|Classification and external resources|
A morbidly obese male. Weight 146 kg/322 lbs, height 177 cm/5 ft 10 in. The body mass index is 46.
Abdominal obesity, also known as belly fat or clinically as central obesity, is excessive abdominal fat around the stomach and abdomen. It can also occur in both children and teenagers if either of their parents have Abdominal obesity. 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. Scientists have come to recognize that body fat, instead of body weight, is the key to evaluating obesity.
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 distractions 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 our understanding of the health risks associated with body fat accumulation. Techniques such as computed tomography and magnetic resonance imaging made it possible to dissect mass of adipose tissue located at the abdominal level into intra-abdominal fat and subcutaneous fat.
The immediate cause of obesity is net energy imbalance—the organism consumes more usable calories than it expends, wastes‚ or discards through elimination. The fundamental cause of obesity is unknown, but is presumably a combination of the organism’s genes and environment. Some studies indicate that visceral adiposity, together with lipid dysregulation and decreased insulin sensitivity, is related to the excessive consumption of fructose. 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 the quality protein intake in a 24-hour period and the times achieving the essential amino acid threshold of approximately 10 g is inversely related to percent 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, due to a combination of low physical activity and high-energy 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.
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 Dr. Eric D. 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 does not just occur 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 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.
 Health risks
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 does not just occur in those who are obese but also affects people who are non-obese and it also contributes to insulin sensitivity.
 Relationship with Diabetes
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.
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.
 Relationship with 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. 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.
 Pathophysiology of Visceral Obesity
There is enough evidence in the scientific community where an impaired non-esterified fatty acid (NEFA) metabolism could give way to the insulin-resistant state of individuals with this type of obesity. Hypertrophy of intra-abdominal adipose cells causes it to be in a hyperlipolytic state in which it is resistant to the antilipolytic effect of insulin. The resulting NEFA flux to the liver causes impairment of liver metabolism which leads to over production of glucose in the liver. Individuals with obesity are more likely to develop weakened non-esterified fatty acid (NEFA), which can weaken the metabolism of the liver causing  high glucose production. An individual is at a higher risk of developing ischemic heart disease if they have hyperinsulinemia-dyslipidemia while being abdominal obese.
Visceral fat, unlike subcutaneous fat, is implicated in many aging-associated diseases. Surgical removal of visceral fat, but not subcutaneous fat, has been shown to extend the mean and maximum lifespan of rodents. Abdominal adipose tissue is a major source of increased inflammatory Interleukin-6 (IL-6) associated with aging. Induction of cellular senescence by visceral fat contributes to the inflammation.
 Relationship with 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, however the relationship between later life obesity and dementia is less clear. A U.S. study reported in May 2010 Annals of Neurology 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.
 Relationship with Pulmonary Function
One study found a relationship between abdominal obesity and lung function. It has been shown with increasing waist circumference, there is a strong correlation with spirometry or breathing results. Also, abdominal obesity affects pulmonary function more in men than in women. 
 Relationship with Alcohol Consumption
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 in men and >88 cm 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)
- Index of Central Obesity
- 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 40 inches (102 cm) or higher. On the other hand, women are considered to be at high risk if their waist measurements are 35 inches (89 cm) 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.
 Sex differences
Abdominal 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. Female sex hormones are believed to cause fat to be stored in the buttocks, thighs, and hips in women. This typical female fat storage may be essential for normal reproductive function. 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 for men. 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 abdominal obesity measured as waist circumference or waists to hip ratio, coronary artery disease rates are identical in men and women.
 Economic Costs of Abdominal Obesity
Højgaard et al. of Danish Institute for Health Services Research at 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 a cost of approximately 397 USD per year compared to a woman in the normal waist circumference group, which is about 22% higher.[clarification needed]
 Prevention and treatments
A permanent routine of exercise, eating healthier‚ and consuming the same number or fewer calories than used will prevent and help fight obesity. A single pound of fat is believed to yield approximately 3500 calories 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.
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.
Abdominal obesity is associated with GH secretion and a cluster of cardiovascular risk factors that characterize the metabolic syndrome. Franco and colleagues, Sahlgrensk University Hospital, Gothenburg, Sweden, had an experiment of GH treatment to forty postmenopausal women with abdominal obesity for 12-month trial. GH treatment reduced visceral fat mass,increase thigh muscle area, and reduced total and low-density lipoprotein cholesterol compared with placebo. Furthermore, a positive correlation was found between changes in GDR and other organs. The researcher Franco said that “In postmenopausal women with abdominal obesity, 1 year of GH treatment improved insulin sensitivity was associated with reduced hepatic fat content.” 
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 abdominal 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 abdominal 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.
The skin flap resulting from extreme central obesity is also called “F.U.P.A.” which is short for “fat upper pubic area.” In common speech, the abbreviation may even be used as a word by itself, as in a picture of a fat woman that shows “the exact shape and size of her fupa.”
Deposits of excess fat at the sides of one’s waistline are commonly referred to as “love handles”.
 Social Views
Besides the health aspect of the subject, obesity has a strong influence on one’s general mood and behaviour. According to an article in the American Journal of Epidemiology, the percentage of depression in people of normal body weight was about 2.79%. 12.51% of people with class 3 obesity, which is classified as a BMI greater or equal to 40, however, were found to suffer from DIS/DSM-III major depression.
 See also
- Bariatrics, the branch of medicine that deals with the causes, prevention, and treatment of obesity
- Gros Ventre
- 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
 Further reading
- Griesemer, Rebecca Lynn (July 25, 2008) (Master’s thesis). Index of Central Obesity as a Parameter to Evaluate Metabolic Syndrome for White, Black, and Hispanic Adults in the United States. Georgia State University. http://digitalarchive.gsu.edu/iph_theses/42.
- 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.
- 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, George, “Obesity, Abdominal Obesity and Alzheimer’s Disease”, Dementia & Genetic Cognitive Disorders, July 2006
- Poehlman, Eric T. (1998). Abdominal obesity: the metabolic multi-risk factor. 9. pp. 469–471.
- Stanhope, Kimber L.; Peter J. Havel (March 2010). “Fructose consumption: Recent results and their potential implications”. Annals of the New York Academy of Science 1190. doi:10.1111/j.1749-6632.2009.05266.x.
- Elliott, Sharon; Nancy L Keim, Judith S Stern, Karen Teff and Peter J Havel (November 2002). “Fructose, weight gain, and the insulin resistance syndrome”. American Journal of Clinical Nutrition 76 (5): 911–922. http://www.ajcn.org/content/76/5/911.full.
- Perez-Pozo, SE; et al (22). “Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response”. International Journal of Obesity 34: 454–461. http://www.gnmhealthcare.com/pdf/12-2009/22/ijo_vaop_ncurrent_gnm_ijo2009259a.pdf.
- Choi, Mary (March 2009). “The Not-so-Sweet Side of Fructose”. JASN. 3 20 (3): 457–459. http://jasn.asnjournals.org/content/20/3/457.full.
- 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. http://www.springerlink.com/content/q5487k0r18162473/.
- Ibrahim, Islam Ahmed Abd El-Hamid. Is the effect of high fat diet on lipid and carbohydrate metabolism related to inflammation?. 4. pp. 203–209. http://www.springerlink.com/content/7630488lpx4j4tk6/.
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- Abdominal obesity and your health. (2006). Retrieved from http://www.health.harvard.edu/fhg/updates/abdominal-obesity-and-your-health.shtml
- 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.
- 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: 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. et al. (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.
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