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This paper explores metabolic syndrome X. The paper gives background information about the condition citing the precursors of the disease and major components as identified by the National Cholesterol Education Program’s Adult Treatment Panel III (ATP III). The paper goes ahead to explain in details the causes and pathogenesis of the disease as well as highlighting its diagnosis and treatment. The article concludes by outlining the prevalence of the condition noting genetic and ethnic factors that determine people at higher risk of getting the disease.
Metabolic Syndrome X is a combination of risk factors that increases chances of developing cardiovascular complications and diabetes. The condition results from body’s resistance to insulin. There are a number of risk factors associated with the condition. These include body’s resistance to insulin, obesity, particularly in the abdominal region, hypertension, lipid, and blood clotting disorders as well as glucose intolerance. The condition is a lifestyle condition whose cause is a genetic component. It is clinically diagnosed in the laboratory, though signs, such as fat deposition along the waistline may serve as strong indicators of its presence. The National Cholesterol Education Program’s Adult Treatment Panel III (ATP III) has identified six components of the condition that strongly relate to cardiovascular diseases. These include insulin resistance, hypertension, atherogenic dyslipidemia, proinflammatory state, visceral obesity, and prothrombotic state (Fogoros, 2008).
Causes and Pathogenesis
This condition traces its etiology in genetic and environmental factors. Family lineage common with type two diabetes, high blood pressure, and early cardiac diseases significantly increase the probability of developing the metabolic syndrome X. Environmental factors, such as individual inactivity and sedentary lifestyle as well as excessive weight gain also plays a major role in progression of metabolic syndrome.
There are three probable etiological components that combine to cause metabolic syndrome i.e. obesity and adipose tissue anomalies, insulin resistance, and independent factors. These components present a complex relationship between themselves leading to the development of the syndrome. Visceral obesity can cause insulin resistance because of abnormal glucose tolerance, high levels of blood glucose, and type II diabetes. There are a number of pathophysiological changes associated with abdominal obesity. These include endocrine changes e.g. activation of renin-angiotensin system and release of adipocytokines into circulation, raised activity of the sympathetic nervous system, and sodium retention and volume expansion (Karst, 2010). Inflammatory markers e.g. C-reactive proteins are also closely associated with obesity and appear to mediate progress of diabetes as well as cardiovascular complications.
Insulin resistance plays more major role in pathogenesis of metabolic syndrome than obesity according to the majority of investigators (Mendelson, 2007). It causes obesity by raising the fat content in the body. In addition, excess nonesterified fatty acids (NEFA) are diverted to the liver, when muscles resistant to insulin are saturated with lipids due to high plasma levels of NEFA. This results to fatty liver and atherogenic dyslipidemia. Other independent factors that cause the condition include lipoprotein metabolism, senility, proinflammatory state, and endocrine factors.
Metabolic Syndrome is clinically diagnosed in the laboratory. A combination of three of the following parameters confirms the presence of the condition: a) abdominal obesity. This leads to an elevated waistline of over 102 centimeters in men and 88 cm and above in women; b) elevated serum triglycerides of 150ml/dl or more; c) low levels of High Density Lipoproteins or good cholesterol i.e. below 40mg/dl in men and below 50mg/dl in women. d) increased blood pressure i.e. 130/85 mm Hg and above and high fasting blood glucose of 110 mg/dl and above.
Metabolic syndrome X is treatable through different therapeutic interventions, such as treating insulin resistance, clotting and lipid disorders and hypertension. Although, there is no direct therapeutic intervention for insulin resistance in metabolic syndrome, the process can be reversed through diet and physical exercise. Weight reduction to within 20% of an individual’s ideal body weight and increased body exercise reverses the situation and hence reduces the probability of developing cardiovascular conditions.
Common lipid anomalies associated with metabolic disorder i.e. low High Density Lipoproteins (HDL), high Low Density Lipoproteins (LDL), and high triglycerides are responsive to exercise and weight loss. However, this does not compensate for drug therapy. Initial drug intervention targets at lowering the LDL followed by the triglycerides and finally increasing the HDL levels. Daily aspirin therapy, on the other hand, lowers chances of intravascular blood clotting, whereas hypertension can be treated using ACE inhibitors and diuretics (Karst, 2010).
The condition is more prevalent in men as compared to women. There is also varying prevalence patterns between ethnic groups, with Mexican-American women having the highest prevalence rate. There is a paradoxical observation among the African Americans. Despite the fact that obesity and high blood pressure are more prevalent in African Americans in comparison to the whites, the latter have high prevalence of metabolic syndrome than the former (Park et al., 2003). In comparison to the whites, males of African American descent have lower incidences of elevated waistline, increased levels of triglycerides, and low levels of ‘good’ cholesterol (HDL). High incidences of high blood pressure are also observed in this group. The ethnic difference in prevalence of this condition is a strong indicator of an inheritable (genetic) factor that contributes to the development of the condition.
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