Abdominal obesity

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Central obesity
Classification and external resources
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, also known as belly fat or clinically as central obesity, is excessive abdominal fat around the stomach and abdomen. There is a strong correlation between central obesity and cardiovascular disease.[1] Abdominal obesity is not confined only to the elderly and obese subjects.[2] Abdominal obesity has been linked to Alzheimer's Disease as well as other metabolic and vascular diseases.[3]

Visceral and central abdominal fat and waist circumference show a strong association with type 2 diabetes.[4]

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.[citation needed]

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 our 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.[5]

Causes[edit]

Excess abdominal fat on a teenage male.

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. 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,[6] is related to the excessive consumption of fructose.[7][8][9] Other environmental factors, such as maternal smoking, estrogenic compounds in the diet‚ and endocrine-disrupting chemicals may be important also.[10] Obesity plays an important role in the impairment of lipid and carbohydrate metabolism shown in high-carbohydrate diets.[11][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[12] 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.[13]

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'.[14]

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,[15] 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.[16][17]

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.[18]

Diagnosis[edit]

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)[19] 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.[20] 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.[21] 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.[22] 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[edit]

Index of Central Obesity (ICO) is the ratio of waist circumference and height first proposed by a Parikh et al. in 2007[23][24] as a better substitute to the widely used waist circumference in defining metabolic syndrome.[25] 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.[26] The same was used in defining metabolic syndrome.[27] 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.[28] Various race specific cutoffs were suggested by different groups.[citation needed] The International Diabetes Federation defined central obesity based on these various race and gender specific cutoffs.[citation needed] 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.[25] 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.[25]

This parameter has been used in the study of metabolic syndrome[29][30] and cardiovascular disease.[31]

Body Volume Index[edit]

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.[32]

Ghroubi et al. (2007) examined whether abdominal circumference is a more reliable indicator than BMI of the presence of knee osteoarthritis in obese patients.[33] 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.[33]

Health risks[edit]

Central obesity is associated with a statistically higher risk of heart disease, hypertension, insulin resistance, and Diabetes Mellitus Type 2 (see below).[34] With an increase in the waist to hip ratio and overall waist circumference the risk of death increases as well.[35] Metabolic syndrome is associated with abdominal obesity, blood lipid disorders, inflammation, insulin resistance, full-blown diabetes, and increased risk of developing cardiovascular disease.[36][37][38][39] It is now generally believed that intra-abdominal fat is the depot that conveys the biggest health risk.[40][41]

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[42] 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[edit]

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.[43][44] Increased adiposity (obesity) raises serum resistin levels,[45][46][47][48] which in turn directly correlate to insulin resistance.[49][50][51][52] Studies have also confirmed a direct correlation between resistin levels and T2DM.[45][53][54][55] 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.[56][57] Conversely, serum resistin levels have been found to decline with decreased adiposity following medical treatment.[58]

Relationship with Asthma[edit]

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.[59] 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.[60]

Pathophysiology of Visceral Obesity[edit]

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.[61] Individuals with obesity are more likely to develop weakened non-esterified fatty acid (NEFA), which can weaken the metabolism of the liver causing [62] high glucose production. An individual is at a higher risk of developing ischemic heart disease if they have hyperinsulinemia-dyslipidemia while being abdominal obese.[63]

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.[64][65] Abdominal adipose tissue is a major source of increased inflammatory Interleukin-6 (IL-6) associated with aging.[66] Induction of cellular senescence by visceral fat contributes to the inflammation.[67]

Relationship with Alzheimer's Disease[edit]

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.[68] 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.[69][70][71] 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.[72]

Relationship with Pulmonary Function[edit]

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.[73] [5]

Relationship with Alcohol Consumption[edit]

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.[74] [6]

Measurement[edit]

Silhouettes and waist circumferences representing normal, overweight, and obese

There are various ways of measuring abdominal obesity including:

Excess abdominal fat on a female.

In those with a BMI under 35, intra-abdominal body fat is related to negative health outcomes independent of total body fat.[76] Intra-abdominal or visceral fat has a particularly strong correlation with cardiovascular disease.[19]

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.[77]

Sex differences[edit]

50% of men and 70% of women in the United States between the ages of 50 and 79 years now exceed the waist circumference threshold for abdominal obesity. [78]

When comparing the body fat of men and women it is seen that men have close to twice the visceral fat as that of pre-menopausal women. [79][80]

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.[81]

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.[82] This typical female fat storage may be essential for normal reproductive function.[83] When women reach menopause and the estrogen produced by ovaries declines, fat migrates from their buttocks, hips‚ and thighs to their belly.[84][85]

Males are more susceptible to upper-body fat accumulation, most likely in the belly, due to sex hormone differences.[86] Abdominal obesity in males is correlated with comparatively low testosterone levels for men.[87] Testosterone administration significantly increased thigh muscle area, reduced subcutaneous fat deposition at all levels measured, but slightly increased the visceral fat area.[88]

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.[89]

Economic Costs of Abdominal Obesity[edit]

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 economic costs that are 22%, of 397 USD, higher per year than a woman with a normal waist circumference.[90]

Prevention and treatments[edit]

A permanent routine of exercise, eating healthier‚ and consuming the same number or fewer calories than used will prevent and help fight obesity.[91] A single pound of fat is believed to yield approximately 3500 calories of energy, and weight loss is achieved by reducing energy intake.[92] 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,[93] the UK,[94] the EU,[95] Australia,[96] Canada,[97] Hong Kong,[98] Thailand,[99] Egypt and Mexico.

A 2006 study published in the International Journal of Sport Nutrition and Exercise Metabolism,[100] 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.[101] 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.[102]

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."[103] The Women's Health Initiative ("the largest and longest randomized, controlled dietary intervention clinical trial"[103]) 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.[104]

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." [105]

Myths[edit]

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.[106]

Colloquialisms[edit]

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.[107][108] 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."

Factors[edit]

There are many factors that can contribute to someone becoming obese. The common assumption is that the person has an unhealthy diet and or inactive, without an exercise routine, meaning that they take in more calories than they burn, and their body stores the excess calories as fat, increasing the total body mass. Lack of sleep is not commonly thought of as a factor, but getting less than seven hours of sleep a night can cause changes in hormones that increase your appetite. You may also crave foods high in calories and carbohydrates to give you lost energy, which can contribute to weight gain. In women, pregnancy can also be a catalyst in becoming obese. During pregnancy, a woman's weight necessarily increases for development of a baby. Some women find this weight difficult to lose after the baby is born. This weight gain may contribute to the development of obesity in women. Certain medication that a person takes can have side effects of gaining weight. These medications include some antidepressants, anti-seizure medications, diabetes medications, and steroids. Obesity can sometimes be traced to a medical cause, such as Cushing's syndrome and other diseases and conditions. Some medical problems, such as arthritis, can lead to the decrease in activity, which usually results in weight gain. A study suggests that low metabolism is unlikely to cause obesity, as is having low thyroid function.[109] Another sets forth a close relationship between hypothyroidism, thermogenesis, lipid metabolism, and obesity.[7]

On the earliest stages of obesity people usually do not feel a lot of discomfort and do not tend to connect their health concerns with their extra weight. During these stages people may take their overweight as a cosmetic defect rather psychological and physical discomfort. However, during these early stages of obesity, it is very important to seek medical attention and start making changes in life-style and eating habits, because the processes of fat accumulation in the body tend to progress and result increased risks of having many lasting health problems.[citation needed]

See also[edit]

  • 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

Further reading[edit]

References[edit]

  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 (9438): 937–52. doi:10.1016/S0140-6736(04)17018-9. PMID 15364185. 
  2. ^ Carey D.G.P. (1998). Abdominal Obesity. Current Opinion in Lipidology. (pp. 35-40). Vol. 9, No 1. Retrieved on April 9, 2012.
  3. ^ Razay, George, "Obesity, Abdominal Obesity and Alzheimer's Disease", Dementia & Genetic Cognitive Disorders, July 2006
  4. ^ http://care.diabetesjournals.org/content/27/12/2948.full
  5. ^ Poehlman, Eric T. (1998). Abdominal obesity: the metabolic multi-risk factor 9 (8). pp. 469–471. 
  6. ^ Stanhope, Kimber L.; Peter J. Havel (March 2010). "Fructose consumption: Recent results and their potential implications". Annals of the New York Academy of Sciences 1190. doi:10.1111/j.1749-6632.2009.05266.x. 
  7. ^ 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. 
  8. ^ 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". International Journal of Obesity 34: 454–461. 
  9. ^ Choi, Mary (March 2009). "The Not-so-Sweet Side of Fructose". JASN. 3 20 (3): 457–459. 
  10. ^ 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. 
  11. ^ Ibrahim, Islam Ahmed Abd El-Hamid. Is the effect of high fat diet on lipid and carbohydrate metabolism related to inflammation? 4 (3). pp. 203–209. 
  12. ^ Cuthbertson, Danie; Kenneth Smith, John Babraj, Graham Leese, Tom Waddell, Philip Atherton,, Henning Wackerhage, Peter M Taylor, and Michael J Rennie (March 2005). "Anabolic deficits underlie amino acid resistance of wasting, aging muscle". The FASEB Journal 19 (3): 422–424. 
  13. ^ Loenneke, Jeremy; Jacob M Wilson, Anssi H Manninen, Mandy E Wray, Jeremy T Barnes and Thomas J Pujol (January 2012). "Quality protein intake is inversely related with abdominal fat". Nutrition & Metabolism 9 (1). 
  14. ^ 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
  15. ^ 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. 
  16. ^ Després, J. (May 2006). Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic risk. Oxford Journals. Retrieved from http://eurheartjsupp.oxfordjournals.org/content/8/suppl_B/B4.full
  17. ^ Carey, David G.P. (February 1998). Abdominal obesity. pp. 35–40. Retrieved 6 April 2012. 
  18. ^ Abdominal obesity and your health. (2006). Retrieved from http://www.health.harvard.edu/fhg/updates/abdominal-obesity-and-your-health.shtml
  19. ^ a b c 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. 
  20. ^ 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. 
  21. ^ 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. 
  22. ^ Poehlman, Eric (1998). "Abdominal obesity: the metabolic multi risk factor". Journal of Coronary Heart Disease 9: 469–471;. 
  23. ^ a b 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. 
  24. ^ 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. 
  25. ^ a b c 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. 
  26. ^ a b 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. 
  27. ^ 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. 
  28. ^ 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. 
  29. ^ 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. 
  30. ^ 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. 
  31. ^ 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. 
  32. ^ 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
  33. ^ a b S. Ghroubi; H. Elleuch; M. Guermazi; N. Kaffel; H. Feki; M. Abid; S. Baklouti; M.H. Elleuch, "Abdominal obesity and knee ostheoarthritis", Annales de readaptation et de medecine physique, date
  34. ^ Westphal, S. A. (2008)
  35. ^ Cameron, A. J., & Zimmet, P. Z. (2008). Expanding evidence for the multiple dangers of epidemic abdominal obesity. International Diabetes Institute, Retrieved from http://circ.ahajournals.org.myaccess.library.utoronto.ca/content/117/13/1624.full
  36. ^ Després, Jean-Pierre, and Isabelle Lemieux. "Review Article Abdominal Obesity and Metabolic Syndrome." Review Article Abdominal Obesity and Metabolic Syndrome 444 (2006) 881-87. Web. 20 Aug. 2012. <http://www.nature.com/nature/journal/v444/n7121/full/nature05488.html?free=2>
  37. ^ "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. 2001. doi:10.1001/jama.285.19.2486. PMID 11368702. 
  38. ^ 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.
  39. ^ "American Heart Association's description of Syndrome X". Americanheart.org. Retrieved 2013-01-05. 
  40. ^ Poehlman E.T. (1998)
  41. ^ 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 3115050. PMID 21461943. 
  42. ^ 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. 
  43. ^ 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.
  44. ^ 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. 
  45. ^ a b Asensio C., Cettour-Rose P., Theander-Carrillo C., Rohner-Jeanrenaud F., 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. 
  46. ^ 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.
  47. ^ 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.
  48. ^ 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.
  49. ^ 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]
  50. ^ Rajala M. W., Qi Y., Patel H. R., Takahashi N, Banerjee R, Pajvani UB, Sinha MK, Gingerich RL, Scherer PE et al.. "Regulation of resistin expression and circulating levels in obesity, diabetes, and fasting". Diabetes 53 (1671–1679): 2004. 
  51. ^ 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: 331–335. 
  52. ^ Smith S. R., Bai F., Charbonneau C., Janderova L., Argyropoulos G. "A promoter genotype and oxidative stress potentially link resistin to human insulin resistance". Diabetes 52 (1611–1618): 2003. 
  53. ^ Fujinami A., Obayashi H., Ohta K, Ichimura T, Nishimura M, Matsui H, Kawahara Y, Yamazaki M, Ogata M et al.. "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. 
  54. ^ McTernan P. G., Fisher F. M., Valsamakis G, Chetty R, Harte A, McTernan CL, Clark PM, Smith SA, Barnett AH et al.. "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. 
  55. ^ 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: 307–312. doi:10.1038/35053000. PMID 11201732. 
  56. ^ McTernan C. L., McTernan P. G., Harte A. L., Levick P. L., Barnett A. H., Kumar S. "Resistin, central obesity, and type 2 diabetes". Lancet 359 (46–47): 2002. doi:10.1016/S0140-6736(02)08836-0. 
  57. ^ 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.
  58. ^ 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.
  59. ^ Shore, S., & Johnston, R. (2006). Obesity and asthma" Pharmacology & Therapeutics 110(1), 83-102. Retrieved August 6, 2012, from the ScienceDirect database.
  60. ^ Thomson, C., Clark, S., & Jr, C. C. (2003). Body Mass Index and Asthma Severity Among Adults Presenting to the Emergency Department. Chest Journal, 124(3), 795-802. Retrieved August 6, 2012, from the CHEST Journal database.
  61. ^ Després, Jean-Pierre and Lemieux, Isabelle, Nature, ISSN 0028-0836, 12/2006, Volume 444, Issue 7121, pp. 881 - 887
  62. ^ Després, Jean-Pierre; Lemieux (14 December 2006). "Isabelle". Abdominal obesity and metabolic syndrome. Nature 444: 881–887. Retrieved March 12, 2012. 
  63. ^ Poelhlman, E. T. Abdominal obesity: the metabolic multi-risk factor. Coronary Heart Disease. Exp. 9:469-471, 1998.
  64. ^ Huffman DM, Barzilai N (2009). "Role of visceral adipose tissue in aging". BIOCHEMICA ET BIOPHYSICA ACTA 1790 (10): 1117–1123. doi:10.1016/j.bbagen.2009.01.008. PMC 2779572. PMID 19364483. 
  65. ^ Zhang H, Wang Y, Zhang J, Potter BJ, Sowers JR, Zhang C (2011). "Bariatric surgery reduces visceral adipose inflammation and improves endothelial function in type 2 diabetic mice". ATHEROSCLEROSIS, THROMBOSIS, AND VASCULAR BIOLOGY 31 (9): 2063–2069. doi:10.1161/ATVBAHA.111.225870. PMC 3158262. PMID 21680898. 
  66. ^ Starr ME, Evers BM, Saito H (2009). "Age-associated increase in cytokine production during systemic inflammation: adipose tissue as a major source of IL-6". JOURNALS OF GERONTOLOGY, SERIES A 64 (7): 723–730. doi:10.1093/gerona/glp046. PMC 2844135. PMID 19377014. 
  67. ^ Villaret A, Galitzky J, Decaunes P, Estève D, Marques MA, Sengenès C, Chiotasso P, Tchkonia T, Lafontan M, Kirkland JL, Bouloumié A (2010). "Adipose tissue endothelial cells from obese human subjects: differences among depots in angiogenic, metabolic, and inflammatory gene expression and cellular senescence". Diabetes (journal) 59 (11): 2755–2763. doi:10.2337/db10-0398. PMC 2963533. PMID 20713685. 
  68. ^ Razay , G., Vreugdenhil, A., and Wilcock, G. (July 14, 2006). Obesity, abdominal obesity and Alzheimer disease. Dementia and geriatric cognitive disorders. 22, 173-176.
  69. ^ "'Beer belly' link to Alzheimer's". BBC News. 2010-05-20. 
  70. ^ Mitchell, Steve (2008-03-26). "Bulging belly now could mean dementia later - Health - Alzheimer's Disease | NBC News". MSNBC. Retrieved 2013-01-05. 
  71. ^ 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]
  72. ^ Razay, George. (2006) Obesity, Abdominal obesity and Alzheimer's disease. Retrieved from http://bf4dv7zn3u.search.serialssolutions.com.myaccess.library.utoronto.ca/?ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info:sid/summon.serialssolutions.com&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Obesity%2C+Abdominal+Obesity+and+Alzheimer+Disease&rft.jtitle=Dementia+and+Geriatric+Cognitive+Disorders&rft.au=Anthea+Vreugdenhil&rft.au=George+Razay&rft.au=Gordon+Wilcock&rft.date=2006-08-01&rft.pub=S.+Karger+AG&rft.issn=1420-8008&rft.volume=22&rft.issue=2&rft.spage=173&rft.externalDocID=1141025081
  73. ^ Pekkarinen, E., Vanninen, E., Lansimies, E., et al. Relation between body composition, abdominal obesity, and lung function. (2012). Clin Physiol Funct Imagining. 32: 83-88.
  74. ^ H. Schro¨der et al. Relationship of abdominal obesity with alcohol consumption. (2007). doi:10.1007/s00394-007-0674-7
  75. ^ 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. 
  76. ^ 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. 
  77. ^ "Abdominal obesity and your health". Health.harvard.edu. Retrieved 2013-01-05. 
  78. ^ [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]
  79. ^ 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: 463–467. 
  80. ^ Carey DGP, 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. 
  81. ^ Wingard DL (1990). "Sex differences and coronary heart disease. A case of comparing apples and pears?". Circulation 81: 1710–12. 
  82. ^ Andersen, Barbara L., and Joseph LeGrand. "Body Image for Women: Conceptualization, Assessment, and a Test of Its Importance to Sexual Dysfunction and Medical Illness." Journal of Sex Research 28.3 (1991) 457-78.
  83. ^ Van Kesteren P. J. M., Lips P., Devillé W., Popp-Snijders C., Asscheman H., Megens J. A. J., Gooren L. J. G. (1996). "The effect of one-year cross-sex hormonal treatment on bone metabolism and serum insulin-like growth factor-I in transsexuals". J. Clin. Endocrinol. Metab 81: 2227–2232. 
  84. ^ [3][dead link]
  85. ^ "Abdominal fat and what to do about it - Harvard Health Publications". Health.harvard.edu. Retrieved 2013-01-05. 
  86. ^ "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. 
  87. ^ [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.]
  88. ^ 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: 513–519. 
  89. ^ 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. 
  90. ^ 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
  91. ^ "Even a Little Exercise Fights Obesity". Webmd.com. 2009-11-06. Retrieved 2013-01-05. 
  92. ^ "Weight Management". Washington.edu. 2012-11-26. Retrieved 2013-01-05. 
  93. ^ 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. 
  94. ^ "Top obesity drug sibutramine being suspended". BBC News. 2010-01-22. Archived from the original on 25 January 2010. Retrieved 2010-01-22. 
  95. ^ (German) Sibutramin-Vertrieb in der Europäischen Union ausgesetzt [4]. Abbott Laboratories in Germany. Press Release 2010-01-21. Retrieved 2010-01-27
  96. ^ "Sibutramine (brand name Reductil) Information - Australia". Abbott Laboratories. 2010. Archived from the original on 14 October 2010. Retrieved 2010-10-08. 
  97. ^ "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. 
  98. ^ "De-registration of pharmaceutical products containing sibutramine" (Press release). info.gov in Hong Kong. November 2, 2010. Retrieved 2010-11-08. 
  99. ^ "Thai FDA reveals voluntary withdrawal of sibutramine from the Thai market" (Press release). Food and Drug Administration of Thailand. October 20, 2010. Retrieved 2010-12-22. 
  100. ^ 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. 
  101. ^ 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. 
  102. ^ 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
  103. ^ a b 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 3041737. PMID 21261939. 
  104. ^ 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: 39–49. doi:10.1001/jama.295.1.39. PMID 16391215. 
  105. ^ Obesity, fitness & wellness week (May 2005). "Abdominal obesity; GH treatment". Factiva. 
  106. ^ 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." 
  107. ^ 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. 
  108. ^ Staff writer (2003-10-12). "Why the beer belly may be a myth". BBC News. 
  109. ^ Crum, R. et al (2003-06-13). "Is Obesity Associated with Major Depression? Results from the Third National Health and Nutrition Examination Survey". American Journal of Epidemiology.