Normal weight obesity: Difference between revisions
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== '''Genetic and Environmental Factors of High Adiposity''' == | == '''Genetic and Environmental Factors of High Adiposity''' == | ||
High adiposity, specifically in abdominal regions, can serve as a positive indicator of the potential risk of cardiac disease and diabetes mellitus. <ref>Despre´s JP (2006) Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic riskEuropean Heart Journal Supplements 8: B4–B12</ref> Both of these diseases along with other conditions are of increased risk when suffering from obesity. This high abdominal adiposity can be independent of body weight, as observed in the normal weight obesity phenotype, and can be evaluated by measuring the waist circumference, or more reliably, the waist-to-hip ratio. <ref>Burkhauser R V, Cawley J (2008) Beyond BMI: The value of more accurate measures of fatness and obesity in social science research Journal of Health Economics 27: 519–529 </ref> | |||
Obesity and fatness are thought to be largely inheritable features <ref> Farooqi, S. and O’Rahilly, S (2005) MONOGENIC OBESITY IN HUMANS Annu. Rev. Med. 2005. 56:443–58 </ref> . <ref>Despre´s JP (2006) Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic riskEuropean Heart Journal Supplements 8: B4–B12</ref> This has been concluded from several family, twin and adoption studies. However, twin studies tend to indicate heritability more so than adoption or family studies. <ref>Maes, H. H. M., Neale, M. C. and Eaves, L. J. (1997) Genetic and Environmental Factors in Relative Body Weight and Human Adiposity. Behavior Genetics, 27: 4</ref> <ref> Farooqi, S. and O’Rahilly, S (2005) MONOGENIC OBESITY IN HUMANS Annu. Rev. Med. 2005. 56:443–58 </ref>… Studies have also recognised genetic variance among fat deposition patterns, showing that some individuals store more fat abdominally than others. Evidence for this comes from studies between monozygotic and dizygotic twins, between biological siblings and adopted siblings and between children living with their biological parents and children living with foster parents. <ref>Hasstedt, S. J., Ramirez, M.E., Kuida,H. and Williams, R. R. (1989) Recessive Inheritance of a Relative Fat Pattern. Am. J. Hum. Genet. 45:917-925</ref> | |||
[[User:Catriona Thompson|Catriona Thompson]] 20:15, 14 November 2011 (UTC) | |||
== '''Disorders linked to NWO''' == | == '''Disorders linked to NWO''' == | ||
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The prevalence of obesity has risen rapidly in recent years and shows no clear signs of slowing down; thus in the USA for example, the prevalence of obesity has increased from ~13% to almost 30% from the 1960s to present time.[1]
To clinically classify a person as being obese, their Body Mass Index (BMI) must be equal to or greater than 30kg/m2. However, the spectrum of obesity is quite large. Normal Weight Obesity (NWO), found in almost half of the American adult population, is when a person has a normal BMI (18.5- 24.9 kg/m2) but also has a high percentage of body fat(>23.1% for men and >33.3% for women) as well as heart and metabolic disturbances. [2]
Measuring BMI does not take into account muscle or bone mass, and as both are denser than fat, people can have an ‘obese’ BMI while they actually have a healthy percentage of body fat. Conversely, a person can have a normal BMI and be in the normal weight range but have unhealthily high adiposity levels. High percentages of body fat tissue are high risk factors for the diseases and disorders linked to obesity, including diabetes, ischemic heart disease, heart failure, hypertension and sleep apnea. [3] Catriona Thompson 19:50, 25 October 2011 (UTC)
Measuring Normal Weight Obesity
The 'gold standard' definition of obesity is considered to be an excess in Body Fat (BF), but the BMI is used by clinicians and epidemiologists as a means of defining the presence of adiposity and/or obesity. The advantages of using the BMI instead of BF values is that it is a lot simpler to use and easy to reproduce. Studies showing the association between extreme BMI values and increased mortality further support its usage. However, this test fails to differentiate between elevated BF and preserved/ increased lean mass in patients with a BMI below 30kg/m2 - i.e. those not clinically classified as obese.
The strong relationship between high adiposity and metabolic disturbances makes it vital to try find a more accurate way in which to determine adiposity other than BMI.
The definition of metabolic syndrome covers the following criteria:
1) Waist circumference (>102 cm in men and >88 cm in women)
2) HDL (<1.04mmol/L in men and <1.03mmol/L in women)
3) Triglycerides (>1.7mmol/L)
4) Blood Pressure (systolic blood pressure >130mmHg or diastolic blood pressure >85mmHg)
5) Fasting Glucose (>5.5mmol/L)
Genetic and Environmental Factors of High Adiposity
High adiposity, specifically in abdominal regions, can serve as a positive indicator of the potential risk of cardiac disease and diabetes mellitus. [4] Both of these diseases along with other conditions are of increased risk when suffering from obesity. This high abdominal adiposity can be independent of body weight, as observed in the normal weight obesity phenotype, and can be evaluated by measuring the waist circumference, or more reliably, the waist-to-hip ratio. [5]
Obesity and fatness are thought to be largely inheritable features [6] . [7] This has been concluded from several family, twin and adoption studies. However, twin studies tend to indicate heritability more so than adoption or family studies. [8] [9]… Studies have also recognised genetic variance among fat deposition patterns, showing that some individuals store more fat abdominally than others. Evidence for this comes from studies between monozygotic and dizygotic twins, between biological siblings and adopted siblings and between children living with their biological parents and children living with foster parents. [10] Catriona Thompson 20:15, 14 November 2011 (UTC)
Disorders linked to NWO
There are a large number of metabolic complications that result from excess body fat, as well as a number of mechanical complications directly associated with excess body fat (table 1 and 2). Studies involving subjects with normal BMI have reported conflicting finding to the widely held belief; that maintaining a normal weight automatically protects against disorders such as increased adiposity and tendency to develop metabolic syndrome, which often causes type 2 diabetes.
Table 1. Metabolic complications of obesity[11]
| Metabolic complications of obesity |
|---|
| Type 2 diabetes |
| Hypertriglyceridemia/
Low HDL cholesterol |
| Hypertension |
| Non-alcoholic fatty liver disease/
Non-alcoholic steatohepatitis |
| Inflammation |
| Hyperuricemia (excess uric acid) |
| Insulin resistance |
| Polycystic ovarian syndrome |
Table 2. Mechanical complications of obesity[11]
| Mechanical complications of obesity |
|---|
| Gastroesophageal reflux disease |
| Obstructive sleep apnea |
| Degenerative joint disease |
The effect of free fatty acids (FFA) on glucose metabolism in human has been studied extensively. Studies have established that obesity and increased plasma FFA concentrations are risk factors for the development of type 2 diabetes. Elevated plasma FFA concentrations upregulate glucose production and impair muscle glucose uptake, oxidation and storage. Increased insulin release can also result, as well as pancreatic beta-cell dysfunction.
In addition to their effects on glucose metabolism and risk of diabetes, increased FFA concentrations have been shown to associated with ischemic heart disease. [11]
To support this increase in insulin secretion, another study showed that adult-onset NWO individuals show hyperinsulinism, and also an increase in fat cell size, compared to obese patients of similar age, height and weight. The subjects in this study also showed hypertriglyceridemia, which is associated with HDL deficiency, atherosclerosis and pancreatitis. [12]
Hypertension and cholesterol cholelithiasis are also associated with obesity, and can also result in NWO individuals. These conditions have been shown to improve with caloric restriction both in obese and NWO patients. It is still not clear how subtle increases in adiposity and/or hyperinsulinism cause pathogenesis of obesity-related metabolic complications in normal weight individuals.[12]
Early inflammation and greater proinflammatory cytokine levels in plasma is also characterized in NWO women, compared to non-obese women. White body fat, or adipose tissue, is functionally similar to dynamic endocrine organ; it secretes various adipokines including proinflammatory factor, such as TNF-alpha, IL-6 and IL-1. Since they play an essential role in the onset of cardiovascular disease, atherosclerotic processes and insulin resistance, this supports the concept that NWO patients may be predisposed to develop metabolic syndrome and CV disease.[13]
Romero-Corral et al. reported that NWO is strongly associated with cardiometabolic dysregulation and a high prevalence of metabolic syndrome in these individuals is similar to that in overweight subjects. The study shows that in women, NWO is independently associated with an increased risk for CV mortality. They also found a correlation between increased waist circumference (>87cm in men and >82cm in women) and CV risk, which is a similar correlation observed with BF%. Since devices for measuring BF are not widely available in clinical practice, this study reinforces the reliability of waist circumference measurement as an alternative method of prognosis, which is easier and inexpensive.[13]
These studies show that a focus on maintaining "a healthy weight" may need to be shifted to maintaining "a healthy body fat percentage". It is important to be aware that even people with normal weight may have excessive body fat, and that they may be at risk of developing diabetes and heart disease.
Treatments and Prevention
Conclusion
References
- ↑ Romero-Corral A et al. (2010) Normal weight obesity: a risk factor for cardiometabolic dysregulation and cardiovascular mortality Eur Heart J 31:737-46 PMID 19933515
- ↑ Romero-Corral A et al. (2010) Normal weight obesity: a risk factor for cardiometabolic dysregulation and cardiovascular mortality Eur Heart J 31:737-46 PMID 19933515
- ↑ Burkhauser R V, Cawley J (2008) Beyond BMI: The value of more accurate measures of fatness and obesity in social science research J Health Economics 27: 519–29
- ↑ Despre´s JP (2006) Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic riskEuropean Heart Journal Supplements 8: B4–B12
- ↑ Burkhauser R V, Cawley J (2008) Beyond BMI: The value of more accurate measures of fatness and obesity in social science research Journal of Health Economics 27: 519–529
- ↑ Farooqi, S. and O’Rahilly, S (2005) MONOGENIC OBESITY IN HUMANS Annu. Rev. Med. 2005. 56:443–58
- ↑ Despre´s JP (2006) Abdominal obesity: the most prevalent cause of the metabolic syndrome and related cardiometabolic riskEuropean Heart Journal Supplements 8: B4–B12
- ↑ Maes, H. H. M., Neale, M. C. and Eaves, L. J. (1997) Genetic and Environmental Factors in Relative Body Weight and Human Adiposity. Behavior Genetics, 27: 4
- ↑ Farooqi, S. and O’Rahilly, S (2005) MONOGENIC OBESITY IN HUMANS Annu. Rev. Med. 2005. 56:443–58
- ↑ Hasstedt, S. J., Ramirez, M.E., Kuida,H. and Williams, R. R. (1989) Recessive Inheritance of a Relative Fat Pattern. Am. J. Hum. Genet. 45:917-925
- ↑ 11.0 11.1 11.2 Jensen M.(2009) Normal weight obesity. International Chair on Cardiometabolic Risk 2(1), 23-30
- ↑ 12.0 12.1 Ruderman N, Chisholm D, Pi-Sunyer X, Schneider S (1998) The metabolically obese, normal-weight individual revisited Diabetes 47:699–713
- ↑ 13.0 13.1 A Romero-Corral, VK Somers, J Sierra-Johnson, Y Korenfeld, S Boarin, J Korinek, MD Jensen, G Parati and F Lopez-Jimenez,(2010) Normal weight obesity: the risk factor for cardiometabolic dysregulation and cardiovascular mortality, European Heart Journal, Vol. 31; 737-746