Perbezaan antara semakan "Obesiti"

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<!-- Penyebab -->
Obesiti kerap kali terjadi disebabkan oleh kombinasi pengambilan tenaga makanan secara keterlaluan, kurangnya aktiviti fizikaljasmani, dan kerentanan genetik.<ref name=WHO2015/> Terdapat kes terpencil didapati disebabkan oleh gen, kecelaruan endokrin, pengubatan, atau penyakit mental.<ref name=Ble2008>{{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 | type = Research Support }}</ref> Tiada bukti kukuh sebenarnya yang menyokong pandangan bahawa orang obes makan sedikit tetapi berat masih bertambah kerana metabolisme yang rendah.<ref name=OUP2011>{{cite book|title=Oxford Handbook of Medical Sciences|date=2011|publisher=OUP Oxford|location=Oxford|isbn=9780191652295|page=180|edition=2nd|url=https://books.google.ca/books?id=RUQKjpkeLugC&pg=PA180}}</ref> Secara kebiasaannya, orang obes mempunyai penggunaan tenaga yang lebih banyak berbanding orang yang kurus kerana banyak tenaga diperlukan untuk mengekalkan jisim badan yang bertambah.<ref name=OUP2011/><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=https://books.google.com/?id=vWjK5etS7PMC |doi= |accessdate=April 5, 2009}}</ref>
 
<!-- Pencegahan dan rawatan -->
 
Dalam kalangan penghidap kegagalan jantung, mereka yang mempunyai BMI antara 30.00 hingga 34.9 memiliki kematian lebih rendah berbanding mereka yang mempunyai berat normal. Hal ini disebabkan oleh hakikat bahawa manusia sering hilang berat badan apabila mereka secara berperingkat-peringkat semakin sakit.<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 | type = Review }}</ref> Penemuan sama juga dilihat pada jenis penyakit jantung lain. Orang yang mempunyai obesiti kelas I dan penyakit jantung tidak mempunyai kadar masalah lanjutan jantung yang lebih besar daripada orang yang mempunyai berat normal yang turut menghidap penyakit jantung. Dalam kalangan orang yang mempunyai darjah obesiti yang lebih besar, walau bagaimanapun, risiko masalah lanjutan kardiovaskular bertambah.<ref>{{cite journal | author = Romero-Corral A, Montori VM, Somers VK, Korinek J, Thomas RJ, Allison TG, Mookadam F, Lopez-Jimenez F | 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 | type = Review }}</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 = | type = Meta-analysis, Review }}</ref> Walaupun selepas pembedahan pintasan koronari arteri, tiada pertambahan kematian dilihat berlaku dalam kalangan orang yang berat terlebih dan obes.<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 | type = Meta-analysis }}</ref> Satu kajian mendapati kemandirian yang bertambah dapat dijelaskan oleh rawatan yang lebih agresif yang diterima oleh orang obes selepas peristiwa kardium.<ref>{{cite journal | author = Diercks DB, Roe MT, Mulgund J, Pollack CV, Kirk JD, Gibler WB, Ohman EM, Smith SC, Boden WE, Peterson ED | 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 | volume = 152 | issue = 1 | pages = 140–8 | date = July 2006 | pmid = 16824844 | doi = 10.1016/j.ahj.2005.09.024 | type = Research Support }}</ref> Satu lagi penemuan mendapati jika seseorang mengalami penyakit pulmonari obstruktif kronik serentak dengan penyakit vaskular periferal, manfaat obesiti tidak lagi wujud.<ref name=paradox2003/>
 
==Penyebab==
Pada peringkat individu, kombinasi pengambilan tenaga makanan secara keterlaluan dan kurangnya aktiviti jasmani difikirkan untuk menjelaskan kebanyakan kes obesiti.<ref name=CADG2006/> Sebilangan kes terpencil berpunca disebabkan oleh genetik, sebab perubatan atau kesakitan psikiatri.<ref name=Ble2008/> Sebagai perbandingan, penambahan kadar obesiti pada tahap kemasyarakatan dirasakan berpunca disebabkan diet makanan mudah didapati dan melazatkan,<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 | type = Review }}</ref> peningkatan kebergantungan terhadap kereta, dan perkilangan berjentera.<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 = | type = Research Support }}</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 | type = Review }}</ref>
 
Ulasan tahun 2006 mengenal pasti sepuluh penyumbang berpotensi lain kepada peningkatan masalah obesiti: (1) tidur yang tidak mencukupi, (2) disruptor endokrin (bahan pencemar persekitaran yang mengganggu metabolisme lipid), (3) berkurangnya keragaman suhu sekeliling, (4) berkurangnya kadar merokok tembakau, kerana merokok menahan selera, (5) bertambahnya penggunaan pengubatan yang menyebabkan peningkatan berat (contohnya, antipsikotik atipikal), (6) proporsional bertambah dalam etnik dan kumpulan umur yang cenderung lebih berat, (7) mengandung pada umur lewat (menyebabkan kerentanan kepada obesiti dalam kalangan kanak-kanak), (8) faktor risiko epigenetik diwariskan kepada generasi seterusnya, (9) pemilihan semula jadi bagi BMI lebih tinggi, dan (10) pasangan sesama ciri menjurus kepada bertambahnya penumpuan faktor risiko obesiti (ini boleh meningkatkan bilangan orang obes dengan meningkatkan kelainan populasi dari segi berat).<ref name="pmid16801930">{{cite journal | author = Keith SW, Redden DT, Katzmarzyk PT, Boggiano MM, Hanlon EC, Benca RM, Ruden D, Pietrobelli A, Barger JL, Fontaine KR, Wang C, Aronne LJ, Wright SM, Baskin M, Dhurandhar NV, Lijoi MC, Grilo CM, DeLuca M, Westfall AO, Allison DB | 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 | type = Review }}</ref> Meskipun terdapat bukti penting yang menyokong pengaruh mekanisme tersebut ke atas bertambahnya kelaziman obesiti, bukti ini masih lagi tidak mempunyai kesimpulan, dan pengarang menyatakan bukti ini kurang berpengaruh berbanding yang dibincangkan pada perenggan sebelumnya.
 
===Diet===
{{Main|Diet dan obesiti}}
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<div class="thumbimage">[[File:World map of Energy consumption 1961,2.svg|200px|alt=(Kiri) Peta dunia di mana negara diwarnakan untuk menggambarkan pengambilan tenaga makanan oleh orangnya pada 1961. Amerika Utara, Eropah, dan Australia secara relatifnya pengambilan tenaga makanan tinggi, manakala Afrika dan Asia kurang mengambil tenaga makanan.]]
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<div class="thumbcaption" style="clear:left">1961
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<div class="thumbimage">[[File:World map of Energy consumption 2001-2003.svg|200px|alt=(Kanan) Peta dunia di mana negara diwarnakan untuk menggambarkan pengambilan tenaga makanan oleh orangnya pada 2001–2003. Pengambilan tenaga makanan di Amerika Utara, Eropah, dan Australia bertambah daripada paras sebelumnya pada 1971. Pengambilan tenaga makanan turut bertambah dengan banyaknya di banyak bahagian Asia. Walau bagaimanapun, pengambilan tenaga makanan di Afrika tetap rendah.]]
</div><div class="thumbcaption" style="clear:left">2001–03
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</div><div class="thumbcaption" style="clear: left; text-align: left; background: transparent">Peta ketersediaan tenaga diet setiap orang setiap hari pada 1961 (kiri) dan 2001–2003 (kanan)<ref name=Earth09/> Kalori setiap orang setiap hari (kilojoule setiap orang setiap hari)
{{Multicol}}
{{legend|#b3b3b3|<small>tiada data</small>}}
{{legend|#ffff65|<small><1,600 (<6,700)</small>}}
{{legend|#fff200|<small>1,600–1,800 (6,700–7,500)</small>}}
{{legend|#ffdc00|<small>1,800–2,000 (7,500–8,400)</small>}}
{{legend|#ffc600|<small>2,000–2,200 (8,400–9,200)</small>}}
{{legend|#ffb000|<small>2,200–2,400 (9,200–10,000)</small>}}
{{legend|#ff9a00|<small>2,400–2,600 (10,000–10,900)</small>}}
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{{legend|#ff8400|<small>2,600–2,800 (10,900–11,700)</small>}}
{{legend|#ff6e00|<small>2,800–3,000 (11,700–12,600)</small>}}
{{legend|#ff5800|<small>3,000–3,200 (12,600–13,400)</small>}}
{{legend|#ff4200|<small>3,200–3,400 (13,400–14,200)</small>}}
{{legend|#ff2c00|<small>3,400–3,600 (14,200–15,100)</small>}}
{{legend|#cb0000|<small>>3,600 (>15,100)</small>}}
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[[File:World Per Person Energy Consumption.png|thumb|upright=1.6|alt=Graf menunjukkan peningkatan beransur-ansur pengambilan tenaga makanan global setiap orang setiap hari antara 1961 hingga 2002.|Purata per kapita pengambilan tenaga serata dunia dari 1961 hingga 2002<ref name=Earth09>{{cite web|url=http://earthtrends.wri.org/searchable_db/index.php?theme=8&variable_ID=212&action=select_countries |title=EarthTrends: Nutrition: Calorie supply per capita |work=World Resources Institute |accessdate=Oct 18, 2009 |archiveurl=https://web.archive.org/web/20110611160708/http://earthtrends.wri.org/searchable_db/index.php?theme=8&variable_ID=212&action=select_countries |archivedate=2011-06-11}}</ref>]]
 
Bekalan tenaga diet per kapita berbeza-beza antara wilayah dan negara yang berbeza. Ia juga berubah dengan nyata sekali mengikut peredaran masa.<ref name=Earth09/> Dari awal 1970-an hingga akhir 1990-an, purata ketersediaan tenaga makanan setiap orang setiap hari (bilangan makanan yang dibeli) bertambah di semua bahagian dunia kecuali Eropah Timur. Amerika Syarikat mempunyai ketersediaan tenaga makanan paling tinggi dengan {{convert|3654|Cal}} setiap orang pada 1996.<ref name=Earth09/> Ini jelas bertambah pada 2003 kepada {{convert|3754|Cal}}.<ref name=Earth09/> Semasa akhir 1990-an, kawasan Eropah mempunyai {{convert|3394|Cal}} setiap orang, di kawasan membangun Asia mempunyai {{convert|2648|Cal}} setiap orang, dan di kawasan sub-Sahara Afrika mempunyai {{convert|2176|Cal}} setiap orang.<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> Jumlah pengambilan tenaga makanan didapati berkait rapat dengan obesiti.<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>
 
Ketersediaan panduan nutrisi pemakanan yang meluas<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> dilihat tidak cukup untuk mengatasi masalah makan terlebih dan pemilihan diet yang tidak berkhasiat.<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> Dari 1971 hingga 2000, kadar obesiti di Amerika Syarikat bertambah dari 14.5% hingga 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]] | volume = 288 | issue = 14 | pages = 1723–1727 | date = October 2002 | pmid = 12365955 | doi = 10.1001/jama.288.14.1723 | url = http://jama.ama-assn.org/cgi/content/full/288/14/1723 }}</ref> Ketika tempoh yang sama, berlaku pertambahan jumlah tenaga makanan yang diambil. Bagi wanita, pertambahan purata ialah {{convert|335|Cal}} setiap hari ({{convert|1542|Cal}} pada 1971 dan {{convert|1877|Cal}} pada 2004), manakala bagi lelaki, pertambahan purata ialah {{convert|168|Cal}} setiap hari ({{convert|2450|Cal}} pada 1971 dan {{convert|2618|Cal}} pada 2004). Kebanyakan lebihan tenaga makanan datang daripada peningkatan pengambilan karbohidrat berbanding pengambilan lemak.<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 | volume = 53 | issue = 4 | pages = 80–2 | date = February 2004 | pmid = 14762332 | url = http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm }}</ref> Sumber asas lebihan karbohidrat ialah minuman manis, di mana sekarang ini meliputi 25 peratus daripada tenaga makanan harian dalam kalangan orang dewasa di Amerika,<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> dan kentang goreng.<ref>{{cite journal | author = Mozaffarian D, Hao T, Rimm EB, Willett WC, Hu FB | title = Changes in Diet and Lifestyle and Long-Term Weight Gain in Women and Men | journal = The New England Journal of Medicine | volume = 364 | issue = 25 | pages = 2392–404 | date = 23 June 2011 | pmid = 21696306 | pmc = 3151731 | doi = 10.1056/NEJMoa1014296 | type = Meta-analysis }}</ref> Pengambilan minuman manis seperti minuman ringan, minuman buah, teh ais, dan minuman air bertenaga dan bervitamin dipercayai menjadi penyumbang kepada peningkatan mendadak kadar obesiti<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 | pmc = 3210834 | doi = | url = http://www.ajcn.org/cgi/content/full/84/2/274 | type = Review }}</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 | type = Review }}</ref> dan meningkatnya risiko sindrom metabolik dan diabetes melitus tahap 2.<ref>{{cite journal |author=Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB |title=Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis |journal=Diabetes Care |volume=33 |issue=11 |pages=2477–83 |date=November 2010 |pmid=20693348 |pmc=2963518 |doi=10.2337/dc10-1079 |url= |type=Meta-analysis, Review}}</ref>
 
Bila mana masyarakat terus-menerus bergantung dengan tenaga makanan yang padat, hidangan yang besar, dan makanan segera, perkaitan antara pengambilan makanan segera dan obesiti menjadi semakin membimbangkan.<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 = | type = Review }}</ref> Di Amerika Syarikat, pengambilan makanan segera bertiga kali ganda dan pengambilan tenaga makanan ini berempat kali ganda antara 1977 hingga 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/aib-agricultural-information-bulletin/aib750.aspx |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>
 
Dasar pertanian dan Revolusi Hijau di Amerika Syarikat dan Eropah telah membawa kepada rendahnya harga makanan. Di Amerika Syarikat, pemberian subsidi jagung, soya, gandum, dan beras melalui undang-undang ladang Amerika Syarikat sememangnya membolehkan sumber utama makanan diproses murah berbanding buah-buahan dan sayur-sayuran.<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> Cubaan undang-undang pengiraan kalori dan label fakta pemakanan dibuat untuk menggalakkan masyarakat memilih makanan yang lebih menyihatkan, termasuklah kesedaran berapa banyak tenaga makanan yang diambil.
 
Orang obes selalunya tidak melaporkan pengambilan makanan mereka berbanding orang yang berat normal.<ref>Kopelman and Caterson 2005:324.</ref> Hal ini turut disokong oleh ujian yang dilakukan ke atas ramai orang di dalam bilik kalorimeter<ref>{{cite book|title=Metabolism alone doesn't explain how thin people stay thin |publisher=The Medical Post |work=John Schieszer}}</ref> dan pemerhatian secara langsung.
 
===Gaya hidup banyak duduk===
{{See also|Gaya hidup banyak duduk|Trend senaman}}
Gaya hidup banyak duduk memainkan peranan penting dalam obesiti.<ref>Seidell 2005 p.10</ref> Di serata dunia, terdapat anjakan besar ke arah kerja yang kurang menggunakan kekuatan jasmani,<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 = | type = Review }}</ref> and currently at least 30% of the world's population gets insufficient exercise.<ref name=WHOExercise/> Hal ini juga didorong oleh peningkatan penggunaan pengangkutan berjentera dan ketersebarluasan teknologi yang menjimatkan tenaga buruh di rumah.<ref name=WHO2009/><ref name=WHOExercise/><ref name=Ness2006/> Dalam kalangan kanak-kanak, kelihatannya berlaku penurunan tahap aktiviti jasmani disebabkan kurangnya berjalan dan pendidikan jasmani.<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 | isbn = 978-3-318-01396-2 | series = Medicine and Sport Science | type = Review }}</ref> Trend dunia meluangkan masa senggang dengan melakukan aktiviti jasmani semakin tidak jelas. Pertubuhan Kesihatan Dunia menunjukkan masyarakat serata dunia kurang aktif berekreasi, manakala kajian dari 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 = | type = Research Support }}</ref> mendapati peningkatan dan kajian dari Amerika Syarikat mendapati masa senggang untuk aktiviti jasmani tidaklah berubah dengan ketara.<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 = | type = Review }}</ref>
 
Dalam kalangan kanak-kanak dan dewasa, terdapat hubung kait antara masa menonton televisyen dengan risiko obesiti.<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 | type = Review }}</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 = | type = Research Support }}</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>
 
===Genetics===
{{Main|Genetics of obesity}}
[[File:La monstrua desnuda (1680), de Juan Carreño de Miranda..jpg|thumb|upright=1.4|alt=A painting of a dark haired pink cheeked obese nude young female leaning against a table. She is holding grapes and grape leaves in her left hand which cover her genitalia.|A 1680 painting by [[Juan Carreno de Miranda]] of a girl presumed to have [[Prader–Willi syndrome]]<ref>{{cite web|url=http://www.esst.org/newsletter2000.htm |title=Case Study: Cataplexy and SOREMPs Without Excessive Daytime Sleepiness in Prader Willi Syndrome. Is This the Beginning of Narcolepsy in a Five Year Old? |author=Mary Jones |publisher=European Society of Sleep Technologists |accessdate=April 6, 2009}}</ref>]]
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, Giles TD, Bray GA, Hong Y, Stern JS, Pi-Sunyer FX, Eckel RH | 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 | type = Review }}</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 = | type = Review }}</ref> The differences in BMI between people that are [[heritability|due 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 | type = Review }}</ref>
 
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 = | type = Review }}</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 | type = Review }}</ref>
 
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> Different people exposed to the same environment have different risks of obesity due to their underlying genetics.<ref>{{cite journal | author = Walley, Andrew J., Asher, Julian E., Froguel, Philippe | title = The genetic contribution to non-syndromic human obesity. | journal = Nat Rev Genet. | volume = 10 | issue = 7 | pages = 431–42 | date = July 2009 | pmid = 19506576 | doi = 10.1038/nrg2594 | url = http://www.nature.com/nrg/journal/v10/n7/full/nrg2594.html | type = Review |quote=However, it is also clear that genetics greatly influences this situation, giving individuals in the same 'obesogenic' environment significantly different risks of becoming obese. }}</ref>
 
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 | type = Review }}</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 journal | author = Wells JC | title = Thrift: A guide to thrifty genes, thrifty phenotypes and thrifty norms | journal = International Journal of Obesity | volume = 33 | issue = 12 | pages = 1331–1338 | year = 2009 | pmid = 19752875 | pmc = | doi = 10.1038/ijo.2009.175 | type = Review }}</ref><ref>{{cite journal | author = Wells JC | title = The thrifty phenotype: An adaptation in growth or metabolism? | journal = American Journal of Human Biology | volume = 23 | issue = 1 | pages = 65–75 | year = 2011 | pmid = 21082685 | pmc = | doi = 10.1002/ajhb.21100 | type = Review }}</ref>
 
===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 | type = Review }}</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>
 
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/>
 
===Social determinants===
{{Main|Social determinants of obesity}}
[[File:Yamai no Soshi - Obesity.JPG|thumb|upright=1.4|The disease scroll (Yamai no soshi, late 12th century) depicts a woman moneylender with obesity, considered a disease of the rich.]]
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.
 
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 | type = Review }}</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 | type = Review }}</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>
 
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, 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 | type = Research Support }}</ref> Stress and perceived low social status appear to increase risk of obesity.<ref name="spirit" /><ref>{{cite journal | author = Björntorp P | title = Do stress reactions cause abdominal obesity and comorbidities? | journal = Obesity Reviews | volume = 2 | issue = 2 | pages = 73–86 | year = 2001 | pmid = 12119665 | doi = 10.1046/j.1467-789x.2001.00027.x }}</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 | type = Research Support }}</ref>
 
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 | type = Review }}</ref>
 
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 | type = Comparative Study }}</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 | type = Review }}</ref>
 
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>
 
[[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 | type = Review }}</ref> Endocrine changes that occur during periods of malnutrition may promote the storage of fat once more food energy becomes available.<ref name=DC2001/>
 
Consistent with [[cognitive epidemiology|cognitive epidemiological]] data, numerous studies confirm that obesity is associated with cognitive deficits.<ref name="Smith2011">{{cite journal | author = Smith E, Hay P, Campbell L, Trollor JN | title = A review of the association between obesity and cognitive function across the lifespan: implications for novel approaches to prevention and treatment | journal = Obesity Reviews | volume = 12 | pages = 740–755 | year = 2011 | pmid = 21991597 | doi = 10.1111/j.1467-789X.2011.00920.x | url = http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2011.00920.x/abstract | issue=9|type=Review}}</ref> Whether obesity causes cognitive deficits, or vice versa is unclear at present.
 
===Infectious agents===
{{See also|Infectobesity}}
The study of the effect of infectious agents on metabolism is still in its early stages. [[Gut flora]] has been shown to differ between lean and obese humans. There is an indication that gut flora in obese and lean individuals can affect the 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 | type = Review }}</ref>
 
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 = | type = Review }}</ref>
 
==Pathophysiology==
[[File:Fatmouse.jpg|thumb|upright=1.4|alt=Two white mice both with similar sized ears, black eyes, and pink noses. The body of the mouse on the left, however, is about three times the width of the normal sized mouse on the right.|A comparison of a mouse unable to produce [[leptin]] thus resulting in obesity (left) and a normal mouse (right)]]
 
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 | volume = 116 | issue = 2 | pages = 337–50 | year = 2004 | pmid = 14744442 | doi = 10.1016/S0092-8674(03)01081-X | type = Review }}</ref> This field of research had been almost unapproached until the [[leptin]] gene was discovered in 1994 by J. M. Friedman's laboratory.<ref>{{cite journal|last1=Zhang|first1=Y|last2=Proenca|first2=R|last3=Maffei|first3=M|last4=Barone|first4=M|last5=Leopold|first5=L|last6=Friedman|first6=JM|title=Positional cloning of the mouse obese gene and its human homologue.|journal=Nature|date=Dec 1, 1994|volume=372|issue=6505|pages=425–32|doi=10.1038/372425a0|pmid=7984236|type=Research Support}}</ref> These investigators postulated that leptin was a satiety factor. In the ob/ob mouse, mutations in the [[leptin]] gene resulted in the obese phenotype opening the possibility of leptin therapy for human obesity. However, soon thereafter [[Jose F. Caro|J. F. Caro's]] laboratory could not detect any mutations in the leptin gene in humans with obesity. On the contrary [[Leptin]] expression was increased proposing the possibility of Leptin-resistance in human obesity.<ref>{{cite journal|last1=Considine|first1=RV|last2=Considine|first2=EL|last3=Williams|first3=CJ|last4=Nyce|first4=MR|last5=Magosin|first5=SA|last6=Bauer|first6=TL|last7=Rosato|first7=EL|last8=Colberg|first8=J|last9=Caro|first9=JF <!--exactly 9 authors--> |title=Evidence against either a premature stop codon or the absence of obese gene mRNA in human obesity.|journal=The Journal of Clinical Investigation|date=Jun 1995|volume=95|issue=6|pages=2986–8|pmid=7769141|doi=10.1172/jci118007|pmc=295988|type=Research Support}}</ref> 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.
 
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 | type = Review }}</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"/>
 
[[File:Leptin.png|thumb|left|upright=1.4|alt=A three dimensional model with two pairs of opposed curling columns attached together at their ends by more linear segments.|A graphic depiction of a [[leptin]] molecule]]
While leptin and ghrelin are produced peripherally, they control appetite through their actions on the [[central nervous system]]. In particular, they and other appetite-related hormones act on the [[hypothalamus]], a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the [[melanocortin]] pathway being the most well understood.<ref name="flier"/> The circuit begins with an area of the hypothalamus, the [[arcuate nucleus]], that has outputs to the [[lateral hypothalamus]] (LH) and [[ventromedial hypothalamus]] (VMH), the brain's feeding and satiety centers, respectively.<ref>{{cite book|author=Boulpaep, Emile L.; Boron, Walter F. |title=Medical physiology: A cellular and molecular approach |publisher=Saunders |location=Philadelphia |year=2003 |page=1227 |isbn=0-7216-3256-4}}</ref>
 
The arcuate nucleus contains two distinct groups of [[neuron]]s.<ref name="flier"/> The first group coexpresses [[neuropeptide Y]] (NPY) and [[agouti-related peptide]] (AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH. The second group coexpresses [[pro-opiomelanocortin]] (POMC) and [[cocaine- and amphetamine-regulated transcript]] (CART) and has stimulatory inputs to the VMH and inhibitory inputs to the LH. Consequently, NPY/AgRP neurons stimulate feeding and inhibit satiety, while POMC/CART neurons stimulate satiety and inhibit feeding. Both groups of arcuate nucleus neurons are regulated in part by leptin. Leptin inhibits the NPY/AgRP group while stimulating the POMC/CART group. Thus a deficiency in leptin signaling, either via leptin deficiency or leptin resistance, leads to overfeeding and may account for some genetic and acquired forms of obesity.<ref name="flier"/>
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