinol. Metab. |volume=89 |issue=6 |pages=2595–600 |year=2004 |pmid=15181029 |doi=10.1210/jc.2004-0372}}</ref>
 
Complications are either directly caused by obesity or indirectly related through 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 of 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.<ref>Seidell 2005 p.9</ref>
 
Health consequences can be categorized by the effects of increased fat mass ([[osteoarthritis]], [[obstructive sleep apnea]], social stigmatization) or by the increased number of [[fat cells]] ([[diabetes mellitus|diabetes]], [[cancer]], [[cardiovascular disease]], [[non-alcoholic fatty liver disease]]).<ref name=HaslamJames/><ref name=Bray2004>{{cite journal |author=Bray GA |title=Medical consequences of obesity |journal=J. Clin. Endocrinol. Metab. |volume=89 |issue=6 |pages=2583–9 |year=2004 |pmid=15181027 |doi=10.1210/jc.2004-0535}}</ref>  Increases in body fat alter the body's response to insulin, potentially leading to [[insulin resistance]]. Increased fat also creates a [[inflammation|proinflammatory state]], increasing the risk of [[thrombosis]].<ref name=Bray2004/>
 
{| class="wikitable"
|-
! Medical field
! Condition
! Medical field
! Condition
|-
<!--Alphabetized-->|width=10%| [[Cardiology]]
|
*[[ischemic heart disease]]:<ref name=Yusuf2004/> [[angina pectoris|angina]] and [[myocardial infarction]]
*[[congestive heart failure]]<ref name=HaslamJames/>
*[[high blood pressure]]<ref name=HaslamJames/>
*[[Dyslipidemia|abnormal cholesterol levels]]<ref name=HaslamJames/>
*[[deep vein thrombosis]] and [[pulmonary embolism]]<ref>{{cite journal |author=Darvall KA, Sam RC, Silverman SH, Bradbury AW, Adam DJ |title=Obesity and thrombosis |journal=Eur J Vasc Endovasc Surg |volume=33 |issue=2 |pages=223–33 |year=2007 |month=February |pmid=17185009 |doi=10.1016/j.ejvs.2006.10.006}}</ref>
| <!--Alphabetized-->[[Dermatology]]
|
*[[stretch mark]]s<ref name=derm2007/>
*[[acanthosis nigricans]]<ref name=derm2007>{{cite journal |author=Yosipovitch G, DeVore A, Dawn A |title=Obesity and the skin: skin physiology and skin manifestations of obesity |journal=J. Am. Acad. Dermatol. |volume=56 |issue=6 |pages=901–16; quiz 917–20 |year=2007 |month=June |pmid=17504714 |doi=10.1016/j.jaad.2006.12.004 |url=}}</ref>
*[[lymphedema]]<ref name=derm2007/>
*[[cellulitis]]<ref name=derm2007/>
*[[hirsutism]]<ref name=derm2007/>
*[[intertrigo]]<ref>{{cite journal |author=Hahler B |title=An overview of dermatological conditions commonly associated with the obese patient |journal=Ostomy Wound Manage |volume=52 |issue=6 |pages=34–6, 38, 40 passim |year=2006 |month=June |pmid=16799182 |doi= |url=}}</ref>
|-
| <!--Alphabetized-->[[Endocrinology]] and [[Reproductive medicine]]
|
*[[diabetes mellitus]]<ref name=HaslamJames/>
*[[polycystic ovarian syndrome]]<ref name=HaslamJames/>
*[[menstruation|menstrual]] disorders<ref name=HaslamJames/>
*[[infertility]]<ref name=HaslamJames/><ref name=OBGYN2008>{{cite journal |author=Arendas K, Qiu Q, Gruslin A |title=Obesity in pregnancy: pre-conceptional to postpartum consequences |journal=J Obstet Gynaecol Can |volume=30 |issue=6 |pages=477–88 |year=2008 |month=June |pmid=18611299 |doi= |url=}}</ref>
* complications during [[pregnancy]]<ref name=HaslamJames/><ref name=OBGYN2008/>
* [[birth defects]]<ref name=HaslamJames/>
*[[Stillbirth|intrauterine fetal death]]<ref name=OBGYN2008/>
| <!--Alphabetized-->[[Gastrointestinal]]
|
*[[gastroesophageal reflux disease]]<ref name=HaslamJames/><ref name=GERD2008>{{cite journal |author=Anand G, Katz PO |title=Gastroesophageal reflux disease and obesity |journal=Rev Gastroenterol Disord |volume=8 |issue=4 |pages=233–9 |year=2008 |pmid=19107097 |doi= |url=http://www.medreviews.com/pubmed.cfm?j=3&v=8&i=4&p=233}}</ref>
*[[non-alcoholic fatty liver disease|fatty liver disease]]<ref name=HaslamJames/>
*[[cholelithiasis]] (gallstones)<ref name=HaslamJames/>
|-
| <!--Alphabetized-->[[Neurology]]
| width=40%|
*[[stroke]]<ref name=HaslamJames/>
*[[meralgia paresthetica]]<ref>{{cite journal |author=Harney D, Patijn J |title=Meralgia paresthetica: diagnosis and management strategies |journal=Pain Med |volume=8 |issue=8 |pages=669–77 |year=2007 |pmid=18028045 |doi=10.1111/j.1526-4637.2006.00227.x |url=}}</ref>
*[[migraines]]<ref>{{cite journal |author=Bigal ME, Lipton RB |title=Obesity and chronic daily headache |journal=Curr Pain Headache Rep |volume=12 |issue=1 |pages=56–61 |year=2008 |month=January |pmid=18417025 |doi= 10.1007/s11916-008-0011-8|url=}}</ref>
*[[carpal tunnel syndrome]]<ref>{{cite journal |author=Sharifi-Mollayousefi A, Yazdchi-Marandi M, Ayramlou H, ''et al'' |title=Assessment of body mass index and hand anthropometric measurements as independent risk factors for carpal tunnel syndrome |journal=Folia Morphol. (Warsz) |volume=67 |issue=1 |pages=36–42 |year=2008 |month=February |pmid=18335412 |doi= |url=}}</ref>
*[[dementia]]<ref>{{cite journal |author=Beydoun MA, Beydoun HA, Wang Y |title=Obesity and central obesity as risk factors for incident dementia and its subtypes: A systematic review and meta-analysis |journal=Obes Rev |volume=9 |issue=3 |pages=204–18 |year=2008 |month=May |pmid=18331422 |doi=10.1111/j.1467-789X.2008.00473.x}}</ref>
*[[idiopathic intracranial hypertension]]<ref>{{cite journal |author=Wall M |title=Idiopathic intracranial hypertension (pseudotumor cerebri) |journal=Curr Neurol Neurosci Rep |volume=8 |issue=2 |pages=87–93 |year=2008 |month=March |pmid=18460275 |doi= 10.1007/s11910-008-0015-0|url=}}</ref>
| <!--Alphabetized-->[[Oncology]]<ref>{{cite journal |author=Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ |title=Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults |journal=N. Engl. J. Med. |volume=348 |issue=17 |pages=1625–38 |year=2003 |month=April |pmid=12711737 |doi=10.1056/NEJMoa021423}}</ref>
|
*[[breast cancer|breast]], [[ovarian cancer|ovarian]]
*[[esophageal cancer|esophageal]], [[colorectal cancer|colorectal]]
*[[hepatocellular carcinoma|liver]], [[pancreatic cancer|pancreatic]]
*[[Gallbladder cancer|gallbladder]], [[stomach cancer|stomach]]
*[[Endometrial cancer|endometrial]], [[cervical cancer|cervical]]
*[[prostate cancer|prostate]], [[Renal cell carcinoma|kidney]]
*[[non-Hodgkin's lymphoma]], [[multiple myeloma]]
|-
| width=10%| <!--Alphabetized-->[[Psychiatry]]
| width=40%|
*[[Major depressive disorder|depression]] in women<ref name=HaslamJames/>
*social stigmatization<ref name=HaslamJames/>
| <!--Alphabetized-->Respirology
|
*[[sleep apnea|obstructive sleep apnea]]<ref name=HaslamJames/><ref name=Poulain>{{cite journal |author=Poulain M, Doucet M, Major GC, ''et al.'' |title=The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies |journal=CMAJ |volume=174 |issue=9 |pages=1293–9 |year=2006 |month=April |pmid=16636330 |pmc=1435949 |doi=10.1503/cmaj.051299 |url=http://www.cmaj.ca/cgi/content/full/174/9/1293}}</ref>
*[[obesity hypoventilation syndrome]]<ref name=HaslamJames/><ref name=Poulain/>
*[[asthma]]<ref name=HaslamJames/><ref name=Poulain/>
*increased complications during [[general anaesthesia]]<ref name=HaslamJames/><ref name=Anes2000>{{cite journal |author=Adams JP, Murphy PG |title=Obesity in anaesthesia and intensive care |journal=Br J Anaesth |volume=85 |issue=1 |pages=91–108 |year=2000 |month=July |pmid=10927998 |doi= 10.1093/bja/85.1.91|url=http://bja.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=10927998}}</ref>
|-
| <!--Alphabetized-->[[Rheumatology]] and [[Orthopedics]]
|
*[[gout]]<ref>{{cite journal |author=Choi HK, Atkinson K, Karlson EW, Curhan G |title=Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow-up study |journal=Arch. Intern. Med. |volume=165 |issue=7 |pages=742–8 |year=2005 |month=April |pmid=15824292 |doi=10.1001/archinte.165.7.742 |url=}}</ref>
*poor mobility<ref>{{cite journal |author=Tukker A, Visscher T, Picavet H |title=Overweight and health problems of the lower extremities: osteoarthritis, pain and disability |journal=Public Health Nutr |volume= |issue= |pages=1–10 |year=2008 |month=April |pmid=18426630 |doi=10.1017/S1368980008002103 |url=}}</ref>
*[[osteoarthritis]]<ref name=HaslamJames/>
*[[low back pain]]<ref>{{cite journal |author=Molenaar EA, Numans ME, van Ameijden EJ, Grobbee DE |title=[Considerable comorbidity in overweight adults: results from the Utrecht Health Project] |language=Dutch; Flemish |journal=Ned Tijdschr Geneeskd |volume=152 |issue=45 |pages=2457–63 |year=2008 |month=November |pmid=19051798 |doi= |url=}}</ref>
| <!--Alphabetized-->[[Urology]] and [[Nephrology]]
|
*[[erectile dysfunction]]<ref>{{cite journal |author=Esposito K, Giugliano F, Di Palo C, Giugliano G, Marfella R, D'Andrea F, D'Armiento M, Giugliano D |title=Effect of lifestyle changes on erectile dysfunction in obese men: A randomized controlled trial |journal=JAMA |volume=291 |issue=24 |pages=2978–84 |year=2004 |pmid=15213209 |doi=10.1001/jama.291.24.2978}}</ref>
*[[urinary incontinence]]<ref>{{cite journal |author=Hunskaar S |title=A systematic review of overweight and obesity as risk factors and targets for clinical intervention for urinary incontinence in women |journal=Neurourol. Urodyn. |volume=27 |issue=8 |pages=749–57 |year=2008 |pmid=18951445 |doi=10.1002/nau.20635 |url=}}</ref>
*[[chronic renal failure]]<ref>{{cite journal |author=Ejerblad E, Fored CM, Lindblad P, Fryzek J, McLaughlin JK, Nyrén O |title=Obesity and risk for chronic renal failure |journal=J. Am. Soc. Nephrol. |volume=17 |issue=6 |pages=1695–702 |year=2006 |pmid=16641153 |doi=10.1681/ASN.2005060638}}</ref>
*[[hypogonadism]]<ref>{{cite journal |author=Makhsida N, Shah J, Yan G, Fisch H, Shabsigh R |title=Hypogonadism and metabolic syndrome: Implications for testosterone therapy |journal=J. Urol. |volume=174 |issue=3 |pages=827–34 |year=2005 |month=September |pmid=16093964 |doi=10.1097/01.ju.0000169490.78443.59}}</ref>
|}
 
===Obesity survival paradox===
Although the negative health consequences of obesity in the general population are well supported by the available evidence, health outcomes in certain subgroups seem to be improved at an increased BMI, a phenomenon known as the obesity survival paradox.<ref name=Schmidt2007>{{cite journal |author=Schmidt DS, Salahudeen AK |title=Obesity-survival paradox-still a controversy? |journal=Semin Dial |volume=20 |issue=6 |pages=486–92 |year=2007 |pmid=17991192 |doi=10.1111/j.1525-139X.2007.00349.x}}</ref> The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis,<ref name=Schmidt2007/> and has subsequently been found in those with [[heart failure]], and [[Peripheral vascular disease|peripheral artery disease]] (PAD).<ref name=paradox2003>{{cite journal |author= |title=Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale |journal=Am Fam Physician |volume=67 |issue=12 |pages=2573–6 |year=2003 |month=June |pmid=12825847 |doi= |url=http://www.aafp.org/afp/20030615/us.html}}</ref>
 
In people with heart failure, those with a BMI between 30.0–34.9 had lower mortality then those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill.<ref>{{cite journal |author=Habbu A, Lakkis NM, Dokainish H |title=The obesity paradox: Fact or fiction? |journal=Am. J. Cardiol. |volume=98 |issue=7 |pages=944–8 |year=2006 |month=October |pmid=16996880 |doi=10.1016/j.amjcard.2006.04.039}}</ref> Similar findings have been made in other types of heart disease. People with class I obesity and 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.<ref>{{cite journal |author=Romero-Corral A, Montori VM, Somers VK, ''et al.'' |title=Association of bodyweight with total mortality and with cardiovascular events in coronary artery disease: A systematic review of cohort studies |journal=Lancet |volume=368 |issue=9536 |pages=666–78 |year=2006 |pmid=16920472 |doi=10.1016/S0140-6736(06)69251-9}}</ref><ref>{{cite journal |author=Oreopoulos A, Padwal R, Kalantar-Zadeh K, Fonarow GC, Norris CM, McAlister FA |title=Body mass index and mortality in heart failure: A meta-analysis |journal=Am. Heart J. |volume=156 |issue=1 |pages=13–22 |year=2008 |month=July |pmid=18585492 |doi=10.1016/j.ahj.2008.02.014 |url=}}</ref>  Even after [[Coronary artery bypass surgery|cardiac bypass surgery]], no increase in mortality is seen in the overweight and obese.<ref>{{cite journal |author=Oreopoulos A, Padwal R, Norris CM, Mullen JC, Pretorius V, Kalantar-Zadeh K |title=Effect of obesity on short- and long-term mortality postcoronary revascularization: A meta-analysis |journal=Obesity (Silver Spring) |volume=16 |issue=2 |pages=442–50 |year=2008 |month=February |pmid=18239657 |doi=10.1038/oby.2007.36}}</ref>  One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event.<ref>{{cite journal| author=Diercks DB, Roe MT, Mulgund J ''et al.'' | title=The obesity paradox in non-ST-segment elevation acute coronary syndromes: Results from the Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the American College of Cardiology/American Heart Association Guidelines Quality Improvement Initiative | journal=Am Heart J | year=2006 | month=July | volume=152 | issue=1 | pages=140–8 | pmid=16824844 | doi=10.1016/j.ahj.2005.09.024}}</ref>  Another found that if one takes into account [[chronic obstructive pulmonary disease]] (COPD) in those with PAD the benefit of obesity no longer exsists.<ref name=paradox2003/>
 
==Causes and mechanisms==
===Lifestyle===
Most researchers have concluded that the combination of an excessive nutrient intake and a [[sedentary lifestyle]] are the main cause for the rapid acceleration of obesity in Western society in the last quarter of the 20th century. <ref>Sara Bleich, David Cutler, Christopher Murray, Alyce Adams. [http://www.nber.org/papers/w12954 ''Why is the Developed World Obese?''] National Bureau of Economic Research Working Paper No. 12954. Issued in March 2007.</ref>
 
Despite the widespread availability of nutritional information in schools, doctors' offices, on the internet and on groceries,<ref>Centers for Disease Control and Prevention. ''[http://www.cdc.gov/nccdphp/dnpa/nutrition/nutrition_for_everyone/index.htm Nutrition For Everyone]''. National Control for Health Statistics. Accessed July 15, 2007.</ref> it is evident that overeating remains a substantial problem. For instance, reliance on [[food energy|energy-dense]] fast-food meals tripled between 1977 and 1995, and calorie intake quadrupled over the same period.<ref>Lin BH, Guthrie J and Frazao E (1999). "Nutrient contribution of food away from home". In: Frazao E (Ed). ''America's Eating Habits: Changes and Consequences''. Agriculture Information Bulletin No. 750, US Department of Agriculture, Economic Research Service, Washington, DC, pp. 213–239. [http://www.ers.usda.gov/publications/aib750/ Fulltext index].</ref>
 
However, dietary intake in itself is insufficient to explain the phenomenal rise in levels of obesity in much of the industrialized world during recent years.  An increasingly sedentary lifestyle also has a significant role to play.  More and more research into [[child obesity]], for example, links such things as [[school run|the school run]], with the current high levels of this disease. <ref>http://politics.guardian.co.uk/publicservices/story/0,,2147839,00.html</ref>
 
Less well established life style issues which may influence obesity include a [[Stress (medicine)|stressful]] mentality and insufficient [[sleep]].
 
===Genetics===
As with many medical conditions, the calorific imbalance that results in obesity often develops from a combination of genetic and environmental factors. [[Polymorphism (biology)|Polymorphism]]s in various [[gene]]s controlling [[appetite]], [[metabolism]], and [[adipokine]] release predispose to obesity, but the condition requires availability of sufficient calories, and possibly other factors, to develop fully. Various genetic conditions that feature obesity have been identified (such as [[Prader-Willi syndrome]], [[Bardet-Biedl syndrome]], [[MOMO syndrome]], [[leptin]] receptor mutations and [[melanocortin receptor]] mutations), but known single-locus mutations have been found in only about 5% of obese individuals. While it is thought that a large proportion of the causative genes are still to be identified, much obesity is likely the result of interactions between multiple genes, and non-genetic factors are likely also important.
 
A 2007 study identified fairly common mutations in the [[FTO gene|''FTO'' gene]]; heterozygotes had a 30% increased risk of obesity, while homozygotes faced a 70% increased risk.<ref>{{cite journal |author=Frayling TM, Timpson NJ, Weedon MN, ''et al'' |title=A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity |journal=Science |volume=316 |issue=5826 |pages=889-94 |year=2007 |pmid=17434869 |doi=10.1126/science.1141634}}</ref>
 
On a population level, the ''[[thrifty gene hypothesis]]'' postulates that certain ethnic groups may be more prone to obesity than others, and the ability to take advantage of rare periods of abundance and use such abundance by storing energy efficiently may have been an evolutionary advantage in times when food was scarce. Individuals with greater adipose reserves were more likely to survive famine. This tendency to store fat is likely maladaptive in a society with stable food supplies.<ref>{{cite journal |author=Chakravarthy MV, Booth FW |title=Eating, exercise, and "thrifty" genotypes: connecting the dots toward an evolutionary understanding of modern chronic diseases |journal=J. Appl. Physiol. |volume=96 |issue=1 |pages=3-10 |year=2004 |pmid=14660491 |doi=10.1152/japplphysiol.00757.2003}}</ref>
 
===Medical illness===
Certain physical and mental illnesses and particular pharmaceutical substances may predispose to obesity. Apart from the fact that correcting these situations may improve the obesity, the presence of increased body weight may complicate the management of others.
 
Medical illnesses that increase obesity risk include several rare congenital syndromes (listed above), [[hypothyroidism]], [[Cushing's syndrome]], [[growth hormone deficiency]].<ref>{{cite journal |author=Rosén T, Bosaeus I, Tölli J, Lindstedt G, Bengtsson BA |title=Increased body fat mass and decreased extracellular fluid volume in adults with growth hormone deficiency |journal=Clin. Endocrinol. (Oxf) |volume=38 |issue=1 |pages=63-71 |year=1993 |pmid=8435887 |doi=}}</ref> [[Smoking cessation]] is a known cause for moderate weight gain, as nicotine suppresses appetite. Certain medications (e.g. [[glucocorticoids|steroids]], [[atypical antipsychotic]]s, some [[fertility medication]]) may cause weight gain.
 
Mental illnesses may also increase obesity risk, specifically some [[eating disorder]]s such as [[bulimia nervosa]], [[binge eating disorder]], and [[compulsive overeating]] (also known as food addiction).
 
===Neurobiological mechanisms===
[[Image:Fatmouse.jpg|thumb|left|350px|Scientists investigating the mechanisms and treatment of obesity may use [[animal model]]s such as mice to conduct experiments.]]
 
Flier<ref name="flier">{{cite journal | author=Flier JS | title=Obesity wars: molecular progress confronts an expanding epidemic | journal=Cell | year=2004 | pages=337-50 | volume=116 | issue=2 | id=PMID 14744442}}</ref> summarizes the many possible [[pathophysiology|pathophysiological]] mechanisms involved in the development and maintenance of obesity. This field of research had been almost unapproached until [[leptin]] was discovered in 1994. Since this discovery, many other hormonal mechanisms have been elucidated that participate in the regulation of [[appetite]] and food intake, storage patterns of [[adipose tissue]], and development of [[insulin resistance]]. Since leptin's discovery, [[ghrelin]], [[orexin]], [[PYY 3-36]], [[cholecystokinin]], [[adiponectin]], and many other mediators have been studied. The [[adipokine]]s 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 appetite, with ghrelin produced by the [[stomach]] modulating short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is stretched). Leptin is produced by adipose tissue to signal fat storage reserves in the body, and mediates long-term appetitive controls (i.e. to eat more when fat storages 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 deficient, many more obese individuals are thought to be leptin resistant. This resistance is thought to explain in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese subjects.
 
While leptin and ghrelin are produced peripherally, they control appetite through their actions on the [[central nervous system]]. In particular, they and other appetite-related hormones act on the [[hypothalamus]], a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the [[melanocortin]] pathway being the most well understood.<ref name="flier"/> The circuit begins with an area of the hypothalamus, the [[arcuate nucleus]], that has outputs to the [[lateral hypothalamus]] (LH) and [[ventromedial hypothalamus]] (VMH), the brain's feeding and satiety centers, respectively.<ref>{{cite book |author=Boulpaep, Emile L.; Boron, Walter F. |title=Medical physiology: a cellular and molecular approach |publisher=Saunders |location=Philadelphia |year=2003 |pages= |isbn=0-7216-3256-4 |oclc= |doi=}}</ref>
 
The arcuate nucleus contains two distinct groups of [[neuron]]s.<ref name="flier"/> The first 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 coexpresses [[pro-opiomelanocortin]] (POMC) and [[cocaine- and amphetamine-regulated transcript]] (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 group while stimulating the POMC/CART group. Thus a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leads to overfeeding and may account for some genetic and acquired forms of obesity.
 
===Microbiological aspects===
The role of [[bacteria]] colonizing the digestive tract in the development of obesity has recently become the subject of investigation. Bacteria participate in digestion (especially of [[fatty acid]]s and [[polysaccharide]]s), and alterations in the proportion of particular strains of bacteria may explain why certain people are more prone to weight gain than others. Human digestive tract are generally either members of the phyla of [[bacteroidetes]] or of [[firmicutes]]. In obese people, there is a relative abundance of firmicutes (which cause relatively high energy absorption), which is restored by weight loss. From these results it cannot yet be concluded whether this imbalance is the cause of obesity or an effect.<ref>{{cite journal |author=Ley RE, Turnbaugh PJ, Klein S, Gordon JI |title=Microbial ecology: human gut microbes associated with obesity |journal=Nature |volume=444 |issue=7122 |pages=1022-3 |year=2006 |pmid=17183309 |doi=10.1038/4441022a}}</ref>


===Social determinants===
{{SK}}  
Some obesity co-factors are resistant to the theory that the "epidemic" is a new phenomenon. In particular, a [[social class|class]] co-factor consistently appears across many studies. Comparing net worth with BMI scores, a 2004 study<ref>Zagorsky JL. Is Obesity as Dangerous to Your Wealth as to Your Health? ''Res Aging'' 2004;26:130-152. [http://roa.sagepub.com/cgi/reprint/26/1/130 PDF fulltext].{{doi|10.1177/0164027503258519}}.<!--No PMID--></ref> found obese American subjects approximately half as wealthy as thin ones. When income differentials were factored out, the inequity persisted—thin subjects were inheriting more wealth than fat ones. A higher rate of a lower level of education and tendencies to rely on cheaper [[fast food]]s is seen as a reason why these results are so dissimilar. Another study finds women who married into higher status are predictably thinner than women who married into lower status.


A 2007 study of more than 32,500 children of the original [[Framingham Heart Study]] cohort followed for 32 years indicated that BMI change in friends, siblings or spouse predicted BMI change in subjects irrespective of geographical distance. The association was strongest among mutual friends and lower among siblings and spouses (although these differences were not statistically significant). The authors concluded from the results that acceptance of body mass plays an important role in changes in body size.<ref>{{cite journal |author=Christakis NA, [[James H. Fowler|Fowler JH]] |title=The Spread of Obesity in a Large Social Network over 32 Years |journal= |volume=357 |issue=4 |pages=370-379 |year=2007 |pmid=17652652 |doi=10.1056/NEJMsa066082}}</ref>
==[[Obesity overview|Overview]]==


== Treatment ==
==[[Obesity historical perspective|Historical Perspective]]==
{{Main|Weight loss#Intentional weight loss|l1=Weight loss}}
The main treatment for obesity is to reduce body fat by [[dieting|eating fewer calories]] and [[Physical exercise|exercising]] more.  A beneficial side effect of exercise is to increase muscle, tendon, and ligament strength, which helps to prevent injury from accidents and vigorous activity.  Diet and exercise programs produce an average weight loss of approximately 8% of total body mass (excluding program drop-outs). Not all dieters are satisfied with these results, but a loss of as little as 5% of body mass can create large health benefits.


Much more difficult than reducing body fat is keeping it off. Eighty to ninety-five percent of those who lose 10% or more of their [[body mass]] by dieting regain all that weight back within two to five years.  The body has systems that maintain its [[homeostasis]] at certain set points, including body weight. Therefore, keeping weight off generally requires making [[Physical exercise|exercise]] and [[Healthy diet|eating right]] a permanent part of a person's [[lifestyle]]. Certain nutrients, such as [[phenylalanine]], are natural appetite suppressants which allow resetting of the body's set point for body weight.
==[[Obesity classification|Classification]]==


== Clinical protocols ==
==[[Obesity pathophysiology|Pathophysiology]]==
In a [[clinical practice guideline]] by the [[American College of Physicians]], the following five recommendations are made:<ref name=Snow2005>{{cite journal | author=Snow V, Barry P, Fitterman N, Qaseem A, Weiss K | title=Pharmacologic and surgical management of obesity in primary care: a clinical practice guideline from the American College of Physicians | journal=Ann Intern Med | year=2005 | pages=525-31 | volume=142 | issue=7 | id=PMID 15809464}} [http://www.annals.org/cgi/content/full/142/7/525 Fulltext].</ref>
# People with a BMI of over 30 should be counseled on diet, exercise and other relevant behavioral interventions, and set a realistic goal for weight loss.
# If these goals are not achieved, pharmacotherapy can be offered. The patient needs to be informed of the possibility of [[Adverse effect (medicine)|side-effects]] and the unavailability of long-term safety and efficacy data.
# Drug therapy may consist of [[sibutramine]], [[orlistat]], [[phentermine]], [[diethylpropion]], [[fluoxetine]], and [[bupropion]]. For more severe cases of obesity, stronger drugs such as [[amphetamine]] and [[methamphetamine]] may be used on a selective basis.  Evidence is not sufficient to recommend [[sertraline]], [[topiramate]], or [[zonisamide]].
# In patients with BMI > 40 who fail to achieve their weight loss goals (with or without medication) and who develop obesity-related complications, referral for [[bariatric surgery]] may be indicated. The patient needs to be aware of the potential complications.
# Those requiring bariatric surgery should be referred to high-volume referral centers, as the evidence suggests that surgeons who frequently perform these procedures have fewer complications.


A [[clinical practice guideline]] by the [[US Preventive Services Task Force]] (USPSTF) concluded that the evidence is insufficient to recommend for or against routine behavioral counseling to promote a healthy diet in unselected patients in primary care settings, but that intensive behavioral dietary counseling is recommended in those with [[hyperlipidemia]] and other known risk factors for cardiovascular and diet-related chronic disease. Intensive counseling can be delivered by primary care clinicians or by referral to other specialists, such as nutritionists or dietitians.<ref>{{cite web |url=http://www.ngc.gov/summary/summary.aspx?ss=15&doc_id=3494 |title=Behavioral counseling in primary care to promote a healthy diet: recommendations and rationale. |accessdate=2007-05-22 |format= |work=}}</ref><ref name="pmid12554027">{{cite journal |author=Pignone MP, Ammerman A, Fernandez L, ''et al'' |title=Counseling to promote a healthy diet in adults: a summary of the evidence for the U.S. Preventive Services Task Force |journal=American journal of preventive medicine |volume=24 |issue=1 |pages=75-92 |year=2003 |pmid=12554027 |doi=}}</ref>
==[[Obesity causes|Causes]]==


=== Exercise ===
==[[Obesity differential diagnosis|Differentiating Obesity from other Diseases]]==
Exercise requires energy (calories).  Calories are stored in body fat. The body breaks down its fat stores in order to provide energy during prolonged [[aerobic exercise]]. The largest muscles in the body are the leg muscles, and naturally these burn the most calories, which make walking, running, and cycling among the most effective forms of exercise for reducing body fat.


A [[meta-analysis]] of [[randomized controlled trials]] by the international [[Cochrane Collaboration]] found that "exercise combined with diet resulted in a greater weight reduction than diet alone".<ref name="pmid17054187">{{cite journal |author=Shaw K, Gennat H, O'Rourke P, Del Mar C |title=Exercise for overweight or obesity |journal=Cochrane database of systematic reviews (Online) |volume= |issue=4 |pages=CD003817 |year=2006 |pmid=17054187 |doi=10.1002/14651858.CD003817.pub3}}</ref>
==[[Obesity epidemiology and demographics|Epidemiology and Demographics]]==


=== Dieting ===
==[[Obesity risk factors|Risk Factors]]==
{{main|Dieting}}


In general, dieting means eating less.  Various dietary approaches have been proposed, some of which have been compared by [[randomized controlled trials]]:
==[[Obesity screening|Screening]]==
* A comparison of [[Atkins diet|Dr. Atkins']], [[Slim-Fast]]'s, [[Weight Watchers]]', and Rosemary Conley's diets found no significant differences.<ref name="pmid16720619">{{cite journal |author=Truby H, Baic S, deLooy A, ''et al'' |title=Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from the BBC "diet trials" |journal=BMJ |volume=332 |issue=7553 |pages=1309-14 |year=2006 |pmid=16720619 |doi=10.1136/bmj.38833.411204.80}}</ref>
* A comparison of [[Atkins diet]], [[Zone diet]], [[Weight Watchers]], and [[Ornish diet]] noted:<ref name="pmid15632335">{{cite journal |author=Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ |title=Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial |journal=JAMA |volume=293 |issue=1 |pages=43-53 |year=2005 |pmid=15632335 |doi=10.1001/jama.293.1.43}}</ref>
: "all 4 diets resulted in modest statistically significant weight loss at 1 year, with no statistically significant differences between diets"
: "The higher discontinuation rates for the Atkins and Ornish diet groups suggest many individuals found these diets to be too extreme"


====Low carbohydrate versus low fat====
==[[Obesity natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
{{main|Medical research related to low-carbohydrate diets}}
Many studies have focused on diets that reduce calories via a low-carbohydrate ([[Atkins diet]], [[Zone diet]]) diet versus a low-fat diet ([[LEARN diet]], [[Ornish diet]]). The [[Nurses' Health Study]], an observational [[cohort study]], found that low carbohydrate diets based on vegetable sources of fat and protein are associated with less [[coronary heart disease]].<ref name="pmid17093250">{{cite journal |author=Halton TL, Willett WC, Liu S, ''et al'' |title=Low-carbohydrate-diet score and the risk of coronary heart disease in women |journal=N. Engl. J. Med. |volume=355 |issue=19 |pages=1991-2002 |year=2006 |pmid=17093250 |doi=10.1056/NEJMoa055317}}</ref>


A [[meta-analysis]] of [[randomized controlled trials]] by the international [[Cochrane Collaboration]] in 2002 concluded<ref name="pmid12076496">{{cite journal |author=Pirozzo S, Summerbell C, Cameron C, Glasziou P |title=Advice on low-fat diets for obesity |journal=Cochrane database of systematic reviews (Online) |volume= |issue=2 |pages=CD003640 |year=2002 |pmid=12076496 |doi=}}</ref> that fat-restricted diets are no better than calorie restricted diets in achieving long term weight loss in overweight or obese people.
==Diagnosis==
[[Obesity history and symptoms|History and Symptoms]] | [[Obesity physical examination|Physical Examination]] | [[Obesity laboratory findings|Laboratory Findings]] | [[Obesity electrocardiogram|Electrocardiogram]] | [[Obesity chest x ray|Chest X Ray]] | [[Obesity CT|CT]] | [[Obesity MRI|MRI]] | [[Obesity echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Obesity other imaging findings|Other Imaging Findings]] | [[Obesity other diagnostic studies|Other Diagnostic Studies]]


A more recent [[meta-analysis]] that included [[randomized controlled trials]] published after the Cochrane review<ref name="pmid12761364">{{cite journal |author=Samaha FF, Iqbal N, Seshadri P, ''et al'' |title=A low-carbohydrate as compared with a low-fat diet in severe obesity |journal=N. Engl. J. Med. |volume=348 |issue=21 |pages=2074–81 |year=2003 |pmid=12761364 |doi=10.1056/NEJMoa022637}}</ref><ref name="pmid12761365">{{cite journal |author=Foster GD, Wyatt HR, Hill JO, ''et al'' |title=A randomized trial of a low-carbohydrate diet for obesity |journal=N. Engl. J. Med. |volume=348 |issue=21 |pages=2082–90 |year=2003 |pmid=12761365 |doi=10.1056/NEJMoa022207}}</ref><ref name="pmid15632335"/> found that "low-carbohydrate, non-energy-restricted diets appear to be at least as effective as low-fat, energy-restricted diets in inducing weight loss for up to 1 year. However, potential favorable changes in triglyceride and high-density lipoprotein cholesterol values should be weighed against potential unfavorable changes in low-density lipoprotein cholesterol values when low-carbohydrate diets to induce weight loss are considered."<ref name="pmid16476868">{{cite journal |author=Nordmann AJ, Nordmann A, Briel M, ''et al'' |title=Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials |journal=Arch. Intern. Med. |volume=166 |issue=3 |pages=285-93 |year=2006 |pmid=16476868 |doi=10.1001/archinte.166.3.285}}</ref>
==Treatment==
[[Obesity medical therapy|Medical Therapy]] | [[Obesity surgery|Surgery]] | [[Obesity primary prevention|Primary Prevention]] | [[Obesity secondary prevention|Secondary Prevention]] | [[Obesity cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Obesity future or investigational therapies|Future or Investigational Therapies]]


The [[Women's Health Initiative]] Randomized Controlled Dietary Modification Trial<ref name="pmid16391215">{{cite journal |author=Howard BV, Manson JE, Stefanick ML, ''et al'' |title=Low-fat dietary pattern and weight change over 7 years: the Women's Health Initiative Dietary Modification Trial |journal=JAMA |volume=295 |issue=1 |pages=39-49 |year=2006 |pmid=16391215 |doi=10.1001/jama.295.1.39}}</ref> found that a diet of total fat to 20% of energy and increasing consumption of vegetables and fruit to at least 5 servings daily and grains to at least 6 servings daily resulted in:
==Case Studies==
* no reduction in cardiovascular disease<ref name="pmid16467234">{{cite journal |author=Howard BV, Van Horn L, Hsia J, ''et al'' |title=Low-fat dietary pattern and risk of cardiovascular disease: the Women's Health Initiative Randomized Controlled Dietary Modification Trial |journal=JAMA |volume=295 |issue=6 |pages=655-66 |year=2006 |pmid=16467234 |doi=10.1001/jama.295.6.655}}</ref>
[[Obesity case study one|Case #1]]
* an insignificant reduction in invasive breast cancer<ref name="pmid16467232">{{cite journal |author=Prentice RL, Caan B, Chlebowski RT, ''et al'' |title=Low-fat dietary pattern and risk of invasive breast cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial |journal=JAMA |volume=295 |issue=6 |pages=629-42 |year=2006 |pmid=16467232 |doi=10.1001/jama.295.6.629}}</ref>
* no reductions in colorectal cancer<ref name="pmid16467233">{{cite journal |author=Beresford SA, Johnson KC, Ritenbaugh C, ''et al'' |title=Low-fat dietary pattern and risk of colorectal cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial |journal=JAMA |volume=295 |issue=6 |pages=643-54 |year=2006 |pmid=16467233 |doi=10.1001/jama.295.6.643}}</ref>


Additional recent [[randomized controlled trials]] have found that:
==Related Chapters==
* A comparison of Atkins, [[Zone diet]], [[Ornish diet]], and [[LEARN diet]] in ''premenopausal women'' found the greatest benefit from the [[Atkins diet]].<ref name="pmid17341711">{{cite journal |author=Gardner CD, Kiazand A, Alhassan S, ''et al'' |title=Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial |journal=JAMA |volume=297 |issue=9 |pages=969-77 |year=2007 |pmid=17341711 |doi=10.1001/jama.297.9.969}}</ref>
 
* The choice of diet for a specific person may be influenced by measuring the invididual's insulin secretion:
:In [[young adults]] "Reducing glycemic [carbohydrate] load may be especially important to achieve weight loss among individuals with high insulin secretion."<ref name="pmid17507345">{{cite journal |author=Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, Ludwig DS |title=Effects of a low-glycemic load vs low-fat diet in obese young adults: a randomized trial |journal=JAMA |volume=297 |issue=19 |pages=2092-102 |year=2007 |pmid=17507345 |doi=10.1001/jama.297.19.2092}}</ref> This is consistent with prior studies of diabetic patients in which low carbohydrate diets were more beneficial.<ref name="pmid15148064">{{cite journal |author=Stern L, Iqbal N, Seshadri P, ''et al'' |title=The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial |journal=Ann. Intern. Med. |volume=140 |issue=10 |pages=778–85 |year=2004 |pmid=15148064 |doi=}}</ref><ref name="pmid7848401">{{cite journal |author=Garg A, Bantle JP, Henry RR, ''et al'' |title=Effects of varying carbohydrate content of diet in patients with non-insulin-dependent diabetes mellitus |journal=JAMA |volume=271 |issue=18 |pages=1421–8 |year=1994 |pmid=7848401 |doi=}}</ref>
 
====Low glycemic index====
"The glycaemic index factor is a ranking of foods based on their overall effect on blood sugar levels. Low glycaemic index foods, such as lentils, provide a slower more consistent source of glucose to the bloodstream, thereby stimulating less insulin release than high glycaemic index foods, such as white bread."<ref name="pmid17636786">{{cite journal |author=Thomas D, Elliott E, Baur L |title=Low glycaemic index or low glycaemic load diets for overweight and obesity |journal= |volume=3 |issue= |pages=CD005105 |year=2007 |pmid=17636786 |doi=10.1002/14651858.CD005105.pub2}}</ref><ref name="pmid6259925">{{cite journal |author=Jenkins DJ, Wolever TM, Taylor RH, ''et al'' |title=Glycemic index of foods: a physiological basis for carbohydrate exchange |journal=Am. J. Clin. Nutr. |volume=34 |issue=3 |pages=362-6 |year=1981 |pmid=6259925 |doi=}}</ref>
 
The glycemic load is "the mathematical product of the glycemic index and the carbohydrate amount".<ref name="pmid12949357">{{cite journal |author=Brand-Miller JC, Thomas M, Swan V, Ahmad ZI, Petocz P, Colagiuri S |title=Physiological validation of the concept of glycemic load in lean young adults |journal=J. Nutr. |volume=133 |issue=9 |pages=2728-32 |year=2003 |pmid=12949357 |doi=}}</ref>
 
In a [[randomized controlled trial]] that compared four diets that varied in carbohydrate amount and glycemic index found complicated results<ref name="pmid16864756">{{cite journal |author=McMillan-Price J, Petocz P, Atkinson F, ''et al'' |title=Comparison of 4 diets of varying glycemic load on weight loss and cardiovascular risk reduction in overweight and obese young adults: a randomized controlled trial |journal=Arch. Intern. Med. |volume=166 |issue=14 |pages=1466-75 |year=2006 |pmid=16864756 |doi=10.1001/archinte.166.14.1466}}</ref>:
* Diet 1 and 2 were high carbohydrate (55% of total energy intake)
** Diet 1 was high-glycemic index
** Diet 2 was low-glycemic index
* Diet 3 and 4 were high protein (25% of total energy intake)
** Diet 3 was high-glycemic index
** Diet 4 was low-glycemic index
 
Diets 2 and 3 lost the most weight and fat mass; however, low density lipoprotein fell in Diet 2 and rose in Diet 3. Thus the authors concluded that the high-carbohydrate, low-glycemic index  diet was the most favorable.
 
A [[meta-analysis]] by the [[Cochrane Collaboration]] concluded that low glycemic index or low glycemic load diets led to more weight loss and better lipid profiles. ''However'', the [[Cochrane Collaboration]] grouped low glycemic index and low glycemic load diets together and did not try to separate the effects of the load versus the index.<ref name="pmid17636786">{{cite journal |author=Thomas DE, Elliott E, Baur L |title=Low glycaemic index or low glycaemic load diets for overweight and obesity |journal=Cochrane database of systematic reviews (Online) |volume= |issue=3 |pages=CD005105 |year=2007 |pmid=17636786 |doi=10.1002/14651858.CD005105.pub2}}</ref>
 
===Drugs===
{{main|Anti-obesity drug}}
 
Medication most commonly prescribed for diet/exercise-resistant obesity is [[orlistat]] (Xenical, which reduces intestinal fat absorption by inhibiting [[pancreas|pancreatic]] [[lipase]]) and [[sibutramine]] (Reductil, Meridia, an [[anorectic]]). Weight loss with these drugs is modest, and over the longer term average weight loss on orlistat is 2.9 kg, sibutramine 4.2 kg and rimonabant 4.7 kg. Orlistat and rimonabant lead to a reduced incidence of diabetes, and all drugs have some effect on [[lipoprotein]]s (different forms of [[cholesterol]]). There is little data, however, on longer-term complications of obesity such as [[myocardial infarction|heart attacks]]. All drugs have side-effects and potential contraindications.<ref>{{cite journal |author=Rucker D, Padwal R, Li SK, Curioni C, Lau DC |title=Long term pharmacotherapy for obesity and overweight: updated meta-analysis |journal=BMJ |volume=335 |issue=7631 |pages=1194–9 |year=2007 |pmid=18006966 |doi=10.1136/bmj.39385.413113.25|http://www.bmj.com/cgi/content/full/335/7631/1194}}</ref> It is common for weight loss drugs to be tried for a period of time (e.g. 3 months), and to discontinue them or change to another agent if no benefit is achieved, such as weight loss less than 5% the total body weight.<ref name=NICECG043/>
 
A [[meta-analysis]] of [[randomized controlled trials]] by the international [[Cochrane Collaboration]] concluded that in ''diabetic'' patients fluoxetine, orlistat and sibutramine could achieve significant but modest weight loss over 12-57 weeks, with long-term health benefits being unclear.<ref name="pmid15674929">{{cite journal |author=Norris SL, Zhang X, Avenell A, Gregg E, Schmid CH, Lau J |title=Pharmacotherapy for weight loss in adults with type 2 diabetes mellitus |journal=Cochrane database of systematic reviews (Online) |volume= |issue=1 |pages=CD004096 |year=2005 |pmid=15674929 |doi=10.1002/14651858.CD004096.pub2}}</ref>
 
Obesity may also influence the choice of drug treatment for diabetes. [[Metformin]] may lead to mild weight reduction (as opposed to [[sulfonylurea]]s and [[insulin]]), and has been demonstrated to reduce the risk of [[cardiovascular disease]] in type 2 diabetics who are obese.<ref name = UKPDS>{{cite journal | author =UK Prospective Diabetes Study (UKPDS) Group | title = Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34) | journal = Lancet | volume = 352 | issue = 9131 | pages = 854–65 | year = 1998 | pmid=9742977 |doi=10.1016/S0140-6736(98)07037-8}}</ref> The [[thiazolidinedione]]s may cause slight weight gain, but decrease the "pathologic" form of abdominal fat and may therefore be used in diabetics with central obesity.<ref>{{cite journal |author=Fonseca V |title=Effect of thiazolidinediones on body weight in patients with diabetes mellitus |journal=Am. J. Med. |volume=115 Suppl 8A |issue= |pages=42S–48S |year=2003 |pmid=14678865 |doi=10.1016/j.amjmed.2003.09.005}}</ref>
 
===Bariatric surgery===
{{main|bariatric surgery}}
''[[Bariatric surgery]]'' (or "weight loss surgery") is the use of surgical interventions in the treatment of obesity. As every surgical intervention may lead to complications, it is regarded as a last resort when dietary modification and pharmacological treatment have proven to be unsuccessful. Weight loss surgery relies on various principles; the most common approaches are reducing the volume of the stomach, producing an earlier sense of satiation (e.g. by [[adjustable gastric band]]ing and [[Vertical banded gastroplasty surgery|vertical banded gastroplasty]]) while others also reduce the length of bowel that food will be in contact with, directly reducing absorption ([[gastric bypass surgery]]). Band surgery is reversible, while bowel shortening operations are not. Some procedures can be performed [[laparoscopic surgery|laparoscopically]]. Complications from weight loss surgery are frequent.<ref name="pmid16862031">{{cite journal |author=Encinosa WE, Bernard DM, Chen CC, Steiner CA |title=Healthcare utilization and outcomes after bariatric surgery |journal=Medical care |volume=44 |issue=8 |pages=706-12 |year=2006 |pmid=16862031 |doi=10.1097/01.mlr.0000220833.89050.ed}}</ref>
 
Two large studies have demonstrated a mortality benefit from bariatric surgery. A marked decrease in the risk of [[diabetes mellitus]], [[cardiovascular disease]] and [[cancer]].<ref name="pmid17715408">{{cite journal |author=Sjöström L, Narbro K, Sjöström CD, ''et al'' |title=Effects of bariatric surgery on mortality in Swedish obese subjects |journal=N. Engl. J. Med. |volume=357 |issue=8 |pages=741-52 |year=2007 |pmid=17715408 |doi=10.1056/NEJMoa066254}}</ref><ref name="pmid17715409">{{cite journal |author=Adams TD, Gress RE, Smith SC, ''et al'' |title=Long-term mortality after gastric bypass surgery |journal=N. Engl. J. Med. |volume=357 |issue=8 |pages=753-61 |year=2007 |pmid=17715409 |doi=10.1056/NEJMoa066603}}</ref> Weight loss was most marked in the first few months after surgery, but the benefit was sustained in the longer term. In one study there was an unexplained increase in deaths from accidents and suicide that did not outweigh the benefit in terms of disease prevention. Gastric bypass surgery was about twice as effective as banding procedures.<ref name="pmid17715409"/>
 
===Counseling===
A [[meta-analysis]] of [[randomized controlled trial]]s concluded that "compared with usual care, dietary counseling interventions produce modest weight losses that diminish over time."<ref name="pmid17606960">{{cite journal |author=Dansinger ML, Tatsioni A, Wong JB, Chung M, Balk EM |title=Meta-analysis: the effect of dietary counseling for weight loss |journal=Ann. Intern. Med. |volume=147 |issue=1 |pages=41-50 |year=2007 |pmid=17606960 |doi=|url=http://www.annals.org/cgi/content/full/147/1/41}}</ref>
 
==Cultural and social significance==
 
===Etymology===
''Obesity'' is the nominal form of ''obese'' which comes from the Latin ''obēsus'', which means "stout, fat, or plump."  ''Ēsus'' is the past participle of ''edere'' (to eat), with ''ob'' added to it. In Classical Latin, this verb is seen only in past participial form. Its first attested usage in English was in 1651, in Noah Biggs's ''Matæotechnia Medicinæ Praxeos''.<ref>''The Oxford English Dictionary'' (website)</ref>
 
===History===
 
[[Image:Italienischer Maler des 17 Jahrhunderts 001.jpg|110px|thumb|left|Obesity was a status symbol in European culture: "The Tuscan General" by Alessandro del Borro, 17th century.]]
In several human cultures, obesity was associated with [[physical attractiveness]], [[physical strength|strength]], and [[fertility]]. Some of the earliest known cultural artifact artifacts, known as Venus figurines, are pocket-sized statuettes representing an obese female figure. Although their cultural significance is unrecorded, their widespread use throughout pre-historic Mediterranean and European cultures suggests a central role for the obese female form in magical rituals, and suggests cultural approval of (and perhaps reverence for) this body form.  This is most likely due to their ability to easily bear children and survive [[famine]].
 
Obesity was considered a symbol of wealth and [[social status]] in cultures prone to food shortages or famine. It was viewed in the same manner well into the early modern period in European cultures as well, but as food security was realized, it came to serve more as a visible signifier of "lust for life", appetite, and immersion in the realm of the erotic.
 
This was especially the case in the visual arts, such as the paintings of Rubens (1577&ndash;1640), whose regular depiction of fat women gives us the description ''Rubenesque''. Obesity can also be seen as a symbol within a system of prestige. "The kind of food, the quantity, and the manner in which it is served are among the important criteria of social class. In most tribal societies, even those with a highly stratified social system, everyone – royalty and the commoners – ate the same kind of food, and if there was famine everyone was hungry. With the ever increasing diversity of foods, food has become not only a matter of social status, but also a mark of one's personality and taste."<ref>Powdermaker H. "An anthropological approach to the problem of obesity." In: ''Food and Culture: A Reader.'' Ed. Carole Counihan and Penny van Esterik. New York: Routledge, 1997;206. ISBN 0-415-91710-7.</ref>
 
===Contemporary culture===
In modern Western culture, the obese body shape is widely regarded as unattractive and many negative stereotypes are commonly associated with obese people. Obese children, teenagers and adults can also face a heavy social stigma. Obese children are frequently the targets of bullies and are often shunned by their peers. Although obesity rates are rising amongst all social classes in the West, obesity is often seen as a sign of lower [[socio-economic status]].<ref>Greg Critser, ''Fat Land''. Houghton Mifflin, NY, 2003. ISBN 0-14101-540-3.</ref> Most obese people have experienced negative thoughts about their body image, and some take drastic steps to try to change their shape including [[dieting]], the use of [[diet pill]]s, and even [[bariatrics|surgery]].
Not all contemporary cultures disapprove of obesity. There are many cultures which are traditionally more approving (to varying degrees) of obesity, including some African, Arabic, Indian, and Pacific Island cultures. Especially in recent decades, obesity has come to be seen more as a medical condition in modern Western culture even being referred to as an epidemic.<ref>{{cite news  | last = Phillips | first = Stone | coauthors = | title = Who's to blame for the U.S. obesity epidemic? | work = | pages = | language = English | publisher = MSNBC | date = 2006-08-18 | url = http://www.msnbc.msn.com/id/14415766/ | accessdate = 2007-06-03 }}</ref>
 
Recently emerging is a small but vocal [[fat acceptance movement]] that seeks to challenge weight-based discrimination. Obesity acceptance and advocacy groups have initiated litigation to defend the rights of obese people and to prevent their social exclusion.
 
Some notable figures within this movement, such as Paul Campos, argue that the social stigma surrounding obesity is founded in cultural [[anxiety]], and that public concern over health risks associated with obesity are inappropriately used as a rationalization for this stigma.<ref> Paul Campos, ''The Diet Myth''. Gotham Books, NY, 2004. ISBN 1-59240-135-X.</ref>
 
Government agencies and private medicine have warned Americans for years of the adverse health effects associated with overweight and obesity.  Despite the warnings, the problem is getting worse.  In 2004, the CDC reported that 66.3% of adults in the United States were overweight or obese. The cause in most cases is a sedentary lifestyle; approximately 40% of adults in the United States do not participate in any leisure-time physical activity and less than 1/3 of adults engage in the recommended amount of physical activity.<ref>Centers for Disease Control and Prevention, National Center for Health Statistics, Fast Facts A to Z. Available at: http://www.cdc.gov/nchs/fastats/overwt.htm . Accessed July 15, 2007</ref> Overweight and obesity are easily determined by using Body Mass Index (BMI); this index uses your weight and height to determine body fat. An index A BMI range of 25 to 29.9 is considered overweight and anything over 30 obese. Individuals with a BMI over 30 increase the risk of several heath hazards.<ref>The Surgeon General's call to action to prevent and decrease overweight and obesity; U.S. Dept. of Health and Human Services, Public Health Service, Office of The Surgeon General; Washington, D.C. Available at: http://www.surgeongeneral.gov/topics/obesity/calltoaction/CalltoAction.pdf. Accessed July 12, 2007</ref>
 
===Popular culture===
 
Various [[stereotype]]s of obese people have found their way into expressions of popular culture. A common stereotype is the obese character who has a warm and dependable personality, or a jolly fat man like Santa Claus. Equally common is the obese vicious bully (such as Dudley Dursley from the Harry Potter book series, Eric Cartman from ''South Park'', Nelson Muntz from ''The Simpsons'').
 
[[Gluttony]] and obesity are commonly depicted together in works of fiction.
 
In cartoons, obesity is often used to comedic effect, with fat animal characters (such as Piggy, Porky Pig, Tummi Gummi, and Podgy Pig) having to squeeze through narrow spaces, frequently getting stuck or even exploding.
 
A more unusual example of obesity-related humour is Bustopher Jones, from T. S. Eliot's poem "Bustopher Jones: The Cat About Town" featured in ''Old Possum's Book of Practical Cats'', and the musical ''Cats'' derived from the poem.  Bustopher's claim to fame is that he is a regular visitor to many gentlemen's clubs including Drones, Blimp's and the Tomb. Due to his constant lunching at these clubs, he is remarkably fat, being described by others as "a twenty-five pounder... And he's putting on weight everyday." Another popular character, Garfield, a cartoon cat, is also obese for humor. When his owner, Jon, puts him on diets, rather than losing weight, Garfield slows down his weight gain.
 
It can be argued that depiction in popular culture adds to and maintains commonly perceived stereotypes, in turn harming the [[self esteem]] of obese people. On the other hand, obesity is often associated with positive characteristics such as good humor.  In addition, some people are [[sexual attraction|sexually attracted]] to obese people (see chubby culture and fat admirer).
 
==Public health and policy==
 
[[Image:bmi30chart.png|thumb|left|250px|Graphic chart comparing obesity percentages of the total population in OECD member countries.]]
 
=== Prevalence ===
 
;United Kingdom
The Health Survey for England predicts that more than 12 million adults and 1 million children will be obese by 2010 if no action is taken.<ref>BBC [http://news.bbc.co.uk/1/hi/health/5282446.stm England to have 13m obese by 2010] [[25 August]] [[2006]]</ref><ref>[http://www.dh.gov.uk/PublicationsAndStatistics/Publications/PublicationsStatistics/PublicationsStatisticsArticle/fs/en?CONTENT_ID=4138630&chk=XVZ/60 Forecasting obesity to 2010]</ref>
 
;United States
The prevalence of overweight and obesity in the United States makes obesity a leading public health problem. The United States has the highest rates of obesity in the developed world.<ref>According to circa 2005 [[OECD]] data.  See [http://titania.sourceoecd.org/vl=13245990/cl=31/nw=1/rpsv/health2007/3-3.htm &sect;3.3, Overweight and obesity, ''Health at a Glance 2007: OECD Indicators''], SourceOECD (accessed on line [[January 12]], [[2008]].)</ref>  From 1980 to 2002, obesity has doubled in adults and overweight prevalence has tripled in children and adolescents.<ref name="pmid16595758">{{cite journal |author=Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM |title=Prevalence of overweight and obesity in the United States, 1999-2004 |journal=JAMA |volume=295 |issue=13 |pages=1549-55 |year=2006 |pmid=16595758 |doi=10.1001/jama.295.13.1549}}</ref> From 2003-2004, "children and adolescents aged 2 to 19 years, 17.1% were overweight...and 32.2% of adults aged 20 years or older were obese."<ref name="pmid16595758"/> The prevalence in the United States continues to rise.<ref name=epidemiologic> [http://www.epidemiologic.org/2006/10/obesity-epidemic-us-temporal-trends.html The rapid epidemic of obesity in individual U.S. states from 1985-2004 can be seen here] and [http://www.cdc.gov/nchs/products/pubs/pubd/hestats/overweight/overwght_child_03.htm here]</ref>
 
;China
Because of the booming economy increasing average incomes, the population of China has recently begun a more sedentary lifestyle and at the same time begun consuming more calorie-rich foods.  From 1991 to 2004 the percentage of adults who are overweight or obese increased from 12.9% to 27.3%.<ref>{{cite news |first=Barry |last= Popkin |authorlink=  |coauthors=  |title= The World Is Fat |url=  |id= {{ISSN|0036-8733}} |pages= 94 |publisher= Scientific American |accessdate=  |date=September, 2007}}</ref>
 
Obesity is a public health and policy problem because of its prevalence, costs and burdens.<ref>U.S. Dept. of Health and Human Services, Public Health Service, Office of Surgeon General, ''The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity 2001'' (2001)</ref> The prevalence of obesity has been continually rising for two decades.<ref>Centers for Disease Control and Prevention, U.S. Obesity Trends 1984 - 2002 [http://www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/index.htm].</ref> This sudden rise in obesity prevalence is attributed to environmental and population factors rather than individual behavior and biology because of the rapid and continual rise in the number of overweight and obese individuals.<ref>Morrill A, Chinn C. The obesity epidemic in the United States. ''J Public Health Policy'' 2004;25:353-366. PMID 15683071.</ref> The current environment produces risk factors for decreased physical activity and for increased calorie consumption. These environmental factors operate on the population to decrease physical activity and increase calorie consumption.
 
===Environmental factors===
While it may often appear obvious why a certain individual gets fat, it is far more difficult to understand why the average weight of certain societies have recently been growing. While genetic causes are central to understanding obesity, they cannot fully explain why one culture grows fatter than another.
 
This is most notable in the United States. In the years from just after the Second World War until 1960 the average person's weight increased, but few were obese. In the two and a half decades since 1980 the growth in the rate of obesity has accelerated markedly and is increasingly becoming a [[public health]] concern.
 
There are a number of theories as to the cause of this change since 1980. Most believe it is a combination of various factors.
 
*''Lack of activity'': obese people are less active in general than lean people, and not just because of their obesity. A controlled increase in calorie intake of lean people did not make them less active; correspondingly when obese people lost weight they did not become more active. Weight change does not affect activity levels, but the converse seems to be the case.<ref>{{cite journal | author=Levine JA, Lanningham-Foster LM, McCrady SK, Krizan AC, Olson LR, Kane PH, Jensen MD, Clark MM | title=Interindividual variation in posture allocation: possible role in human obesity | journal=Science | year=2005 | pages=584-6 | volume=307 | issue=5709 | id=PMID 15681386 {{doi|10.1126/science.1106561}}}}</ref>
 
*''Lower relative cost of foodstuffs'': massive changes in agricultural policy in the United States and Europe have led to food prices for consumers being lower than at any point in history. This can raise costs for consumers in some areas but greatly lower it in others.  Current debates into trade policy highlight disagreements on the effects of subsidies. In the United States, production of corn, soy, wheat and rice is subsidized through the U.S. farm bill. Corn and soy, which are main sources of the sugars and fats in processed food, are thus cheap compared to fruits and vegetables.<ref>{{cite news|author=Pollan, Michael|title=You Are What You Grow|work=New York Times|url=http://www.nytimes.com/2007/04/22/magazine/22wwlnlede.t.html?ex=1186027200&en=bbe0f6a2c10e3b3c&ei=5070|date= April 22, 2007|accessdate= 2007-07-30}}</ref>
 
*''Increased marketing'' has also played a role.  In the early 1980s in America the Reagan administration lifted most regulations pertaining to sweets and fast food advertising to children. As a result, the number of advertisements seen by the average child increased greatly, and a large proportion of these were for fast food and sweets.<ref> [[Brian Wansink]] and [[Mike Huckabee]] (2005), “De-Marketing Obesity,” California Management Review, 47:4 (Summer), 6-18.</ref>
 
*The ''changing workforce'' as each year a greater percent of the population spends their entire workday behind a desk or computer, seeing virtually no exercise.  In the kitchen the microwave oven has seen sales of calorie-dense frozen convenience foods skyrocket and has encouraged more elaborate snacking.
 
*A social cause that is believed by many to play a role is the increasing number of ''two income households'' in which one parent no longer remains home to look after the house. This increases the number of restaurant and take-out meals.
 
*''Urban sprawl'' may be a factor: obesity rates increase as urban sprawl increases, possibly due to less walking and less time for cooking.<ref>{{cite journal | author=Lopez R | title=Urban sprawl and risk for being overweight or obese | journal=Am J Public Health | year=2004 | pages=1574-9 | volume=94 | issue=9 | id=PMID 15333317}}</ref>
 
*Since 1980 ''fast food restaurants'' have seen dramatic growth in terms of the number of outlets and customers served.  Low food costs, and intense competition for market share, led to increased portion sizes—for example, McDonalds french fries portions rose from 200 calories (840 [[joule|kilojoules]]) in 1960 to over 600 calories (2,500 kJ) today.
 
===Public health and policy responses===
[[Image:Wide Chair.jpg|thumb|left|250px|Some U.S. [[Kaiser Permanente]] facilities now provide oversized chairs such as this one at [[Richmond Medical Center]], for obese patients.]]
 
Public health and policy responses to obesity seek to understand and correct the environmental factors responsible for shifts in the prevalence of overweight and obesity in a population. Obesity and overweight are, currently, primarily policy problems in the United States. Policy and public health solutions look to change the environmental factors that promote calorie dense, low nutrient food consumption and that inhibit physical activity.
 
In the United States, policy has focused primarily on controlling [[childhood obesity]] which has the most serious long-term public health implication. Efforts have been underway to target schools. There are efforts underway to reform federally-reimbursed meal programs, limit food marketing to children, and ban or limit access to sugar sweetened beverages. In Europe, policy has focused on limiting marketing to children. There has been international focus on sugar policy and the role of agriculture policy in producing food environments that produce overweight and obesity in a population. To confront physical activity, efforts have examined zoning and access parks and safe routes in cities.
 
In the United Kingdom, a 2004 report by the [[Royal College of Physicians]], the [[Faculty of Public Health]] and the  [[Royal College of Paediatrics and Child Health]], titled "Storing up Problems",<ref>{{cite book |title=Storing up problems; the medical case for a slimmer nation |url=http://www.rcplondon.ac.uk/pubs/contents/ca4032bf-7b10-4e2f-8701-b24874f84514.pdf |format=PDF |date=2004-02-11 |publisher=Royal College of Physicians |location= London|isbn=1-86016-200-2}}</ref> was followed by a report by the British House of Commons [[Health Select Committee]] - the "the most comprehensive inquiry" ever by that body - on the impact of obesity on health and society in the UK and possible approaches to the problem.<ref>{{cite book |author=Great Britain Parliament House of Commons Health Committee |title=Obesity - Volume 1 - HCP 23-I, Third Report of session 2003-04. Report, together with formal minutes |url=http://www.publications.parliament.uk/pa/cm200304/cmselect/cmhealth/23/2302.htm |accessdate=2007-12-17|year=2004 |month= May|publisher=TSO (The Stationery Office) |location=London, UK |isbn=0-21501-737-4}}</ref> 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 implications for non-healthcare organizations such as local councils.<ref name=NICECG043/> A 2007 report produced by Sir Derek Wanless for the [[King's Fund]] warned that unless further action was taken, obesity had the capacity to cripple the [[National Health Service]] financially.<ref>{{cite book |last=Wanless |first=Sir Derek |coauthors=John Appleby, Anthony Harrison, Darshan Patel |title=Our Future Health Secured? A review of NHS funding and performance |url=http://www.kingsfund.org.uk/publications/kings_fund_publications/our_future.html|accessdate=2007-12-17 |year=2007 |publisher=The King's Fund |location=London, UK |isbn=185717562X}}</ref>
 
===Non-medical consequences===
Besides increases in disease and mortality there are other implications of the present world trend in obesity. Among these are:
* Increased pressure on airline revenues (or increased fares) due to lobbying efforts to increase seating width on commercial airplanes, and due to higher fuel costs: in 2000, extra weight of obese passengers cost airlines and consumers US$275,000,000.<ref>{{cite journal |author=Dannenberg AL, Burton DC, Jackson RJ |title=Economic and environmental costs of obesity: the impact on airlines |journal=American journal of preventive medicine |volume=27 |issue=3 |pages=264 |year=2004 |pmid=15450642 |doi=10.1016/j.amepre.2004.06.004}}</ref>
* Increased litigation by obese persons suing restaurants (for causing obesity)<ref>109th U.S. Congress (2005-2006) H.R. 554: 109th U.S. Congress (2005-2006) H.R. 554: Personal Responsibility in Food Consumption Act of 2005</ref> and airlines (over airline seating width)[http://www.forbes.com/2002/10/24/cx_ld_1024obese.html] [http://www.cbc.ca/story/news/national/2000/12/12/Consumers/airlines_lawsuit001212.html].  The ''[[Personal Responsibility in Food Consumption Act]] of 2005'' was motivated by a need to reduce litigation from obesity activists.
* Sizable societal economic costs attributable to obesity, with medical costs attributable to obesity rising to 78.5 billion dollars or 9.1 percent of all medical expenditures in the U.S. as of 1998<ref>{{cite journal |author=Finkelstein EA, Fiebelkorn IA, Wang G |title=National medical spending attributable to overweight and obesity: how much, and who’s paying |journal=National medical spending attributable to overweight and obesity: how much, and who's paying |volume=Online |issue=May |pages=|year=2003 | url=http://content.healthaffairs.org/cgi/content/full/hlthaff.w3.219v1/DC1}}</ref><ref>{{cite web |url=http://www.cdc.gov/nccdphp/dnpa/obesity/economic_consequences.htm |title=Obesity and Overweight: Economic Consequences | publisher=CDC | pubdate=22 May 2007 | accessdate=2007-09-05}}</ref>
* Decreased worker productivity as measured by usage of disability leave and absenteeism at work.<ref>[http://www.dhs.ca.gov/ps/cdic/cpns/press/downloads/CostofObesityToplineReport.pdf The Economic Costs of Physical Inactivity, Obesity, and Overweight in California Adults], report by Chenoweth & Associates Inc. for the Cancer Prevention and Nutrition Section, California Center for Physical Activity, California Department of Health Services, Sacramento, CA, 2005.</ref>
* A study examining Duke University employees found that those with a BMI>40 filed twice as many workers compensation claims as workers whose BMI was 18.5-24.9, and had more than 12 times as many lost work days. The most common injuries were due to falls and lifting, and affected the lower extremities, wrists or hands, and backs.<ref>{{cite journal |author=Ostbye T, Dement JM, Krause KM |title=Obesity and workers' compensation: results from the Duke Health and Safety Surveillance System |journal=Arch. Intern. Med. |volume=167 |issue=8 |pages=766-73 |year=2007 |pmid=17452538 |doi=10.1001/archinte.167.8.766}}</ref>
 
==See also==
*[[Body image]]
*[[Body image]]
*[[Healthy diet]]
*[[Healthy diet]]
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*[[Overeaters Anonymous]]
*[[Overeaters Anonymous]]


==References==
{{reflist|2}}
==External links==
{{Wiktionary}}
* [http://www.who.int/topics/obesity/en/ World Health Organization] - Obesity pages
* [http://www.who.int/nutrition/topics/dietnutrition_and_chronicdiseases/en/ Diet, Nutrition and the prevention of chronic diseases] (including obesity) by a Joint [[WHO]]/[[FAO]] Expert consultation (2003).
* [http://www.endotext.org/obesity/index.htm Obesity at Endotext.org]
* [http://www.iotf.org/ International Task Force on Obesity]
* [http://www.naaso.org The Obesity Society] (USA)
* [http://www.nationalobesityforum.org.uk/ National Obesity Forum] (UK)
* [http://www.asso.org.au Australasian Society for the Study of Obesity]
{{SIB}}
{{Nutritional pathology}}
{{Nutritional pathology}}
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[[Category:Metabolic disorders]]
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