|beer belly, beer gut, pot belly, spare tyre|
A centrally obese male. Weight 182 kg/400 lbs, height 185 cm/6 ft 1 in. The body mass index is 53.
|Classification and external resources|
Abdominal obesity, also known as central obesity, is when excessive abdominal fat around the stomach and abdomen has built up to the extent that it is likely to have a negative impact on health. There is a strong correlation between central obesity and cardiovascular disease. Abdominal obesity is not confined only to the elderly and obese subjects. Abdominal obesity has been linked to Alzheimer's disease as well as other metabolic and vascular diseases.
Visceral fat, also known as organ fat or intra-abdominal fat, is located inside the peritoneal cavity, packed in between internal organs and torso, as opposed to subcutaneous fat‚ which is found underneath the skin, and intramuscular fat‚ which is found interspersed in skeletal muscle. Visceral fat is composed of several adipose depots including mesenteric, epididymal white adipose tissue (EWAT) and perirenal fat. An excess of visceral fat is known as central obesity, the "pot belly" or "beer belly" effect, in which the abdomen protrudes excessively. This body type is also known as "apple shaped‚" as opposed to "pear shaped‚" in which fat is deposited on the hips and buttocks.
Researchers first started to focus on abdominal obesity in the 1980s when they realized that it had an important connection to cardiovascular disease, diabetes, and dyslipidemia. Abdominal obesity was more closely related with metabolic dysfunctions connected with cardiovascular disease than was general obesity. In the late 1980s and early 1990s insightful and powerful imaging techniques were discovered that would further help advance the understanding of the health risks associated with body fat accumulation. Techniques such as computed tomography and magnetic resonance imaging made it possible to categorize mass of adipose tissue located at the abdominal level into intra-abdominal fat and subcutaneous fat.
- 1 Health risks
- 2 Causes
- 3 Diagnosis
- 4 Prevention and treatments
- 5 Society and culture
- 6 See also
- 7 References
- 8 Further reading
Central obesity is associated with a statistically higher risk of heart disease, hypertension, insulin resistance, and Diabetes Mellitus Type 2 (see below). With an increase in the waist to hip ratio and overall waist circumference the risk of death increases as well. Metabolic syndrome is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance, full-blown diabetes, and increased risk of developing cardiovascular disease. It is now generally believed that intra-abdominal fat is the depot that conveys the biggest health risk.
Central obesity can be a feature of lipodystrophies, a group of diseases that is either inherited, or due to secondary causes (often protease inhibitors, a group of medications against AIDS). Central obesity is a symptom of Cushing's syndrome 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.
There are numerous theories as to the exact cause and mechanism in 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 adipokines that may possibly impair glucose tolerance. But adiponectin which is found in lower concentration in obese and diabetic individuals has shown to be beneficial and protective in Type 2 diabetes mellitus.
Insulin resistance is a major feature of Diabetes Mellitus Type 2 (T2DM), and central obesity is correlated with both insulin resistance and T2DM itself. Increased adiposity (obesity) raises serum resistin levels, which in turn directly correlate to insulin resistance. Studies have also confirmed a direct correlation between resistin levels and T2DM. 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. Conversely, serum resistin levels have been found to decline with decreased adiposity following medical treatment.
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. It is commonly seen that people who are obese breathe quickly and often, while inhaling small volumes of air. 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.
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. 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. 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.
The currently prevalent belief is that the immediate cause of obesity is net energy imbalance—the organism consumes more usable calories than it expends, wastes‚ or discards through elimination. Some studies indicate that visceral adiposity, together with lipid dysregulation and decreased insulin sensitivity, is related to the excessive consumption of fructose. Greater meat consumption has also been positively associated with greater weight gain, and specifically abdominal obesity, even when accounting for calories. Other environmental factors, such as maternal smoking, estrogenic compounds in the diet‚ and endocrine-disrupting chemicals may be important also. Obesity plays an important role in the impairment of lipid and carbohydrate metabolism shown in high-carbohydrate diets.[unreliable source?] It has also been shown that quality protein intake during a 24-hour period and the number of times the essential amino acid threshold of approximately 10 g has been achieved is inversely related to the percentage of central abdominal fat. Quality protein uptake is defined as the ratio of essential amino acids to daily dietary protein.
Visceral fat cells will release their metabolic by-products in the portal circulation, where the blood leads straight to the liver. Thus, the excess of triglycerides and fatty acids created by the visceral fat cells will go into the liver and accumulate there. In the liver, most of it will be stored as fat. This concept is known as 'lipotoxicity'.
Hypercortisolism, such as in Cushing's syndrome, also leads to central obesity. Many prescription drugs, such as dexamethasone and other steroids, can also have side effects resulting in central obesity, especially in the presence of elevated insulin levels.
The prevalence of abdominal obesity is increasing in western populations, possibly due to a combination of low physical activity and high-calorie diets, and also in developing countries, where it is associated with the urbanization of populations.
Waist measurement is more prone to errors than measuring height and weight. It is recommended to use both standards. BMI will illustrate the best estimate of your total body fatness, while waist measurement gives an estimate of visceral fat and risk of obesity-related disease.
A study has shown that alcohol consumption is directly associated with waist circumference and with a higher risk of abdominal obesity in men, but not in women, in the present population. Excluding energy under-reporters slightly attenuated these associations. After controlling for energy under-reporting, it was observed that increasing alcohol consumption significantly increased the risk of exceeding recommended energy intakes in male participants – but not in the small number of female participants (2.13%) with elevated alcohol consumption, even after establishing a lower number of drinks per day to characterize women as consuming a high quantity of alcohol. Further study is needed to determine whether a significant relationship between alcohol consumption and abdominal obesity exists among women who consume higher amounts of alcohol. 
There are various ways of measuring abdominal obesity including:
- Absolute waist circumference (>102 cm (40 in) in men and >88 cm (35 in) in women)
- Waist–hip ratio (the circumference of the waist divided by that of the hips of >0.9 for men and >0.85 for women)
- Waist-to-height ratio
- Sagittal Abdominal Diameter
In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat. Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.
Men are considered to be at high risk from abdominal obesity if their waist measurements are 102 cm (40 in)or higher, while women are considered to be at high risk if their waist measurements are >88 cm (35 in) or higher. BMI and waist measurements are well recognized ways to characterize obesity. However, waist measurements are not as accurate as BMI measurements. For this reason, it is recommended to use both methods of measurements.
While central obesity can be obvious just by looking at the naked body (see the picture), the severity of central obesity is determined by taking waist and hip measurements. The absolute waist circumference 102 centimetres (40 in) in men and 88 centimetres (35 in) in women) and the waist-hip ratio (>0.9 for men and >0.85 for women) are both used as measures of central obesity. A differential diagnosis includes distinguishing central obesity from ascites and intestinal bloating. In the cohort of 15,000 people participating in the National Health and Nutrition Examination Survey (NHANES III), waist circumference explained obesity-related health risk better than the body mass index (or BMI) when metabolic syndrome was taken as an outcome measure and this difference was statistically significant. In other words, excessive waist circumference appears to be more of a risk factor for metabolic syndrome than BMI. Another measure of central obesity which has shown superiority to BMI in predicting cardiovascular disease risk is the Index of Central Obesity (waist-to-height ratio - WHtR), where a ratio of >=0.5 (i.e. a waist circumference at least half of the individual's height) is predictive of increased risk. Another diagnosis of obesity is the analysis of intra-abdominal fat having the most risk to one's personal health. The increased amount of fat in this region relates to the higher levels of plasma lipid and lipoproteins as per studies mentioned by Eric Poehlman (1998) review. An increasing acceptance of the importance of central obesity within the medical profession as an indicator of health risk has led to new developments in obesity diagnosis such as the Body Volume Index, which measures central obesity by measuring a person's body shape and their weight distribution. 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
Index of central obesity
Index of Central Obesity (ICO) is the ratio of waist circumference and height first proposed by a Parikh et al. in 2007 as a better substitute to the widely used waist circumference in defining metabolic syndrome. The National Cholesterol Education Program Adult Treatment Panel III suggested cut off of 102 cm (40 in) and 88 cm (35 in) for males and females as a marker of central obesity. The same was used in defining metabolic syndrome. Misra et al. suggested that these cutoffs are not applicable among Indians and the cutoffs be lowered to 90 cm (35 in) and 80 cm (31 in) for males and females. Various race specific cutoffs were suggested by different groups. The International Diabetes Federation defined central obesity based on these various race and gender specific cutoffs. The other limitation of waist circumference is that it can not be applied in children.[dubious ]
Parikh et al. looked at the average heights of various races and suggested that by using ICO various race- and gender-specific cutoffs of waist circumference can be discarded. An ICO cutoff of 0.5 was suggested as a criterion to define central obesity. Parikh et al. further tested a modified definition of metabolic syndrome in which waist circumference was replaced with ICO in the National Health and Nutrition Examination Survey (NHANES) database and found the modified definition to be more specific and sensitive.
Body volume index
BVI is based upon the principle that excess abdominal weight, measured by part volume as a percentage of total volume, constitutes a greater health risk. Recent validation has concluded that total and regional body volume estimates correlate positively and significantly with biomarkers of cardiovascular risk and BVI calculations correlate significantly with all biomarkers of cardio-vascular risk.
Ghroubi et al. (2007) examined whether abdominal circumference is a more reliable indicator than BMI of the presence of knee osteoarthritis in obese patients. 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.
Central obesity is positively associated with coronary heart disease risk in women and men. It has been hypothesized that the sex differences in fat distribution may explain the sex difference in coronary heart disease risk.
There are sex-dependent differences in regional fat distribution. In women, estrogen is believed to cause fat to be stored in the buttocks, thighs, and hips. When women reach menopause and the estrogen produced by ovaries declines, fat migrates from their buttocks, hips‚ and thighs to their belly.
Males are more susceptible to upper-body fat accumulation, most likely in the belly, due to sex hormone differences. Abdominal obesity in males is correlated with comparatively low testosterone levels. Testosterone administration significantly increased thigh muscle area, reduced subcutaneous fat deposition at all levels measured, but slightly increased the visceral fat area.
Even with the differences, at any given level of central obesity measured as waist circumference or waists to hip ratio, coronary artery disease rates are identical in men and women.
Prevention and treatments
A permanent routine of exercise, eating healthier‚ and, during periods of overweight, consuming the same number or fewer calories than used will prevent and help fight obesity. A single pound of fat (0.454 kg) yields approximately 3500 calories (14644kJ) of energy, and weight loss is achieved by reducing energy intake. Adjunctive therapies which may be prescribed by a physician are orlistat or sibutramine, although the latter has been associated with increased cardiovascular events and strokes and has been withdrawn from the market in the United States, the UK, the EU, Australia, Canada, Hong Kong, Thailand, Egypt and Mexico.
A 2006 study published in the International Journal of Sport Nutrition and Exercise Metabolism, suggests that combining cardiovascular (aerobic) exercise with resistance training is more effective than cardiovascular training alone in getting rid of abdominal fat. An additional benefit to exercising is that it reduces stress and insulin levels, which reduces the presence of cortisol, a hormone that leads to more belly fat deposits.
Self-motivation by understanding the risks associated with abdominal obesity is widely regarded as being far more important than worries about cosmetics. In addition, understanding the health issues linked with abdominal obesity can help in the self-motivation process of losing the abdominal fat. As mentioned above, abdominal fat is linked with cardiovascular disease, diabetes, and cancer. Specifically it's the deepest layer of belly fat (the fat you cannot see or grab) that poses health risks, as these "visceral" fat cells produce hormones that can affect health (e.g. increased insulin resistance and/or breast cancer risk). The risk increases considering the fact that they are located in the proximity or in between organs in the abdominal cavity. For example, fat next to the liver drains into it, causing a fatty liver, which is a risk factor for insulin resistance, setting the stage for Type 2 diabetes.
In the presence of diabetes mellitus type 2, the physician might instead prescribe metformin and thiazolidinediones (rosiglitazone or pioglitazone) as antidiabetic drugs rather than sulfonylurea derivatives. Thiazolidinediones may cause slight weight gain but decrease "pathologic" abdominal fat (visceral fat), and therefore may be prescribed for diabetics with central obesity. Thiazolidinedione has been associated with heart failure and increased cardiovascular risk; so it has been withdrawn from the market in Europe by EMA in 2010.
Low-fat diets may not be an effective long-term intervention for obesity: as Bacon and Aphramor wrote, "The majority of individuals regain virtually all of the weight that was lost during treatment." The Women's Health Initiative ("the largest and longest randomized, controlled dietary intervention clinical trial") found that long-term dietary intervention increased the waist circumference of both the intervention group and the control group, though the increase was smaller for the intervention group. The conclusion was that mean weight decreased significantly in the intervention group from baseline to year 1 by 2.2 kg (P<.001) and was 2.2 kg less than the control group change from baseline at year 1. This difference from baseline between control and intervention groups diminished over time, but a significant difference in weight was maintained through year 9, the end of the study.
Society and culture
There is a common misconception that spot exercise (that is, exercising a specific muscle or location of the body) most effectively burns fat at the desired location, but this is not the case. Spot exercise is beneficial for building specific muscles, but it has little effect, if any, on fat in that area of the body, or on the body's distribution of body fat. The same logic applies to sit-ups and belly fat. Sit-ups, crunches and other abdominal exercises are useful in building the abdominal muscles, but they have little effect, if any, on the adipose tissue located there.
Several colloquial terms used to refer to central obesity, and to people who have it, refer to beer drinking. However, there is little scientific evidence that beer drinkers are more prone to central obesity, despite its being known colloquially as "beer belly‚" "beer gut‚" or "beer pot". One of the few studies conducted on the subject did not find that beer drinkers are more prone to central obesity than nondrinkers or drinkers of wine or spirits. Chronic alcoholism can lead to cirrhosis, symptoms of which include gynecomastia (enlarged breasts) and ascites (abdominal fluid). These symptoms can suggest the appearance of central obesity.
Deposits of excess fat at the sides of one's waistline are commonly referred to as "love handles."
Researchers in Copenhagen examined the relationship between waist circumferences and costs among 31,840 subjects aged 50–64 years of age with different waist circumferences. Their study showed that an increase in just an additional centimetre above normal waistline caused a 1.25% and 2.08% rise in health care costs in women and men respectively. To put this in perspective, a woman with a waistline of 95 cm. and without underlying health problems or co-morbidities can incur economic costs that are 22%, of 397 USD, higher per year than a woman with a normal waist circumference.
- Bariatrics, the branch of medicine that deals with the causes, prevention, and treatment of obesity
- Lipoatrophy, the term describing the localized loss of fat tissue
- Lipodystrophy, a medical condition characterized by abnormal or degenerative conditions of the body's adipose tissue.
- Sagittal Abdominal Diameter (SAD), a measure of visceral obesity
- Steatosis, also called fatty change, fatty degeneration or adipose degeneration
- 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. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study". Lancet. 364 (9438): 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185.
- Carey D.G.P. (1998). Abdominal Obesity. Current Opinion in Lipidology. (pp. 35-40). Vol. 9, No 1. Retrieved on April 9, 2012.
- Razay, G.; Vreugdenhil, A.; Wilcock, G. (2006). "Obesity, abdominal obesity and Alzheimer disease". Dementia and Geriatric Cognitive Disorders. 22 (2): 173–176. doi:10.1159/000094586. PMID 16847377.
- Anjana, M.; Sandeep, S.; Deepa, R.; Vimaleswaran, K. S.; Farooq, S.; Mohan, V. (2004). "Visceral and Central Abdominal Fat and Anthropometry in Relation to Diabetes in Asian Indians". Diabetes Care. 27 (12): 2948–53. doi:10.2337/diacare.27.12.2948. PMID 15562212.
- Poehlman, Eric T. (1998). "Abdominal Obesity: The Metabolic Multi-risk Factor". Coronary Heart Disease. Exp. 9 (8): 469–471. doi:10.1097/00019501-199809080-00001.
- Westphal, S. A. (2008). "Obesity, Abdominal Obesity, and Insulin Resistance". Clinical Cornerstone. 9 (1): 23–29; discussion 30–1. doi:10.1016/S1098-3597(08)60025-3. PMID 19046737.
- Cameron, A. J.; Zimmet, P. Z. (2008). "Expanding evidence for the multiple dangers of epidemic abdominal obesity". Circulation. International Diabetes Institute. 117 (13): 1624–1626. doi:10.1161/CIRCULATIONAHA.108.775080.
- Després, Jean-Pierre; Lemieux, Isabelle (2006). "Abdominal Obesity and Metabolic Syndrome". Nature. 444 (7121): 881–887. doi:10.1038/nature05488.
- Expert Panel On Detection, Evaluation (2001). "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)". JAMA: the Journal of the American Medical Association. 285 (19): 2486–97. doi:10.1001/jama.285.19.2486. PMID 11368702.
- 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.
- "American Heart Association's description of Syndrome X". Americanheart.org. Retrieved 2013-01-05.
- Morkedal B, Romundstad PR, Vatten LJ (June 2011). "Informativeness of indices of blood pressure, obesity and serum lipids in relation to ischaemic heart disease mortality: the HUNT-II study". European Journal of Epidemiology. 26 (6): 457–61. doi:10.1007/s10654-011-9572-7. PMC . PMID 21461943.
- Bujalska IJ, Kumar S, Stewart PM (1997). "Does central obesity reflect "Cushing's disease of the omentum"?". Lancet. 349 (9060): 1210–3. doi:10.1016/S0140-6736(96)11222-8. PMID 9130942.
- Ghoshal, Kakali (2015). "Adiponectin: Probe of the molecular paradigm associating diabetes and obesity". World Journal of Diabetes. 6 (1): 151–66. doi:10.4239/wjd.v6.i1.151. PMC . PMID 25685286.
- Darabi, Hossein; Raeisi, Alireza; Kalantarhormozi, Mohammad Reza; Ostovar, Afshin; Assadi, Majid; Asadipooya, Kamyar; Vahdat, Katayoun; Dobaradaran, Sina; Nabipour, Iraj (2015). "Adiponectin as a Protective Factor Against the Progression Toward Type 2 Diabetes Mellitus in Postmenopausal Women". Medicine. 94 (33): e1347. doi:10.1097/md.0000000000001347. PMC . PMID 26287420.
- Duman BS, Turkoglu C, Gunay D, Cagatay P, Demiroglu C, Buyukdevrim AS (2003). "The interrelationship between insulin secretion and action in type 2 diabetes mellitus with different degrees of obesity: evidence supporting central obesity". Diabetes Butr Metab. 16 (4): 243–250.
- Gabriely I.; Ma X. H.; Yang X. M.; Atzmon G; Rajala MW; Berg AH; Sherer P; Rossetti L; Barzilai N. (October 2002). "Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process?". Diabetes. 51 (2951–2958): 2951–8. doi:10.2337/diabetes.51.10.2951. PMID 12351432.
- Asensio C.; Cettour-Rose P.; Theander-Carrillo C.; Rohner-Jeanrenaud F.; Muzzin P. (May 2004). "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". Endocrinology. 145 (2206–2213): 2206–13. doi:10.1210/en.2003-1679. PMID 14962997.
- Degawa-Yamauchi MBJE; Juliar BE; Watson W; Kerr K; Jones RM; Zhu Q; Considine RV (2003). "Serum resistin (FIZZ3) protein is increased in obese humans". Journal of Clinical Endocrinology and Metabolism. 88 (11): 5452–5455. doi:10.1210/jc.2002-021808. PMID 14602788.
- Lee J. H.; Bullen Jr J. W.; Stoyneva V. L.; Mantzoros C. S. (2005). "Circulating resistin in lean, obese and insulin-resistant mouse models: lack of association with insulinemia and glycemia". Am. J. Physiol. Endocrinol. Metab. 288 (3): E625–E632. doi:10.1152/ajpendo.00184.2004. PMID 15522996.
- Vendrell J, Broch M, Vilarrasa N, Molina A, Gomez JM, Gutierrez C, Simon I, Soler J, Richart C (2004). "Resistin, adiponectin, ghrelin, leptin, and proinflammatory cytokines: relationships in obesity". Obesity Research. 12 (6): 962–971. doi:10.1038/oby.2004.118. PMID 15229336.
- Hirosumi J, Tuncman G, Chang L, Gorgun CZ, Uysal KT, Maeda K, Karin M, Hotamisligil GS (2002). "A central role for JNK in obesity and insulin resistance". Nature. 420 (6913): 333–336. doi:10.1038/nature01137. PMID 12447443.
- Rajala M. W.; Qi Y.; Patel H. R.; Takahashi N; Banerjee R; Pajvani UB; Sinha MK; Gingerich RL; Scherer PE; et al. (July 2004). "Regulation of resistin expression and circulating levels in obesity, diabetes, and fasting". Diabetes. 53 (1671–1679): 1671–9. doi:10.2337/diabetes.53.7.1671. PMID 15220189.
- Silha JV, Krsek M, Skrha JV, Sucharda P, Nyomba BL, Murphy LJ (2003). "Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance". Eur. J. Endocrinol. 149 (4): 331–335. doi:10.1530/eje.0.1490331. PMID 14514348.
- Smith S. R.; Bai F.; Charbonneau C.; Janderova L.; Argyropoulos G. (July 2003). "A promoter genotype and oxidative stress potentially link resistin to human insulin resistance". Diabetes. 52 (1611–1618): 1611–8. doi:10.2337/diabetes.52.7.1611. PMID 12829623.
- Fujinami A.; Obayashi H.; Ohta K; Ichimura T; Nishimura M; Matsui H; Kawahara Y; Yamazaki M; Ogata M; et al. (January 2004). "Enzyme-linked immunosorbent assay for circulating human resistin: resistin concentrations in normal subjects and patients with type 2 diabetes". Clin. Chim. Acta. 339 (57–63): 57–63. doi:10.1016/j.cccn.2003.09.009. PMID 14687894.
- McTernan P. G.; Fisher F. M.; Valsamakis G; Chetty R; Harte A; McTernan CL; Clark PM; Smith SA; Barnett AH; et al. (December 2003). "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". J. Clin. Endocrinol. Metab. 88 (6098–6106): 6098–106. doi:10.1210/jc.2003-030898. PMID 14671216.
- Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, Patel HR, Ahima RS, Lazar MA, et al. (2001). "The hormone resistin links obesity to diabetes". Nature. 409 (6818): 307–312. doi:10.1038/35053000. PMID 11201732.
- McTernan C. L.; McTernan P. G.; Harte A. L.; Levick P. L.; Barnett A. H.; Kumar S. (2002). "Resistin, central obesity, and type 2 diabetes". Lancet. 359 (46–47): 2002–2003. doi:10.1016/S0140-6736(02)08836-0.
- McTernan P. G.; McTernan C. L.; Chetty R; Jenner K; Fisher FM; Lauer MN; Crocker J; Barnett AH; Kumar S. (2002). "Increased resistin gene and protein expression in human abdominal adipose tissue". J. Clin. Endocrinol. Metab. 87 (5): 2407. doi:10.1210/jc.87.5.2407.
- Valsamakis G.; McTernan P. G.; Chetty R; Al Daghri N; Field A; Hanif W; Barnett AH; Kumar S. (2004). "Modest weight loss and reduction in waist circumference after medical treatment are associated with favourable changes in serum adipocytokines". Metab. Clin. Exp. 53 (4): 430–434. doi:10.1016/j.metabol.2003.11.022. PMID 15045687.
- Shore, S.; Johnston, R. (2006). "Obesity and asthma". Pharmacology & Therapeutics. 110 (1): 83–102. doi:10.1016/j.pharmthera.2005.10.002.
- Thomson, Carey C.; Clark, Sunday; Camargo, Carlos A., Jr. (2003). "Body Mass Index and Asthma Severity Among Adults Presenting to the Emergency Department". Chest. 124 (3): 795–802. doi:10.1378/chest.124.3.795.
- Debette, Stéphanie; Beiser, Alexa; Hoffmann, Udo; et al. (2010). "Visceral fat is associated with lower brain volume in healthy middle-aged adults". Annals of Neurology. 68 (2): 136–144. doi:10.1002/ana.22062.
- "'Beer belly' link to Alzheimer's". BBC News. 2010-05-20.
- Mitchell, Steve (2008-03-26). "Bulging belly now could mean dementia later". NBC News. Retrieved 2013-01-05.
- Stanhope, Kimber L.; Havel, Peter J. (March 2010). "Fructose consumption: Recent results and their potential implications". Annals of the New York Academy of Sciences. 1190: 15–24. doi:10.1111/j.1749-6632.2009.05266.x. PMC . PMID 20388133.
- Elliott, Sharon; Keim, Nancy L.; Stern, Judith S.; Teff, Karen; Havel, Peter J. (November 2002). "Fructose, weight gain, and the insulin resistance syndrome". American Journal of Clinical Nutrition. 76 (5): 911–922. PMID 12399260.
- Perez-Pozo, SE; et al. (22 December 2009). "Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response" (PDF). International Journal of Obesity. 34 (3): 454–461. doi:10.1038/ijo.2009.259. PMID 20029377.
- Choi, Mary (March 2009). "The Not-so-Sweet Side of Fructose". JASN. 3. 20 (3): 457–459. doi:10.1681/asn.2009010104. PMID 19244571.
- Vergnaud, Anne-Claire; Norat, Teresa; Romaguera, Dora; Mouw, Traci; May, Anne M.; Travier, Noemie; Luan, Jian'an; Wareham, Nick; Slimani, Nadia (2010-08-01). "Meat consumption and prospective weight change in participants of the EPIC-PANACEA study". The American Journal of Clinical Nutrition. 92 (2): 398–407. doi:10.3945/ajcn.2009.28713. ISSN 1938-3207. PMID 20592131.
- Vergnaud, Anne-Claire; Norat, Teresa; Romaguera, Dora; Peeters, Petra HM (2010-11-01). "Reply to A Astrup et al". The American Journal of Clinical Nutrition. 92 (5): 1275–1276. doi:10.3945/ajcn.110.000786. ISSN 0002-9165.
- Heindel, Jerrold (2011). "The Obesogen Hypothesis of Obesity: Overview and Human Evidence". Endocrine updates. 4. 30: 355–365. doi:10.1007/978-1-4419-7034-3_17. ISBN 978-1-4419-7033-6.
- Ibrahim, Islam Ahmed Abd El-Hamid (2011). "Is the effect of high fat diet on lipid and carbohydrate metabolism related to inflammation?". Mediterranean Journal of Nutrition and Metabolism. 4 (3): 203–209. doi:10.1007/s12349-011-0056-9.
- Cuthbertson, Daniel; Smith, Kenneth; Babraj, John; Leese, Graham; Waddell, Tom; Atherton, Philip; Wackerhage, Henning; Taylor, Peter M.; Rennie, Michael J. (March 2005). "Anabolic deficits underlie amino acid resistance of wasting, aging muscle". The FASEB Journal. 19 (3): 422–424. doi:10.1096/fj.04-2640fje.
- Loenneke, Jeremy; Wilson, Jacob M.; Manninen, Anssi H.; Wray, Mandy E.; Barnes, Jeremy T.; Pujol, Thomas J. (January 2012). "Quality protein intake is inversely related with abdominal fat". Nutrition & Metabolism. 9 (1).
- President and fellows of Harvard College. (2006). Abnormal obesity and your health. Retrieved from http://www.health.harvard.edu/fhg/updates/abdominal-obesity-and-your-health.shtml
- Bujalska, Iwona; et al. (26 April 1997). "Does central obesity reflect "Cushing's disease of the omentum"?". The Lancet. 349 (9060,): 1210–1213. doi:10.1016/S0140-6736(96)11222-8. PMID 9130942.
- Després, J. (2006). "Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic risk". European Heart Journal. 8 (Supplements): B4–B12. doi:10.1093/eurheartj/sul002.
- Abdominal obesity and your health. (2006). Retrieved from http://www.health.harvard.edu/fhg/updates/abdominal-obesity-and-your-health.shtml
- H. Schroder; et al. (2007). "Relationship of abdominal obesity with alcohol consumption". European Journal of Nutrition. 46 (7): 369–376. doi:10.1007/s00394-007-0674-7. PMID 17885722.
- National Cholesterol Education Program (2002). Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III Final Report). National Institutes of Health. p. II–17.
- 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. (2004). "Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): Case-control study". Lancet. 364 (9438): 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185.
- Parikh, Rakesh M; Menon, Padmavathy S; Shah, Nalini S; Shah, N (2007). "Index of central obesity – A novel parameter". Medical Hypotheses. 68 (6): 1272–5. doi:10.1016/j.mehy.2006.10.038. PMID 17156939.
- Iribarren, Carlos; Darbinian, Jeanne A.; Lo, Joan C.; Fireman, Bruce H.; Go, Alan S. (2006). "Value of the Sagittal Abdominal Diameter in Coronary Heart Disease Risk Assessment: Cohort Study in a Large, Multiethnic Population". American Journal of Epidemiology. 164 (12): 1150–9. doi:10.1093/aje/kwj341. PMID 17041127.
- U.S. Preventive Services Task Force Evidence Syntheses (2000). HSTAT: Guide to Clinical Preventive Services, 3rd Edition: Recommendations and Systematic Evidence Reviews, Guide to Community Preventive Services.
- "Abdominal obesity and your health". Health.harvard.edu. Retrieved 2013-01-05.
- Smith, Sidney C.; Haslam, David (2007). "Abdominal obesity, waist circumference and cardiometabolic risk: awareness among primary care physicians, the general population and patients at risk – the Shape of the Nations survey". Current Medical Research and Opinion. 23 (1): 379–84. doi:10.1185/030079906X159489. PMID 17261236.
- Knowles, K. M.; Paiva, L. L.; Sanchez, S. E.; Revilla, L.; Lopez, T.; Yasuda, M. B.; Yanez, N. D.; Gelaye, B.; Williams, M. A. (2011). "Waist Circumference, Body Mass Index, and Other Measures of Adiposity in Predicting Cardiovascular Disease Risk Factors among Peruvian Adults". International Journal of Hypertension. 2011: 1–10. doi:10.4061/2011/931402.
- Méthot, Julie; Houle, Julie; Poirier, Paul (2010). "Obesity: how to define central adiposity?". Expert Review of Cardiovascular Therapy. 8 (5): 639–44. doi:10.1586/erc.10.38. PMID 20450297.
- Parikh, Rakesh M.; Joshi, Shashank R.; Pandia, Kirti (2009). "Index of Central Obesity Is Better Than Waist Circumference in Defining Metabolic Syndrome". Metabolic Syndrome and Related Disorders. 7 (6): 525–8. doi:10.1089/met.2008.0102. PMID 19558273.
- National Cholesterol Education Program (2002). Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III Final Report). National Institutes of Health. p. II–27.
- Misra, Anoop; Wasir, Jasjeet S.; Vikram, Naval K.; Pandey, Ravindra M.; Kumar, Pawan (2010). "Cutoffs of Abdominal Adipose Tissue Compartments as Measured by Magnetic Resonance Imaging for Detection of Cardiovascular Risk Factors in Apparently Healthy Adult Asian Indians in North India". Metabolic Syndrome and Related Disorders. 8 (3): 243–7. doi:10.1089/met.2009.0046. PMID 20156066.
- Alberti KG, Zimmet P, Shaw J, IDF Epidemiology Task Force Consensus Group (2005). "The metabolic syndrome—a new worldwide definition". Lancet. 366 (9491): 1059–1062. doi:10.1016/S0140-6736(05)67402-8. PMID 16182882.
- Joshi, P. P. (2008). "Is Waist to Height Ratio a Better and More Practical Measure of Obesity to Assess Cardiovascular or Diabetes risk in Indians?". Journal of Association of Physicians of India. 56: 202–3; author reply 203–4. PMID 18700281.
- Veigas, Nina Maria; Dharmalingam, Mala; Marcus, Sara Rani (2011). "Oxidative Stress in Obesity and Metabolic Syndrome in Asian Indians". Journal of Medical Biochemistry. 30 (2): 115–20. doi:10.2478/v10011-011-0006-6.
- Gupta, R; Rastogi, Priyanka; Sarna, M; Gupta, VP; Sharma, SK; Kothari, K (2007). "Body-Mass Index, Waist-Size, Waist-Hip Ratio and Cardiovascular Risk Factors in Urban Subejcts". Journal of Association of Physicians of India. 55: 621–7. PMID 18051732.
- 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
- Ghroubi, S.; Elleuch, H.; Guermazi, M.; Kaffel, N.; Feki, H.; Abid, M.; Baklouti, S.; Elleuch, M. H. (2007). "Abdominal obesity and knee ostheoarthritis". Annales de Réadaptation et de Médecine Physique. 50 (8): 661–666. doi:10.1016/j.annrmp.2007.03.005.
- [Li C, Ford ES, McGuire LC, Mokdad AH. Increasing trends in waist circumference and abdominal obesity among US adults. Obesity (Silver Spring) 2007;15 (1) 216- 224]
- Lemieux S, Prudhomme D, Bouchard C, Tremblay A, Despres JP (1993). "Sex differences in the relation of visceral adipose tissue to total body fatness". Am J Clin Nutr. 58 (4): 463–467. PMID 8379501.
- Carey DG, Campbell LV, Chisholm DJ (1996). "Is visceral fat (intra-abdominal and hepatic) a major determinant of gender differences in insulin resistance and dyslipidaemia?". Diabetes. 45: 110A.
- Wingard DL (1990). "Sex differences and coronary heart disease. A case of comparing apples and pears?". Circulation. 81 (5): 1710–12. doi:10.1161/01.cir.81.5.1710.
- Andersen Barbara L.; LeGrand Joseph (1991). "Body Image for Women: Conceptualization, Assessment, and a Test of Its Importance to Sexual Dysfunction and Medical Illness". Journal of Sex Research. 28 (3): 457–78. doi:10.1080/00224499109551619.
-  Archived October 24, 2007, at the Wayback Machine.
- "Abdominal fat and what to do about it - Harvard Health Publications". Health.harvard.edu. Retrieved 2013-01-05.
- "Effects of sex steroid hormones on regional fat depots as assessed by magnetic resonance imaging in transsexuals". Ajpendo.physiology.org. 1999-02-01. Retrieved 2013-01-05.
- [Seidell J. C.,Björntorp P.,Sjöstrom L.,Kvist H.,Sannerstedt R. (1990) Visceral fat accumulation in men is positively associated with insulin, glucose, and C-peptide levels, but negatively with testosterone levels. Metabolism 39:897–901.]
- Tchernof A.; Després J.-P.; Bélanger A.; Dupont A.; Prud'homme D.; Moorjani S.; Lupien P. J.; Labrie F. (1995). "Reduced testosterone, and adrenal C19 steroid levels in obese men". Metabolism. 44 (4): 513–519. doi:10.1016/0026-0495(95)90060-8. PMID 7723675.
- Barrett-Connor E (1997). "Sex differences in coronary heart disease. Why are women so superior? The 1995 Ancel Keys Lecture". Circulation. 95 (1): 252–264. doi:10.1161/01.cir.95.1.252. PMID 8994444.
- "Even a Little Exercise Fights Obesity". Webmd.com. 2009-11-06. Retrieved 2013-01-05.
- "Weight Management". Washington.edu. 2012-11-26. Archived from the original on February 9, 2013. Retrieved 2013-01-05.
- Rockoff, Jonathan D.; Dooren, Jennifer Corbett (October 8, 2010). "Abbott Pulls Diet Drug Meridia Off US Shelves". The Wall Street Journal. Archived from the original on 11 October 2010. Retrieved 8 October 2010.
- "Top obesity drug sibutramine being suspended". BBC News. 2010-01-22. Archived from the original on 25 January 2010. Retrieved 2010-01-22.
- (German) Sibutramin-Vertrieb in der Europäischen Union ausgesetzt . Abbott Laboratories in Germany. Press release 2010-01-21. Retrieved 2010-01-27
- "Sibutramine (brand name Reductil) Information - Australia". Abbott Laboratories. 2010. Archived from the original on 14 October 2010. Retrieved 2010-10-08.
- "Health Canada Endorsed Important Safety Information on MERIDIA (Sibutramine Hydrochloride Monohydrate): Subject: Voluntary withdrawal of Meridia® (sibutramine) capsules from the Canadian market". Hc-sc.gc.ca. 2010-10-14. Retrieved 2013-01-05.
- "De-registration of pharmaceutical products containing sibutramine" (Press release). info.gov in Hong Kong. November 2, 2010. Retrieved 2010-11-08.
- "Thai FDA reveals voluntary withdrawal of sibutramine from the Thai market" (PDF) (Press release). Food and Drug Administration of Thailand. October 20, 2010. Retrieved 2010-12-22.
- Arciero, PJ; Gentile, CL (August 16, 2006). "Increased dietary protein and combined high intensity aerobic and resistance exercise improves body fat distribution and cardiovascular risk factors.". International Journal of Sport Nutrition and Exercise Metabolism.
- Kelley, George A.; Kelley, Kristi S.; Roberts, Susan; Haskell, William (2012). "Combined Effects of Aerobic Exercise and Diet on Lipids and Lipoproteins in Overweight and Obese Adults: A Meta-Analysis". Journal of Obesity. 2012: 1–16. doi:10.1155/2012/985902.
- Fonseca V (2003). "Effect of thiazolidinediones on body weight in patients with diabetes mellitus". Am. J. Med. 115 Suppl 8A (8): 42S–48S. doi:10.1016/j.amjmed.2003.09.005. PMID 14678865.
- 23/09/2010 European Medicines Agency recommends suspension of Avandia, Avandamet and Avaglim http://www.ema.europa.eu/ema/index.jsp?curl=pages/news_and_events/news/2010/09/news_detail_001119.jsp&mid=WC0b01ac058004d5c1
- Bacon, Linda; Aphramor, Lucy (January 24, 2011). "Weight Science: Evaluating the Evidence for a Paradigm Shift". Nutr J. 10 (9). doi:10.1186/1475-2891-10-9. PMC . PMID 21261939.
- Howard BV, Manson JE, Stefanick ML, Beresford SA, Frank G, Jones B, Rodabough RJ, Snetselaar L, Thomson C, Tinker L, et al. (2006). "Low-fat dietary pattern and weight change over 7 years: the Women's Health Initiative Dietary Modification Trial.". JAMA. 295 (1): 39–49. doi:10.1001/jama.295.1.39. PMID 16391215.
- Michael Jensen, M.D. (2007-01-19). "Belly fat in men: What you need to know". Mayoclinic.com. Archived from the original on 23 March 2008. Retrieved 2008-04-07.
Sit-ups will make your abdominal muscles stronger, sure. And, you may look thinner by building your abdominal muscles because you can hold in your belly fat better. But strengthening your stomach muscles alone will not specifically reduce belly fat.
- Bobak M, Skodova Z, Marmot M (2003). "Beer and obesity: a cross-sectional study". Eur J Clin Nutr. 57 (10): 1250–3. doi:10.1038/sj.ejcn.1601678. PMID 14506485.
- Staff writer (2003-10-12). "Why the beer belly may be a myth". BBC News.
- Economic costs of abdominal obesity; Højgaard, Betina and Olsen, Kim Rose and Søgaard, Jes and Sørensen, Thorkild I A and Gyrd-Hansen, Dorte; Obesity facts, ISSN 1662-4025, 2008, Volume 1, Issue 3, pp. 146 - 154
|Wikimedia Commons has media related to Abdominal obesity.|
- Griesemer, Rebecca Lynn (July 25, 2008). Index of Central Obesity as a Parameter to Evaluate Metabolic Syndrome for White, Black, and Hispanic Adults in the United States (Master's thesis). Georgia State University.
- Lee, Kayoung; Song, Yun-Mi; Sung, Joohon (2008). "Which Obesity Indicators Are Better Predictors of Metabolic Risk?: Healthy Twin Study". Obesity. 16 (4): 834–40. doi:10.1038/oby.2007.109. PMID 18239595.
- Shao, J.; Yu, L.; Shen, X.; Li, D.; Wang, K. (2010). "Waist-to-height ratio, an optimal predictor for obesity and metabolic syndrome in Chinese adults". The Journal of Nutrition, Health & Aging. 14 (9): 782–5. doi:10.1007/s12603-010-0106-x. PMID 21085910.