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Metabolic Syndrome: Contributing Factors and Treatment Strategies

Posted on: Saturday, 20 August 2005, 03:00 CDT

Abstract: Metabolic syndrome is associated with increased risk for cardiovascular and cerebrovascular disease. The World Health Organization and National Cholesterol Education Program Adult Treatment Panel III have identified physiologic abnormalities associated with metabolic syndrome, including impaired glucose metabolism, high blood pressure, elevated cholesterol levels, and abdominal obesity. It is estimated that 47 million Americans have metabolic syndrome. A variety of therapies may help reduce the incidence and risk, including diet, weight loss, physical exercise, glycemic control, and pharmacological treatments. Nursing care is focused on developing an individualized plan of care that includes family members and providing education, psychosocial support, close monitoring, and continued follow-up to ensure adherence and success in achieving patient outcomes.

An aggregate of several metabolic and nonmetabolic abnormalities characterizes metabolic syndrome, which predisposes individuals to atherosclerotic disease, including cerebrovascular disease (Grundy, 2002; Isomaa et al., 2001). Many other names, including syndrome X, dysmetabolic syndrome, insulin resistance syndrome, plurimetabolic syndrome, and the deadly quartet have been used to describe this condition. This article discusses the history, definition, prevalence, etiology, and consequences of metabolic syndrome. A multifaceted treatment approach that includes neuroscience nursing patient education and support also is discussed.

History and Definitions

Metabolic syndrome was first described early in the 20th century as a clustering of several vascular risk factors, including hypertension, obesity, and gout. The syndrome was reintroduced as syndrome X in the 1980s, defined as the concurrence of hypertension, dyslipidemia, abnormal glucose metabolism, and obesity (Barnard, Roberts, Varon, & Berger, 1998). In 1988, the World Health Organization (WHO) proposed a unifying definition for metabolic syndrome that was later modified in 1999 (World Health Organization, 1999). According to the newer WHO definition, a person with metabolic syndrome has abnormal glucose metabolism (type 2 diabetes, glucose intolerance, or insulin resistance), plus two additional physiologic abnormalities. Additional physiologic abnormalities may include hypertension (> 140/90 mmHg), dyslipidemia (triglycrides > 1.7 mmol/1 or high-density lipoproteins < 0.9 in men and < 1 in women), obesity (body mass index [BM] > 30 kg/m^sup 2^ or waist/hip ratio [WHR] > 0.9 in men and > .85 in women), and microalbuminuria (albumin excretion > 20 ug/min; Alberti & Zimmet, 1998).

Proposed modifications to this definition have included changing the cutoff for the WHR to > 1 in men and > 0.9 in women. In 2001, a simpler and more easily applicable working diagnosis was proposed by the National Cholesterol Education Program (NCEP). This definition was based on the presence of any three of the following: fasting serum glucose > 6.1mmol/l, hypertension > 130/85 mmHg, hypertriglyceridemia > 1.7 mmol/1, low high-density lipoproteins HDL < 1 mmol/1 in men and <1.3 mmol/1 in women, and central obesity with waist circumference > 102 cm in men and > 88 cm in women (Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults, 2001).

Obesity, a major component in metabolic syndrome, is measured according to BMI as weight in kilograms divided by the square of height in meters (kg/m^sup 2^). Obesity is defined as a WHR > .90 in men and > .85 in women. In metabolic syndrome, waist circumference is important as a diagnostic tool because it most accurately predicts the absolute amount of visceral adipose tissue.

Along with the core components of metabolic syndrome- hypertension, abnormal glucose metabolism, dyslipidemia, and obesity- additional metabolic abnormalities have been identified. These associated abnormalities include microalbuminuria, hyperuricemia, fatty liver disease, deficient fibrinolysis with elevated fibrinogen and plasminogen activator inhibitor levels, and evidence of chronic inflammation, such as increased C-reactive protein (CRP) levels (Bray & Champagne, 2004; Eckel, Barouch, & Ershow, 2002).

Prevalence and Demographics

The exact prevalence of metabolic syndrome varies, depending on the definition used. Prevalence was recently assessed using the WHO and NCEP definitions. According to the WHO definition, 25.1% of the U.S. population meets the diagnostic criteria for metabolic syndrome; with the NCEP definition, this prevalence becomes 23.9% (Ford & Giles, 2003).

Men generally are at increased risk for metabolic syndrome, and certain populations, particularly Black men, have been found to have a greater incidence of metabolic syndrome (Fords & Giles, 2003). In other studies, Mexican women and persons from the Indian subcontinent also had increased frequency of metabolic syndrome (Das, 2002; Ford, Giles, & Dietz, 2002).

Population sample studies have demonstrated the prevalence of metabolic syndrome increases with age. In one investigation, 6.7% of persons younger than 30 years of age were diagnosed with metabolic syndrome, whereas 40% of people 60 years of age and older met the criteria for diagnosis (Cleveland Clinic Health Information Center, 2003; Ford, Giles, & Dietz, 2002). Approximately 25% U.S. of the population has metabolic syndrome, or one in four adults (Ninomiya et al., 2004). According to recent estimates, 47 million Americans have metabolic syndrome (Isomaa, 2003).

Contributing Factors

Metabolic syndrome is associated with risk for vascular alterations. Various theories have been proposed to explain the clustering of multiple vascular risk factors in persons with the metabolic syndrome. Underlying theories have included endothelial dysfunction, systemic inflammation, sympatho-adrenal abnormalities, and the interplay between genetic predisposition and environmental factors.

Vascular endothelium is a dynamic tissue with multiple functions, including vascular tone regulation, platelet adhesion, coagulation activity, and fibrinolysis. Endothelial dysfunction implies alterations in one or more of these functions, but impaired tone is believed to be a particular consequence of metabolic syndrome. This finding may be due to loss of nitric oxide, which normally relaxes the vascular wall (Isomaa, 2003).

Low-grade systemic inflammation is believed to contribute to the pathophysiology of various components of metabolic syndrome. Markers of systemic inflammation, such as C-reactive protein (CRP), have been positively correlated with hypertension, abnormal glucose metabolism, hyperlipidemia, and obesity (Das, 2002). Adipose tissue can activate inflammatory mediators such as cytokines, which increase CRP levels (Bray & Champagne, 2004; Keller & Lemberg, 2003). Adipose tissue also has been linked to increased plasminogen activator inhibitor-1 activity, which prevents fibrinolysis (Bray & Champagne, 2004; Ecke et al, 2002). Accordingly, the beneficial effects of exercise and aspirin on metabolic syndrome and its components have been attributed at least partially to anti- inflammatory effects, though the mechanism for exercise remains unknown.

Psychological stress, which activates the sypatho-adrenal system and results in chronically increased cortisol levels and sympathetic tone, also has been evaluated as a potential contributor to metabolic syndrome. Clinical and biochemical similarities have been noted between hypercortisolism and metabolic syndrome by previous investigators (Isomaa, 2003).

Heredity is believed to play a major role in the predisposition towards metabolic syndrome. Heredity already has been identified as a risk factor in hypertension, glucose dysmetabolism, dyslipidemia, and obesity. Candidate genes for metabolic syndrome have included regulators of lipolysis and those affecting obesity and insulin sensitivity. Genetic adaptation to rural environments with low or unstable food supplies, which induces maximal energy storage in the form of adipose tissue, has been proposed as an explanation for the frequent occurrence of metabolic syndrome in persons who move to urban environments with more reliable and consistent food sources (Groop & Orho-Melander, 2001).

Modern-day sedentary lifestyles and concurrent low cardiorespiratory fitness levels have been linked to an increased frequency of metabolic syndrome. Conversely, physical activity has been shown to decrease the risk of developing metabolic syndrome due to decreased body fat and increased cardiovascular fitness (Rennie, McCarthy, Yazdgerdi, Marmot, & Brunner, 2003).

Metabolic Syndrome Effects

Metabolic syndrome has been associated with a threefold increase in the prevalence of coronary artery disease and ischemic cerebrovascular disease, and an overall increase in mortality (Bonora et al., 2003; Ginsberg, 2003). Clinical studies on the effect of metabolic syndrome upon coronary artery disease and ultrasound studies of the progression of carotid atherosclerotic disease have demonstrated markedly increased risks in persons with metabolic syndrome compared with nonmetabolic syndrome controls (Bonora et al., 2003). Even in women younger than 45 years of age, metabolic syndrome has been found to be a dominant predictor of nonfatal myocardial infarction (Amowitz, Ridker, Rifai, Loughrey, & K\omaroff, 2004).

Treatment Strategies

There is no predefined standard of care for metabolic syndrome. Treatment is multifaceted and involves collaborative efforts from a multidisciplinary team that includes registered nurses, dietitians, physical and exercise therapists, physicians, pharmacists, and social workers. Developing the plan of care by setting realistic goals and progressive, personalized activity schedules are key to success. Early diagnosis is critical to reverse or slow the development of vascular complications. Treatment strategies have focused on individual components of the condition, and have included lifestyle modifications and medication-directed therapies. Rennie McCarthy, Yazdgerdt, Marmoth, and Brumer (2003) found that lifestyle changes that include dietary modifications and regular exercise have reduced obesity and the incidence of diabetes dramatically, in addition to lowering lipid levels and blood pressure.

A carbohydrate-rich, low fat diet is recommended for dyslipidemia management. In addition, Davy and Melby (2003) suggest ingesting 3- 10 grams of soluble fiber daily to optimize serum lipid and lipoprotein concentrations. Such measures have been found to decrease obesity and lower risk for cardiovascular disease, cerebrovascular disease, diabetes, and cancer.

Both the eating habits and exercise patterns of children must be monitored to detect and deter them from developing metabolic syndrome (Mooney, 2004). Efforts to break the cycle of overweight children becoming overweight adolescents and overweight adults are critical to decrease the incidence of metabolic syndrome. The rate of metabolic syndrome is increasing among very young people; some studies have demonstrated a lower incidence of hypertension, diabetes, and obesity in breast-fed infants (Das, 2002). All members of the healthcare team need to highlight the complications of obesity and diabetes (which often go unrecognized) to both children and their parents.

Weight must be monitored and the BMI calculated before treatment begins, and reassessed after treatment ends. Because central abdominal adiposity is a measure of obesity, waist circumference also should be measured and monitored. A combination of proper diet and adequate exercise is recommended to enhance weight loss potential. Inform patients that weight loss also can result in a decrease in total cholesterol, low-density lipoprotein (LDL), and triglyceride levels, as well as improved blood pressure with an increase in HDL cholesterol. Ultimately, glucose tolerance and insulin sensitivity increase, and plasminogen activator inhibitor-1 levels are lowered (Bray, 2002).

Because low physical activity levels can increase a person's likelihood of developing insulin resistance and type 2 diabetes, it is a key target area for treatment. Neuroscience nurses can provide patient education on the importance of regular exercise, facilitate referrals to rehabilitation specialists, and assess patients' interests and abilities in physical activity. Rennie et al. (2003) found that moderate and vigorous physical activities are associated with a decreased risk of metabolic syndrome, independent of age, smoking habits, and alcohol use. A safe, progressive fitness program, which is critical to minimizing risk, will help ensure success in achieving weight loss goals and decrease the risk for vascular disease. Nurses should educate patients on risks and benefits of physical activity throughout the activity monitoring process.

Patients with metabolic syndrome may be prescribed medications to treat hypertension, diabetes, and dyslipidemia. Antithrombotic therapy also may be necessary. Antihypertensive drugs have been found to decrease cardiovascular mortality and vascular events (myocardial infarction, cerebral infarction, vascular mortality) by approximately 25%-40% (Ginsberg, 2003). Thiazide diuretics and angiotensin converting enzyme (ACE) inhibitors have been shown to be especially effective in preventing ischemic cerebrovascular disease. Current national guidelines suggest maintaining blood pressure below 120/80 mmHg, with prehypertension defined as 130-139/80-89 mmHg, and below 130/80 mmHg in diabetic patients (Chobanian et al., 2003). No guideline is designated specifically for obesity and metabolic syndrome.

Educating patients on actions, side effects, and dosing schedules is an important role for all nurses. Compliance is enhanced with education, blood pressure monitoring, dosage adjustments, and necessary medication changes.

Statin medications have recently shown dramatic efficacy for reducing major cardiovascular and cerebrovascular events, and for decreasing vascular mortality in patients with preexisting cerebral and cardiac vascular disease. Statin therapy is advocated to achieve appropriate LDL goals. LDL goals are individualized, but general recommendations by the Expert Panel on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (2001) include < 100 mg/dL as an optimal level, and 100-129 mg/dL for near-optimal/ above-optimal levels. If triglycerides are higher than 200 mg/dL, treatment is recommended to achieve a non-HDL goal that is 30 mg/dL higher than the LDL goal (Zelis, 2003).

Fibrate medications, such as gemfibrozil (Lopid) and fenofibrate (TriCor), have shown similar efficacy in one trial, and niacin has been found effective in decreasing LDL/triglyceride levels and increasing HDL levels (Ginsberg, 2003). Tight glycemic control with blood glucose levels between 60-100 mg/mL and stringent management of cardiovascular risk factors is advocated for diabetic patients (Campbell, 2003).

Anticoagulation with warfarin is indicated for patients with atrial fibrillation, and antiplatelet agents are used for patients with coronary artery disease or ischemic cerebrovascular disease. Antiplatelet agents include aspirin alone, clopidogrel alone, aspirin plus clopidogrel, or a combination of aspirin and extended- release dipyridamole. Of these agents, aspirin and aspirin- containing products have been hypothesized to work by both inhibiting platelet aggregation and decreasing systemic inflammation. Of the medications previously discussed, ACE inhibitors and statin agents also have been hypothesized to possess anti-inflammatory properties, and, subsequently, reduce stroke risk.

Family members and significant others need to be involved in the teaching and plan of care for individuals with metabolic syndrome and those at risk for its development. Education and psychosocial support to encourage therapeutic adherence to dietary changes, increased physical activity, and risk factor management are essential parts of patient care (Berra, 2003; Minehira & Tappy, 2002).

Stress is a contributing factor for metabolic syndrome; consequently, it is important to identify stressors and effective strategies to decrease or alter a person's response to stress, if the stressors cannot be eliminated. Referrals to mental health specialists may be warranted. Support groups appropriate for individual situations and stressors also may be suggested.

Close monitoring and continued follow-up are key to treatment success. Insurance issues may at times limit availability of preventive strategies. Therefore, neuroscience nurses are challenged to be collaborative and creative in their approaches to individualized patient care.

Summary

Metabolic syndrome is a complex syndrome of abnormal metabolic and physiologic parameters that increases a person's risk for cardiovascular and cerebrovascular disease. Education and lifestyle changes, however, may reduce the incidence of metabolic syndrome. Neuroscience nurses are in key positions to facilitate collaborative interventions that decrease risk for metabolic syndrome and associated diseases.

Modern-day sedentary lifestyles and concurrent low cardiorespiratory fitness levels have been linked to an increased frequency of metabolic syndrome.

References

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Questions or comments about this article may be directed to Susan B. Fowler, PhD, RN, CNRN, 163 Essex Ave., Unit 106, Metuchen, NJ 08840, or via e-mail to njfowlers761@msn.com. She is associate professor/nurse scientist, University of Medicine and Dentistry of New Jersey School of Nursing, The University Hospital, Newark, NJ.

Michael Moussouttas, MD, is assistant professor of Neurology, Cerebrovascular and General Neurology, New Jersey Neuroscience Institute, Seton Hall University, Edison, NJ.

Barbara Mancini, MBA RN CNRN CNNA, is director, Neurosciences Services, Inova Fairfax Hospital, Falls Church, VA.

Copyright 2005 American Association of Neuroscience Nurses 0047- 2606/05/4/00220$5.00

Copyright American Association of Neurosurgical Nurses Aug 2005

Source: Journal of Neuroscience Nursing

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