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https://studentshare.org/nursing/1471380-metabolic-syndrome.
The most used criteria are those of the NCEP-ATP III, and IDF. According to the research carried out on US residents using the NCEP-ATP III standards, the unadjusted and age-adjusted prevalence of MetS were 21.8% and 23.7%, respectively (Byrne, 2011). Prevalence is higher when using IDF standards than using the NCEP-ATP III standards. For instance, in the comparison of the two organization’s standards, the age-adjusted prevalence of MetS established by NCEP-ATP III was 24.5%, whereas that of IDF was 43.4%. In other words, the prevalence of MetS rises consistently with increasing age unconventionally of sex, from 6.
7% in individuals aged 20 to 29 years, to 43.5% for individuals aged 60 to 69 years, and 42% for individual aged 70 years and older (Byrne, 2011). In addition, although there is no postulated information for adolescents and children, the overall prevalence of MetS in these groups is approximated to be 4.2% (6.1% for boys and 2.1 for girls), increasing to 6.8% amongst overweight and 28.7% in obese adolescents. Also, the study indicates that, the prevalence of MetS are similar for men and women, however, higher in black women than men, and lower in white women than men (Codario, 2011).
The underlying pathophysiology for MetS is still an issue of concern amongst various professional organizations resulting to inconsistencies in the way MetS is defined. Each definition has its benefit and drawbacks. However, insulin resistance and obesity has been identified to be the key contributing factors. Although insulin resistance is the core cause of glucose and fatty acid tolerance, it does not enlighten the alterations seen in endothelial dysfunction, lipid metabolism, systemic inflammation, blood pressure, and hypercoagulability.
Laboratory measurement of insulin resistance is challenging, and, however, researches have indicated fasting insulin levels as a substitute, absence of analyze standardization makes this approach impractical (Awad, 2010). On the other hand, other exponents have suggested that although abdominal obesity may be the key cause of MetS, still insulin resistance occur in up to 15% of non-obese individuals. High free fatty acids can promote hypercholesterolemia, impact endothelial dysfunction, and impair insulin sensitivity, thus encouraging hypertension (Kurian, & Thompson, 2012).
Adipose tissue has been denoted to be an active endocrine organ that impacts inflammatory cytokines, generates adipokines, affects insulin resistance, and influence CV risk by playing a role in impaired glucose tolerance, hypertension, and dyslipidemia, thus strengthening the link between inflammatory and obesity (Kurian, & Thompson, 2012). All these approaches have been attributed to the pathophysiology of MetS. However, the question is, “why is the pathophysiology of metabolic syndrome significant?
” Metabolic syndrome raises the individual risk of coronary artery disease (CAD), even beyond CAD caused by high LDL cholesterol alone. This helps the patient and all healthcare providers to take measures of preventing and managing CAD immediately (Preedy, & Watson, 2010). Metabolic syndrome is described by several signs and symptoms. These involve elevated triglycerides, large waist circumferences (abdominal obesity), low levels of HDL, high blood pressure, and high fasting blood glucose. As suggested by NCEP-ATP III, criteria used in diagnosis for metabolic syndrome involve body size, level of blood glucose, individual’
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