Abdominal obesity

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Central obesity
Classification and external resources
File:Obesity6.JPG
A morbidly obese male. Weight 146 kg/322 lbs, height 177 cm/5 ft 10 in. The body mass index is 46.
ICD-10 E66
ICD-9 278

Abdominal obesity, colloquially known as belly fat or clinically as central obesity, is the accumulation of abdominal fat resulting in an increase in waist size. There is a strong correlation between central obesity and cardiovascular disease.[1]

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.

Causes

The immediate cause of obesity is net energy imbalance — the organism consumes more usable calories than it expends, wastes, or discards via elimination. The fundamental cause of obesity is not well understood, but is presumably a combination of the organism's genes and environment. The specific cause of central distribution of fat is also not well understood[citation needed].

In humans, central obesity is correlated with overeating and a sedentary lifestyle. Hypercortisolism, such as in Cushing's syndrome also leads to central obesity. Many prescription drugs can also have side effects resulting in obesity.

Because fat in the midsection contain the greatest amount of cortisol receptors, fat is created and stored in the midsection, specifically in fat cell deposits deep in the abdomen.[2]

Diagnosis

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)[3] 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.[4]

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.

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 cardio-vascular risk and BVI calculations correlate significantly with all biomarkers of cardio-vascular risk.[5]

Chronic alcoholism can lead to cirrhosis, symptoms of which include gynecomastia (enlarged breasts) and ascites (abdominal fluid). These symptoms can simulate the appearance of central obesity.[citation needed]

Health risks

File:IMAG0042-1.jpg
Excess adipose tissue on a male

Central obesity is associated with a statistically higher risk of heart disease, hypertension, insulin resistance, and Diabetes Mellitus Type 2 (see below). Belly fat is a symptom of metabolic syndrome, and is an indicator used in the diagnosis of that disorder.[6][7][8][9]

Central obesity can be a feature of lipodystrophies, a group of diseases which 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[10] and is also common in patients with polycystic ovary syndrome (PCOS). Central obesity is associated with glucose intolerance and dyslipidemia.

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.[11][12] Increased adiposity (obesity) raises serum resistin levels[13][14][15][16], which in turn directly correlate to insulin resistance[17][18][19][20]. Studies have also confirmed a direct correlation between resistin levels and T2DM.[13][21][22][23]. 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.[24][25] Conversely, serum resistin levels have been found to decline with decreased adiposity following medical treatment.[26]

Relationship with Alzheimer's Disease

A US 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.[27][28][29]

Waist–hip ratio

File:Obesity-waist circumference.svg
Silhouettes and waist circumferences representing normal, overweight, and obese

The absolute waist circumference (>102 cm in men and >88 cm in women) and the waist–hip ratio (the circumference of the waist divided by that of the hips of >0.9 for men and >0.85 for women) are both used as measures of central obesity.[3]

In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat.[30] Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.[3]

Sex differences

Female sex hormone causes fat to be stored in the buttocks, thighs, and hips in women. Men are more likely to have fat stored in the belly due to sex hormone differences. When women reach menopause and the estrogen produced by ovaries declines, fat migrates from their buttocks, hips and thighs to their waists;[31] later fat is stored in the belly.[32]

Prevention and treatments

Performing adequate aerobic exercise and eating a healthy diet can prevent central obesity, and losing weight via these methods is the main way to reverse the condition.[33]

Adjunctive therapies which may be prescribed by a physician are orlistat or sibutramine. In the presence of diabetes mellitus type 2, the physician might instead prescribe metformin and thiazolidinediones (rosiglitazone or pioglitazone) as anti-diabetic drugs rather than sulfonylurea derivatives. Thiazolidinediones may cause slight weight gain but decrease "pathologic" abdominal fat, and therefore may be prescribed for diabetics with central obesity.[34]

Sit-ups myth

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 on fat in that area of the body, or on the body's distribution of body fat. The same thing 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 on the adipose tissue located there.[35]

Slang terms

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 it 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.[36][37] (However, these alcohol-related terms might not always have referred to abdominal fat. Chronic, heavy drinkers suffering from liver damage caused by their drinking may develop ascites, a condition involving fluid buildup in the abdomen due to poor liver function, resulting in an enlarged belly.) [38]

"Love handles" is a colloquial term for a layer of fat that is deposited around a person's midsection, especially visible on the sides over the abdominal external oblique muscle.

"Muffin top" is a pejorative term used for a person whose midsection spills over the waistline of his or her trousers in a manner that resembles the top of a muffin spilling over its baking pan.

See also

References

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Hypoalimentation/
malnutrition
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Mineral overload

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drug(A8/11/12)

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de:Stammfettsucht nl:Bierbuik no:Bukfett pl:Otyłość brzuszna fi:Keskivartalolihavuus sv:Bukfetma tl:Bilbil (taba) zh-yue:大肚腩

zh:肚腩贅肉
  1. ↑ 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: 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185. 
  2. ↑ Cortisol and Belly Fat
  3. ↑ 3.0 3.1 3.2 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: 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185. 
  4. ↑ Janssen I, Katzmarzyk PT, Ross R (2004). "Waist circumference and not body mass index explains obesity-related health risk". Am. J. Clin. Nutr. 79 (3): 379–84. doi:10.1185/030079906X159489. PMID 14985210. 
  5. ↑ 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
  6. ↑ Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. 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 2001;285:2486-97. PMID 11368702.
  7. ↑ 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.
  8. ↑ American Heart Association's description of Syndrome X
  9. ↑ "> 'How to Lose Belly Fat' from Real Weight Loss Tips
  10. ↑ 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. 
  11. ↑ Duman BS, Turkoglu C, Gunay D, Cagatay P, Demiroglu C, Buyukdevrim AS. 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, 2003.
  12. ↑ Gabriely, I., Ma, X. H., Yang, X. M., Atzmon G, Rajala MW, berg AH, Sherer P, Rossetti L, Barzilai N. Removal of visceral fat prevents insulin resistance and glucose intolerance of aging: an adipokine-mediated process? Diabetes. 51: 2951–2958, 2002.
  13. ↑ 13.0 13.1 Asensio, C., Cettour-Rose, P., Theander-Carrillo, C., Rohner-Jeanrenaud, F. and Muzzin, P. 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, 2004.
  14. ↑ Degawa-Yamauchi MBJE, Juliar BE, Watson W, Kerr K, Jones RM, Zhu Q & Considine RV. Serum resistin (FIZZ3) protein is increased in obese humans. Journal of Clinical Endocrinology and Metabolism. 88: 5452–5455, 2003.
  15. ↑ Lee, J. H., Bullen, Jr, J. W., Stoyneva, V. L. and Mantzoros, C. S. Circulating resistin in lean, obese and insulin-resistant mouse models: lack of association with insulinemia and glycemia. Am. J. Physiol. Endocrinol. Metab. 288: E625–E632, 2005.
  16. ↑ Vendrell J, Broch M, Vilarrasa N, Molina A, Gomez JM, Gutierrez C, Simon I, Soler J & Richart C. Resistin, adiponectin, ghrelin, leptin, and proinflammatory cytokines: relationships in obesity. Obesity Research. 12: 962–971, 2004.
  17. ↑ Hirosumi J, Tuncman G, Chang L, Gorgun CZ, Uysal KT, Maeda K, Karin M, Hotamisligil GS. A central role for JNK in obesity and insulin resistance. Nature. 420: 333-336, 2002. [1]
  18. ↑ Rajala, M. W., Qi, Y., Patel, H. R., Takahashi N, Banerjee R, Pajvani UB, Sinha MK, Gingerich RL, Scherer PE, Ahima RS. Regulation of resistin expression and circulating levels in obesity, diabetes, and fasting. Diabetes. 53: 1671–1679, 2004.
  19. ↑ Silha JV, Krsek M, Skrha JV, Sucharda P, Nyomba BL and Murphy LJ. Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance. Eur. J. Endocrinol. 149: 331-335, 2003.
  20. ↑ Smith, S. R., Bai, F., Charbonneau, C., Janderova, L. and Argyropoulos, G. A promoter genotype and oxidative stress potentially link resistin to human insulin resistance. Diabetes 52, 1611–1618, 2003.
  21. ↑ 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. 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, 2004.
  22. ↑ McTernan, P. G., Fisher, F. M., Valsamakis, G, Chetty R, Harte A, McTernan CL, Clark PM, Smith SA, Barnett AH, Kumar S. 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, 2003.
  23. ↑ Steppan CM, Bailey ST, Bhat S, Brown EJ, Banerjee RR, Wright CM, Patel HR, Ahima RS, Lazar MA. The hormone resistin links obesity to diabetes. Nature. 409:307-312, 2001.
  24. ↑ McTernan, C. L., McTernan, P. G., Harte, A. L., Levick, P. L., Barnett, A. H. and Kumar, S. Resistin, central obesity, and type 2 diabetes. Lancet. 359: 46–47, 2002.
  25. ↑ McTernan, P. G., McTernan, C. L., Chetty, R, Jenner K, Fisher FM, Lauer MN, Crocker J, Barnett AH, Kumar S. Increased resistin gene and protein expression in human abdominal adipose tissue. J. Clin. Endocrinol. Metab. 87: 2407, 2002.
  26. ↑ Valsamakis, G., McTernan, P. G., Chetty, R, Al Daghri N, Field A, Hanif W, Barnett AH, Kumar S. Modest weight loss and reduction in waist circumference after medical treatment are associated with favourable changes in serum adipocytokines. Metab. Clin. Exp. 53:430–434, 2004.
  27. ↑ http://news.bbc.co.uk/2/hi/health/8693947.stm
  28. ↑ http://www.msnbc.msn.com/id/23800703/
  29. ↑ Stéphanie Debette, MD, PhD, et al "Visceral fat is associated with lower brain volume in healthy middle-aged adults" Annals of Neurology published online 20May2010 [2]
  30. ↑ 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. ISBN url=http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=hstat3.section.36199 Check |isbn= value: invalid character (help). 
  31. ↑ Researchers think that the lack of estrogen at menopause play a role in driving our fat northward [3]
  32. ↑ Abdominal fat and what to do about it
  33. ↑ Christian Finn, M.Sc. "The Best Way To Lose Belly Fat". thefactsaboutfitness.com. Retrieved 2010-04-08. There's a growing body of research to show that the fastest way to lose abdominal fat is with a combination of resistance training and aerobic exercise. 
  34. ↑ Fonseca V (2003). "Effect of thiazolidinediones on body weight in patients with diabetes mellitus". Am. J. Med. 115 Suppl 8A: 42S–48S. doi:10.1016/j.amjmed.2003.09.005. PMID 14678865. 
  35. ↑ Michael Jensen, M.D. (2007-01-19). "Belly fat in men: What you need to know". Mayoclinic.com. 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.  line feed character in |quote= at position 70 (help)
  36. ↑ Bobak M, Skodova Z, Marmot M. Beer and obesity: a cross-sectional study. Eur J Clin Nutr 2003;57:1250–3.
  37. ↑ Staff writer (2003-10-12). "Why the beer belly may be a myth". BBC News. 
  38. ↑ Netional Library of Medicine. "Ascites." From http://www.nlm.nih.gov/medlineplus/ency/article/000286.htm. Accessed July 1, 2010.
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