Difference between revisions of "Obesity"

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{{SI}}
  
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'''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.<ref name="WHO 2000 p.6">WHO 2000 p.6</ref><ref name=HaslamJames/> People are considered obese when their [[body mass index]] (BMI),<ref name="WHO 2000 p.9">WHO 2000 p.9</ref> a measurement obtained by dividing a person's weight by the square of the person's height, exceeds 30 kg/m2.
  
'''Obesity''' is a condition in which the body stores excess energy in the form of [[adipose tissue|fatty tissue]] of [[human]]s and [[mammal]]s, is increased to a point where it is thought to be a risk factor for certain health conditions or increased mortality.  
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[[File:Obesity.jpg|left|600px]]
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Obesity increases the likelihood of [[Obesity-associated morbidity|various diseases]], particularly [[heart disease|heart disease]], [[diabetes mellitus type 2|type 2 diabetes]], [[obstructive sleep apnea|sleep apnea]], certain types of [[cancer]], and [[osteoarthritis]].<ref name=HaslamJames/> Obesity is most commonly caused by a combination of excessive [[food energy]] intake, lack of physical activity, and [[Polygenic inheritance|genetic susceptibility]], although a few cases are caused primarily by [[gene]]s, [[endocrine]] disorders, [[medication]]s 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.<ref>{{cite book|author=Kushner, Robert |title=Treatment of the Obese Patient (Contemporary Endocrinology) |publisher=Humana Press |location=Totowa, NJ |year=2007 |page=158 |isbn=1-59745-400-1 |url=http://books.google.com/?id=vWjK5etS7PMC |doi= |accessdate=April 5, 2009}}</ref><ref name=Anes2000>{{cite journal|last=Adams |first=PG |last2=Murphy |title=Obesity in anaesthesia and intensive care |journal=Br J Anaesth |volume=85 |issue=1 |pages=91–108 |date=July 2000 |pmid=10927998 |doi=10.1093/bja/85.1.91 |url=http://bja.oxfordjournals.org/cgi/content/full/85/1/91 |first2=PG |author-separator=,}}</ref>
  
==How do we get obese?==
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[[Dieting]] and [[physical exercise]] are the mainstays of treatment 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]]. [[Anti-obesity drug]]s may be taken to reduce appetite or decrease fat absorption when used together with a suitable diet. If diet, exercise and medication are not effective, a [[gastric balloon]] may assist with weight loss, or [[bariatric surgery|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.<ref>NICE 2006 p.10–11</ref><ref name=balloon2008>{{cite journal|last=Imaz |first=I |last2=Martínez-Cervell |first2=C |last3=García-Alvarez |first3=EE |last4=Sendra-Gutiérrez |first4=JM |last5=González-Enríquez |first5=J |title=Safety and effectiveness of the intragastric balloon for obesity. A meta-analysis |journal=Obes Surg |volume=18 |issue=7 |pages=841–6 |date=July 2008 |pmid=18459025 |doi=10.1007/s11695-007-9331-8 |display-authors=3 |author-separator=,}}</ref>
  
Excess [[weight gain]] that leads to obesity has many causes. Excessive body weight has been shown to correlate with various [[diseases]], particularly [[metabolic syndrome]], [[cardiovascular disease]], [[type 2 diabetes|diabetes mellitus type 2]], [[sleep apnea]], and [[osteoarthritis]]. U.S. Dept. of Health and Human Services, National Institutes of Health, 'The Practical Guide: Identification, Evaluation and Treatment of Overweight and Obesity in Adults 5 (2000) [http://www.nhlbi.nih.gov/guidelines/obesity/prctgd_c.pdf PDF]. Obesity is both an individual clinical condition and is increasingly viewed as a serious public health problem.
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Obesity is a leading [[preventable causes of death|preventable cause of death]] worldwide, with increasing rates in adults and [[childhood obesity|children]]. Authorities view it as one of the most serious [[public health]] problems of the 21st&nbsp;century.<ref name=Barn1999>{{cite journal|last=Barness |first=LA |last2=Opitz |first2=JM |last3=Gilbert-Barness |first3=E |title=Obesity: genetic, molecular, and environmental aspects |journal=American Journal of Medical Genetics |volume=143A |issue=24 |pages=3016–34 |date=December 2007 |pmid=18000969 |doi=10.1002/ajmg.a.32035 |url=|author-separator=,}}</ref> Obesity is [[Weight stigma|stigmatized]] in much of the modern world (particularly in the [[Western world]]), though it was widely seen as a symbol of wealth and fertility at other times in history, and still is in some parts of the world.<ref name=HaslamJames/><ref name=Woodhouse/> In 2013, the [[American Medical Association]] classified obesity as a disease.<ref name=NYTimes20130618>{{cite news|url=http://www.nytimes.com/2013/06/19/business/ama-recognizes-obesity-as-a-disease.html?_r=0 |title=A.M.A. Recognizes Obesity as a Disease |last=Pollack |first=Andrew |date=June 18, 2013 |newspaper=New York Times |archiveurl=http://www.webcitation.org/6Hav05TK0 |archivedate=June 18, 2013}}</ref><ref>{{cite web|url=http://www.hhnmag.com/hhnmag/HHNDaily/HHNDailyDisplay.dhtml?id=5870001020 |title=The Facts About Obesity |last1=Weinstock |first1=Matthew |date=June 21, 2013 |website=H&HN |publisher=[[American Hospital Association]] |accessdate=June 24, 2013}}</ref>
{{1-5}}
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==Definition==  
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==Classification==
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{{Main|Classification of obesity}}
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Obesity is a [[medical condition]] in which excess [[body fat]] has accumulated to the extent that it may have an adverse effect on health.<ref name="WHO 2000 p.6"/> It is defined by [[body mass index|body mass index (BMI)]] and further evaluated in terms of fat distribution via the [[waist-hip ratio|waist–hip ratio]] and total cardiovascular risk factors.<ref>{{cite journal|journal=Nutr J |year=2007 |volume=6 |page=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 |pmc=2164947 |issue=1}}</ref><ref>NHLBI p.xiv</ref>  BMI is closely related to both [[Body fat percentage|percentage body fat]] and total body fat.<ref>{{cite journal|last=Gray |first=DS |last2=Fujioka |first2=K |title=Use of relative weight and Body Mass Index for the determination of adiposity |journal=J Clin Epidemiol |volume=44 |issue=6 |pages=545–50 |year=1991 |pmid=2037859 |doi=10.1016/0895-4356(91)90218-X |author-separator=,}}</ref>
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In children, a healthy weight varies with age and sex. Obesity in children and adolescents is defined not as an absolute number but in relation to a historical normal group, such that obesity is a BMI greater than the 95th&nbsp;[[percentile]].<ref name="cdc.gov">{{cite web|url=http://www.cdc.gov/nccdphp/dnpa/healthyweight/assessing/bmi/childrens_BMI/about_childrens_BMI.htm |title=Healthy Weight: Assessing Your Weight: BMI: About BMI for Children and Teens |publisher=[[Center for disease control and prevention]] |accessdate=April 6, 2009}}</ref>  The reference data on which these percentiles were based date from 1963 to 1994, and thus have not been affected by the recent increases in weight.<ref name="Flegal KM, Ogden CL, Wei R, Kuczmarski RL, Johnson CL 2001 1086–93">{{cite journal|last=Flegal |first=KM |last2=Ogden |first2=CL |last3=Wei |first3=R |last4=Kuczmarski |first4=RL |last5=Johnson |first5=CL |title=Prevalence of overweight in US children: comparison of US growth charts from the Centers for Disease Control and Prevention with other reference values for body mass index |journal=Am. J. Clin. Nutr. |volume=73 |issue=6 |pages=1086–93 |date=June 2001 |pmid=11382664 |doi= |url=http://www.ajcn.org/cgi/content/full/73/6/1086 |display-authors=3 |author-separator=,}}</ref>
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{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
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|-
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! BMI (kg/m<sup>2</sup>) !! Classification<ref>{{cite web|title=BMI classification|url=http://apps.who.int/bmi/index.jsp?introPage=intro_3.html|work=World Health Organization|accessdate=15 February 2014}}</ref>
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|-
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|width=50%| < 18.50 ||underweight
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|-
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|18.50–24.99 || normal weight
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|-
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|25.00–29.99 || overweight
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|-
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|30.00–34.99 || class I obesity
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|-
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|35.00–39.99 || class II obesity
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|-
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|≥ 40.00 || &nbsp;&nbsp;class III obesity&nbsp;&nbsp;
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|}
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BMI is defined as the subject's weight divided by the square of their height and is calculated as follows.
  
In the clinical setting, obesity is typically evaluated by measuring BMI (Body Mass Index), waist circumference, and evaluating the presence of risk factors and [[morbidity|comorbidities]]. In [[epidemiology|epidemiological]] studies BMI alone is used to define obesity.
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:<math>\mathrm{BMI}= \frac{m}{h^2}</math>
  
===Body Mass Index===
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:where ''m'' and ''h'' are the subject's weight in kilograms and height in meters respectively.
  
[[Body mass index]] is a practical and simple way to measure a persons body weight relative to their height. Although not perfect or without flaws, BMI is a reliable indicator of body fatness for most people except for heavy body builders. It is calculated based on your weight relative to your height.
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BMI is usually expressed in kilograms per square metre. To convert from pounds per square inch multiply by {{nowrap|703 (kg/m<sup>2</sup>)/(lb/sq in)}}.<ref>{{nowrap|1 (lb/sq in)}} is more precisely {{nowrap|703.06957964 (kg/m<sup>2</sup>)}}.</ref>
  
BMI was developed by the [[Belgium|Belgian]] statistician and [[anthropometry|anthropometrist]] [[Adolphe Quetelet]] :
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The most commonly used definitions, established by the [[World Health Organization]] (WHO) in 1997 and published in 2000, provide the values listed in the table at right.<ref name="WHO 2000 p.9"/>
* 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''
 
  
BMI is a simple and widely used method for estimating body fat, although there are more accurate measures such as DEXA scan etc. to look at a person's level of [[adiposity]]. BMI as an indicator of a clinical condition is used in conjunction with other clinical assessments. 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. In [[epidemiology|epidemiological analyses]] BMI alone is used as an indicator of [[prevalence]] and [[incidence]].
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Some modifications to the WHO definitions have been made by particular bodies. The surgical literature breaks down "class III" obesity into further categories whose exact values are still disputed.<ref name=morbid2007>{{cite journal|author=Sturm R |title=Increases in morbid obesity in the USA: 2000–2005 |journal=Public Health |volume=121 |issue=7 |pages=492–6 |date=July 2007 |pmid=17399752 |pmc=2864630 |doi=10.1016/j.puhe.2007.01.006 |author-separator=,}}</ref>
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* Any BMI ≥ 35 or 40&nbsp;kg/m<sup>2</sup> is ''severe obesity''
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* A BMI of ≥ 35&nbsp;kg/m<sup>2</sup> and experiencing obesity-related health conditions or ≥40–44.9&nbsp;kg/m<sup>2</sup> is ''morbid obesity''
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* A BMI of ≥ 45 or 50&nbsp;kg/m<sup>2</sup> is ''super obesity''
  
=== Waist Circumference ===
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As Asian populations develop negative health consequences at a lower BMI than Caucasians, some nations have redefined obesity; the Japanese have defined obesity as any BMI greater than 25&nbsp;kg/m<sup>2</sup><ref>{{cite journal|last=Kanazawa |first=M |last2=Yoshiike |first2=N |last3=Osaka |first3=T |last4=Numba |first4=Y |last5=Zimmet |first5=P |last6=Inoue |first6=S |title=Criteria and classification of obesity in Japan and Asia-Oceania |journal=Asia Pac J Clin Nutr |volume=11 Suppl 8 |issue= |pages=S732–S737 |date=December 2002 |pmid=12534701 |doi=10.1046/j.1440-6047.11.s8.19.x |display-authors=3 |author-separator=,}}</ref> while China uses a BMI of greater than 28&nbsp;kg/m<sup>2</sup>.<ref>{{cite journal|author=Bei-Fan Z |author2=Cooperative Meta-Analysis Group of Working Group on Obesity in China |title=Predictive values of body mass index and waist circumference for risk factors of certain related diseases in Chinese adults: study on optimal cut-off points of body mass index and waist circumference in Chinese adults |journal=Asia Pac J Clin Nutr |volume=11 Suppl 8 |issue= |pages=S685–93 |date=December 2002 |pmid=12534691 |doi=10.1046/j.1440-6047.11.s8.9.x |author-separator=,}}</ref>
  
Another important measure to know your risk related to excess weight is to know your waist to hip ratio or simply your waist circumference as a big waist circumference is associated with higher risk of developing obesity-related conditions:
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==Effects on health==
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<!-- [[Effects of obesity on health]] links here, please make corresponding changes if altering this section title or removing the anchor tag. -->
  
* A man with a waist circumference of 40 inches
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Excessive body [[Human weight|weight]] is associated with various [[diseases]], particularly [[cardiovascular diseases]], [[diabetes mellitus type 2]], [[obstructive sleep apnea]], certain types of [[cancer]], [[osteoarthritis]]<ref name=HaslamJames/> and [[asthma]].<ref name=HaslamJames/><ref name=Poulain/> As a result, obesity has been found to reduce [[life expectancy]].<ref name=HaslamJames/>
* A woman whose waist circumference is more than 35 inches (lower in Asians)
 
  
Excessive abdominal or belly fat increases the risk for developing obesity-related conditions, such as Type 2 Diabetes, high blood cholesterol, high triglycerides, high blood pressure, and coronary artery disease.
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===Mortality===
  
===Online BMI calculator===
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Obesity is one of the leading [[preventable causes of death]] worldwide.<ref name=Barn1999/><ref>{{cite journal|last=Mokdad |first=AH |last2=Marks |first2=JS |last3=Stroup |first3=DF |last4=Gerberding |first4=JL |title=Actual causes of death in the United States, 2000 |journal=[[JAMA (journal)|JAMA]] |volume=291 |issue=10 |pages=1238–45 |date=March 2004 |pmid=15010446 |doi=10.1001/jama.291.10.1238 |url=http://www.csdp.org/research/1238.pdf |format=PDF |display-authors=3 |author-separator=,}}</ref><ref name=Allison>{{cite journal|last=Allison |first=DB |last2=Fontaine |first2=KR |last3=Manson |first3=JE |authorlink3=JoAnn E. Manson |last4=Stevens |first4=J |last5=VanItallie |first5=TB |title=Annual deaths attributable to obesity in the United States |journal=[[JAMA (journal)|JAMA]] |volume=282 |issue=16 |pages=1530–8 |date=October 1999 |pmid=10546692 |doi=10.1001/jama.282.16.1530 |url=http://jama.ama-assn.org/cgi/content/full/282/16/1530 |display-authors=3 |author-separator=,}}</ref>  Large-scale American and European studies have found that mortality risk is lowest at a BMI of 20–25&nbsp;kg/m<sup>2</sup><ref name=NEJM10/><ref name=Lancet2009>{{cite journal|author=Whitlock G |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 |date=March 2009 |pmid=19299006 |doi=10.1016/S0140-6736(09)60318-4 |url= |pmc=2662372 |author2=Lewington S |author3=Sherliker P |last4=Sherliker |first4=P |last5=Clarke |first5=R |last6=Emberson |first6=J |last7=Halsey |first7=J |last8=Qizilbash |first8=N |last9=Collins |first9=R |first10=R |display-authors=3 |author-separator=,}}</ref> in non-smokers and at 24–27&nbsp;kg/m<sup>2</sup> in current smokers, with risk increasing along with changes in either direction.<ref>{{cite journal|last=Calle |first=EE |last2=Thun |first2=MJ |last3=Petrelli |first3=JM |last4=Rodriguez |first4=C |last5=Heath |first5=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 |date=October 1999 |pmid=10511607 |doi=10.1056/NEJM199910073411501 |url=http://content.nejm.org/cgi/content/full/341/15/1097 |display-authors=3 |author-separator=,}}</ref><ref name=Euro2008>{{cite journal|author=Pischon T |title=General and abdominal adiposity and risk of death in Europe |journal=N. Engl. J. Med. |volume=359 |issue=20 |pages=2105–20 |date=November 2008 |pmid=19005195 |doi=10.1056/NEJMoa0801891 |url= |author2=Boeing H |author3=Hoffmann K |last4=Bergmann |first4=M. |last5=Schulze |first5=M.B. |last6=Overvad |first6=K. |last7=Van Der Schouw |first7=Y.T. |last8=Spencer |first8=E. |last9=Moons |first9=K.G.M. |first10=A. |first11=J. |first14=F. |first15=M.-C. |first16=V. |first17=J. |first18=R. |first19=A. |first20=D. |first21=C. |first24=R. |first25=P. |first26=S. |first27=P.H.M. |first28=A.M. |first29=H.B. |first30=F.J.B. |display-authors=3 |author-separator=,}}</ref>  A BMI above 32&nbsp;kg/m<sup>2</sup> has been associated with a doubled [[mortality rate]] among women over a 16-year period.<ref>{{cite journal|author=Manson JE |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 |author2=Willett WC |author3=Stampfer MJ |last4=Colditz |first4=Graham A. |last5=Hunter |first5=David J. |last6=Hankinson |first6=Susan E. |last7=Hennekens |first7=Charles H. |last8=Speizer |first8=Frank E. |display-authors=3 |author-separator=,}}</ref>  In the United States obesity is estimated to cause 111,909 to 365,000 deaths per year,<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><ref name=Allison/> while 1 million (7.7%) of deaths in Europe are attributed to excess weight.<ref name=EuroG2008/><ref name=Euro2007>{{cite journal|author=Fried M |title=Inter-disciplinary European guidelines on surgery of severe obesity |journal=Int J Obes (Lond) |volume=31 |issue=4 |pages=569–77 |date=April 2007 |pmid=17325689 |doi=10.1038/sj.ijo.0803560 |url= |author2=Hainer V |author3=Basdevant A |last4=Buchwald |first4=H |last5=Deitel |first5=M |last6=Finer |first6=N |last7=Greve |first7=J W M |last8=Horber |first8=F |last9=Mathus-Vliegen |first9=E |first10=N |first11=R |first14=K |display-authors=3 |author-separator=,}}</ref>  On average, obesity reduces life expectancy by six to seven&nbsp;years,<ref name=HaslamJames/><ref>{{cite journal|last=Nedcom |first=A |last2=Barendregt |first2=JJ |last3=Willekens |first3=F |last4=Mackenbach |first4=JP |last5=Al Mamun |first5=A |last6=Bonneux |first6=L |title=Obesity in adulthood and its consequences for life expectancy: A life-table analysis |journal=Annals of Internal Medicine |volume=138 |issue=1 |pages=24–32 |date=January 2003 |pmid=12513041 |doi=10.7326/0003-4819-138-1-200301070-00008 |url=http://www.annals.org/cgi/reprint/138/1/24 |format=PDF |display-authors=3 |author-separator=,}}</ref> a BMI of 30–35&nbsp;kg/m<sup>2</sup> reduces life expectancy by two to four&nbsp;years,<ref name=Lancet2009/> while severe obesity (BMI&nbsp;>&nbsp;40&nbsp;kg/m<sup>2</sup>) reduces life expectancy by ten&nbsp;years.<ref name=Lancet2009/>
* [http://www.w8md.com/81-w8md-patient-portal/76-w8md-bmi-calculator Adult BMI Calculator]
 
  
===Waist circumference===
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===Morbidity===
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. ...Learn more on risk of [http://www.youtube.com/watch?v=D6tXDis4C3w belly fat], or [http://www.pinterest.com/w8md/52-weeks-of-weight-loss-and-wellness/ abdominal weight gain]
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{{Main|Obesity-associated morbidity}}
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Obesity increases the risk of many physical and mental conditions. These comorbidities are most commonly shown in [[metabolic syndrome]],<ref name=HaslamJames/>  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>
  
{{causes}}
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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>
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 are both used as measures of central obesity.
 
  
===Body fat measurement===
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{{blame}}
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.
 
  
===Gestalt===
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Health consequences fall into two broad categories: those attributable to the effects of increased fat mass (such as [[osteoarthritis]], [[obstructive sleep apnea]], social stigmatization) and those due to 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]],<ref>{{cite journal|last=Shoelson |first=SE |last2=Herrero |first2=L |last3=Naaz |first3=A |title=Obesity, inflammation, and insulin resistance |journal=Gastroenterology |volume=132 |issue=6 |pages=2169–80 |date=May 2007 |pmid=17498510 |doi=10.1053/j.gastro.2007.03.059 |author-separator=,}}</ref><ref>{{cite journal|author=Shoelson SE, Lee J, Goldfine AB |title=Inflammation and insulin resistance |journal=J. Clin. Invest. |volume=116 |issue=7 |pages=1793–801 |date=July 2006 |pmid=16823477 |pmc=1483173 |doi=10.1172/JCI29069 |url=http://www.jci.org/articles/view/29069}}</ref> and a [[thrombosis|prothrombotic]] state.<ref name=Bray2004/><ref>{{cite journal|author=Dentali F, Squizzato A, Ageno W |title=The metabolic syndrome as a risk factor for venous and arterial thrombosis |journal=Semin. Thromb. Hemost. |volume=35 |issue=5 |pages=451–7 |date=July 2009 |pmid=19739035 |doi=10.1055/s-0029-1234140}}</ref>
In practice, in most examples of overweight that may designate risk, both doctor and patient can see "by eye" whether excess fat is a concern. In these cases, [[Body mass index|BMI]] thresholds provide simple targets all patients can understand.
 
  
===Risk factors and comorbidities===
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{| class="wikitable"
The presence of risk factors and diseases associated with obesity are also used to establish a clinical diagnosis. Coronary heart disease, Type II diabetes, and sleep apnea are possible life-threatening risk factors that would indicate clinical treatment of obesity. Smoking, hypertension, age and family history are other risk factors that may indicate treatment Diabetes and heart disease are risk factors used in epidemiological studies of obesity.
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|-
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! Medical field
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! Condition
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! Medical field
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! Condition
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|-
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<!--Alphabetized-->|width=10%| [[Cardiology]]
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|
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* [[ischemic heart disease]]:<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=Lancet |year=2004 |pages=937–52 |volume=364 |pmid=15364185 |doi=10.1016/S0140-6736(04)17018-9 |issue=9438}}</ref> [[angina pectoris|angina]] and [[myocardial infarction]]
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* [[congestive heart failure]]<ref name=HaslamJames/>
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* [[high blood pressure]]<ref name=HaslamJames/>
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* [[Dyslipidemia|abnormal cholesterol levels]]<ref name=HaslamJames/>
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* [[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 |date=February 2007 |pmid=17185009 |doi=10.1016/j.ejvs.2006.10.006}}</ref>
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| <!--Alphabetized-->[[Dermatology]]
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|
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* [[stretch marks]]<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 |date=June 2007 |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 |date=June 2006 |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 |date=June 2008 |pmid=18611299 |doi= |url=}}</ref>
 +
* [[Maternal obesity|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]]
 +
| style="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 |date=January 2008 |pmid=18417025 |doi=10.1007/s11916-008-0011-8 |url=}}</ref>
 +
* [[carpal tunnel syndrome]]<ref>{{cite journal|author=Sharifi-Mollayousefi A |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 |date=February 2008 |pmid=18335412 |doi= |url=|author-separator=, |author2=Yazdchi-Marandi M |author3=Ayramlou H |last4=Heidari |first4=P |last5=Salavati |first5=A |last6=Zarrintan |first6=S |last7=Sharifi-Mollayousefi |first7=A |display-authors=3}}</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 |date=May 2008 |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 |date=March 2008 |pmid=18460275 |doi=10.1007/s11910-008-0015-0 |url=}}</ref>
 +
* [[multiple sclerosis]]<ref>{{cite journal|last1=Munger |first1=KL |last2=Chitnis |first2=T |last3=Ascherio |first3=A. |year=2009 |title=Body size and risk of MS in two cohorts of US women |url= |journal=Neurology |volume=73 |issue=19 |pages=1543–50 |doi=10.1212/WNL.0b013e3181c0d6e0 |pmc=2777074 |pmid=19901245 |author-separator=, |author-name-separator=}}</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 |date=April 2003 |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]]
 +
|-
 +
| style="width:10%;"| <!--Alphabetized-->[[Psychiatry]]
 +
| style="width:40%;"|
 +
* [[Major depressive disorder|depression]] in women<ref name=HaslamJames/>
 +
* social [[Social stigma|stigmatization]]<ref name=HaslamJames/>
 +
| <!--Alphabetized-->[[Respirology]]
 +
|
 +
* [[sleep apnea|obstructive sleep apnea]]<ref name=HaslamJames/><ref name=Poulain>{{cite journal|author=Poulain M |title=The effect of obesity on chronic respiratory diseases: pathophysiology and therapeutic strategies |journal=CMAJ |volume=174 |issue=9 |pages=1293–9 |date=April 2006 |pmid=16636330 |pmc=1435949 |doi=10.1503/cmaj.051299 |url=http://www.cmaj.ca/cgi/content/full/174/9/1293 |author-separator=, |author2=Doucet M |author3=Major GC |last4=Drapeau |first4=V |last5=Sériès |first5=F |last6=Boulet |first6=LP |last7=Tremblay |first7=A |last8=Maltais |first8=F |display-authors=3}}</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/>
 +
|-
 +
| <!--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 |date=April 2005 |pmid=15824292 |doi=10.1001/archinte.165.7.742}}</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=12 |issue=3 |pages=1–10 |date=April 2008 |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 |date=November 2008 |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 (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 |date=September 2005 |pmid=16093964 |doi=10.1097/01.ju.0000169490.78443.59}}</ref>
 +
* [[buried penis]]<ref name="pmid19935302">{{cite journal|author=Pestana IA, Greenfield JM, Walsh M, Donatucci CF, Erdmann D |title=Management of "buried" penis in adulthood: an overview |journal=Plast. Reconstr. Surg. |volume=124 |issue=4 |pages=1186–95 |date=October 2009 |pmid=19935302 |doi=10.1097/PRS.0b013e3181b5a37f}}</ref>
 +
|}
  
==Childhood obesity==
+
{{1-5}}
 +
===Survival paradox===
 +
{{See also|Obesity 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=U.S. Preventive Services Task Force |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 |date=June 2003 |pmid=12825847 |doi=}}</ref>
  
* Obesity and extreme obesity among U.S. low-income, preschool-aged children went down for the first time in recent years, according to CDC’s first national study.
+
In people with heart failure, those with a BMI between 30.0 and 34.9 had lower mortality than 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 |date=October 2006 |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, the risk of further cardiovascular events is increased.<ref>{{cite journal|author=Romero-Corral A |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 |author-separator=, |author2=Montori VM |author3=Somers VK |last4=Korinek |first4=Josef |last5=Thomas |first5=Randal J |last6=Allison |first6=Thomas G |last7=Mookadam |first7=Farouk |last8=Lopez-Jimenez |first8=Francisco |display-authors=3}}</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 |date=July 2008 |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 |date=February 2008 |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 |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 |date=July 2006 |volume=152 |issue=1 |pages=140–8 |pmid=16824844 |doi=10.1016/j.ahj.2005.09.024| author-separator=, |author2=Roe MT |author3=Mulgund J |last4=Pollack |first4=Charles V. |last5=Kirk |first5=J. Douglas |last6=Gibler |first6=W. Brian |last7=Ohman |first7=E. Magnus |last8=Smith |first8=Sidney C. |last9=Boden |first9=William E. |display-authors=3 |first10=Eric D.}}</ref>  Another found that if one takes into account [[chronic obstructive pulmonary disease]] (COPD) in those with PAD, the benefit of obesity no longer exists.<ref name=paradox2003/>
   
 
* From 2003 through 2010, the prevalence of obesity decreased slightly from 15.21% to 14.94%. Similarly, the prevalence of extreme obesity decreased from 2.22% to 2.07%.
 
  
* However, from 1998 through 2003, the prevalence of obesity increased from 13.05% to 15.21%, and the prevalence of extreme obesity increased from 1.75% to 2.22%.
+
==Causes==
 +
At an individual level, a combination of excessive [[food energy]] intake and a lack of [[physical activity]] is thought to explain most cases of obesity.<ref name=CADG2006/>  A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness.<ref>{{cite journal|author=Bleich S, Cutler D, Murray C, Adams A |title=Why is the developed world obese? |journal=Annu Rev Public Health |volume=29 |pages=273–95 |year=2008 |pmid=18173389 |doi=10.1146/annurev.publhealth.29.020907.090954}}</ref>  In contrast, increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet,<ref>{{cite journal|author=Drewnowski A, Specter SE |title=Poverty and obesity: the role of energy density and energy costs |journal=Am. J. Clin. Nutr. |volume=79 |issue=1 |pages=6–16 |date=January 2004 |pmid=14684391 |doi= |url=http://www.ajcn.org/cgi/content/full/79/1/6}}</ref> increased reliance on cars, and mechanized manufacturing.<ref>{{cite journal|author=Nestle M, Jacobson MF |title=Halting the obesity epidemic: a public health policy approach |journal=Public Health Rep |volume=115 |issue=1 |pages=12–24 |year=2000 |pmid=10968581 |pmc=1308552 |doi=10.1093/phr/115.1.12 |url=}}</ref><ref name=James2008>{{cite journal|author=James WP |title=The fundamental drivers of the obesity epidemic |journal=Obes Rev |volume=9 |issue=Suppl 1 |pages=6–13 |date=March 2008 |pmid=18307693 |doi=10.1111/j.1467-789X.2007.00432.x}}</ref>
  
* Extreme obesity significantly decreased among all racial groups except American Indians/Alaska Natives. The greatest decrease was among 2-year old and Asian/Pacific Islander children.
+
{{causes}}
  
*The data for this study is from the Pediatric Nutrition Surveillance System (PedNSS), which includes almost 50% of preschool children eligible for federally funded maternal and child health and nutrition programs, primarily the WIC Program. The study population included 27.5 million children aged 2 through 4 years from 30 states and the District of Columbia that consistently reported data to PedNSS from 1998 -2010.
+
A 2006 review identified ten other possible contributors to the recent increase of obesity: (1) insufficient sleep, (2) [[endocrine disruptor]]s (environmental [[pollutant]]s that interfere with lipid metabolism), (3) decreased variability in ambient temperature, (4) decreased rates of [[tobacco smoking|smoking]], because smoking suppresses appetite, (5) increased use of medications that can cause weight gain (e.g., [[atypical antipsychotics]]), (6) proportional increases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may cause susceptibility to obesity in children), (8) [[epigenetic]] risk factors passed on generationally, (9) [[natural selection]] for higher BMI, and (10) [[assortative mating]] leading to increased concentration of obesity risk factors (this would  increase the number of obese people by increasing population variance in weight).<ref name="pmid16801930">{{cite journal|author=Keith SW |title=Putative contributors to the secular increase in obesity: Exploring the roads less traveled |journal=Int J Obes (Lond) |volume=30 |issue=11 |pages=1585–94 |year=2006 |pmid=16801930 |doi=10.1038/sj.ijo.0803326 |url=http://www.nature.com/ijo/journal/v30/n11/full/0803326a.html |author-separator=, |author2=Redden DT |author3=Katzmarzyk PT |last4=Boggiano |first4=M M |last5=Hanlon |first5=E C |last6=Benca |first6=R M |last7=Ruden |first7=D |last8=Pietrobelli |first8=A |last9=Barger |first9=J L |display-authors=3 |first10=K R |first11=C |first14=M |first15=N V |first16=M C |first17=C M |first18=M |first19=A O |first20=D B}}</ref> While there is substantial evidence supporting the influence of these mechanisms on the increased prevalence of obesity, the evidence is still inconclusive, and the authors state that these are probably less influential than the ones discussed in the previous paragraph.
  
== Obesity rates among all children in the United States ==
+
===Diet===
+
{{Main|Diet and obesity}}
* Approximately 17% (or 12.5 million) of children and adolescents aged 2—19 years are obese.
+
{{Double image|right|World map of Energy consumption 1961,2.svg|200|World map of Energy consumption 2001-2003.svg|200|alt=(Left) A world map with countries colored to reflect the food energy consumption of their people in 1961. North America, Europe, and Australia have relatively high intake, while Africa and Asia consume much less.(Right) A world map with countries colored to reflect the food energy consumption of their people in 2001–2003. Consumption in North America, Europe, and Australia has increased with respect to previous levels in 1971. Food consumption has also increased substantially in many parts of Asia. However, food consumption in Africa remains low.|Map of dietary energy availability per person per day in 1961 (left) and 2001–2003 (right)<ref name=Earth09/> Calories per person per day (kilojoules per person per day)
* Since 1980, obesity prevalence among children and adolescents has almost tripled.
+
{{Multicol}}
* There are significant racial and ethnic disparities in obesity prevalence among U.S. children and adolescents. In 2007—2008, Hispanic boys, aged 2 to 19 years,were significantly more likely to be obese than non-Hispanic white boys, and non-Hispanic black girls were significantly more likely to be obese than non-Hispanic white girls.
+
{{legend|#b3b3b3|no data}}
 +
{{legend|#ffff65|<1,600 (<6,700)}}
 +
{{legend|#fff200|1,600–1,800 (6,700–7,500)}}
 +
{{legend|#ffdc00|1,800–2,000 (7,500–8,400)}}
 +
{{legend|#ffc600|2,000–2,200 (8,400–9,200)}}
 +
{{legend|#ffb000|2,200–2,400 (9,200–10,000)}}
 +
{{legend|#ff9a00|2,400–2,600 (10,000–10,900)}}
 +
{{Multicol-break}}
 +
{{legend|#ff8400|2,600–2,800 (10,900–11,700)}}
 +
{{legend|#ff6e00|2,800–3,000 (11,700–12,600)}}
 +
{{legend|#ff5800|3,000–3,200 (12,600–13,400)}}
 +
{{legend|#ff4200|3,200–3,400 (13,400–14,200)}}
 +
{{legend|#ff2c00|3,400–3,600 (14,200–15,100)}}
 +
{{legend|#cb0000|>3,600 (>15,100)}}
 +
{{Multicol-end}}
 +
}}
  
==Obesity rates among all children in the United States==
+
[[Dietary energy supply]] per capita varies markedly between different regions and countries. It has also changed significantly over time.<ref name=Earth09/> From the early 1970s to the late 1990s the average food energy available per person per day (the amount of food bought) increased in all parts of the world except Eastern Europe. The United States had the highest availability with {{convert|3654|Cal}} per person in 1996.<ref name=Earth09/> This increased further in 2003 to {{convert|3754|Cal}}.<ref name=Earth09/>  During the late 1990s Europeans had {{convert|3394|Cal}} per person, in the developing areas of Asia there were {{convert|2648|Cal}} per person, and in sub-Saharan Africa people had {{convert|2176|Cal}} per person.<ref name=Earth09/><ref>{{cite web|url=http://www.scribd.com/doc/1470965/USDA-frsept99b |title=USDA: frsept99b |work=[[United States Department of Agriculture]] |accessdate=January 10, 2009}}</ref>  Total food energy consumption has been found to be related to obesity.<ref>{{cite web|url=http://www.statcan.gc.ca/pub/82-003-x/2009004/article/10933-eng.htm |title=Diet composition and obesity among Canadian adults |work=Statistics Canada |accessdate=}}</ref>
  
Approximately 17% (or 12.5 million) of children and adolescents aged 2—19 years are obese.
+
The widespread availability of [[Nutrition#Advice and guidance|nutritional guidelines]]<ref>{{cite web|author=National Control for Health Statistics |title=Nutrition For Everyone |publisher=Centers for Disease Control and Prevention |url=http://www.cdc.gov/nccdphp/dnpa/nutrition/nutrition_for_everyone |accessdate=2008-07-09}}</ref> has done little to address the problems of overeating and poor dietary choice.<ref>{{cite journal|author=Marantz PR, Bird ED, Alderman MH |title=A call for higher standards of evidence for dietary guidelines |journal=Am J Prev Med |volume=34 |issue=3 |pages=234–40 |date=March 2008 |pmid=18312812 |doi=10.1016/j.amepre.2007.11.017 |url=}}</ref> From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%.<ref name=Flegal2002>{{cite journal|author=Flegal KM, Carroll MD, Ogden CL, Johnson CL |title=Prevalence and trends in obesity among US adults, 1999–2000 |journal=[[JAMA (journal)|JAMA]] |date=October 2002 |volume=288 |pages=1723–1727 |url=http://jama.ama-assn.org/cgi/content/full/288/14/1723 |doi=10.1001/jama.288.14.1723 |pmid=12365955 |issue=14}}</ref> During the same period, an increase occurred in the average amount of food energy consumed. For women, the average increase was {{convert|335|Cal}} per day ({{convert|1542|Cal}} in 1971 and {{convert|1877|Cal}} in 2004), while for men the average increase was {{convert|168|Cal}} per day ({{convert|2450|Cal}} in 1971 and {{convert|2618|Cal}} in 2004). Most of this extra food energy came from an increase in carbohydrate consumption rather than fat consumption.<ref>{{cite journal|author=Wright JD, Kennedy-Stephenson J, Wang CY, McDowell MA, Johnson CL |title=Trends in intake of energy and macronutrients—United States, 1971–2000 |journal=MMWR Morb Mortal Wkly Rep |date=February 2004 |volume=53 |issue=4 |pages=80–2 |url=http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm |pmid=14762332}}</ref>  The primary sources of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily food energy in young adults in America,<ref name=Caballero>{{cite journal|author=Caballero B |title=The global epidemic of obesity: An overview |journal=Epidemiol Rev |volume=29 |issue= |pages=1–5 |year=2007 |pmid=17569676 |doi=10.1093/epirev/mxm012 |url=}}</ref> and potato chips.<ref>{{cite journal|last=Mozaffarian |first=D |last2=Hao |first2=T |last3=Rimm |first3=EB |last4=Willett |first4=WC |last5=Hu |first5=FB |title=Changes in Diet and Lifestyle and Long-Term Weight Gain in Women and Men |journal=The New England Journal of Medicine |date=23 June 2011 |volume=364 |issue=25 |pages=2392–404 |pmid=21696306 |doi=10.1056/NEJMoa1014296 |pmc=3151731 |author-separator=, |display-authors=3}}</ref>  Consumption of sweetened drinks is believed to be contributing to the rising rates of obesity.<ref>{{cite journal|author=Malik VS, Schulze MB, Hu FB |title=Intake of sugar-sweetened beverages and weight gain: a systematic review |journal=Am. J. Clin. Nutr. |volume=84 |issue=2 |pages=274–88 |date=August 2006 |pmid=16895873 |doi= |url=http://www.ajcn.org/cgi/content/full/84/2/274 |pmc=3210834}}</ref><ref>{{cite journal|author=Olsen NJ, Heitmann BL |title=Intake of calorically sweetened beverages and obesity |journal=Obes Rev |volume=10 |issue=1 |pages=68–75 |date=January 2009 |pmid=18764885 |doi=10.1111/j.1467-789X.2008.00523.x |url=}}</ref>
Since 1980, obesity prevalence among children and adolescents has almost tripled.
 
There are significant racial and ethnic disparities in obesity prevalence among U.S. children and adolescents. In 2007—2008, Hispanic boys, aged 2 to 19 years
 
  
==Causes of weight gain==
+
As societies become increasingly reliant on [[food energy|energy-dense]], big-portions, and fast-food meals, the association between fast-food consumption and obesity becomes more concerning.<ref>{{cite journal|author=Rosenheck R |title=Fast food consumption and increased caloric intake: a systematic review of a trajectory towards weight gain and obesity risk |journal=Obes Rev |volume=9 |issue=6 |pages=535–47 |date=November 2008 |pmid=18346099 |doi=10.1111/j.1467-789X.2008.00477.x |url=}}</ref>  In the United States consumption of fast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.<ref>{{cite book|author=Lin BH, Guthrie J and Frazao E |editor=Frazão E |title=Agriculture Information Bulletin No. 750: America's Eating Habits: Changes and Consequences |url=http://www.ers.usda.gov/publications/aib750/ |year=1999 |publisher=US Department of Agriculture, Economic Research Service |location=Washington, DC |pages=213–239 |chapter=Nutrient contribution of food away from home}}</ref>
* See causes of [[weight gain]].
 
* Understand the anabolic effects of [[insulin]], and the role of the all too common [[insulin resistance]] that leads to [[central obesity|belly fat]],
 
* Check to see if you might have a metabolic cause for your [[weight gain]] using this free online [http://w8md.com/w8md-tools-for-w8loss insulin resistance calculator].
 
  
When [[food energy]] intake exceeds energy expenditure, fat cells (and to a lesser extent muscle and [[liver]] cells) throughout the body take in the energy and store it as fat. In its simplest conception, therefore, obesity is only made possible when the lifetime energy intake exceeds lifetime energy expenditure by more than it does for individuals of "normal weight".
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[[Agricultural policy]] and [[Green Revolution (agriculture)|techniques]] in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the [[U.S. farm bill]] has made the main sources of processed food 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=22 April 2007 |accessdate=2007-07-30}}</ref>  [[Calorie count laws]] and [[nutrition facts label]]s attempt to steer people toward making healthier food choices, including awareness of how much food energy is being consumed.
  
In all individuals, the excess energy utilized to generate fat reserves is minute relative to the total number of calories consumed. This means that very fine perturbations in the energy balance can lead to large fluctuations in weight over time. To illustrate, an obese 40 year old who carries 100 lb of adipose tissue has only consumed about 25 more calories per day than he has burned on average - or the equivalent of an apple every three days. In comparison a very lean 40-year-old who carries only 15 lb of body fat will have exceeded his daily energy expenditure by about four calories a day - the equivalent of an apple every 18 days.  
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Obese people consistently under-report their food consumption as compared to people of normal weight.<ref>Kopelman and Caterson 2005:324.</ref>  This is supported both by tests of people carried out in a [[calorimeter]] room<ref>{{cite book|title=Metabolism alone doesn't explain how thin people stay thin |publisher=The Medical Post |work=John Schieszer}}</ref> and by direct observation.
  
Factors that have been suggested to contribute to the development of obesity include:
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===Sedentary lifestyle===
* Sedentary lifestyle
+
{{See also|Sedentary lifestyle|Exercise trends}}
* A high [[glycemic index|glycemic]] diet (i.e. a diet that consists of meals that give high postprandial [[blood sugar]])
+
A [[sedentary lifestyle]] plays a significant role in obesity.<ref>Seidell 2005 p.10</ref> Worldwide there has been a large shift towards less physically demanding work,<ref name=WHO2009>{{cite web|url=http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/ |title=WHO: Obesity and overweight |work=[[World Health Organization]] |accessdate=January 10, 2009 |archiveurl=https://web.archive.org/web/20081218104805/http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/ |archivedate=December 18, 2008}}</ref><ref name=WHOExercise>{{cite web|url=http://www.who.int/dietphysicalactivity/factsheet_inactivity/en/index.html |title=WHO &#124; Physical Inactivity: A Global Public Health Problem |work=[[World Health Organization]] |accessdate=February 22, 2009}}</ref><ref name=Ness2006>{{cite journal|author=Ness-Abramof R, Apovian CM |title=Diet modification for treatment and prevention of obesity |journal=Endocrine |volume=29 |issue=1 |pages=5–9 |date=February 2006 |pmid=16622287 |doi=10.1385/ENDO:29:1:135 |url=}}</ref> and currently at least 30% of the world's population gets insufficient exercise.<ref name=WHOExercise/> This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home.<ref name=WHO2009/><ref name=WHOExercise/><ref name=Ness2006/>  In children, there appear to be declines in levels of physical activity due to less walking and physical education.<ref>{{cite journal|author=Salmon J, Timperio A |title=Prevalence, trends and environmental influences on child and youth physical activity |journal=Med Sport Sci |volume=50 |issue= |pages=183–99 |year=2007 |pmid=17387258 |doi=10.1159/000101391 |series=Medicine and Sport Science |isbn=978-3-318-01396-2}}</ref>  World trends in active leisure time [[physical activity]] are less clear.  The [[World Health Organization]] indicates people worldwide are taking up less active recreational pursuits, while a study from Finland<ref>{{cite journal|author=Borodulin K, Laatikainen T, Juolevi A, Jousilahti P |title=Thirty-year trends of physical activity in relation to age, calendar time and birth cohort in Finnish adults |journal=Eur J Public Health |volume=18 |issue=3 |pages=339–44 |date=June 2008 |pmid=17875578 |doi=10.1093/eurpub/ckm092 |url=}}</ref> found an increase and a study from the United States found leisure-time physical activity has not changed significantly.<ref>{{cite journal|author=Brownson RC, Boehmer TK, Luke DA |title=Declining rates of physical activity in the United States: what are the contributors? |journal=Annu Rev Public Health |volume=26 |issue= |pages=421–43 |year=2005 |pmid=15760296 |doi=10.1146/annurev.publhealth.26.021304.144437 |url=}}</ref>
* Weight cycling, caused by repeated attempts to lose weight by dieting
 
* Underlying illness (e.g. [[hypothyroidism]])
 
* [[Genetic disorders]] (e.g. [[Prader-Willi syndrome]])
 
* [[Eating disorder]]s (such as [[binge eating disorder]])
 
* [[Stress (medicine)|Stressful]] mentality
 
* Insufficient [[sleep]]
 
* Certain medications (e.g. [[atypical antipsychotic]]s)
 
* [[Smoking cessation]]
 
* [[genetics|Genetic]] factors
 
  
As with many medical conditions, the caloric imbalance that results in obesity often develops from a combination of genetic and environmental factors. [[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 abnormalities that predispose to obesity have been identified (such as [[Prader-Willi syndrome]] and [[leptin]] 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.  
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In both children and adults, there is an association between television viewing time and the risk of obesity.<ref>{{cite journal|author=Gortmaker SL, Must A, Sobol AM, Peterson K, Colditz GA, Dietz WH |title=Television viewing as a cause of increasing obesity among children in the United States, 1986–1990 |journal=Arch Pediatr Adolesc Med |volume=150 |issue=4 |pages=356–62 |date=April 1996 |pmid=8634729 |doi=10.1001/archpedi.1996.02170290022003}}</ref><ref>{{cite journal|author=Vioque J, Torres A, Quiles J |title=Time spent watching television, sleep duration and obesity in adults living in Valencia, Spain |journal=Int. J. Obes. Relat. Metab. Disord. |volume=24 |issue=12 |pages=1683–8 |date=December 2000 |pmid=11126224 |doi=10.1038/sj.ijo.0801434 |url=}}</ref><ref>{{cite journal|author=Tucker LA, Bagwell M |title=Television viewing and obesity in adult females |journal=Am J Public Health |volume=81 |issue=7 |pages=908–11 |date=July 1991 |pmid=2053671 |pmc=1405200 |doi=10.2105/AJPH.81.7.908 |url=http://www.ajph.org/cgi/reprint/81/7/908 |format=PDF}}</ref>  A review found 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.<ref>{{cite web|url=http://ipsdweb.ipsd.org/uploads/IPPC/CSM%20Media%20Health%20Report.pdf |title=Media + Child and Adolescent Health: A Systematic Review |publisher=Common Sense Media |year=2008 |format=PDF |work=Ezekiel J. Emanuel |accessdate=April 6, 2009}}</ref>
  
Some eating disorders are associated with obesity, especially binge eating disorder (BED). As the name indicates, patients with this disorder are prone to overeat, often in binges. A proposed mechanism is that the eating serves to reduce [[anxiety]], and some parallels with [[substance abuse]] can be drawn. An important additional factor is that BED patients often lack the ability to recognize [[hunger]] and [[satiety]], something that is normally learned in childhood. [[Learning theory (education)|Learning theory]] suggests that early childhood conceptions may lead to an association between food and a calm mental state.
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===Genetics===
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{{Main|Genetics of obesity}}
  
{{blame}}
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Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. [[Polymorphism (biology)|Polymorphisms]] in various [[gene]]s controlling [[appetite]] and [[metabolism]] predispose to obesity when sufficient food energy is present.  As of 2006, more than 41 of these sites on the human genome have been linked to the development of obesity when a favorable environment is present.<ref>{{cite journal|author=Poirier P |title=Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss |journal=Arterioscler. Thromb. Vasc. Biol. |volume=26 |issue=5 |pages=968–76 |date=May 2006 |pmid=16627822 |doi=10.1161/01.ATV.0000216787.85457.f3 |url=|author-separator=, |author2=Giles TD |author3=Bray GA |last4=Hong |first4=Y |last5=Stern |first5=JS |last6=Pi-Sunyer |first6=FX |last7=Eckel |first7=RH |display-authors=3}}</ref> People with two copies of the [[FTO gene]] (fat mass and obesity associated gene) have been found on average to weigh 3–4&nbsp;kg more and have a 1.67-fold greater risk of obesity compared with those without the risk [[allele]].<ref>{{cite journal|author=Loos RJ, Bouchard C |title=FTO: the first gene contributing to common forms of human obesity |journal=Obes Rev |volume=9 |issue=3 |pages=246–50 |date=May 2008 |pmid=18373508 |doi=10.1111/j.1467-789X.2008.00481.x |url=}}</ref>  The percentage of obesity that can be attributed to genetics varies, depending on the population examined, from 6% to 85%.<ref>{{cite journal|author=Yang W, Kelly T, He J |title=Genetic epidemiology of obesity |journal=Epidemiol Rev |volume=29 |issue= |pages=49–61 |year=2007 |pmid=17566051 |doi=10.1093/epirev/mxm004}}</ref>
  
===Evolutionary aspects===
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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.)<ref name="pmid19506576">{{cite journal|author=Walley AJ, Asher JE, Froguel P |title=The genetic contribution to non-syndromic human obesity |journal=Nature Reviews Genetics |volume=10 |issue=7 |pages=431–42 |date=June 2009 |pmid=19506576 |doi=10.1038/nrg2594 |url=}}</ref> In people with early-onset severe obesity (defined by an onset before 10&nbsp;years of age and body mass index over three [[standard deviation]]s above normal), 7% harbor a single point DNA mutation.<ref>{{cite journal|author=Farooqi S, O'Rahilly S |title=Genetics of obesity in humans |journal=Endocr. Rev. |volume=27 |issue=7 |pages=710–18 |date=December 2006 |pmid=17122358 |doi=10.1210/er.2006-0040 |url=http://edrv.endojournals.org/cgi/content/full/27/7/710}}</ref>
Although there is no definitive explanation for the recent increase of obesity, the [[thrifty gene hypothesis]] provides some understanding of this phenomenon, and suggests why certain populations and individuals may be more prone to obesity than others. In times when food was scarce, the ability to take advantage of rare periods of abundance and use such abundance by storing energy efficiently was undoubtedly an evolutionary advantage. Individuals with greater adipose reserves were more likely to survive famine. This tendency to store fat is likely maladaptive in a society with adequate and stable food supplies. Although many people likely have a genetic propensity towards obesity, in most cases this propensity requires the modern environment with increased caloric availability and decreased requirements for physical labor in order to be expressed fully.
 
  
===Neurobiological mechanisms===
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Studies that have focused on inheritance patterns rather than on specific genes have found that 80% of the offspring of two [[parental obesity|obese parents]] were also obese, in contrast to less than 10% of the offspring of two parents who were of normal weight.<ref>{{cite book|author=Kolata,Gina |title=Rethinking thin: The new science of weight loss&nbsp;– and the myths and realities of dieting |publisher=Picador |location= |year=2007 |page=122 |isbn=0-312-42785-9}}</ref>
  
Flier 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]], 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.
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The [[thrifty gene hypothesis]] postulates that, due to dietary scarcity during human evolution, people are prone to obesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would be more likely to survive [[famine]]. This tendency to store fat, however, would be maladaptive in societies 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> This theory has received various criticisms, and other evolutionarily-based theories such as the [[drifty gene hypothesis]] and the [[thrifty phenotype|thrifty phenotype hypothesis]] have also been proposed.<ref>{{cite doi|10.1038/ijo.2009.175}}</ref><ref>{{cite doi|10.1002/ajhb.21100}}</ref>
  
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, and this resistance has been implicated in obesity in some people, is thought to explain in part why administration of leptin has not been shown to be effective in suppressing appetite in most obese subjects.
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===Other illnesses===
 +
Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: [[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=10.1111/j.1365-2265.1993.tb00974.x}}</ref> and the [[eating disorder]]s: [[binge eating disorder]] and [[night eating syndrome]].<ref name=HaslamJames/> However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the [[Diagnostic and Statistical Manual of Mental Disorders|DSM-IVR]] as a psychiatric illness.<ref>{{cite journal|author=Zametkin AJ, Zoon CK, Klein HW, Munson S |title=Psychiatric aspects of child and adolescent obesity: a review of the past 10 years |journal=J Am Acad Child Adolesc Psychiatry |volume=43 |issue=2 |pages=134–50 |date=February 2004 |pmid=14726719 |doi=10.1097/00004583-200402000-00008}}</ref> The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.<ref>{{cite journal|author=Chiles C, van Wattum PJ |title=Psychiatric aspects of the obesity crisis |journal=Psychiatr Times |year=2010 |volume=27 |issue=4 |pages=47–51}}</ref>
  
[[Neuroscience|Neuroscientific]] approaches hinge on the action of the aforementioned mediators on the [[hypothalamus]], the part of the brain that is thought to process signals related to metabolic state and energy storage and to shift the energy balance in either a positive or negative direction, primarily by acting on appetite and energy expenditure. [[Lesion|Lesion studies]] in the 1940s and 1950s identified two regions of the hypothalamus &mdash; the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH) &mdash; as the brain's hunger and satiety centers, respectively. Specific lesions to a mouse's LH suppressed its appetite while damaging the VMH caused overeating.
+
Certain medications may cause weight gain or changes in [[body composition]]; these include [[insulin]], [[sulfonylurea]]s, [[thiazolidinedione]]s, [[atypical antipsychotic]]s, [[antidepressant]]s, [[glucocorticoids|steroids]], certain [[anticonvulsant]]s ([[phenytoin]] and [[valproate]]), [[pizotifen]], and some forms of [[hormonal contraception]].<ref name=HaslamJames/>
  
Studies of the distribution of the leptin receptor in the mid-1990s cast doubt upon this dual center theory of hunger and satiety. Leptin's effect on the [[arcuate nucleus]] melanocortin system is now considered central to the regulation of feeding and metabolism.
+
===Social determinants===
{{exercise}}
+
{{Main|Social determinants of obesity}}
 +
While genetic influences are important to understanding obesity, they cannot explain the current dramatic increase seen within specific countries or globally.<ref>{{cite journal|author=Yach D, Stuckler D, Brownell KD |title=Epidemiologic and economic consequences of the global epidemics of obesity and diabetes |journal=Nat. Med. |volume=12 |issue=1 |pages=62–6 |date=January 2006 |pmid=16397571 |doi=10.1038/nm0106-62 |url=}}</ref> Though it is accepted that energy consumption in 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 much debated. There are a number of theories as to the cause but most believe it is a combination of various factors.
  
===Poverty link===
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The correlation between [[social class]] and BMI varies globally. A review in 1989 found that in developed countries women of a high social class were less likely to be obese. No significant differences were seen among men of different social classes. In the developing world, women, men, and children from high social classes had greater rates of obesity.<ref>{{cite journal|author=Sobal J, Stunkard AJ |title=Socioeconomic status and obesity: A review of the literature |journal=Psychol Bull |volume=105 |issue=2 |pages=260–75 |date=March 1989 |pmid=2648443 |doi=10.1037/0033-2909.105.2.260}}</ref> An update of this review carried out in 2007 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of [[globalization]].<ref name=McLaren2007>{{cite journal|author=McLaren L |title=Socioeconomic status and obesity |journal=Epidemiol Rev |volume=29 |issue= |pages=29–48 |year=2007 |pmid=17478442 |doi=10.1093/epirev/mxm001}}</ref> Among developed countries, levels of adult obesity, and percentage of teenage children who are overweight, are correlated with [[economic inequality|income inequality]]. A similar relationship is seen among US states: more adults, even in higher social classes, are obese in more unequal states.<ref name="spirit">{{cite book|title=[[The Spirit Level: Why More Equal Societies Almost Always Do Better]] |last1=Wilkinson |first1=Richard |authorlink1=Richard G. Wilkinson |last2=Pickett |first2=Kate |publisher=Allen Lane |location=London |isbn=978-1-84614-039-6 |year=2009 |pages=91–101}}</ref>
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 [http://roa.sagepub.com/cgi/reprint/26/1/130 study] found obese American subjects approximately half as wealthy as thin ones. When income differentials were factored out, the inequity persisted &mdash; thin subjects were inheriting more wealth than fat ones. Another study finds women who married into higher status predictably thinner than women who married into lower status.
 
  
==Health Consequences of Obesity==
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Many explanations have been put forth for associations between BMI and social class. It is thought that in developed countries, the wealthy are able to afford more nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for [[physical fitness]]. In [[undeveloped countries]] the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns.<ref name=McLaren2007/> Attitudes toward body weight held by people in one's life may also play a role in obesity. A correlation in BMI changes over time has been found among friends, siblings, and spouses.<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=New England Journal of Medicine |volume=357 |issue=4 |pages=370–379 |year=2007 |pmid=17652652 |doi=10.1056/NEJMsa066082}}</ref>  Stress and perceived low social status appear to increase risk of obesity.<ref name="spirit" /><ref>{{cite journal|author=Bjornstop P |title=Do stress reactions cause abdominal obesity and comorbidities? |journal=Obesity Reviews |volume=2 |issue=2 |pages=73–86 |year=2001 |doi=10.1046/j.1467-789x.2001.00027.x |pmid=12119665}}</ref><ref>{{cite journal|author=Goodman E, Adler NE, Daniels SR, Morrison JA, Slap GB, Dolan LM |title=Impact of objective and subjective social status on obesity in a biracial cohort of adolescents |journal=Obesity Reviews |volume=11 |issue=8 |pages=1018–26 |year=2003 |pmid=12917508 |doi=10.1038/oby.2003.140}}</ref>
Obesity increases the risk of over 50 health conditions, including, but not limited to the following:
 
* [[Metabolic syndrome]]
 
* [[Coronary heart disease]]
 
* [[Stroke]],  
 
* {{High blood pressure]]
 
* [[Prediabetes]]
 
* [[Type 2 diabetes]]
 
* [[Cancer]]s, such as endometrial, breast, and colon cancer.
 
* [[Hypercholesterolemia]]
 
* [[High triglceredemia]]
 
* [[Fatty liver]]
 
* [[Gall stones]]
 
* [[Polycystic ovaries]]
 
* [[Sleep apnea]], [[Asthma]] and respiratory problems.
 
* [[Osteoarthritis]]
 
* Reproductive health complications such as infertility.
 
* Mental health conditions.
 
  
In fact, [[losing weight]] has many [http://w8md.com/w8d-healthy-living/benefits-of-losing-weight preventive benefits] that up to 90 percent of [[diabetes]], 80 percent of [[cardiovascular diseases]] and 60% of [[cancer]]s could be prevented with [[weight loss]] and other lifestyle interventions according research.  
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Smoking has a significant effect on an individual's weight. Those who quit smoking gain an average of 4.4&nbsp;kilograms (9.7&nbsp;lb) for men and 5.0&nbsp;kilograms (11.0&nbsp;lb) for women over ten years.<ref>{{cite journal|author=Flegal KM, Troiano RP, Pamuk ER, Kuczmarski RJ, Campbell SM |title=The influence of smoking cessation on the prevalence of overweight in the United States |journal=N. Engl. J. Med. |volume=333 |issue=18 |pages=1165–70 |date=November 1995 |pmid=7565970 |doi=10.1056/NEJM199511023331801 |url=http://content.nejm.org/cgi/content/full/333/18/1165}}</ref>  However, changing rates of smoking have had little effect on the overall rates of obesity.<ref>{{cite journal|author=Chiolero A, Faeh D, Paccaud F, Cornuz J |title=Consequences of smoking for body weight, body fat distribution, and insulin resistance |journal=Am. J. Clin. Nutr. |volume=87 |issue=4 |pages=801–9 |date=1 April 2008 |pmid=18400700 |url=http://www.ajcn.org/cgi/content/full/87/4/801}}</ref>
  
==Cost of Obesity==
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In the United States the number of children a person has is related to their risk of obesity. A woman's risk increases by 7% per child, while a man's risk increases by 4% per child.<ref>{{cite journal|author=Weng HH, Bastian LA, Taylor DH, Moser BK, Ostbye T |title=Number of children associated with obesity in middle-aged women and men: results from the health and retirement study |journal=J Women's Health (Larchmt) |volume=13 |issue=1 |pages=85–91 |year=2004 |pmid=15006281 |doi=10.1089/154099904322836492}}</ref>  This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.<ref>{{cite journal|author=Bellows-Riecken KH, Rhodes RE |title=A birth of inactivity? A review of physical activity and parenthood |journal=Prev Med |volume=46 |issue=2 |pages=99–110 |date=February 2008 |pmid=17919713 |doi=10.1016/j.ypmed.2007.08.003}}</ref>
In 2008, overall medical care [http://storify.com/w8md/annual-cost-of-obesity-or-overweight-in-usa costs related to obesity] for U.S. adults were estimated to be as high as $147 billion. People who were obese had medical costs that were $1,429 higher than the cost for people of normal body weight. [[Obesity]] also has been linked with reduced worker productivity and chronic absence from work. [[Obesity]] also comes at a steep individual cost as one study from George Washington University found that the average annual [http://www.w8md.com/how-w8md-weight-loss-works/why-lose-weight cost of obesity] can as high as  $4,879 for a woman, $2,646 for a man!
 
  
==Complications==
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In the developing world urbanization is playing a role in increasing rate of obesity.  In [[China]] overall rates of obesity are below 5%; however, in some cities rates of obesity are greater than 20%.<ref>{{cite web|url=http://www.who.int/dietphysicalactivity/media/en/gsfs_obesity.pdf |title=Obesity and Overweight |format=PDF |publisher=[[World Health Organization]] |accessdate=February 22, 2009}}</ref>
Obesity, especially [[central obesity]] (male-type or waist-predominant obesity), is an important risk factor for the "[[metabolic syndrome]]" ("syndrome X"), the clustering of a number of diseases and risk factors that heavily predispose for [[cardiovascular disease]]. These are [[diabetes mellitus|diabetes mellitus type 2]], [[arterial hypertension|high blood pressure]], [[hypercholesterolemia|high blood cholesterol]], and [[hypertriglyceridemia|triglyceride levels]] ([[combined hyperlipidemia]]). An [[inflammation|inflammatory state]] is present, which &mdash; together with the above &mdash; has been implicated in the high prevalence of [[atherosclerosis]] (fatty lumps in the arterial wall), and a [[thrombosis|prothrombotic]] state may further worsen cardiovascular risk.
 
  
Apart from the metabolic syndrome, obesity is also [[correlation|correlated]] (in population studies) with a variety of other complications. For many of these complaints, it has not been clearly established to what extent they are caused directly by obesity itself, or have some other cause (such as limited exercise) that causes obesity as well. Most confidence in a direct cause is given to the mechanical complications in the following list, compiled by the [[American Medical Association]] for general physicians:
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[[Malnutrition]] in early life is believed to play a role in the rising rates of obesity in the [[developing world]].<ref name=DC2001>{{cite journal|author=Caballero B |title=Introduction. Symposium: Obesity in developing countries: biological and ecological factors |journal=J. Nutr. |volume=131 |issue=3 |pages=866S–870S |date=March 2001 |pmid=11238776 |doi= |url=http://jn.nutrition.org/cgi/content/full/131/3/866S}}</ref>  Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more food energy becomes available.<ref name=DC2001/>
* ''[[Cardiovascular]]'': [[congestive heart failure]], [[cardiomegaly|enlarged heart]] and its associated [[arrhythmia]] and dizziness, [[cor pulmonale]], [[varicose veins]], and [[pulmonary embolism]]
 
*''[[Endocrine]]'': [[polycystic ovarian syndrome]] (PCOS), [[menstruation|menstrual]] disorders, and [[infertility]]
 
* ''[[Gastrointestinal]]'': [[gastroesophageal reflux disease]] (GERD), [[non-alcoholic steatohepatitis|fatty liver disease]], [[cholelithiasis]] (gallstones), [[hernia]], and [[colorectal cancer]]
 
* ''Renal and [[genitourinary]]'': [[urinary incontinence]], [[glomerulopathy]], [[hypogonadism]] (male), [[breast cancer]] (female), [[endometrial cancer|uterine cancer]] (female), [[stillbirth]]
 
* ''[[Integument]]'' (skin and appendages): [[stretch mark]]s, [[acanthosis nigricans]], [[lymphedema]], [[cellulitis]], [[carbuncle]]s, [[intertrigo]]
 
* ''Musculoskeletal'': [[hyperuricemia]] (which predisposes to [[gout]]), immobility, [[osteoarthritis]], [[low back pain]]
 
* ''Neurologic'': [[stroke]], [[meralgia paresthetica]], [[headache]], [[carpal tunnel syndrome]], [[dementia]]{{mnb|Whitmer|10}}
 
* ''[[Respiratory]]'': [[dyspnea]], [[obstructive sleep apnea]], [[hypoventilation]] syndrome, [[Pickwickian syndrome]], [[asthma]]
 
* ''[[Psychological]]'': [[Clinical depression|Depression]], low [[self esteem]], [[body image disorder]], social stigmatization
 
  
While being severely obese has many health ramifications, those who are somewhat overweight face little increased [[mortality]] or [[morbidity]]. Some studies suggest that the somewhat "overweight" tend to live longer than those at their "ideal" weight [http://www.chron.com/cs/CDA/ssistory.mpl/nation/3142605]. This may in part be attributable to lower mortality rates in diseases where death is either caused or contributed to by significant weight loss due to the greater risk of being underweight experienced by those in the ideal category. Another factor which may confound mortality data is smoking, since obese individuals are less likely to smoke. [[Osteoporosis]] is known to occur less in slightly overweight people.
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Consistent with [[cognitive epidemiology|cognitive epidemiological]] data, numerous studies confirm that obesity is  associated with cognitive deficits.<ref name="Smith2011">{{cite doi|10.1111/j.1467-789X.2011.00920.x}}</ref> Whether obesity causes cognitive deficits, or vice versa is unclear at present.
{{5 proven}}
 
  
==Therapy==
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===Infectious agents===
The mainstay of treatment for obesity is an energy-limited [[dieting|diet]] and increased exercise. In studies, diet and exercise programs have consistently produced an average weight loss of approximately 8% of total body mass on average (excluding study drop-outs). While not all dieters will be satisfied with this outcome, studies have shown that a loss of as little as 5% of body mass can create enormous health benefits.  
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{{See also|Infectobesity}}
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The study of the effect of infectious agents on metabolism is still in its early stages.  [[Gut flora]] has been shown to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the metabolic potential. This apparent alteration of the metabolic potential is believed to confer a greater capacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result of obesity has yet to be determined unequivocally.<ref>{{cite journal|author=DiBaise JK, Zhang H, Crowell MD, Krajmalnik-Brown R, Decker GA, Rittmann BE |title=Gut microbiota and its possible relationship with obesity |journal=Mayo Clinic proceedings. Mayo Clinic |volume=83 |issue=4 |pages=460–9 |date=April 2008 |pmid=18380992 |doi=10.4065/83.4.460}}</ref>
  
A more intractable therapeutic problem appears to be weight loss maintenance. Of dieters who manage to lose 10% or more of their body mass in studies, 80-95% will regain that weight within two to five years. It appears that the [[homeostasis|homeostatic]] mechanisms regulating body weight are very robust (see [[leptin]], for example), and vigorously defend against weight loss. Much important research is now being devoted to determining what factors can improve the currently dismal weight loss maintenance rates.  
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An association between [[viruses]] and obesity has been found in humans and several different animal species. The amount that these associations may have contributed to the rising rate of obesity is yet to be determined.<ref>{{cite journal|author=Falagas ME, Kompoti M |title=Obesity and infection |journal=Lancet Infect Dis |volume=6 |issue=7 |pages=438–46 |date=July 2006 |pmid=16790384 |doi=10.1016/S1473-3099(06)70523-0 |url=}}</ref>
  
Recent scientific research has cast some doubt over whether or not dieting actually improves health, with some studies indicating that dieting may in fact be more detrimental than remaining overweight.
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==Pathophysiology==
  
In a [[clinical practice guideline]] by the [[American College of Physicians]], the following five recommendations are made:
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There are many possible [[pathophysiology|pathophysiological]] mechanisms involved in the development and maintenance of obesity.<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 |pmid=14744442 |doi=10.1016/S0092-8674(03)01081-X}}</ref> 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]], [[insulin]], [[orexin]], [[PYY 3-36]], [[cholecystokinin]], [[adiponectin]], as well as 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.
# 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.
 
  
Much research focuses on new [[medication|drugs]] to combat obesity, which is seen as the biggest health problem facing developed countries. Nutritionists and many doctors feel that these research funds would be better devoted to advice on good [[nutrition]], healthy eating, and promoting a more active lifestyle.
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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, most obese individuals are thought to be leptin resistant and have been found to have high levels of leptin.<ref>{{cite journal|author=Hamann A, Matthaei S |title=Regulation of energy balance by leptin |journal=Exp. Clin. Endocrinol. Diabetes |volume=104 |issue=4 |pages=293–300 |year=1996 |pmid=8886745 |doi=10.1055/s-0029-1211457}}</ref> 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 people.<ref name="flier"/>
  
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]]). In the presence of [[diabetes mellitus]], there is evidence that the [[anti-diabetic drug]] [[metformin]] (Glucophage®) can assist in [[weight loss]] &mdash; rather than [[sulfonylurea]] derivatives and [[insulin]], which often lead to further weight gain.  The [[thiazolidinedione]]s ([[rosiglitazone]] or [[pioglitazone]]) can cause slight weight gain, but decrease the "pathologic" form of abdominal fat, and are therefore often used in obese [[diabetes mellitus|diabetics]].
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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 physiologya: A cellular and molecular approach |publisher=Saunders |location=Philadelphia |year=2003 |page=1227 |isbn=0-7216-3256-4}}</ref>
  
Although ''[[bariatric surgery]]'' is being used sometimes to combat obesity, there are many non-surgical [[weight loss]] options for [[losing weight]]. The most common weight loss surgery in [[Europe]] and [[Australia]] is the [[adjustable gastric band]] where a silicone ring is placed around the top of the stomach to help restrict the amount of food eaten in a sitting. This surgery has been FDA approved in the United States since [[2001]] but has been being used in other parts of the world since the early 1990s.  It is considered the safest and least invasive of the available weight loss surgeries such as [[Roux-en-Y gastric bypass surgery]] (RNY), [[biliopancreatic diversion]], and [[stomach stapling]] (also known as "vertical banded gastroplasty", VBG). Unlike those more invasive techniques the band surgery does not cut into or reroute any of the digestive tract and is completely reversible. Removing the implant returns the stomach to its pre-surgical norm. All of these surgeries can be done [[laparoscopic surgery|laparoscopically]].  The more invasive of the surgeries usually bypass or remove some portion of the patient's intestines which causes  [[malabsorption]] and [[Gastric dumping syndrome|dumping]].
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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.<ref name="flier"/>
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{{clear}}
  
All of these surgeries come with risk to the patient. For instance a recent study by the U.S. Department of Health and Human Service showed a 40% complication rate within 180 days of bariatric surgery. Moreover these surgeries do not guarantee either successful weight loss or reduced morbidity and mortality. Patients are also required to to make lifelong changes to their diet if they are to keep the lost weight off in the long term. Therefore, as with any major surgery, patients needs to carefully evalute the long term ramifications of their choice.
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==Public health==
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The [[World Health Organization]] (WHO) predicts that [[overweight]] and obesity may soon replace more traditional [[public health]] concerns such as [[undernutrition]] and [[infectious diseases]] as the most significant cause of poor health.<ref>{{cite book|author=Loscalzo, Joseph; Fauci, Anthony S.; Braunwald, Eugene; Dennis L. Kasper; Hauser, Stephen L; Longo, Dan L. |title=Harrison's principles of internal medicine |publisher=McGraw-Hill Medical |location= |year=2008 |pages= |isbn=0-07-146633-9 |oclc= |doi= |accessdate=}}</ref> Obesity is a public health and policy problem because of its prevalence, costs, and health effects.<ref>{{cite book|author=Satcher D |title=The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity |year=2001 |publisher=U.S. Dept. of Health and Human Services, Public Health Service, Office of Surgeon General |url=http://www.ncbi.nlm.nih.gov/books/NBK44206/ |isbn=978-0-16-051005-2}}</ref> The [[United States Preventive Services Task Force]] recommends screening for all adults followed by behavioral interventions in those who are obese.<ref>{{cite journal|author1=Moyer, VA |author2=U.S. Preventive Services Task Force |title=Screening for and management of obesity in adults: U.S. Preventive Services Task Force recommendation statement |journal=Annals of Internal Medicine |date=4 September 2012 |volume=157 |issue=5 |pages=373–8 |pmid=22733087 |doi=10.7326/0003-4819-157-5-201209040-00475}}</ref> Public health efforts seek to understand and correct the environmental factors responsible for the increasing prevalence of obesity in the population. Solutions look at changing the factors that cause excess food energy consumption and inhibit physical activity. Efforts include federally reimbursed meal programs in schools, limiting direct [[junk food]] marketing to children,<ref>{{cite news|author=Brook Barnes |title=Limiting Ads of Junk Food to Children |url=http://www.nytimes.com/2007/07/18/business/18food.html |work=New York Times |date=2007-07-18 |accessdate=2008-07-24}}</ref> and decreasing access to sugar-sweetened beverages in schools.<ref>{{cite web|url=http://www.healthfinder.gov/news/newsstory.aspx?docID=625759 |title=Fewer Sugary Drinks Key to Weight Loss - healthfinder.gov |work=U.S. Department of Health and Human Services |accessdate=Oct 18,2009}}</ref>  When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.<ref>{{cite journal|author=Brennan Ramirez LK |title=Indicators of activity-friendly communities: An evidence-based consensus process |journal=Am J Prev Med |date=December 2006 |issue=6 |pages=530–32 |pmid=17169714 |url= |doi=10.1016/j.amepre.2006.07.026 |volume=31 | author-separator=, |author2=Hoehner CM |author3=Brownson RC |last4=Cook |first4=R |last5=Orleans |first5=C |last6=Hollander |first6=M |last7=Barker |first7=D |last8=Bors |first8=P |last9=Ewing |first9=R |display-authors=3 |first10=R |first11=K}}</ref>
  
==Cultural and social significance==
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Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelines were published, titled "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report".<ref>{{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=1998 |isbn=1-58808-002-1 |oclc= |url=http://www.nhlbi.nih.gov/guidelines/obesity/ob_gdlns.pdf |format=PDF}}</ref> In 2006 the [[Canadian Obesity Network]] published the "Canadian Clinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children". This is a comprehensive evidence-based guideline to address the management and prevention of overweight and obesity in adults and children.<ref>{{cite journal|author=Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E |title=2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children summary |journal=CMAJ |volume=176 |issue=8 |pages=S1–13 |date=April 2007 |pmid=17420481 |pmc=1839777 |doi=10.1503/cmaj.061409 |url=http://www.cmaj.ca/cgi/content/full/176/8/S1}}</ref>
===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 language|English]] was in [[1651]], in [[Noah Biggs]]'s ''Matæotechnia Medicinæ Praxeos''
 
  
===Culture and obesity===
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In 2004, the United Kingdom [[Royal College of Physicians]], the [[Faculty of Public Health]] and the [[Royal College of Paediatrics and Child Health]] released the report "Storing up Problems", which highlighted the growing problem of obesity in the UK.<ref>{{cite book|title=Storing up problems; the medical case for a slimmer nation |date=2004-02-11 |publisher=Royal College of Physicians |location=London |isbn=1-86016-200-2 |author=}}</ref> The same year, the [[British House of Commons|House of Commons]] [[Health Select Committee]] published its "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in the UK and possible approaches to the problem.<ref name =GB2004>{{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 |date=May 2004 |publisher=TSO (The Stationery Office) |location=London, UK |isbn=978-0-215-01737-6}}</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>{{cite web|url=http://www.nice.org.uk/nicemedia/pdf/CG43NICEGuideline.pdf |title=Obesity: guidance on the prevention, identification, assessment and management of overweight and obesity in adults and children |publisher=[[National Health Services]] (NHS) |year=2006 |format=PDF |work=National Institute for Health and Clinical Excellence(NICE) |accessdate=April 8, 2009}}</ref> 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 |last2=Appleby |first2=John |last3=Harrison |first3=Anthony |last4=Patel |first4=Darshan |title=Our Future Health Secured? A review of NHS funding and performance |year=2007 |publisher=The King's Fund |location=London, UK |isbn=1-85717-562-X}}</ref>
  
In several human cultures, obesity is associated with [[physical attractiveness]], [[physical strength|strength]], and [[fertility]]. Some of the earliest known cultural [[artifact (archaeology)|artifact]]s, known as [[Venus figurines]], are pocket-sized [[statue]]ttes representing an obese female figure. Although their cultural significance is unrecorded, their widespread use throughout pre-historic Mediterranean and [[Europe]]an cultures suggests a central role for the obese female form in [[magic and religion|magical]] rituals, and suggests cultural approval of (and perhaps reverence for) this body formThis is most likely due to their ability to easily bear children and survive [[famine]].
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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 prevent obesity, and 'downstream' policies try to treat currently afflicted people.<ref>{{cite journal|last=Sacks |first=G |last2=Swinburn |first2=B |last3=Lawrence |first3=M |title=Obesity Policy Action framework and analysis grids for a comprehensive policy approach to reducing obesity |journal=Obes Rev |volume=10 |issue=1 |pages=76–86 |date=January 2009 |pmid=18761640 |doi=10.1111/j.1467-789X.2008.00524.X |author-separator=, |display-authors=3}}</ref>
  
In contrast, in modern [[Western culture]], a more slender body shape is more typically considered desirable. "Thinness" is often considered more important for women than men.  
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==Management==
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{{Main|Management of obesity}}
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(Xenical), the most commonly used medication to treat obesity, and [[sibutramine]] (Meridia), a medication recently withdrawn due to cardiovascular side effects]]
 +
The main treatment for obesity consists of [[dieting]] and [[physical exercise]].<ref name=CADG2006>{{cite journal|author=Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E |title=2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children summary |journal=CMAJ |volume=176 |issue=8 |pages=S1–13 |date=April 2007 |pmid=17420481 |pmc=1839777 |doi=10.1503/cmaj.061409 |url=}}</ref> Diet programs may produce [[weight loss]] over the short term,<ref name=Strychar>{{cite journal|author=Strychar I |title=Diet in the management of weight loss |journal=CMAJ |volume=174 |issue=1 |pages=56–63 |date=January 2006 |pmid=16389240 |pmc=1319349 |doi=10.1503/cmaj.045037 |url=http://www.cmaj.ca/cgi/content/full/174/1/56}}</ref> but maintaining this weight loss is frequently difficult and often requires making exercise and a lower food energy diet a permanent part of a person's lifestyle.<ref>{{cite journal|author=Shick SM, Wing RR, Klem ML, McGuire MT, Hill JO, Seagle H |title=Persons successful at long-term weight loss and maintenance continue to consume a low-energy, low-fat diet |journal=J Am Diet Assoc |volume=98 |issue=4 |pages=408–13 |date=April 1998 |pmid=9550162 |doi=10.1016/S0002-8223(98)00093-5}}</ref><ref>{{cite journal|author=Tate DF, Jeffery RW, Sherwood NE, Wing RR |title=Long-term weight losses associated with prescription of higher physical activity goals. Are higher levels of physical activity protective against weight regain? |journal=Am. J. Clin. Nutr. |volume=85 |issue=4 |pages=954–9 |date=1 April 2007 |pmid=17413092 |url=http://www.ajcn.org/cgi/content/full/85/4/954}}</ref> Success rates of long-term weight loss maintenance with lifestyle changes are low, ranging from 2–20%.<ref>{{cite journal|author=Wing RR, Phelan, S |title=Science-Based Solutions to Obesity: What are the Roles of Academia, Government, Industry, and Health Care? Proceedings of a symposium, Boston, Massachusetts, USA, 10–11 March 2004 and Anaheim, California, USA, 2 October 2004 |journal=Am. J. Clin. Nutr. |volume=82 |issue=1 Suppl |pages=207S–273S |date=1 July 2005 |pmid=16002825 |url=http://www.ajcn.org/cgi/content/full/82/1/222S}}</ref> Dietary and lifestyle changes are effective in limiting excessive weight gain in [[pregnancy]] and improve outcomes for both the mother and the child.<ref>{{cite journal|last=Thangaratinam |first=S |last2=Rogozinska |first2=E |last3=Jolly |first3=K |last4=Glinkowski |first4=S |last5=Roseboom |first5=T |last6=Tomlinson |first6=JW |last7=Kunz |first7=R |last8=Mol |first8=BW |last9=Coomarasamy |first9=A |last10=Khan |first10=KS |title=Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence |journal=BMJ (Clinical research ed.) |date=16 May 2012 |volume=344 |pages=e2088 |pmid=22596383 |pmc=3355191 |doi=10.1136/bmj.e2088 |author-separator=, |display-authors=3}}</ref>
  
Obesity was occasionally considered a [[symbol]] of [[wealth]] and [[social status]] in cultures prone to food shortages or famine. Well into the early modern period in European cultures, it often served this role. But as food security was realised, it came to serve more as a visible signifier of "lust for life", appetite, and immersion in the realm of the [[eroticism|erotic]]. This was especially the case in the visual arts, such as the paintings of [[Peter Paul Rubens|Rubens]] ([[1577]]&ndash;[[1640]]), whose regular use of the full female figures gives us the description ''Rubenesque'' for plumpness. 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."
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Three medication, [[orlistat]] (Xenical), [[lorcaserin]] (Belviq) and a combination of [[Phentermine/topiramate|phentermine and topiramate]] (Qsymia) are currently available and have evidence for long term use.<ref name=Yan2014>{{cite journal|last=Yanovski|first=SZ|coauthors=Yanovski, JA|title=Long-term drug treatment for obesity: a systematic and clinical review.|journal=JAMA : the journal of the American Medical Association|date=2014 Jan 1|volume=311|issue=1|pages=74-86|pmid=24231879}}</ref> Weight loss with orlistat is modest, an average of 2.9&nbsp;kg (6.4&nbsp;lb) at 1 to 4&nbsp;years.<ref name=Orli07>{{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=1194–99 |year=2007 |pmid=18006966 |doi=10.1136/bmj.39385.413113.25 |url=http://www.bmj.com/cgi/content/full/335/7631/1194 |pmc=2128668}}</ref> Its use is associated with high rates of gastrointestinal side effects<ref name=Orli07/> and concerns have been raised about negative effects on the kidneys.<ref>{{cite web|last=Wood |first=Shelley |title=Diet Drug Orlistat Linked to Kidney, Pancreas Injuries |url=http://www.medscape.com/viewarticle/740855?src=mp&spon=30 |work=Medscape |publisher=Medscape News |accessdate=26 April 2011}}</ref> The other two medications are available in the United States but not Europe.<ref name=EMA2013>{{cite journal|last=Wolfe |first=SM |title=When EMA and FDA decisions conflict: differences in patients or in regulation? |journal=BMJ (Clinical research ed.) |date=21 August 2013 |volume=347 |pages=f5140 |pmid=23970394 |doi=10.1136/bmj.f5140 |author-separator=, |display-authors=3}}</ref> Lorcaserin results in an average 3.1&nbsp;kg weight loss (3% of body weight) greater than placebo over a year;<ref>{{cite journal|last=Bays |first=HE |title=Lorcaserin: drug profile and illustrative model of the regulatory challenges of weight-loss drug development |journal=Expert review of cardiovascular therapy |date=March 2011 |volume=9 |issue=3 |pages=265–77 |pmid=21438803 |doi=10.1586/erc.10.22}}</ref> however it may increase heart valve problems.<ref name=EMA2013/> A combination of phentermine and topiramate is also somewhat effective;<ref>{{cite journal|author=Bays HE, Gadde KM |title=Phentermine/topiramate for weight reduction and treatment of adverse metabolic consequences in obesity |journal=Drugs Today |volume=47 |issue=12 |pages=903–14 |date=December 2011 |pmid=22348915 |doi=10.1358/dot.2011.47.12.1718738 |url=|author-separator=, |display-authors=3}}</ref> however, it may be associated with heart problems.<ref name=EMA2013/> There is no information on how these drugs affect longer-term complications of obesity such as cardiovascular disease or death.<ref name=Yan2014/>
  
Not all contemporary cultures disapprove of obesity, although the Western preference for thinness is increasingly being exported worldwide as part of the process of globalization. Few cultures have escaped the "Westernization" of body shape preference, though cultures which are traditionally more approving (to varying degrees), include some African, Arabic, Indian, and Pacific Island cultures. Especially in the past decades, obesity has come to be seen more as a medical condition. There is also a small but vocal [[fat acceptance movement]] that seeks to challenge weight-based [[discrimination]].
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The most effective treatment for obesity is [[bariatric surgery]].<ref>{{cite journal|last=Colquitt |first=JL |last2=Picot |first2=J |last3=Loveman |first3=E |last4=Clegg |first4=AJ |title=Surgery for obesity |journal=Cochrane database of systematic reviews (Online) |date=15 April 2009 |issue=2 |pages=CD003641 |pmid=19370590 |doi=10.1002/14651858.CD003641.pub3 |author-separator=, |display-authors=3 |editor1-last=Colquitt |editor1-first=Jill L |editor-separator=,}}</ref> Surgery for severe obesity is associated with long-term weight loss, improvement in obesity related conditions,<ref name=Chang2013>{{cite journal|last=Chang |first=Su-Hsin |last2=Stoll |first2=Carolyn R. T. |last3=Song |first3=Jihyun |last4=Varela |first4=J. Esteban |last5=Eagon |first5=Christopher J. |last6=Colditz |first6=Graham A. |title=The Effectiveness and Risks of Bariatric Surgery |journal=JAMA Surgery |date=18 December 2013 |doi=10.1001/jamasurg.2013.3654 |author-separator=, |display-authors=3}}</ref> and decreased overall mortality. One study found a weight loss of between 14% and 25% (depending on the type of procedure performed) at 10&nbsp;years, and a 29% reduction in all cause mortality when compared to standard weight loss measures.<ref>{{cite journal|author=Sjöström L |title=Effects of bariatric surgery on mortality in Swedish obese subjects |journal=N. Engl. J. Med. |volume=357 |issue=8 |pages=741–52 |date=August 2007 |pmid=17715408 |doi=10.1056/NEJMoa066254 |url=|author-separator=, |author2=Narbro K |author3=Sjöström CD |last4=Karason |first4=Kristjan |last5=Larsson |first5=Bo |last6=Wedel |first6=Hans |last7=Lystig |first7=Ted |last8=Sullivan |first8=Marianne |last9=Bouchard |first9=Claude |display-authors=3 |first10=Björn |first11=Calle |first14=Peter |first15=Jan |first16=Anna-Karin |first17=Hans |first18=Ingmar |first19=Torsten |first20=Kaj |first21=Jarl |first24=Study}}</ref> Complications occur in about 17% of cases and reoperation is needed in 7% of cases.<ref name=Chang2013/> Due to its cost and risks, researchers are searching for other effective yet less invasive treatments.
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{{clear}}
  
===Popular culture===
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==Epidemiology==
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{{Main|Epidemiology of obesity}}
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{{Double image|right|World map of Male Obesity, 2008.svg|200|World map of Female Obesity, 2008.svg|200|World obesity prevalence among males (left) and females (right).<ref name=IOTF2008>{{cite web|url=http://www.iotf.org/database/documents/GlobalPrevalenceofAdultObesity16thDecember08.pdf |title=Global Prevalence of Adult Obesity |format=PDF |work=[[International Obesity Taskforce]] |accessdate=January 29, 2008}}</ref>
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|alt=A map of the world with countries colored to reflect the percentage of men who are obese.  Obese males and females have higher prevalence (above 30%) in the U.S. and some Middle Eastern and Oceanian countries, medium prevalence in the rest of North America and Europe, and lower prevalence (<5%) in most of Asia and Africa.||}}
  
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, but equally common is the obese vicious [[bullying|bully]]. [[Gluttony]] and obesity are commonly depicted together in works of fiction. In cartoons, obesity is often used to comedic effect, with fat [[cartoon]] characters having to squeeze through narrow spaces, frequently getting stuck or even exploding.
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Before the 20th&nbsp;century, obesity was rare;<ref name=Haslam2007/> in 1997 the WHO formally recognized obesity as a global epidemic.<ref name=Caballero/> As of 2008 the WHO estimates that at least 500&nbsp;million adults (greater than 10%) are obese, with higher rates among women than men.<ref name=WHO2009a>{{cite web|url=http://www.who.int/mediacentre/factsheets/fs311/en/index.html |title=Obesity and overweight |work=World Health Organization |accessdate=April 8, 2009}}</ref>  The rate of obesity also increases with age at least up to 50 or 60&nbsp;years old<ref>Seidell 2005 p.5</ref> and severe obesity in the United States, Australia, and Canada is increasing faster than the overall rate of obesity.<ref name=morbid2007/><ref>{{cite journal|last=Howard |first=NJ |last2=Taylor |first2=AW |last3=Gill |first3=TK |last4=Chittleborough |first4=CR |title=Severe obesity: Investigating the socio-demographics within the extremes of body mass index |journal=Obesity Research & Clinical Practice |volume=2 |issue=1 |pages=51–59 |date=March 2008 |pmid= |doi=10.1016/j.orcp.2008.01.001 |author-separator=, |display-authors=3}}</ref><ref name=Tjepkema2005>{{cite book|author=Tjepkema M |chapter=Measured Obesity–Adult obesity in Canada: Measured height and weight |title=Nutrition: Findings from the Canadian Community Health Survey |publisher=Statistics Canada |date=2005-07-06 |location=Ottawa, Ontario |url=http://www.statcan.gc.ca/pub/82-620-m/2005001/article/adults-adultes/8060-eng.htm}}</ref>
  
It can be argued that depiction in popular culture adds to and maintains commonly perceived stereotypes, in turn harming [[self esteem]] of obese people. A charge of [[discrimination]] on the basis of appearance could be leveled against these depictions.
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Once considered a problem only of high-income countries, obesity rates are rising worldwide and affecting both the developed and developing world.<ref name=EuroG2008>{{cite journal|author=Tsigosa Constantine |title=Management of Obesity in Adults: European Clinical Practice Guidelines |journal=The European Journal of Obesity |volume=1 |date=April 2008 |pmid=20054170 |doi=10.1159/000126822 |url=http://www.gojaznost.org/gs/dodatak/OMTFManagementofObesityinAdults2008.pdf |first2=Vojtech |issue=2 |first3=Arnaud |first4=Nick |first5=Martin |first6=Elisabeth |first7=Dragan |first8=Maximo |first9=Gabriela |pages=106–16 |last2=Hainer |last3=Basdevant |last4=Finer |last5=Fried |last6=Mathus-Vliegen |last7=Micic |last8=Maislos |last9=Roman |display-authors=3 |first10=Yves |first11=Hermann |first12=Barbara}}</ref> These increases have been felt most dramatically in urban settings.<ref name=WHO2009a/>  The only remaining region of the world where obesity is not common is [[sub-Saharan Africa]].<ref name=HaslamJames/>
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{{clear}}
  
On the other hand, obesity is often associated with positive characteristics such as good [[humour|humor]] (the stereotype of the jolly fat man like [[Santa Claus]]), and some people are more [[sexual attraction|sexually attracted]] to obese people than to slender people (see [[chubby culture]], [[fat admirer]]).
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==History==
  
==Public health and policy==
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===Etymology===
The prevalence of overweight and obesity in the United States makes obesity a leading public health problem. From 1980 to 2002, obesity prevalence has doubled in adults and overweight prevalence has has tripled in children and adolescents.
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''Obesity'' is from the [[Latin]] ''obesitas'', which means "stout, fat, or plump".  ''Ēsus'' is the past participle of ''edere'' (to eat), with ''ob'' (over) added to it.<ref name=etymol>{{cite web|url=http://www.etymonline.com/index.php?term=obesity |title=Online Etymology Dictionary: Obesity |work=Douglas Harper |accessdate=December 31, 2008}}</ref>  ''[[The Oxford English Dictionary]]'' documents its first usage in 1611 by [[Randle Cotgrave]].<ref>{{cite web|url=http://www.oed.com/ |title=Obesity, n |work=[[Oxford English Dictionary]] 2008 |accessdate=March 21, 2009}}</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.
 
The prevalence in the United States continues to rise.
 
  
===Environmental causes of obesity===
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===Historical trends===
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.
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The [[Greeks]] were the first to recognize obesity as a medical disorder.<ref name=Haslam2007>{{cite journal|author=Haslam D |title=Obesity: a medical history |journal=Obes Rev |volume=8 Suppl 1 |issue= |pages=31–6 |date=March 2007 |pmid=17316298 |doi=10.1111/j.1467-789X.2007.00314.x |url=}}</ref> [[Hippocrates]] wrote that "Corpulence is not only a disease itself, but the harbinger of others".<ref name=HaslamJames/> The Indian surgeon [[Sushruta]] (6th century BCE) related obesity to diabetes and heart disorders.<ref name=Dwivedi&Dwivedi07/> He recommended physical work to help cure it and its side effects.<ref name=Dwivedi&Dwivedi07>{{cite web|url=http://medind.nic.in/iae/t07/i4/iaet07i4p243.pdf |format=PDF |title=History of Medicine: Sushruta – the Clinician – Teacher par Excellence |accessdate=2008-09-19 |work=Dwivedi, Girish & Dwivedi, Shridhar |publisher= |year=2007}}</ref> For most of human history mankind struggled with food scarcity.<ref>{{cite book|author=Theodore Mazzone; Giamila Fantuzzi |title=Adipose Tissue And Adipokines in Health And Disease (Nutrition and Health) |publisher=Humana Press |location=Totowa, NJ |year=2006 |page=222 |isbn=1-58829-721-7 |oclc= |doi= |accessdate=}}</ref> Obesity has thus historically been viewed as a sign of wealth and prosperity. It was common among high officials in Europe in the [[Middle Ages]] and the [[Renaissance]]<ref name=Zach2003/> as well as in Ancient East Asian civilizations.<ref>Keller p. 49</ref>
  
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.  
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With the onset of the [[industrial revolution]] it was realized that the military and economic might of nations were dependent on both the body size and strength of their soldiers and workers.<ref name=Caballero/> Increasing the average body mass index from what is now considered underweight to what is now the normal range played a significant role in the development of industrialized societies.<ref name=Caballero/> Height and weight thus both increased through the 19th&nbsp;century in the developed world. During the 20th century, as populations reached their genetic potential for height, weight began increasing much more than height, resulting in obesity.<ref name=Caballero/> In the 1950s increasing wealth in the developed world decreased child mortality, but as body weight increased heart and kidney disease became more common.<ref name=Caballero/><ref>{{cite journal|doi=10.2105/AJPH.42.9.1116 |author=Breslow L |title=Public Health Aspects of Weight Control |journal=Am J Public Health Nations Health |date=September 1952 |volume=42 |issue=9 |pages=1116–20 |pmid=12976585 |pmc=1526346}}</ref>
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During this time period insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.<ref name=HaslamJames/>
  
There are a number of theories as to the cause of this change since 1980. Most believe it is a combination of various factors.
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Many cultures throughout history have viewed obesity as the result of a character flaw. The ''obesus'' or fat character in [[Greek comedy]] was a glutton and figure of mockery. During Christian times food was viewed as a gateway to the sins of [[Sloth (deadly sin)|sloth]] and [[lust]].<ref name=Woodhouse/> In modern Western culture, excess weight is often regarded as unattractive, and obesity is commonly associated with various negative stereotypes. People of all ages can face social stigmatization, and may be targeted by bullies or shunned by their peers. Obesity is once again a reason for discrimination.<ref name=Bias2001>{{cite journal|author=Puhl R, Brownell KD |title=Bias, discrimination, and obesity |journal=Obes. Res. |volume=9 |issue=12 |pages=788–805 |date=December 2001 |pmid=11743063 |doi=10.1038/oby.2001.108 |url=}}</ref>
{{exercise}}
 
*''Lack of activity'': obese people appear to be 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.
 
  
*One of the most important is the much ''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. [[Sugar]] and [[corn syrup]], two huge sources of food energy, are some of the most [[subsidy|subsidized]] products by the United States government. This can raise costs for consumers in some areas but greatly lower it in othersCurrent debates into trade policy highlight disagreements on the effects of subsidies.
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Public perceptions in Western society regarding healthy body weight differ from those regarding the weight that is considered ideal &nbsp;– and both have changed since the beginning of the 20th century. The weight that is viewed as an ideal has become lower since the 1920s. This is illustrated by the fact that the average height of Miss America pageant winners increased by 2% from 1922 to 1999, while their average weight decreased by 12%.<ref>{{cite journal|author=Rubinstein S, Caballero B |title=Is Miss America an undernourished role model? |journal=[[JAMA (journal)|JAMA]] |volume=283 |issue=12 |page=1569 |year=2000 |pmid=10735392 |doi=10.1001/jama.283.12.1569 |url=}}</ref>  On the other hand, people's views concerning healthy weight have changed in the opposite direction. In Britain the weight at which people considered themselves to be overweight was significantly higher in 2007 than in 1999.<ref name=John2008>{{cite journal|author=Johnson F, Cooke L, Croker H, Wardle J |title=Changing perceptions of weight in Great Britain: comparison of two population surveys |journal=BMJ |volume=337 |issue= |pages=a494 |year=2008 |pmid=18617488 |pmc=2500200 |doi=10.1136/bmj.a494 |url=http://www.bmj.com/cgi/content/full/337/jul10_1/a494}}</ref> These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being normal.<ref name=John2008/>
  
*''Increased marketing'' has also played a role.  In the early 1980s in America the [[Ronald Reagan|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]].
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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.<ref name=HaslamJames/>
  
*Changes in ''the price of [[mineral oil]] and [[gasoline|petrol]]'' are also believed to have had an effect, as unlike during the [[1970s]] it is now affordable in the United States to drive everywhere &mdash; at a time when [[public transit]] goes underused. At the same time more areas have been built without [[sidewalk]]s and parks.
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===The arts===
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The first sculptural representations of the human body 20,000–35,000&nbsp;years ago depict obese females. Some attribute the [[Venus figurines]] to the tendency to emphasize fertility while others feel they represent "fatness" in the people of the time.<ref name=Woodhouse/> Corpulence is, however, absent in both Greek and Roman art, probably in keeping with their ideals regarding moderation. This continued through much of Christian European history, with only those of low socioeconomic status being depicted as obese.<ref name=Woodhouse/>
  
*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 food|frozen convenience foods]] skyrocket and has encouraged more elaborate [[snack]]ing.
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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 del Borro]].<ref name=Woodhouse>{{cite journal|author=Woodhouse R |title=Obesity in art: A brief overview |journal=Front Horm Res |volume=36 |issue= |pages=271–86 |year=2008 |isbn=978-3-8055-8429-6 |pmid=18230908 |doi=10.1159/000115370 |url=http://books.google.com/?id=nXRU4Ea1aMkC&pg=PA271&lpg=PA271 |series=Frontiers of Hormone Research}}</ref> [[Peter Paul Rubens|Rubens]] (1577–1640) regularly depicted full-bodied women in his pictures, from which derives the term [[Rubenesque]]. These women, however, still maintained the "hourglass" shape with its relationship to fertility.<ref name=Fumento>{{cite book|author=Fumento, Michael |title=The Fat of the Land: Our Health Crisis and How Overweight Americans Can Help Themselves |publisher=Penguin (Non-Classics) |year=1997 |page=126 |isbn=0-14-026144-3}}</ref> During the 19th&nbsp;century, views on obesity changed in the Western world. After centuries of obesity being synonymous with wealth and social status, slimness began to be seen as the desirable standard.<ref name=Woodhouse/>
  
*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.
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==Society and culture==
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===Economic impact===
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In addition to its health impacts, obesity leads to many problems including disadvantages in employment<ref name="Puhl R. p.29">Puhl R., Henderson K., and Brownell K. 2005 p.29</ref><ref>{{cite journal|doi=10.1016/j.ehb.2009.01.008 |author=Johansson E, Bockerman P, Kiiskinen U, Heliovaara M |title=Obesity and labour market success in Finland: The difference between having a high BMI and being fat |journal=Economics and Human Biology |volume=7 |issue=1 |pages=36–45 |year=2009 |pmid=19249259}}</ref> and increased business costs.  These effects are felt by all levels of society from individuals, to corporations, to governments.
  
*''[[Urban sprawl]]'' may be a factor: obesity rates increase as urban sprawl increases, possibly due to less walking and less time for cooking.  
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In 2005, the medical costs attributable to obesity in the US were an estimated $190.2&nbsp;billion or 20.6% of all medical expenditures,<ref name=medical-costs>{{cite journal|last=Cawley |first=J |last2=Meyerhoefer |first2=C |title=The medical care costs of obesity: An instrumental variables approach |journal=Journal of Health Economics |date=January 2012 |volume=31 |issue=1 |pages=219–230 |accessdate=2 August 2012 |doi=10.1016/j.jhealeco.2011.10.003 |pmid=22094013 |author-separator=,}}</ref><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=Health Affairs |volume=Online |issue=May |pages= |date=1 January 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=[[Centers for Disease Control and Prevention]] |date=22 May 2007 |accessdate=2007-09-05}}</ref> while the cost of obesity in Canada was estimated at CA$2 billion in 1997 (2.4% of total health costs).<ref name="CADG2006"/> The total annual direct cost of overweight and obesity in Australia in 2005 was A$21 billion. Overweight and obese Australians also received A$35.6 billion in government subsidies.<ref name=MJA2009>{{Cite journal|title=The cost of overweight and obesity in Australia |url=http://www.mja.com.au/public/issues/192_05_010310/col10841_fm.html |year=2009 |author=Colagiuri, Stephen |journal=The Medical Journal of Australia |accessdate=2011-06-18 |last2=Lee |first2=Crystal M. Y. |last3=Colagiuri |first3=Ruth |display-authors=3 |author5=<Please add first missing authors to populate metadata.>}}</ref> The estimate range for annual expenditures on diet products is $40&nbsp;billion to $100&nbsp;billion in the US alone.<ref>{{cite news|last=Cummings |first=Laura |title=The diet business: Banking on failure |publisher=BBC News |date=5 February 2003 |url=http://news.bbc.co.uk/2/hi/business/2725943.stm |accessdate=25 February 2009}}</ref>
  
*Since 1980 both sit-in and ''[[fast food]] [[restaurant]]s'' 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 &mdash; for example, [[McDonalds]] [[french fries]] portions rose from 200 Calories (840 [[joule|kilojoules]]) in 1960 to over 600 Calories (2,500 kJ) today.
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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 obesity may improve the public's health, but it is unlikely to reduce overall health spending.<ref>{{cite journal|author=van Baal PH |title=Lifetime Medical Costs of Obesity: Prevention No Cure for Increasing Health Expenditure |journal=PLoS Med. |volume=5 |issue=2 |pages=e29 |date=February 2008 |pmid=18254654 |pmc=2225430 |doi=10.1371/journal.pmed.0050029 |url=http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0050029 |author-separator=, |author2=Polder JJ |author3=de Wit GA |last4=Hoogenveen |first4=Rudolf T. |last5=Feenstra |first5=Talitha L. |last6=Boshuizen |first6=Hendriek C. |last7=Engelfriet |first7=Peter M. |last8=Brouwer |first8=Werner B. F. |display-authors=3}}</ref>
  
*''Increased food production'' is a probable factor. The U.S. produces three times more food than U.S. residents eat.
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Obesity can lead to social stigmatization and disadvantages in employment.<ref name="Puhl R. p.29"/> When compared to their normal weight counterparts, obese workers on average have higher rates of absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity.<ref>{{cite journal|author=Neovius K, Johansson K, Kark M, Neovius M |title=Obesity status and sick leave: a systematic review |journal=Obes Rev |volume=10 |issue=1 |pages=17–27 |date=January 2009 |pmid=18778315 |doi=10.1111/j.1467-789X.2008.00521.x |url=}}</ref> A study examining Duke University employees found that people with a BMI over 40&nbsp;kg/m<sup>2</sup> filed twice as many [[workers' compensation]] claims as those whose BMI was 18.5–24.9&nbsp;kg/m<sup>2</sup>. They also had more than 12&nbsp;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.<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> The Alabama State Employees' Insurance Board approved a controversial plan to charge obese workers $25 a month for health insurance that would otherwise be free unless they take steps to lose weight and improve their health. These measures started in January 2010 and apply to those state workers whose BMI exceeds 35&nbsp;kg/m<sup>2</sup> and who fail to make improvements in their health after one year.<ref>{{cite web|url=http://www.webmd.com/diet/news/20080825/alabama-obesity-penalty-stirs-debate |title=Alabama "Obesity Penalty" Stirs Debate |work=Don Fernandez |accessdate=April 5, 2009}}</ref>
  
*Increasing ''affluence'' itself (including many of the above factors as accompaniments of affluence) may be a cause, or contributing factor since obesity tends to flourish as a [[diseases of affluence|disease of affluence]] in countries which are developing and becoming westernised [http://www.iotf.org/]. This is supported by a dip in American GDP after 1990, the year of the [[Gulf War]], followed by an exponential increase. U.S. obesity statistics followed the same pattern, offset by two years [http://www.cdc.gov/brfss/].
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Some research shows that obese people are less likely to be hired for a job and are less likely to be promoted.<ref name=Bias2001/> Obese people are also paid less than their non-obese counterparts for an equivalent job; obese women on average make 6% less and obese men make 3% less.<ref>Puhl R., Henderson K., and Brownell K. 2005 p.30</ref>
  
*An aging population may also be a major factor, as the likelihood of becoming obese increases with age. Beyond their twenties, the older a person becomes the slower their metabolism becomes, reducing the amount of calories required to sustain the body, thus if a person does not reduce their intake of food with age, they will become obese over time. As the average age of individuals within a society increases, the rate of obesity also increases. This situation is exacerbated by the [[Post-WW2 baby boom|baby boom]] generation, which represents a disproportionately large portion of the population in many countries and is currently nearing the latter end of the typical lifespan in affluent nations, and therefore is in the high-risk zone for obesity.
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Specific industries, such as the airline, healthcare and food industries, have special concerns. Due to rising rates of obesity, airlines face higher fuel costs and pressures to increase seating width.<ref>{{cite web|author=Lisa DiCarlo |url=http://www.forbes.com/2002/10/24/cx_ld_1024obese.html |title=Why Airlines Can't Cut The Fat |work=Forbes.com |date=2002-10-24 |accessdate=2008-07-23}}</ref> In 2000, the extra weight of obese passengers cost airlines US$275&nbsp;million.<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 |page=264 |year=2004 |pmid=15450642 |doi=10.1016/j.amepre.2004.06.004}}</ref>  The healthcare industry has had to invest in special facilities for handling severely obese patients, including special lifting equipment and [[bariatric ambulance]]s.<ref>{{cite web|url=http://abcnews.go.com/Health/Diet/obese-health-care-bariatric-ambulances/story?id=7981746 |title=Who Should Pay for Obese Health Care? |author=Lauren Cox |publisher=ABC News |date=July 2, 2009 |accessdate=2012-08-06}}</ref> Costs for restaurants are increased by litigation accusing them of causing obesity.<ref name=Govtrack>{{cite web|url=http://www.govtrack.us/congress/bill.xpd?bill=h109-554 |title=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 |publisher=GovTrack.us |accessdate=2008-07-24}}</ref> In 2005 the US Congress discussed legislation to prevent civil lawsuits against the food industry in relation to obesity; however, it did not become law.<ref name=Govtrack/>
  
Interestingly an increase in the number of Americans who [[exercise]] and [[dieting|diet]] occurred before the increase in obesity, and some scholars have even argued that these trends actually encouraged obesity. Nearly all diets fail, with participants resuming their previous eating habits or even engaging in binge eating.  Many then see an overall increase in their weight.  If the diet is then repeated and abandoned again, a pattern of rising and falling weight is established, known as weight cycling.  Similarly those who work out but then stop can end up being heavier than those who never exercised.
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With the [[American Medical Association]]'s 2013 classification of obesity as chronic disease,<ref name=NYTimes20130618/> it is thought that health insurance companies will more likely pay for obesity treatment, counseling and surgery, and the cost of research and development of fat treatment pills or gene therapy treatments should be more affordable if insurers help to subsidize their cost.<ref name=WashPost20130620/>  The AMA classification is not legally binding, however, so health insurers still have the right to reject coverage for a treatment or procedure.<ref name=WashPost20130620>{{cite web|url=http://www.washingtonpost.com/blogs/innovations/wp/2013/06/20/a-changing-battlefield-in-the-fight-against-fat/?wpisrc=nl_tech_b |title=A changing battlefield in the fight against fat |last=Basulto |first=Dominic |date=June 20, 2013 |website=The Washington Post |publisher= |accessdate=June 20, 2013}} ([http://www.webcitation.org/6HWwftXgI WebCite archive])</ref>
{{w8md}}
 
===Public health and policy responses to obesity===
 
On top of controversies about the causes of obesity, and about its precise health implications, come policy controversies about the correct [[policy]] approach to obesity. The main debate is between "personal responsibility" advocates, who resist regulatory attempts to intervene in citizen's private dietary habits, and "public interest" advocates, who promote regulations, on the same public health grounds as the restrictions applied to tobacco products. In the U.S., a recent bout in this controversy involves the so-called [[Cheeseburger Bill]], an attempt to indemnify food industry businesses from what some consider to be frivolous lawsuits by obese clients.
 
  
"Personal responsibility" advocates work on the basis that, as the [[microbiologist]] [[Rene Dubos]] once said, health ought not to be considered an end in itself, but "the condition best suited to reach goals that each individual formulates for himself" [http://www.spiked-online.com/Articles/0000000CA7A4.htm]. Any other definition permits authorities to curtail the autonomy of the self-determining individual, imposing quantity over quality of life onto them, undermining their civil liberties. As much as principled doctors, personal responsibility arguments have also been offered by food producer lobbies. In 1961, for example, as President [[John F Kennedy]] raised concerns about a lack of fitness in American society, a spokesman for the U.S. Dairy industry, Frank R. Neu, wrote [[advertorial]]s warning ''We May Be Sitting Ourselves To Death'' [http://www.theatlantic.com/issues/61nov/neu.htm]. Not food regulation, but personal exercising, is moved as the solution.
+
===Size acceptance===
 +
{{See also|Fat acceptance movement|Social stigma of obesity}}
 +
The principal goal of the fat acceptance movement is to decrease discrimination against people who are overweight and obese.<ref>{{cite web|url=http://www.capitalnaafa.org/whatisnaafa.html |title=What is NAAFA |work=[[National Association to Advance Fat Acceptance]] |accessdate=February 17, 2009}}</ref><ref>{{cite web|url=http://www.size-acceptance.org/mission.html |title=ISAA Mission Statement |work=[[International Size Acceptance Association]] |accessdate=February 17, 2009}}</ref> However, some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes.<ref name=Pulver2007>{{cite book|author=Pulver, Adam |title=An Imperfect Fit: Obesity, Public Health, and Disability Anti-Discrimination Law |publisher=Social Science Electronic Publishing |location= |year=2007 |pages= |isbn= |oclc= |doi= |url=http://papers.ssrn.com/sol3/papers.cfm?abstract_id=1316106 |accessdate=January 13, 2009}}</ref>
  
When it comes to [[childhood obesity]], personal responsibility also means parental responsibility. A survey by the nonpartisan group [[Public Agenda]] found 68 percent of American parents said it was "absolutely essential" to teach their children good eating habits, but only 40 percent believe they had succeeded. Fewer parents say it's essential to teach their children about physical fitness (51 percent), but more believe they have succeeded (53 percent). Overall, parents said they found it difficult to protect their children from negative social messages on a range of topics, including bad nutrition.
+
A number of organizations exist that promote the acceptance of obesity. They have increased in prominence in the latter half of the 20th&nbsp;century.<ref>{{cite journal|author=Neumark-Sztainer D |title=The weight dilemma: a range of philosophical perspectives |journal=Int. J. Obes. Relat. Metab. Disord. |volume=23 Suppl 2 |issue= |pages=S31–7 |date=March 1999 |pmid=10340803 |doi=10.1038/sj.ijo.0800857 |url=}}</ref> The US-based [[National Association to Advance Fat Acceptance]] (NAAFA) was formed in 1969 and describes itself as a civil rights organization dedicated to ending size discrimination.<ref>{{cite web|author=National Association to Advance Fat Acceptance |url=http://www.naafaonline.com/dev2/ |title=We come in all sizes |publisher=NAAFA |year=2008 |accessdate=2008-07-29}}</ref>
  
 +
The [[International Size Acceptance Association]] (ISAA) is a [[non-governmental organization]] (NGO) which was founded in 1997. It has more of a global orientation and describes its mission as promoting size acceptance and helping to end weight-based discrimination.<ref>{{cite web|url=http://www.size-acceptance.org/ |title=International Size Acceptance Association – ISAA |work=International Size Acceptance Association |accessdate=January 13, 2009}}</ref> These groups often argue for the recognition of obesity as a disability under the US [[Americans With Disabilities Act]] (ADA). The American legal system, however, has decided that the potential public health costs exceed the benefits of extending this anti-discrimination law to cover obesity.<ref name=Pulver2007/>
  
On [[July 16]], [[2004]], the [[United States Department of Health and Human Services]] officially classified obesity as a disease. Speaking to a Senate committee, [[Tommy Thompson]], the Secretary of Health and Human Services, stated that Medicare would cover obesity-related health problems. However, reimbursement would not be given if a treatment was not proven to be effective.
+
==Childhood obesity==
 +
{{Main|Childhood obesity}}
 +
The healthy BMI range varies with the age and sex of the child. Obesity in children and adolescents is defined as a BMI greater than the 95th&nbsp;[[percentile]].<ref name="cdc.gov"/> The reference data that these percentiles are based on is from 1963 to 1994 and thus has not been affected by the recent increases in rates of obesity.<ref name="Flegal KM, Ogden CL, Wei R, Kuczmarski RL, Johnson CL 2001 1086–93"/> Childhood obesity has reached epidemic proportions in 21st&nbsp;century, with rising rates in both the developed and developing world. Rates of obesity in Canadian boys have increased from 11% in 1980s to over 30% in 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children.<ref name=flynn2006/>
  
==See also==
+
As with obesity in adults, many different factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believed to be the two most important in causing the recent increase in the rates.<ref>{{cite journal|author=Dollman J, Norton K, Norton L |title=Evidence for secular trends in children's physical activity behaviour |journal=Br J Sports Med |volume=39 |issue=12 |pages=892–7; discussion 897 |date=December 2005 |pmid=16306494 |pmc=1725088 |doi=10.1136/bjsm.2004.016675 |url=}}</ref> Because childhood obesity often persists into adulthood and is associated with numerous chronic illnesses, children who are obese are often tested for [[hypertension]], [[diabetes]], [[hyperlipidemia]], and [[fatty liver]].<ref name=CADG2006/> Treatments used in children are primarily lifestyle interventions and behavioral techniques, although efforts to increase activity in children have had little success.<ref>{{cite journal|last=Metcalf |first=B. |last2=Henley |first2=W. |last3=Wilkin |first3=T. |title=Effectiveness of intervention on physical activity of children: systematic review and meta-analysis of controlled trials with objectively measured outcomes (EarlyBird 54) |journal=BMJ |date=27 September 2012 |volume=345 |issue=sep27 1 |pages=e5888–e5888 |doi=10.1136/bmj.e5888 |author-separator=, |display-authors=3}}</ref> In the United States, medications are not FDA approved for use in this age group.<ref name=flynn2006>{{cite journal|author=Flynn MA |title=Reducing obesity and related chronic disease risk in children and youth: a synthesis of evidence with 'best practice' recommendations |journal=Obes Rev |volume=7 Suppl 1 |issue= |pages=7–66 |date=February 2006 |pmid=16371076 |doi=10.1111/j.1467-789X.2006.00242.x |url=|author-separator=, |author2=McNeil DA |author3=Maloff B |last4=Mutasingwa |first4=D. |last5=Wu |first5=M. |last6=Ford |first6=C. |last7=Tough |first7=S. C. |display-authors=3}}</ref>
*[[Weight loss]]
 
*[[Insulin resistance]]
 
*[[Metabolic syndrome]]
 
*[[Body image]]
 
*[[Body mass index]]
 
*[[Cardiovascular disease]]
 
*[[Childhood obesity]]
 
*[[Chubby culture]]
 
*[[Dieting]]
 
*[[Fat acceptance movement]]
 
*[[Fat admirer]]
 
*[[Feeder (fetish)|Feederism]]
 
*[[Healthy eating]]
 
*''[[Honey we're killing the kids]]''
 
*[[Human weight]]
 
*[[Junk food]]
 
*[[List of the most obese humans]]
 
*[[MOMO syndrome]]
 
*[[National Weight Control Registry]]
 
*[[Overweight]]
 
*[[Physical activity]]
 
*[[Pickwickian syndrome]]
 
*[[Weight gain]]
 
*[[Metabolic syndrome]]
 
*[[Type 2 diabetes]]
 
*''[[Super Size Me]]''
 
  
{{links}}
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'''[[County obesity rate]] in the [[United States]]'''
  
{{states}}
+
{{obesity-state}}
  
{{telemed}}
+
'''Also see'''
  
{{social}}
+
* Causes of [[weight gain]]
 +
* [[Metabolic syndrome]]
 +
* [[Insulin resistance]]
 +
* [[Racial disparities in obesity]]
 +
* Proven measures for [[losing weight]]
  
==External links==
+
{{adapted}}
  
* [http://www.who.int/topics/obesity/en/ World Health Organization] - Obesity pages
+
{{w8md}}
* [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.greenfacts.org/en/diet-nutrition/l-2/5-obesity-bmi.htm Summary] by [[GreenFacts]].
 
* [http://www.endotext.org/obesity/index.htm Obesity at Endotext.org]
 
* [http://www.iotf.org/ International Task Force on Obesity]
 
* [http://www.yaleruddcenter.org/ Rudd Center for Food Policy and Obesity at Yale University]
 
* [http://www.asso.org.au Australasian Society for the Study of Obesity]
 
  
{{health}}
+
[[Category:Obesity]]
[[Category:Obesity|Obesity]]
+
[[Category:Bariatrics]]
[[Category:Weight loss]]
+
[[Category:Body shape]]
[[Category:Diet]]
 
[[Category:Metabolic disorders]]
 
[[Category:Health risks]]
 
 
[[Category:Nutrition]]
 
[[Category:Nutrition]]
[[Category:Bariatrics]]
 
[[Category:Social stigma]]
 

Revision as of 13:03, 26 March 2019


Editor-In-Chief: Prab R. Tumpati M.D.. Founder, WikiMD and W8MD Weight Loss, Sleep and MedSpa Centers. Dr. Tumpati is board certified physician practicing sleep medicine, obesity medicine, aesthetic medicine and internal medicine. Dr. Tumpati’s passion is prevention rather than cure. As a physician with fellowship training in Obesity Medicine, Dr. Tumpati has a unique approach to wellness, weight loss, aesthetics with a focus on prevention rather than cure. Dr. Tumpati believes in educating the public on the true science and art of medicine, nutrition, wellness and beauty.

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List of terms related to Obesity

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] 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/m2.

Obesity.jpg

Obesity increases the likelihood of various diseases, particularly heart disease, type 2 diabetes, 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 physical exercise are the mainstays of treatment 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. Anti-obesity drugs may be taken to reduce appetite or decrease fat absorption when used together with a suitable diet. 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]

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 is stigmatized in much of the modern world (particularly in the Western world), though it was widely seen as a symbol of wealth and fertility at other times in history, and still is in some parts of the world.[2][9] In 2013, the American Medical Association classified obesity as a disease.[10][11]

Classification

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

In children, a healthy weight varies with age and sex. Obesity in children and adolescents is defined not as an absolute number but in relation to a historical normal group, such that obesity is a BMI greater than the 95th percentile.[15] The reference data on which these percentiles were based date from 1963 to 1994, and thus have not been affected by the recent increases in weight.[16]

BMI (kg/m2) Classification[17]
< 18.50 underweight
18.50–24.99 normal weight
25.00–29.99 overweight
30.00–34.99 class I obesity
35.00–39.99 class II obesity
≥ 40.00   class III obesity  

BMI is defined as the subject's weight divided by the square of their height and is calculated as follows.

<math>\mathrm{BMI}= \frac{m}{h^2}</math>
where m and h are the subject's weight in kilograms and height in meters respectively.

BMI is usually expressed in kilograms per square metre. To convert from pounds per square inch multiply by 703 (kg/m2)/(lb/sq in).[18]

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

Some modifications to the WHO definitions have been made by particular bodies. The surgical literature breaks down "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 morbid obesity
  • 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 nations have redefined obesity; the Japanese have defined obesity as any BMI greater than 25 kg/m2[20] while China uses a BMI of greater than 28 kg/m2.[21]

Effects on health

Excessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetes mellitus 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

Obesity is one of the leading preventable causes of death worldwide.[8][23][24] Large-scale American and European studies have found that mortality risk is lowest at a BMI of 20–25 kg/m2[25][26] in non-smokers and at 24–27 kg/m2 in current smokers, with risk increasing along with changes in either direction.[27][28] A BMI above 32 kg/m2 has been associated with a doubled mortality rate among women over a 16-year period.[29] In the United States obesity is estimated to cause 111,909 to 365,000 deaths per year,[2][24] while 1 million (7.7%) of deaths in Europe are attributed to excess weight.[30][31] On average, obesity reduces life expectancy by six to seven years,[2][32] a BMI of 30–35 kg/m2 reduces life expectancy by two to four 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 commonly shown 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.[33]

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.[34]


What went wrong with our diet?

Instead of blaming the victim for obesity, or yourself for obesity, it is important to understand what drives the weight gain, such as insulin resistance that affects up to 71 percent of the entire population out of which 35 percent already have metabolic syndrome.

Confusing choices

With over 20,000 books written on this topic with so much misleading information, let a trained practicing weight loss physician, Dr Prab R. Tumpati,MD educate you on the true science and art of obesity medicine.

Why the food pyramid failed?

The now withdrawn and failed food guide pyramid was a disaster as it advocated a low fat, but glycemic diet that leads to increased risk of insulin resistance which in turn causes weight gain.

Metabolic starvation in the obese

Most people that gain weight are not on a mission to gain weight intentionally. It is the paradoxical metabolic starvation that happens in the obese due to insulin resistance with a compensatory increase in the anabolic hormone called insulin that drives weight gain, hunger and metabolic starvation leading to food cravings, and weight gain!

3 things wrong with our diet | How insulin resistance causes weight gain? | Causes of weight gain | Skin tags and insulin resistance | Sugar rush and crash | How to lose weight? | Weight loss information

Ted Talks: Why blaming the obese is blaming the victim?

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Health consequences fall into two broad categories: those attributable to the effects of increased fat mass (such as osteoarthritis, obstructive sleep apnea, social stigmatization) and those due to the increased number of fat cells (diabetes, cancer, cardiovascular disease, non-alcoholic fatty liver disease).[2][35] Increases in body fat alter the body's response to insulin, potentially leading to insulin resistance. Increased fat also creates a proinflammatory state,[36][37] and a prothrombotic state.[35][38]

Medical field Condition Medical field Condition
Cardiology Dermatology
Endocrinology and Reproductive medicine Gastrointestinal
Neurology Oncology[51]
Psychiatry Respirology
Rheumatology and Orthopedics Urology and Nephrology

Obesity trends

According to the CDC, up to 70 percent of the population are either overweight or obese. WikiMD brings the latest science and art of treating obesity moderated by a Weight loss doctor

Science and art of losing weight

Secret for losing weight

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Weight loss articles | Body mass index | Obesity | Weight gain | Childhood 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.[60] The paradox was first described in 1999 in overweight and obese people undergoing hemodialysis,[60] and has subsequently been found in those with heart failure and peripheral artery disease (PAD).[61]

In people with heart failure, those with a BMI between 30.0 and 34.9 had lower mortality than those with a normal weight. This has been attributed to the fact that people often lose weight as they become progressively more ill.[62] 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, the risk of further cardiovascular events is increased.[63][64] Even after cardiac bypass surgery, no increase in mortality is seen in the overweight and obese.[65] One study found that the improved survival could be explained by the more aggressive treatment obese people receive after a cardiac event.[66] Another found that if one takes into account chronic obstructive pulmonary disease (COPD) in those with PAD, the benefit of obesity no longer exists.[61]

Causes

At an individual level, a combination of excessive food energy intake and a lack of physical activity is thought to explain most cases of obesity.[67] A limited number of cases are due primarily to genetics, medical reasons, or psychiatric illness.[68] In contrast, increasing rates of obesity at a societal level are felt to be due to an easily accessible and palatable diet,[69] increased reliance on cars, and mechanized manufacturing.[70][71]

What’s causing your weight gain?

  • Up to 70 percent of the population in the United States deals with being overweight or obese
  • 35 percent of all adults, according to Centers for Disease Control (CDC) are prediabetic and have significant insulin resistance while another 36 percent have some signs of insulin resistance
  • Diabetes has increased by over 500 percent in the last 50 years or so and now affects 8 percent of the population.

Could insulin resistance explain your weight gain?

What really causes your weight gain?

STOP Blaming The Victim For Obesity

52 weeks of weight loss and wellness videos

3 things wrong with our diet | How insulin resistance causes weight gain? | Causes of weight gain | Skin tags and insulin resistance | Sugar rush and crash | Causes of weight gain | Weight loss information

Is low vitamin D due to unhealthy belly fat?

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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) decreased variability 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) proportional increases in ethnic and age groups that tend to be heavier, (7) pregnancy at a later age (which may cause susceptibility to obesity in children), (8) epigenetic risk factors passed on generationally, (9) natural selection for higher BMI, and (10) assortative mating leading to increased concentration of obesity risk factors (this would increase the number of obese people by increasing population variance in weight).[72] While there is substantial evidence supporting the influence of these mechanisms on the increased prevalence of obesity, the evidence is still inconclusive, and the authors state that these are probably less influential than the ones discussed in the previous paragraph.

Diet

Template:Double image

Dietary energy supply per capita varies markedly between different regions and countries. It has also changed significantly over time.[73] From the early 1970s to the late 1990s the average food energy available per person per day (the amount of food bought) increased in all parts of the world except Eastern Europe. The United States had the highest availability with 3,654 calories (15,290 kJ) per person in 1996.[73] This increased further in 2003 to 3,754 calories (15,710 kJ).[73] During the late 1990s Europeans had 3,394 calories (14,200 kJ) per person, in the developing areas of Asia there were 2,648 calories (11,080 kJ) per person, and in sub-Saharan Africa people had 2,176 calories (9,100 kJ) per person.[73][74] Total food energy consumption has been found to be related to obesity.[75]

The widespread availability of nutritional guidelines[76] has done little to address the problems of overeating and poor dietary choice.[77] From 1971 to 2000, obesity rates in the United States increased from 14.5% to 30.9%.[78] During the same period, an increase occurred in the average amount of food energy consumed. For women, the average increase was 335 calories (1,400 kJ) per day (1,542 calories (6,450 kJ) in 1971 and 1,877 calories (7,850 kJ) in 2004), while for men the average increase was 168 calories (700 kJ) per day (2,450 calories (10,300 kJ) in 1971 and 2,618 calories (10,950 kJ) in 2004). Most of this extra food energy came from an increase in carbohydrate consumption rather than fat consumption.[79] The primary sources of these extra carbohydrates are sweetened beverages, which now account for almost 25 percent of daily food energy in young adults in America,[80] and potato chips.[81] Consumption of sweetened drinks is believed to be contributing to the rising rates of obesity.[82][83]

As societies become increasingly reliant on energy-dense, big-portions, and fast-food meals, the association between fast-food consumption and obesity becomes more concerning.[84] In the United States consumption of fast-food meals tripled and food energy intake from these meals quadrupled between 1977 and 1995.[85]

Agricultural policy and techniques in the United States and Europe have led to lower food prices. In the United States, subsidization of corn, soy, wheat, and rice through the U.S. farm bill has made the main sources of processed food cheap compared to fruits and vegetables.[86] Calorie count laws and nutrition facts labels attempt to steer people toward making healthier food choices, including awareness of how much food energy is being consumed.

Obese people consistently under-report their food consumption as compared to people of normal weight.[87] This is supported both by tests of people carried out in a calorimeter room[88] and by direct observation.

Sedentary lifestyle

A sedentary lifestyle plays a significant role in obesity.[89] Worldwide there has been a large shift towards less physically demanding work,[90][91][92] and currently at least 30% of the world's population gets insufficient exercise.[91] This is primarily due to increasing use of mechanized transportation and a greater prevalence of labor-saving technology in the home.[90][91][92] In children, there appear to be declines in levels of physical activity due to less walking and physical education.[93] World trends in active leisure time physical activity are less clear. The World Health Organization indicates people worldwide are taking up less active recreational pursuits, while a study from Finland[94] found an increase and a study from the United States found leisure-time physical activity has not changed significantly.[95]

In both children and adults, there is an association between television viewing time and the risk of obesity.[96][97][98] A review found 63 of 73 studies (86%) showed an increased rate of childhood obesity with increased media exposure, with rates increasing proportionally to time spent watching television.[99]

Genetics

Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism predispose to obesity when sufficient food energy is present. As of 2006, more than 41 of these sites on the human genome have been linked to the development of obesity when a favorable environment is present.[100] People with two copies of the FTO gene (fat mass and obesity associated gene) have been found on average to weigh 3–4 kg more and have a 1.67-fold greater risk of obesity compared with those without the risk allele.[101] The percentage of obesity that can be attributed to genetics varies, depending on the population examined, from 6% to 85%.[102]

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.)[103] In people with early-onset severe obesity (defined by an onset before 10 years of age and body mass index over three standard deviations above normal), 7% harbor a single point DNA mutation.[104]

Studies that have focused on inheritance patterns rather than on specific genes have found that 80% of the offspring of two obese parents were also obese, in contrast to less than 10% of the offspring of two parents who were of normal weight.[105]

The thrifty gene hypothesis postulates that, due to dietary scarcity during human evolution, people are prone to obesity. Their ability to take advantage of rare periods of abundance by storing energy as fat would be advantageous during times of varying food availability, and individuals with greater adipose reserves would be more likely to survive famine. This tendency to store fat, however, would be maladaptive in societies with stable food supplies.[106] This theory has received various criticisms, and other evolutionarily-based theories such as the drifty gene hypothesis and the thrifty phenotype hypothesis have also been proposed.[107][108]

Other illnesses

Certain physical and mental illnesses and the pharmaceutical substances used to treat them can increase risk of obesity. Medical illnesses that increase obesity risk include several rare genetic syndromes (listed above) as well as some congenital or acquired conditions: hypothyroidism, Cushing's syndrome, growth hormone deficiency,[109] and the eating disorders: binge eating disorder and night eating syndrome.[2] However, obesity is not regarded as a psychiatric disorder, and therefore is not listed in the DSM-IVR as a psychiatric illness.[110] The risk of overweight and obesity is higher in patients with psychiatric disorders than in persons without psychiatric disorders.[111]

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, they cannot explain the current dramatic increase seen within specific countries or globally.[112] Though it is accepted that energy consumption in 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 much debated. There are a number of theories as to the cause but most believe it is a combination of various factors.

The correlation between social class and BMI varies globally. A review in 1989 found that in developed countries women of a high social class were less likely to be obese. No significant differences were seen among men of different social classes. In the developing world, women, men, and children from high social classes had greater rates of obesity.[113] An update of this review carried out in 2007 found the same relationships, but they were weaker. The decrease in strength of correlation was felt to be due to the effects of globalization.[114] Among developed countries, levels of adult obesity, and percentage of teenage children who are overweight, are correlated with income inequality. A similar relationship is seen among US states: more adults, even in higher social classes, are obese in more unequal states.[115]

Many explanations have been put forth for associations between BMI and social class. It is thought that in developed countries, the wealthy are able to afford more nutritious food, they are under greater social pressure to remain slim, and have more opportunities along with greater expectations for physical fitness. In undeveloped countries the ability to afford food, high energy expenditure with physical labor, and cultural values favoring a larger body size are believed to contribute to the observed patterns.[114] Attitudes toward body weight held by people in one's life may also play a role in obesity. A correlation in BMI changes over time has been found among friends, siblings, and spouses.[116] Stress and perceived low social status appear to increase risk of obesity.[115][117][118]

Smoking has a significant effect on an individual's weight. Those who quit smoking gain an average of 4.4 kilograms (9.7 lb) for men and 5.0 kilograms (11.0 lb) for women over ten years.[119] However, changing rates of smoking have had little effect on the overall rates of obesity.[120]

In the United States the number of children a person has is related to their risk of obesity. A woman's risk increases by 7% per child, while a man's risk increases by 4% per child.[121] This could be partly explained by the fact that having dependent children decreases physical activity in Western parents.[122]

In the developing world urbanization is playing a role in increasing rate of obesity. In China overall rates of obesity are below 5%; however, in some cities rates of obesity are greater than 20%.[123]

Malnutrition in early life is believed to play a role in the rising rates of obesity in the developing world.[124] Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more food energy becomes available.[124]

Consistent with cognitive epidemiological data, numerous studies confirm that obesity is associated with cognitive deficits.[125] 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 to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the metabolic potential. This apparent alteration of the metabolic potential is believed to confer a greater capacity to harvest energy contributing to obesity. Whether these differences are the direct cause or the result of obesity has yet to be determined unequivocally.[126]

An association between viruses and obesity has been found in humans and several different animal species. The amount that these associations may have contributed to the rising rate of obesity is yet to be determined.[127]

Pathophysiology

There are many possible pathophysiological mechanisms involved in the development and maintenance of obesity.[128] 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, insulin, orexin, PYY 3-36, cholecystokinin, adiponectin, as well as many other mediators have been studied. The adipokines are mediators produced by adipose tissue; their action is thought to modify many obesity-related diseases.

Leptin and ghrelin are considered to be complementary in their influence on 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, most obese individuals are thought to be leptin resistant and have been found to have high levels of leptin.[129] 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 people.[128]

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.[128] 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.[130]

The arcuate nucleus contains two distinct groups of neurons.[128] 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.[128]

Public health

The World Health Organization (WHO) predicts that overweight and obesity may soon replace more traditional public health concerns such as undernutrition and infectious diseases as the most significant cause of poor health.[131] Obesity is a public health and policy problem because of its prevalence, costs, and health effects.[132] The United States Preventive Services Task Force recommends screening for all adults followed by behavioral interventions in those who are obese.[133] Public health efforts seek to understand and correct the environmental factors responsible for the increasing prevalence of obesity in the population. Solutions look at changing the factors that cause excess food energy consumption and inhibit physical activity. Efforts include federally reimbursed meal programs in schools, limiting direct junk food marketing to children,[134] and decreasing access to sugar-sweetened beverages in schools.[135] When constructing urban environments, efforts have been made to increase access to parks and to develop pedestrian routes.[136]

Many countries and groups have published reports pertaining to obesity. In 1998 the first US Federal guidelines were published, titled "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report".[137] In 2006 the Canadian Obesity Network published the "Canadian Clinical Practice Guidelines (CPG) on the Management and Prevention of Obesity in Adults and Children". This is a comprehensive evidence-based guideline to address the management and prevention of overweight and obesity in adults and children.[138]

In 2004, the United Kingdom Royal College of Physicians, the Faculty of Public Health and the Royal College of Paediatrics and Child Health released the report "Storing up Problems", which highlighted the growing problem of obesity in the UK.[139] The same year, the House of Commons Health Select Committee published its "most comprehensive inquiry [...] ever undertaken" into the impact of obesity on health and society in the UK and possible approaches to the problem.[140] 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.[141] 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.[142]

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 prevent obesity, and 'downstream' policies try to treat currently afflicted people.[143]

Management

(Xenical), the most commonly used medication to treat obesity, and sibutramine (Meridia), a medication recently withdrawn due to cardiovascular side effects]] The main treatment for obesity consists of dieting and physical exercise.[67] Diet programs may produce weight loss over the short term,[144] but maintaining this weight loss is frequently difficult and often requires making exercise and a lower food energy diet a permanent part of a person's lifestyle.[145][146] Success rates of long-term weight loss maintenance with lifestyle changes are low, ranging from 2–20%.[147] Dietary and lifestyle changes are effective in limiting excessive weight gain in pregnancy and improve outcomes for both the mother and the child.[148]

Three medication, orlistat (Xenical), lorcaserin (Belviq) and a combination of phentermine and topiramate (Qsymia) are currently available and have evidence for long term use.[149] Weight loss with orlistat is modest, an average of 2.9 kg (6.4 lb) at 1 to 4 years.[150] Its use is associated with high rates of gastrointestinal side effects[150] and concerns have been raised about negative effects on the kidneys.[151] The other two medications are available in the United States but not Europe.[152] Lorcaserin results in an average 3.1 kg weight loss (3% of body weight) greater than placebo over a year;[153] however it may increase heart valve problems.[152] A combination of phentermine and topiramate is also somewhat effective;[154] however, it may be associated with heart problems.[152] There is no information on how these drugs affect longer-term complications of obesity such as cardiovascular disease or death.[149]

The most effective treatment for obesity is bariatric surgery.[155] Surgery for severe obesity is associated with long-term weight loss, improvement in obesity related conditions,[156] and decreased overall mortality. One study found a weight loss of between 14% and 25% (depending on the type of procedure performed) at 10 years, and a 29% reduction in all cause mortality when compared to standard weight loss measures.[157] Complications occur in about 17% of cases and reoperation is needed in 7% of cases.[156] Due to its cost and risks, researchers are searching for other effective yet less invasive treatments.

Epidemiology

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Before the 20th century, obesity was rare;[158] in 1997 the WHO formally recognized obesity as a global epidemic.[80] As of 2008 the WHO estimates that at least 500 million adults (greater than 10%) are obese, with higher rates among women than men.[159] The rate of obesity also increases with age at least up to 50 or 60 years old[160] and severe obesity in the United States, Australia, and Canada is increasing faster than the overall rate of obesity.[19][161][162]

Once considered a problem only of high-income countries, obesity rates are rising worldwide and affecting both the developed and developing world.[30] These increases have been felt most dramatically in urban settings.[159] The only remaining region of the world where obesity is not common 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 (to eat), with ob (over) added to it.[163] The Oxford English Dictionary documents its first usage in 1611 by Randle Cotgrave.[164]

Historical trends

The Greeks were the first to recognize obesity as a medical disorder.[158] Hippocrates wrote that "Corpulence is not only a disease itself, but the harbinger of others".[2] The Indian surgeon Sushruta (6th century BCE) related obesity to diabetes and heart disorders.[165] He recommended physical work to help cure it and its side effects.[165] For most of human history mankind struggled with food scarcity.[166] Obesity has thus historically been viewed as a sign of wealth and prosperity. It was common among high officials in Europe in the Middle Ages and the Renaissance[167] as well as in Ancient East Asian civilizations.[168]

With the onset of the industrial revolution it was realized that the military and economic might of nations were dependent on both the body size and strength of their soldiers and workers.[80] Increasing the average body mass index from what is now considered underweight to what is now the normal range played a significant role in the development of industrialized societies.[80] Height and weight thus both increased through the 19th century in the developed world. During the 20th century, as populations reached their genetic potential for height, weight began increasing much more than height, resulting in obesity.[80] In the 1950s increasing wealth in the developed world decreased child mortality, but as body weight increased heart and kidney disease became more common.[80][169] During this time period insurance companies realized the connection between weight and life expectancy and increased premiums for the obese.[2]

Many cultures throughout history have viewed obesity as the result of a character flaw. The obesus or fat character in Greek comedy was a glutton and figure of mockery. During Christian times food was viewed as a gateway to the sins of sloth and lust.[9] In modern Western culture, excess weight is often regarded as unattractive, and obesity is commonly associated with various negative stereotypes. People of all ages can face social stigmatization, and may be targeted by bullies or shunned by their peers. Obesity is once again a reason for discrimination.[170]

Public perceptions in Western society regarding healthy body weight differ from those regarding the weight that is considered ideal  – and both have changed since the beginning of the 20th century. The weight that is viewed as an ideal has become lower since the 1920s. This is illustrated by the fact that the average height of Miss America pageant winners increased by 2% from 1922 to 1999, while their average weight decreased by 12%.[171] On the other hand, people's views concerning healthy weight have changed in the opposite direction. In Britain the weight at which people considered themselves to be overweight was significantly higher in 2007 than in 1999.[172] These changes are believed to be due to increasing rates of adiposity leading to increased acceptance of extra body fat as being normal.[172]

Obesity is still seen as a sign of wealth and well-being in many parts of Africa. This has become particularly common since the HIV epidemic began.[2]

The arts

The first sculptural representations of the human body 20,000–35,000 years ago depict obese females. Some attribute the Venus figurines to the tendency to emphasize fertility while others feel they represent "fatness" in the people of the time.[9] Corpulence is, however, absent in both Greek and Roman art, probably in keeping with their ideals regarding moderation. This continued through much of Christian European history, with only those of low socioeconomic status being 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 del Borro.[9] Rubens (1577–1640) regularly depicted full-bodied women in his pictures, from which derives the term Rubenesque. These women, however, still maintained the "hourglass" shape with its relationship to fertility.[173] During the 19th century, views on obesity changed in the Western world. After centuries of obesity being synonymous with wealth and social status, slimness began to be seen as the desirable standard.[9]

Society and culture

Economic impact

In addition to its health impacts, obesity leads to many problems including disadvantages in employment[174][175] and increased business costs. These effects are felt by all levels of society from individuals, 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 all medical expenditures,[176][177][178] while the cost of obesity in Canada was estimated at CA$2 billion in 1997 (2.4% of total health costs).[67] The total annual direct cost of overweight and obesity in Australia in 2005 was A$21 billion. Overweight and obese Australians also received A$35.6 billion in government subsidies.[179] The estimate range for annual expenditures on diet products is $40 billion to $100 billion in the US alone.[180]

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 obesity may improve the public's health, but it is unlikely to reduce overall health spending.[181]

Obesity can lead to social stigmatization and disadvantages in employment.[174] When compared to their normal weight counterparts, obese workers on average have higher rates of absenteeism from work and take more disability leave, thus increasing costs for employers and decreasing productivity.[182] A study examining Duke University employees found that people with a BMI over 40 kg/m2 filed twice as many 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.[183] The Alabama State Employees' Insurance Board approved a controversial plan to charge obese workers $25 a month for health insurance that would otherwise be free unless they take steps to lose weight and improve 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 after one year.[184]

Some research shows that obese people are less likely to be hired for a job and are less likely to be promoted.[170] Obese people are also paid less than their non-obese counterparts for an equivalent job; obese women on average make 6% less and obese men make 3% less.[185]

Specific industries, such as the airline, healthcare and food industries, have special concerns. Due to rising rates of obesity, airlines face higher fuel costs and pressures to increase seating width.[186] In 2000, the extra weight of obese passengers cost airlines US$275 million.[187] The healthcare industry has had to invest in special facilities for handling severely obese patients, including special lifting equipment and bariatric ambulances.[188] Costs for restaurants are increased by litigation accusing them of causing obesity.[189] In 2005 the US Congress discussed legislation to prevent civil lawsuits against the food industry in relation to obesity; however, it did not become law.[189]

With the American Medical Association's 2013 classification of obesity as chronic disease,[10] it is thought that health insurance companies will more likely pay for obesity treatment, counseling and surgery, and the cost of research and development of fat treatment pills or gene therapy treatments should be more affordable if insurers help to subsidize their cost.[190] The AMA classification is not legally binding, however, so health insurers still have the right to reject coverage for a treatment or procedure.[190]

Size acceptance

The principal goal of the fat acceptance movement is to decrease discrimination against people who are overweight and obese.[191][192] However, some in the movement are also attempting to challenge the established relationship between obesity and negative health outcomes.[193]

A number of organizations exist that promote the acceptance of obesity. They have increased in prominence in the latter half of the 20th century.[194] The US-based National Association to Advance Fat Acceptance (NAAFA) was formed in 1969 and describes itself as a civil rights organization dedicated to ending size discrimination.[195]

The International Size Acceptance Association (ISAA) is a non-governmental organization (NGO) which was founded in 1997. It has more of a global orientation and describes its mission as promoting size acceptance and helping to end weight-based discrimination.[196] These groups often argue for the recognition of obesity as a disability under the US Americans With Disabilities Act (ADA). The American legal system, however, has decided that the potential public health costs exceed the benefits of extending this anti-discrimination law to cover obesity.[193]

Childhood obesity

The healthy BMI range varies with the age and sex of the child. Obesity in children and adolescents is defined as a BMI greater than the 95th percentile.[15] The reference data that these percentiles are based on is from 1963 to 1994 and thus has not been affected by the recent increases in rates of obesity.[16] Childhood obesity has reached epidemic proportions in 21st century, with rising rates in both the developed and developing world. Rates of obesity in Canadian boys have increased from 11% in 1980s to over 30% in 1990s, while during this same time period rates increased from 4 to 14% in Brazilian children.[197]

As with obesity in adults, many different factors contribute to the rising rates of childhood obesity. Changing diet and decreasing physical activity are believed to be the two most important in causing the recent increase in the rates.[198] Because childhood obesity often persists into adulthood and is associated with numerous chronic illnesses, children who are obese are often tested for hypertension, diabetes, hyperlipidemia, and fatty liver.[67] Treatments used in children are primarily lifestyle interventions and behavioral techniques, although efforts to increase activity in children have had little success.[199] In the United States, medications are not FDA approved for use in this age group.[197]

County obesity rate in the United States

In the United States, the prevalence of obesity was 39.8% and affected about 93.3 million of US adults in 2015, according to the data from Centers for Disease Control. Obesity-related conditions include heart disease, stroke, type 2 diabetes and certain types of cancer that are some of the leading causes of preventable, premature death. The estimated annual medical cost of obesity in the United States was $147 billion in 2008 US dollars; the medical cost for people who have obesity was $1,429 higher than those of normal weight.

Obesity statistics, strategies, and treatment options by State and Territory in the United States.

Prevalence of Self-Reported Obesity by State and Territory in the United States, BRFSS, 2017
Obesity statistics
US State Obesity Prevalence 95% Confidence Interval
Alabama 36.3 (34.7, 38.0)
Alaska 34.2 (31.4, 37.1)
Arizona 29.5 (28.5, 30.5)
Arkansas 35.0 (32.6, 37.5)
California 25.1 (23.8, 26.4)
Colorado 22.6 (21.6, 23.7)
Connecticut 26.9 (25.6, 28.1)
Delaware 31.8 (29.7, 34.0)
District of Columbia 23.0 (21.4, 24.7)
Florida 28.4 (27.0, 29.9)
Georgia 31.6 (30.0, 33.2)
Guam 34.3 (31.2, 37.6)
Hawaii 23.8 (22.4, 25.2)
Idaho 29.3 (27.5, 31.2)
Illinois 31.1 (29.5, 32.7)
Indiana 33.6 (32.5, 34.7)
Iowa 36.4 (35.1, 37.7)
Kansas 32.4 (31.5, 33.2)
Kentucky 34.3 (32.6, 36.0)
Louisiana 36.2 (34.4, 38.1)
Maine 29.1 (27.7, 30.6)
Maryland 31.3 (30.0, 32.6)
Massachusetts 25.9 (24.1, 27.7)
Michigan 32.3 (31.1, 33.4)
Minnesota 28.4 (27.5, 29.4)
Mississippi 37.3 (35.3, 39.3)
Missouri 32.5 (30.9, 34.0)
Montana 25.3 (23.8, 26.9)
Nebraska 32.8 (31.6, 34.0)
Nevada 26.7 (24.5, 29.0)
New Hampshire 28.1 (26.3, 29.9)
New Jersey 27.3 (25.8, 28.7)
New Mexico 28.4 (26.8, 30.0)
New York 25.7 (24.6, 26.9)
North Carolina 32.1 (30.4, 34.0)
North Dakota 33.2 (31.6, 34.7)
Ohio 33.8 (32.5, 35.1)
Oklahoma 36.5 (34.9, 38.1)
Oregon 29.4 (27.9, 30.9)
Pennsylvania 31.6 (30.0, 33.2)
Puerto Rico 32.9 (31.0, 34.9)
Rhode Island 30.0 (28.1, 31.9)
South Carolina 34.1 (32.8, 35.4)
South Dakota 31.9 (29.8, 34.1)
Tennessee 32.8 (31.1, 34.6)
Texas 33.0 (31.2, 34.9)
Utah 25.3 (24.2, 26.4)
Vermont 27.6 (26.0, 29.2)
Virginia 30.1 (28.7, 31.4)
Washington 27.7 (26.6, 28.7)
West Virginia 38.1 (36.4, 39.7)
Wisconsin 32.0 (30.3, 33.8)
Wyoming 28.8 (27.1, 30.6)

Also see

Portions of content adapted from Wikipedias article on Obesity licensed under GNU FDL.

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