Editing Abdominal obesity (section)

== Health risks ==
===Heart disease===
Abdominal obesity is typically associated with a statistically higher risk of [[heart disease]], [[hypertension]], [[insulin resistance]], and [[Diabetes Mellitus Type 2|type 2 diabetes]] (see below).<ref>{{cite journal | vauthors = Westphal SA | title = Obesity, abdominal obesity, and insulin resistance | journal = Clinical Cornerstone | volume = 9 | issue = 1 | pages = 23–29; discussion 30–1 | year = 2008 | pmid = 19046737 | doi = 10.1016/S1098-3597(08)60025-3 }}</ref> With an increase in the waist to hip ratio and overall waist circumference the risk of death increases as well.<ref>{{cite journal | vauthors = Cameron AJ, Zimmet PZ | title = Expanding evidence for the multiple dangers of epidemic abdominal obesity | journal = Circulation | volume = 117 | issue = 13 | pages = 1624–6 | date = April 2008 | pmid = 18378623 | doi = 10.1161/CIRCULATIONAHA.108.775080 | doi-access = free }}</ref> [[Metabolic syndrome]] is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance, type 2 diabetes, and an increased risk of developing cardiovascular disease.<ref name="Després">{{cite journal | vauthors = Després JP, Lemieux I | title = Abdominal obesity and metabolic syndrome | journal = Nature | volume = 444 | issue = 7121 | pages = 881–7 | date = December 2006 | pmid = 17167477 | doi = 10.1038/nature05488 | s2cid = 11944065 | bibcode = 2006Natur.444..881D }}</ref><ref>{{cite journal | title = Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III) | journal = JAMA | volume = 285 | issue = 19 | pages = 2486–97 | date = May 2001 | pmid = 11368702 | doi = 10.1001/jama.285.19.2486 | last1 = Expert Panel On Detection | first1 = Evaluation }}</ref><ref name="Grundy">[http://circ.ahajournals.org/cgi/reprint/109/3/433.pdf Grundy SM, Brewer HB, Cleeman JI, Smith SC, Lenfant D, for the Conference Participants. Definition of metabolic syndrome: report of the National, Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition.] Circulation. 2004;109:433-438.</ref><ref>{{cite web|url=http://www.americanheart.org/presenter.jhtml?identifier=4756 |title=American Heart Association's description of Syndrome X |publisher=Americanheart.org |access-date=2013-01-05}}</ref> It is now generally believed that intra-abdominal fat is the depot that conveys the biggest health risk.<ref name="Poehlman1998" /><ref>{{cite journal | vauthors = Mørkedal B, Romundstad PR, Vatten LJ | title = Informativeness of indices of blood pressure, obesity and serum lipids in relation to ischaemic heart disease mortality: the HUNT-II study | journal = European Journal of Epidemiology | volume = 26 | issue = 6 | pages = 457–61 | date = June 2011 | pmid = 21461943 | pmc = 3115050 | doi = 10.1007/s10654-011-9572-7 }}</ref>

Recent validation has concluded that total and regional body volume estimates correlate positively and significantly with biomarkers of cardiovascular risk and that [[Body Volume Index|BVI]] calculations correlate significantly with all biomarkers of cardiovascular risk.<ref>Romero-Corral, A. Somers, V. Lopez-Jimenez, F. Korenfeld, Y. Palin, S. Boelaert, K. Boarin, S. Sierra-Johnson, J. Rahim, A. (2008) 3-D Body Scanner, Body Volume Index: A Novel, Reproducible and Automated Anthropometric Tool Associated with Cardiometabolic Biomarkers ''Obesity A Research Journal'' 16 (1) 266-P</ref>

=== Diabetes ===
There are numerous theories as to the exact cause and mechanism in [[Diabetes Mellitus Type 2|type 2 diabetes]]. Central obesity is known to predispose individuals for insulin resistance. Abdominal fat is especially active hormonally, secreting a group of hormones called [[adipokine]]s that may possibly [[Impaired glucose tolerance|impair glucose tolerance]]. But [[adiponectin]], an anti-inflammatory adipokine, which is found in lower concentration in obese and diabetic individuals has shown to be beneficial and protective in type 2 diabetes mellitus (T2DM).<ref>{{cite journal | vauthors = Ghoshal K, Bhattacharyya M | title = Adiponectin: Probe of the molecular paradigm associating diabetes and obesity | journal = World Journal of Diabetes | volume = 6 | issue = 1 | pages = 151–66 | date = February 2015 | pmid = 25685286 | pmc = 4317307 | doi = 10.4239/wjd.v6.i1.151 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Darabi H, Raeisi A, Kalantarhormozi MR, Ostovar A, Assadi M, Asadipooya K, Vahdat K, Dobaradaran S, Nabipour I | display-authors = 6 | title = Adiponectin as a Protective Factor Against the Progression Toward Type 2 Diabetes Mellitus in Postmenopausal Women | journal = Medicine | volume = 94 | issue = 33 | pages = e1347 | date = August 2015 | pmid = 26287420 | pmc = 4616451 | doi = 10.1097/md.0000000000001347 }}</ref>

[[Insulin resistance]] is a major feature of diabetes mellitus type 2, and central obesity is correlated with both insulin resistance and T2DM itself.<ref>{{cite journal |vauthors=Duman BS, Turkoglu C, Gunay D, Cagatay P, Demiroglu C, Buyukdevrim AS | year = 2003 | title = The interrelationship between insulin secretion and action in type 2 diabetes mellitus with different degrees of obesity: evidence supporting central obesity | journal = Diabetes Butr Metab | volume = 16 | issue = 4| pages = 243–250 }}</ref><ref>{{cite journal | vauthors = Gabriely I, Ma XH, Yang XM, Atzmon G, Rajala MW, Berg AH, Scherer P, Rossetti L, Barzilai N | display-authors = 6 | title = Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process? | journal = Diabetes | volume = 51 | issue = 10 | pages = 2951–8 | date = October 2002 | pmid = 12351432 | doi = 10.2337/diabetes.51.10.2951 | doi-access = free }}</ref>  Increased [[adiposity]] (obesity) raises serum [[resistin]] levels,<ref name=Asensio2004>{{cite journal | vauthors = Asensio C, Cettour-Rose P, Theander-Carrillo C, Rohner-Jeanrenaud F, Muzzin P | title = Changes in glycemia by leptin administration or high- fat feeding in rodent models of obesity/type 2 diabetes suggest a link between resistin expression and control of glucose homeostasis | journal = Endocrinology | volume = 145 | issue = 5 | pages = 2206–13 | date = May 2004 | pmid = 14962997 | doi = 10.1210/en.2003-1679 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Degawa-Yamauchi M, Bovenkerk JE, Juliar BE, Watson W, Kerr K, Jones R, Zhu Q, Considine RV | display-authors = 6 | title = Serum resistin (FIZZ3) protein is increased in obese humans | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 88 | issue = 11 | pages = 5452–5 | date = November 2003 | pmid = 14602788 | doi = 10.1210/jc.2002-021808 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Lee JH, Bullen JW, Stoyneva VL, Mantzoros CS | title = Circulating resistin in lean, obese, and insulin-resistant mouse models: lack of association with insulinemia and glycemia | journal = American Journal of Physiology. Endocrinology and Metabolism | volume = 288 | issue = 3 | pages = E625-32 | date = March 2005 | pmid = 15522996 | doi = 10.1152/ajpendo.00184.2004 | s2cid = 20609673 }}</ref><ref>{{cite journal | vauthors = Vendrell J, Broch M, Vilarrasa N, Molina A, Gómez JM, Gutiérrez C, Simón I, Soler J, Richart C | display-authors = 6 | title = Resistin, adiponectin, ghrelin, leptin, and proinflammatory cytokines: relationships in obesity | journal = Obesity Research | volume = 12 | issue = 6 | pages = 962–71 | date = June 2004 | pmid = 15229336 | doi = 10.1038/oby.2004.118 | doi-access = free }}</ref> which in turn directly correlate to insulin resistance.<ref>{{cite journal | vauthors = Hirosumi J, Tuncman G, Chang L, Görgün CZ, Uysal KT, Maeda K, Karin M, Hotamisligil GS | display-authors = 6 | title = A central role for JNK in obesity and insulin resistance | journal = Nature | volume = 420 | issue = 6913 | pages = 333–6 | date = November 2002 | pmid = 12447443 | doi = 10.1038/nature01137 | url = http://www.hsph.harvard.edu/GSH-LAB/tnf-ins.html | s2cid = 1659156 | bibcode = 2002Natur.420..333H }}</ref><ref>{{cite journal | vauthors = Rajala MW, Qi Y, Patel HR, Takahashi N, Banerjee R, Pajvani UB, Sinha MK, Gingerich RL, Scherer PE, Ahima RS | display-authors = 6 | title = Regulation of resistin expression and circulating levels in obesity, diabetes, and fasting | journal = Diabetes | volume = 53 | issue = 7 | pages = 1671–9 | date = July 2004 | pmid = 15220189 | doi = 10.2337/diabetes.53.7.1671 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Silha JV, Krsek M, Skrha JV, Sucharda P, Nyomba BL, Murphy LJ | title = Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance | journal = European Journal of Endocrinology | volume = 149 | issue = 4 | pages = 331–5 | date = October 2003 | pmid = 14514348 | doi = 10.1530/eje.0.1490331 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Smith SR, Bai F, Charbonneau C, Janderová L, Argyropoulos G | title = A promoter genotype and oxidative stress potentially link resistin to human insulin resistance | journal = Diabetes | volume = 52 | issue = 7 | pages = 1611–8 | date = July 2003 | pmid = 12829623 | doi = 10.2337/diabetes.52.7.1611 | doi-access = free }}</ref> Studies have also confirmed a direct correlation between resistin levels and T2DM.<ref name=Asensio2004/><ref>{{cite journal | vauthors = Fujinami A, Obayashi H, Ohta K, Ichimura T, Nishimura M, Matsui H, Kawahara Y, Yamazaki M, Ogata M, Hasegawa G, Nakamura N, Yoshikawa T, Nakano K, Ohta M | display-authors = 6 | title = Enzyme-linked immunosorbent assay for circulating human resistin: resistin concentrations in normal subjects and patients with type 2 diabetes | journal = Clinica Chimica Acta; International Journal of Clinical Chemistry | volume = 339 | issue = 1–2 | pages = 57–63 | date = January 2004 | pmid = 14687894 | doi = 10.1016/j.cccn.2003.09.009 }}</ref><ref>{{cite journal | vauthors = McTernan PG, Fisher FM, Valsamakis G, Chetty R, Harte A, McTernan CL, Clark PM, Smith SA, Barnett AH, Kumar S | display-authors = 6 | title = Resistin and type 2 diabetes: regulation of resistin expression by insulin and rosiglitazone and the effects of recombinant resistin on lipid and glucose metabolism in human differentiated adipocytes | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 88 | issue = 12 | pages = 6098–106 | date = December 2003 | pmid = 14671216 | doi = 10.1210/jc.2003-030898 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, Patel HR, Ahima RS, Lazar MA | display-authors = 6 | title = The hormone resistin links obesity to diabetes | journal = Nature | volume = 409 | issue = 6818 | pages = 307–12 | date = January 2001 | pmid = 11201732 | doi = 10.1038/35053000 | s2cid = 4358808 | bibcode = 2001Natur.409..307S }}</ref>  And it is waistline adipose tissue (central obesity) which seems to be the foremost type of fat deposits contributing to rising levels of serum resistin.<ref>{{cite journal | vauthors = LiPuma JJ, Spilker T, Coenye T, Gonzalez CF | title = An epidemic Burkholderia cepacia complex strain identified in soil | journal = Lancet | volume = 359 | issue = 9322 | pages = 2002–3 | date = June 2002 | pmid = 12076559 | doi = 10.1016/S0140-6736(02)08836-0 | s2cid = 8649208 | url = https://biblio.ugent.be/publication/162874/file/8172364 }}</ref><ref>{{cite journal | vauthors = McTernan PG, McTernan CL, Chetty R, Jenner K, Fisher FM, Lauer MN, Crocker J, Barnett AH, Kumar S | display-authors = 6 | title = Increased resistin gene and protein expression in human abdominal adipose tissue | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 87 | issue = 5 | pages = 2407 | date = May 2002 | pmid = 11994397 | doi = 10.1210/jc.87.5.2407 | doi-access = free }}</ref> Conversely, serum resistin levels have been found to ''decline'' with decreased adiposity following medical treatment.<ref>{{cite journal | vauthors = Valsamakis G, McTernan PG, Chetty R, Al Daghri N, Field A, Hanif W, Barnett AH, Kumar S | display-authors = 6 | title = Modest weight loss and reduction in waist circumference after medical treatment are associated with favorable changes in serum adipocytokines | journal = Metabolism | volume = 53 | issue = 4 | pages = 430–4 | date = April 2004 | pmid = 15045687 | doi = 10.1016/j.metabol.2003.11.022 }}</ref>

=== Asthma ===

Developing asthma due to abdominal obesity is also a main concern. As a result of breathing at low lung volume, the muscles are tighter and the airway is narrower.  Obesity causes decreased [[tidal volume]]s due to a reduction in chest expansion that is caused both by the weight on the chest itself and the effect of abdominal obesity on flattening the diaphragm.<ref>{{cite journal | vauthors = Mohanan S, Tapp H, McWilliams A, Dulin M | title = Obesity and asthma: pathophysiology and implications for diagnosis and management in primary care | journal = Experimental Biology and Medicine | volume = 239 | issue = 11 | pages = 1531–40 | date = November 2014 | pmid = 24719380 | pmc = 4230977 | doi = 10.1177/1535370214525302 }}</ref> It is commonly seen that people who are obese breathe quickly and often, while inhaling small volumes of air.<ref>{{cite journal | vauthors = Shore SA, Johnston RA | title = Obesity and asthma | journal = Pharmacology & Therapeutics | volume = 110 | issue = 1 | pages = 83–102 | date = April 2006 | pmid = 16297979 | doi = 10.1016/j.pharmthera.2005.10.002 }}</ref> People with obesity are also more likely to be hospitalized for asthma. A study has stated that 75% of patients treated for asthma in the emergency room were either overweight or obese.<ref>{{cite journal | vauthors = Thomson CC, Clark S, Camargo CA | title = Body mass index and asthma severity among adults presenting to the emergency department | journal = Chest | volume = 124 | issue = 3 | pages = 795–802 | date = September 2003 | pmid = 12970000 | doi = 10.1378/chest.124.3.795 | s2cid = 13138899 }}</ref>

=== Alzheimer's disease ===
Based on studies, it is evident that obesity has a strong association with vascular and metabolic disease which could potentially be linked to Alzheimer's disease. Recent studies have also shown an association between mid-life obesity and dementia, but the relationship between later life obesity and dementia is less clear.<ref name="Razay2006">{{cite journal | vauthors = Razay G, Vreugdenhil A, Wilcock G | title = Obesity, abdominal obesity and Alzheimer disease | journal = Dementia and Geriatric Cognitive Disorders | volume = 22 | issue = 2 | pages = 173–6 | year = 2006 | pmid = 16847377 | doi = 10.1159/000094586 | s2cid = 24351283 }}</ref> A study by Debette et al. (2010) examining over 700 adults found evidence to suggest higher volumes of visceral fat, regardless of overall weight, were associated with smaller brain volumes and increased risk of [[dementia]].<ref>{{cite journal | vauthors = Debette S, [[Alexa Beiser|Beiser A]], Hoffmann U, Decarli C, O'Donnell CJ, Massaro JM, Au R, Himali JJ, Wolf PA, Fox CS, Seshadri S | display-authors = 6 | title = Visceral fat is associated with lower brain volume in healthy middle-aged adults | journal = Annals of Neurology | volume = 68 | issue = 2 | pages = 136–44 | date = August 2010 | pmid = 20695006 | pmc = 2933649 | doi = 10.1002/ana.22062 }}</ref><ref>{{cite news |url=http://news.bbc.co.uk/2/hi/health/8693947.stm |publisher=BBC News |title='Beer belly' link to Alzheimer's |date=2010-05-20 }}</ref><ref>{{cite web | vauthors = Mitchell S |url=http://www.nbcnews.com/id/23800703 |archive-url=https://web.archive.org/web/20150318143512/http://www.nbcnews.com/id/23800703/ |url-status=dead |archive-date=18 March 2015 |title=Bulging belly now could mean dementia later |publisher=NBC News |date=2008-03-26 |access-date=2013-01-05}}</ref> Alzheimer's disease and abdominal obesity has a strong correlation and with metabolic factors added in, the risk of developing Alzheimer's disease was even higher. Based on logistic regression analyses, it was found that obesity was associated with an almost 10-fold increase risk of Alzheimer's disease.<ref name="Razay2006" />

===Other health risks===

Central obesity can be a feature of [[lipodystrophy|lipodystrophies]], a group of diseases that is either [[genetic disorder|inherited]], or due to secondary causes (often [[protease inhibitor (pharmacology)|protease inhibitor]]s, a group of [[medication]]s against [[AIDS]]). Central obesity is a symptom of [[Cushing's syndrome]]<ref name="Does central obesity reflect Cushi">{{cite journal | vauthors = Bujalska IJ, Kumar S, Stewart PM | title = Does central obesity reflect "Cushing's disease of the omentum"? | journal = Lancet | volume = 349 | issue = 9060 | pages = 1210–3 | date = April 1997 | pmid = 9130942 | doi = 10.1016/S0140-6736(96)11222-8 | s2cid = 24643796 }}</ref> and is also common in patients with [[polycystic ovary syndrome]] (PCOS). Central obesity is associated with [[glucose intolerance]] and [[dyslipidemia]]. Once dyslipidemia becomes a severe problem, an individual's abdominal cavity would generate elevated free fatty acid flux to the liver. The effect of abdominal adiposity occurs not just in those who are obese, but also affects people who are non-obese and it also contributes to insulin sensitivity.<ref>{{Cite journal |last1=Lukács |first1=Anita |last2=Horváth |first2=Edina |last3=Máté |first3=Zsuzsanna |last4=Szabó |first4=Andrea |last5=Virág |first5=Katalin |last6=Papp |first6=Magor |last7=Sándor |first7=János |last8=Ádány |first8=Róza |last9=Paulik |first9=Edit |date=2019-11-15 |title=Abdominal obesity increases metabolic risk factors in non-obese adults: a Hungarian cross-sectional study |journal=BMC Public Health |volume=19 |issue=1 |pages=1533 |doi=10.1186/s12889-019-7839-1 |issn=1471-2458 |pmc=6858760 |pmid=31730482 |doi-access=free }}</ref>

Ghroubi et al. (2007) examined whether abdominal circumference is a more reliable indicator than [[Body mass index|BMI]] or the presence of [[knee osteoarthritis]] in obese patients.<ref name="Ghroubi2007">{{cite journal | vauthors = Ghroubi S, Elleuch H, Guermazi M, Kaffel N, Feki H, Abid M, Baklouti S, Elleuch MH | display-authors = 6 | title = [Abdominal obesity and knee ostheoarthritis] | journal = Annales de Réadaptation et de Médecine Physique | volume = 50 | issue = 8 | pages = 661–6 | date = November 2007 | pmid = 17445932 | doi = 10.1016/j.annrmp.2007.03.005 }}</ref> They found that it actually appears to be a factor linked with the presence of knee pain as well as osteoarthritis in obese study subjects. Ghroubi et al. (2007) concluded that a high abdominal circumference is associated with great functional repercussion.<ref name="Ghroubi2007"/>

Research published in [[The Lancet]] (2023) found that high levels of visceral fat were related to poorer cognitive performance. The findings suggest that maintaining a healthy weight and metabolic health may be important for preserving cognitive function.<ref>{{Cite web |last=Dolan |first=Eric W. |date=2023-06-04 |title=New research indicates visceral fat has a profoundly negative effect on cognitive abilities |url=https://www.psypost.org/2023/06/new-research-indicates-visceral-fat-has-a-profoundly-negative-effect-on-cognitive-abilities-164382 |access-date=2023-06-04 |website=PsyPost |language=en-US}}</ref>