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SECTION 2 Chronic and Acute Illness CHAPTER CHAPTER 5 Insulin Resistance and the Metabolic Syndrome Chapter Topics Introduction Insulin Resistance and the Metabolic Syndrome Risk Factors, Prevention, and Management of the Metabolic Syndrome The Role of Hyperinsulinemia in the Metabolic Syndrome Causes and Management of Gout Causes and Management of the Polycystic Ovary Syndrome Medication Issues with Insulin Resistance The Role of the Nurse or Other Health Care Professional in Prevention and Management of the Metabolic Syndrome Objectives After completing this chapter, you should be able to: ■ Describe the metabolic syndrome. ■ Identify individuals at risk for the metabolic syndrome. ■ Recognize an appropriate lifestyle plan for preventing and managing insulin resistance. ■ Explain the application of the Dietary Guidelines in managing insulin resistance. Terms to Identify Acanthosis nigricans Glucagon Lipoprotein lipase Androgens Glycemic index Metabolic obesity Atherosclerosis Gout Nonalcoholic fatty liver C-peptide Hirsutism disease C-reactive protein (CRP) Hyperglycemia Oral glucose tolerance test Central obesity Hyperinsulinemia (OGTT) Cutaneous papilloma Hypoglycemia Polycystic Ovary Syndrome (PCOS) Dyslipidemia Impaired fasting glucose Prediabetes Endometrial hyperplasia Impaired glucose tolerance Thrifty gene Ferritin Insulin resistance 151 152 SECTION 2 Chronic and Acute Illness INTRODUCTION It has been over 10 years since the metabolic syndrome received ofﬁcial recognition. It was considered a theory before then. The metabolic syndrome, also known as the insulin resistance syndrome, was initially called Syndrome X. Insulin resistance describes a condition in which the body cells resist the action of insulin, leading to poor use of blood glucose at the cellular level. Various causes have been suggested, from hormonal and enzymatic factors to issues of inflammation and problems with cellular structures. It is now well recognized that lifestyle and diet exert their influence on individuals with a genetic tendency toward insulin resistance. Obesity and lack of physical activity are known to worsen the genetic predisposition to insulin resistance. The metabolic syndrome is often discussed in terms of the common gene theory because it is commonly found. An estimated 40% of U.S. adults between the ages of 40 and 74 have prediabetes (see later section). The rate of insulin resistance in some populations is as high as 60%. Insulin resistance is also associated with the common gene theory because it is the underlying cause of many chronic health problems. About one third of persons with insulin resistance go on to develop type 2 diabetes. Most individuals with type 2 diabetes still have hyperinsulinemia. However, the amount of insulin produced is not adequate to overcome the resistance at the cellular level. The result is high blood glucose levels or diabetes mellitus (see Chapter 8). The World Health Organization (WHO) has estimated that there will be around 300 million persons with diabetes by 2025. It is anticipated that Asia will be at the forefront because of a genetic tendency for insulin resistance along with changing lifestyles. Obesity is now an epidemic throughout the world and is found with the health problems of the metabolic syndrome, including type 2 diabetes, hypertension, and hyperlipidemia (see Chapter 7). The medical community faces an emerging epidemic of type 2 diabetes in children and adolescents as the obesity epidemic continues (Miller and Silverstein, 2005). It is further predicted there will be an epidemic of early cardiovascular morbidity and mortality in years to come unless the epidemic of obesity is stemmed (Pontiroli, 2004). This chapter provides an overview of the metabolic syndrome. Other chapters in Section Two expand on the speciﬁc health problems associated with this syndrome, including central obesity, coronary heart disease, and diabetes, with the resulting adverse effects on the kidneys. Research is expanding on other health conditions associated with the metabolic syndrome, such as certain forms of cancer. As this section points out, the health problems associated with insulin resistance are realized only through environmental factors, with diet playing a large role. WHAT IS THE METABOLIC SYNDROME? The National Cholesterol Education Program’s Adult Treatment Panel III deﬁnition uses easily measured clinical ﬁndings of increased abdominal circumference, elevated triglycerides, low levels of high-density–lipoprotein cholesterol (HDL-C), elevated fasting blood glucose, and/or elevated blood pressure. Three of these ﬁve are required for diagnosis of the syndrome. Gout (a condition related to high levels of uric acid; see later in this chapter) is often found with the metabolic syndrome as well. Insulin Resistance and the Metabolic Syndrome CHAPTER 5 153 There are different deﬁnitions of the criteria to use in making the diagnosis of the metabolic syndrome. The American Association of Clinical Endocrinologists has identiﬁed the following risk factors: ■ Obesity or overweight body mass index (BMI) >25 (especially with central obesity or metabolic obesity—carrying weight in the abdomen or having a high waist-to-hip ratio; see Chapter 6) ■ Elevated triglycerides: 150 mg/dL (1.69 mmol/L) ■ Low HDL cholesterol Men <40 mg/dL (1.04 mmol/L) Women <50 mg/dL (1.29 mmol/L) ■ Elevated blood pressure ≥130/85 mm Hg ■ 2-Hour postglucose challenge >140 mg/dL (199 mg/dL; prediabetes) ■ Fasting glucose between 110 and 126 mg/dL (6.15 and 7.05 mmol/L; prediabetes) ■ Other risk factors: Family history of type 2 diabetes, hypertension, or cardiovascular disease (CVD) Polycystic ovary syndrome (PCOS): a clinical diagnosis based on high levels of male hormones, male pattern hair growth, and ovarian cysts (see later in this chapter) Sedentary lifestyle Advancing age Ethnic groups having high risk for type 2 diabetes or CVD Diagnosis depends on clinical judgment based on risk factors. One condition found with the metabolic syndrome includes atherosclerosis (a buildup of plaque in the arteries and blood vessels; see Chapter 7). Although there are a variety of causes of atherosclerosis, an association with diabetes is well known. Because atherosclerosis generally is noted before the diagnosis of diabetes, it is believed that excess insulin related to insulin resistance promotes the plaque buildup. An increased tendency to form clots is also found with the metabolic syndrome and type 2 diabetes and can cause a variety of circulatory problems. Therefore persons with the metabolic syndrome are at increased risk of heart disease. Certain cancers have been associated with the metabolic syndrome. Known cancers related to the metabolic syndrome include cancers of the breast, pancreas, liver, and colon and uterine (endometrial) cancer. An epidemic pattern of colon cancer and type 2 diabetes among Japanese persons has been noted. However, rates for colon cancer among Japanese in the United States are even higher than among those living in Japan. It is believed that the rise of colon cancer reflects the westernization of food intake (Kuriki et al., 2004). Newer research has linked prostate and ovarian cancers with the metabolic syndrome (see Chapter 10). Other health problems that have recently been connected with the metabolic syndrome and insulin resistance include Nonalcoholic fatty liver disease—a condition of fat buildup in the liver (Brea et al., 2005) and hypothyroidism (Dessein et al., 2004). WHAT MEASUREMENTS CAN HELP DIAGNOSE INSULIN RESISTANCE? A fasting blood glucose between 100 and 125 mg/dL is referred to as impaired fasting glucose and is indicative of prediabetes. Another test that can help diagnose prediabetes is the 2-hour oral glucose tolerance test (OGTT) (blood glucose test 154 SECTION 2 Chronic and Acute Illness performed 2 hours after a 75-g carbohydrate drink). An OGTT blood glucose level of 140 to 199 mg/dL is referred to as impaired glucose tolerance and is indicative of insulin resistance and prediabetes. As hyperinsulinemia is found with insulin resistance, measurements of insulin levels can help conﬁrm the diagnosis of the metabolic syndrome. Insulin is measured using different techniques. One is the ratio of fasting glucose levels to fasting insulin levels. It has been found that a fasting glucose-to-insulin ratio less than 7 may serve as an early identiﬁcation of children at risk for complications of insulin resistance (Silfen et al., 2001). One indirect measure of insulin production is C-peptide. Another lab value increasingly taken into account is the level of C-reactive protein (CRP) (a type of protein found with inflammation). Low-grade chronic inflammation reflected by increased CRP can identify those at risk for type 2 diabetes and coronary heart disease. Over one third of children and adolescents with the metabolic syndrome have been found to have high levels of CRP (Ford et al., 2005). Overweight children and adolescents with a BMI over the 85th percentile (see Chapters 6 and 12) have been found to have elevated CRP and fasting insulin levels (Kelly et al., 2004). Women with PCOS (see section later in this chapter) are often insulin resistant with increased risk for type 2 diabetes and coronary heart disease. Women with PCOS have shown signiﬁcantly elevated CRP concentrations (Kelly et al., 2001). Research is linking high levels of ferritin (a substance that holds iron in the blood) with insulin resistance. High iron stores have been linked to the metabolic syndrome (Jehn et al., 2004). The association between heme iron and diabetes risk may be a result of a relationship between hepatic iron overload and insulin resistance (Piperno et al., 2004). High hemoglobin levels are associated with excess weight, hypertension, hyperlipidemia (see Chapter 7), and hyperinsulinemia (Choi et al., 2003). Heme-iron intake from red meat sources has been positively associated with the risk of type 2 diabetes (Jiang et al., 2004). Body weight measurement is another means of assessment. Individuals in the upper normal weight range (BMI over 23) and mildly overweight range (BMI over 25) are at increased risk for having the metabolic syndrome, and screening is advised to help prevent diabetes and cardiovascular disease (St-Onge et al., 2004). What Do We Know about Risks for Insulin Resistance? Historically, thinking has generally focused on the development of obesity as the cause of insulin resistance and the listed health conditions. This is reflected in warnings that obesity can cause diabetes. However, research continues to indicate that insulin resistance has a strong genetic link. Thus, not everyone with obesity will develop diabetes. Persons who have inherited a genetic predisposition to insulin resistance probably have ancestors who survived repeated bouts of famine. It is likely that several thousands of years ago, before there were restaurants, corner grocery stores, refrigeration, and transportation, many of our ancestors faced continual cycles of famine. Those who were able to survive likely had the ability to be thrifty with food kilocalories. In fact, insulin resistance is often referred to as the thrifty gene theory (being thrifty in calorie expenditure; see Chapter 6 for management of obesity related to insulin resistance). Insulin Resistance and the Metabolic Syndrome CHAPTER 5 155 Many of us have the genetic legacy of those survivors of famine, in that persons who inherit the thrifty gene gain body fat easily in times of plenty. They also tend to have a difﬁcult time losing weight, whether through self-imposed dieting or environmental factors that reduce the food supply. This would have been a survival advantage before a stable food intake could be relied on, but in current times it can result in obesity, type 2 diabetes, and other health problems found with the metabolic syndrome. The Pima Indians of Arizona are the classic example of why it is believed genetic predisposition and environmental conditions allow for the development of the metabolic syndrome. The Pima Indians in the Southwest United States have the highest reported occurrence of obesity and non–insulin-dependent diabetes mellitus in the world. This situation developed only about 100 years ago with the abrupt changes in lifestyle accompanying the rerouting of the Gila River to provide irrigation waters for California. As these Pimas could no longer grow their own foods and their activity levels went down, their lifestyles and dietary intake drastically changed. This has resulted in an epidemic of obesity and diabetes. However, this is in contrast to the low rates of obesity and diabetes among the Pimas living in Mexico (Valencia et al., 2005). The lower rate of diabetes among the Mexican Pimas is attributed to their higher physical activity levels and maintenance of a more traditional diet that emphasizes high-ﬁber foods and low reliance on meat and processed foods. There is some evidence that the risk of the metabolic syndrome may be set in utero. Large babies who were exposed prenatally to their mother’s gestational diabetes or obesity have been noted to be at increased risk for developing the metabolic syndrome in later childhood (Boney et al., 2005). Excess kilocalorie intake during pregnancy is suspected to predispose the infant to later development of the metabolic syndrome (Armitage et al., 2005). Therefore counseling women during pregnancy to avoid excess weight gain and having screening for gestational diabetes with appropriate management may help reduce the rate of diabetes for future generations. See Chapter 11 for pregnancy guidelines. What Population Groups Are Known to Have High Levels of Insulin Resistance? Genetically, certain population groups are known to have high rates of insulin resistance. Native Americans, in general, have a high prevalence of type 2 diabetes. South Paciﬁc Islanders are also at high risk for insulin resistance. Other known groups with high rates of the insulin resistance syndrome include persons with Spanish (i.e., Hispanic and Latino) and South Asian heritage. In Mexico there is an epidemic of obesity, type 2 diabetes, and cardiovascular disease linked with the metabolic syndrome (Sanchez-Castillo et al., 2004). Asian populations may become more susceptible to the metabolic syndrome as a Western diet and lifestyle are adopted. WHO Expert Consultation has advised a BMI (see Chapter 6) of 22 to 25 among the Asian population to reduce the adverse health outcomes of the metabolic syndrome (Rakugi and Ogihara, 2005). Persons with African heritage have a high rate of insulin resistance. Among African-American children a higher rate of type 2 diabetes, along with hyperinsulinemia, obesity, acanthosis nigricans (a skin condition with dark patches related to diabetes—see Figure 5-1 and Chapter 8), and family history of diabetes has been noted as compared to their Caucasian 156 SECTION 2 Chronic and Acute Illness B Figure 5-1 Acanthosis nigricans causes dark patches to A occur on the skin, often in the underarm area as shown, or on the neck; cutaneous papillomas or “skin tags” are also commonly found with insulin resistance and diabetes. counterparts (Arslanian, 2002). Cutaneous papillomas or skin tags are also found with insulin resistance and type 2 diabetes (Figure 5-1). There is a general trend for higher rates of insulin resistance among persons with heritage from regions nearer the equator, such as the Paciﬁc Islanders. There are exceptions to this because insulin resistance is known to occur in all ethnic groups. Finland is one northern country with a relatively high rate of diabetes (Ilanne-Parikka et al., 2004). Among an Irish population the prevalence of glucose intolerance and type 2 diabetes was noted to be almost 15% (Smith et al., 2003). In a study of French families, the metabolic syndrome was found to increase with age (Maumus et al., 2005). Native Hawaiians have been advocating a return to more traditional diets and lifestyles. This is a result, in part, of the recognition of high numbers of chronic illnesses including diabetes, obesity, hypertension, heart disease, and cancer. Family is very important to native Hawaiians, along with respect for one’s ancestors. As part of this, traditional foods are viewed with respect. Arguments or negative comments about traditional foods, such as poi, are frowned on as being disrespectful to ancestors. Attempts to improve the health of native Insulin Resistance and the Metabolic Syndrome CHAPTER 5 157 Hawaiians is best done from a family perspective, rather than an individual one, and should include exercise, cooking, and eating together. ■ How Can the Metabolic Syndrome Be Prevented or Managed? Genetically, a family history of type 2 diabetes and the other health conditions found with the metabolic syndrome increase one’s own risk of developing diabetes. However, even though there may be an increased genetic risk, there are ways to minimize this. Physically active, nonsmoking persons of normal weight with moderately low intake of carbohydrate and alcohol have been found to have a lower risk of developing the metabolic syndrome (Zhu et al., 2004). Lifestyle changes have shown prevention of diabetes by over 40% among persons with prediabetes (Orchard et al., 2005). One study found that individuals who increased their level of physical activity were about 65% less likely to develop diabetes (Laaksonen et al., 2005). The nutritional factors to lower risk for developing the health conditions found with insulin resistance are summarized as follows: ■ Aim for meals with lower glycemic index and glycemic load (McKeown et al., 2004). ■ Include at least 20 g of dietary ﬁber daily, with emphasis on soluble ﬁber (Davy and Melby, 2003). ■ Aim for six meals daily to lower insulin release (Farshchi et al., 2005). ■ Reduce intake of sweetened beverages to control kilocalories (Schulze et al., 2004; Yoo et al., 2004). ■ Avoid excess intake of high-fructose corn syrup as found in commercially sweetened products to control triglyceride levels (Basciano et al., 2005). ■ Include magnesium-rich foods to reduce inflammation (McCarty, 2005). ■ Increase foods rich in vitamin C and beta carotene to lower CRP levels (Fredrikson et al., 2004). ■ Include folate and vitamin B12 to improve insulin resistance (Setola et al., 2004). ■ Emphasize nuts and olive oil versus a low-fat diet, but within a controlled kilocalorie intake (Esposito et al., 2004). ■ Limit intake of saturated fats and trans fats (Musso et al., 2005; Schulze and Hu, 2005). ■ Increase the amount of omega-3 fats to lower blood pressure, serum insulin, and triglycerides (Aguilera et al., 2004; Hulbert et al., 2005). ■ Aim for weight loss as needed, physical activity, and a diet moderate in fat and carbohydrate, with emphasis on monounsaturated fats and omega-3 fatty acids to control triglyceride and blood glucose levels (Carson, 2003). ■ For those who already drink, include moderate amounts (Carnethon et al., 2004; Djousse et al., 2004). What Is the Role of Magnesium in Controlling Insulin Resistance? Insulin resistance may be promoted by magnesium deﬁciency because of adverse changes to metabolic enzymes (Higashiura and Shimamoto, 2005). As reviewed in Chapter 3, magnesium is related to the production of 300 metabolic enzymes. Hyperinsulinemia, as generally found with insulin resistance, promotes excess loss of magnesium. Severe magnesium deﬁciency has been shown to cause a clinical inflammatory syndrome that can be controlled with increasing intake of 158 SECTION 2 Chronic and Acute Illness magnesium. Magnesium deﬁciency contributes to conditions found with the metabolic syndrome, including hyperlipidemia, and hypertension related to cardiovascular disease and cancer (Rayssiguier and Mazur, 2005). Magnesium is found in dark green, leafy vegetables, as it is part of the chlorophyll molecule, and is also found in high amounts in legumes, the germ portion of whole grains, nuts, milk and milk products, and ﬁsh. FALLACY: A person with a strong family history of diabetes is doomed to develop this condition. FACT: Studies show that groups at risk of developing diabetes can help prevent or delay the development of type 2 diabetes if there is regular physical activity, maintenance of a healthy weight, and emphasis on foods high in ﬁber and low in saturated fat. ■ WHAT IS THE ROLE OF HYPERINSULINEMIA IN THE INSULIN RESISTANCE SYNDROME? A person with a genetic predisposition to insulin resistance tends to have an altered insulin response. With insulin resistance there is often a delayed production of meal-related insulin. This can result in a transient state of hyperglycemia (high levels of blood glucose). When the body does respond to the hyperglycemia, it is often with excess insulin production over a prolonged period. Persons with insulin resistance have been noted to produce up to 10 times the amount of insulin to control blood glucose levels as compared with other insulin-sensitive individuals. This hyperinsulinemia can result in symptoms of hypoglycemia (low levels of blood glucose; see Chapter 8) if meals are delayed. The symptoms of reactive hypoglycemia are common among persons with insulin resistance, but medically the condition is rarely diagnosed. The blood glucose criteria for diagnosis of reactive hypoglycemia are more stringent than for persons with diabetes on medication. Physicians generally will not make the diagnosis unless blood glucose levels are below 50 mg/dL. Symptoms of hypo- glycemia, however, may occur years before the onset of diabetes and are likely because of hyperinsulinemia and excess release of counterregulatory hormones (see Chapter 4). Counterregulatory hormones correct hypoglycemia by causing the liver to release its stored sugar, called glycogen. The symptoms that occur because of these hormones, however, can be unpleasant. Altered glucagon (a counterregulatory hormone that is the ﬁrst one produced in response to low levels of blood glucose) secretion has been noted in reactive hypoglycemia. Glucagon in excess leads to feelings of nausea. Glucagon release is inhibited with hyperinsulinemia. It may be for this reason that persons with insulin resistance experience the symptoms of hypoglycemia as the body needs to release other counterregulatory hormones such as adrenalin (epinephrine). Adrenalin causes an increased heart rate and physical tremors, which is an unpleasant and potentially frightening experience if the person has not associated it with the need to eat a carbohydrate source. The symptoms of hypoglycemia do affect the quality of life. However, most persons with hypoglycemia symptoms are not in an immediate health emergency. Insulin Resistance and the Metabolic Syndrome CHAPTER 5 159 Severe hypoglycemia requiring medical assistance is usually limited to persons taking insulin or insulin-stimulating medications such as the sulfonylurea medications (see Chapter 8). Hyperinsulinemia is found with central obesity. It is still, however, a bit of a chicken-and-egg question. Which came ﬁrst? Hyperinsulinemia and central obesity are known to worsen insulin resistance. However, it may be that the genetic predisposition to insulin resistance is what ﬁrst sets up excess production of insulin in relation to carbohydrate intake. Some health care professionals suggest that hyperinsulinemia encourages the gain of abdominal weight in the ﬁrst place. This is the basis of the low-carbohydrate diets (see Chapter 6). Within a group of obese children, 40% were found to have hyperinsulinemia, and over 10% had impaired glucose tolerance as based on an OGTT. About one third of obese children had dyslipidemia (disordered fats in the blood; generally referring to elevated triglycerides and low levels of HDL-C) and hypertension. The metabolic syndrome was found in 30% of children under 12 years of age (Viner et al., 2005). With regard to dyslipidemia (see Chapter 7), it has been clearly shown that the enzyme lipoprotein lipase (an enzyme that helps the breakdown of triglycerides) is altered in the presence of hyperinsulinemia. This results in reduced breakdown of triglycerides, leading to high serum triglyceride levels. Thus elevated triglyceride levels in the blood are generally associated with hyperinsulinemia, especially if the person also has central obesity. This occurs even in childhood, with triglyceride levels correlating with insulin levels in children (Reinehr et al., 2005). Reduction in hyperinsulinemia generally improves dyslipidemia. One study showed that an intake of 250 mg EPA/DHA omega-3 fats for only 6 weeks signiﬁcantly decreased both fasting and postprandial triglyceride levels (Brady et al., 2004). Hypertension is now a well-recognized aspect of insulin resistance and the metabolic syndrome. There are still unanswered questions regarding the speciﬁc mechanism related to hypertension and the underlying cause of insulin resistance. The role of hyperinsulinemia is being suggested as the link, as a result of altered vasodilation. Therefore advice to follow a low-glycemic index diet may contribute to management of hypertension (Kopp, 2005). A person with central obesity and hypertension likely has insulin resistance (Figure 5-2). Hyperinsulinemia is now believed to be related to early heart disease, because of the incidence of heart disease occurring before the diagnosis of diabetes. It is well known that diabetes is associated with increased risk of atherosclerosis (see Chapter 7). Type 2 diabetes is described as a relative insufﬁciency of insulin production. Hyperinsulinemia is usually present with type 2 diabetes; there just is not enough insulin for the demand or to overcome severe insulin resistance at the cellular level. However, hyperinsulinemia can worsen insulin resistance, making it more difﬁcult for the body to regulate blood glucose levels. Certain cancers are found with the metabolic syndrome. Middle-aged men with the metabolic syndrome were found to be more likely to develop prostate cancer (Laukkanen et al., 2004). Excess weight in women is found with hyperinsulinemia, low HDL-C, increased levels of estrogen, and breast cancer (Furberg et al., 2005). See Chapter 10 for more on the role of hyperinsulinemia in the development of cancer. 160 SECTION 2 Chronic and Acute Illness Figure 5-2 Hypertension is commonly found with excess abdominal weight. WHAT IS GOUT, AND WHAT ARE ITS RISK FACTORS AND MANAGEMENT? Gout is the medical condition related to high levels of uric acid. The buildup of uric acid causes crystals to form. Uric acid crystals can cause severe pain in various joints in which the crystals tend to collect. Commonly the big toe is involved, but other joints may be affected. Damage to the kidneys is known to occur with uric acid deposition in this organ. The incidence of gout is increasing, especially with older adults, with men having this condition three to four times more frequently than women (Wallace et al., 2004). A high level of uric acid is associated with insulin resistance (Cohn et al., 2005). Historically, higher uric acid levels are believed to have been helpful to maintain adequate blood pressure levels when intake of sodium was too low. As the Westernized diet has become increasingly prevalent, there has been an increase in both hypertension and gout (Johnson et al., 2005). Traditional medical nutritional therapy for gout has been aimed at lowering intake of purines as found in legumes and other protein-based foods. Generally the use of medications such as allopurinol and colchicines is the primary intervention. With the newer recognition of gout as part of the metabolic syndrome, the goals of medical nutrition therapy (MNT) for managing insulin resistance may be more effective. Moderate amounts of legumes may be tolerated and help meet the goal Insulin Resistance and the Metabolic Syndrome CHAPTER 5 161 for increased intake of ﬁber and magnesium. Slow weight loss, avoidance of excess alcohol, and good fluid intake can be of help. Data from the Third National Health and Nutrition Examination Survey were analyzed and showed that total protein intake was not related to the serum uric acid levels. However, meat and seafood intake appears to increase levels, whereas milk and yogurt consumption was related to lower levels (Choi et al., 2005). WHAT IS THE POLYCYSTIC OVARY SYNDROME, AND WHAT IS ITS MANAGEMENT? PCOS can be related to hyperinsulinemia. There are different causes of PCOS. When PCOS is found in conjunction with central obesity and other risk factors for insulin resistance, hyperinsulinemia is the most likely cause. In the presence of excess levels of insulin, male-type hormones, called androgens, may be formed. This results in the masculinization of some women, leading to hirsutism (excessive male-type body hair), ovarian cysts, and irregular menstrual cycles. In one outpatient adolescent clinic 5% were diagnosed with PCOS including excess androgen levels, hirsutism, acanthosis nigricans (a skin condition; see Figure 5-1), and obesity (Omar et al., 2004). Of women with unwanted hair growth, it was found that about half had excess androgen levels and PCOS. Women with hirsutism are advised to have ovulatory function assessed even if the menstrual cycle is normal (Souter et al., 2004). Women with PCOS are at high risk for impaired glucose tolerance and type 2 diabetes. This is especially true of minority women. A 2-hour OGTT for screening women with PCOS at high risk for diabetes, rather than fasting glucose levels alone, can better identify health risk. An increased potential for endometrial hyperplasia (thickening of the endometrial layer of the uterus) and cancer is associated with anovulation (Richardson, 2003). This underscores the need for prompt identiﬁcation and treatment of PCOS. Women with PCOS generally beneﬁt with the same goals of MNT to control insulin resistance as described earlier in the chapter. One area of concern, however, is normalizing food intake. A higher prevalence of bulimia nervosa (see Chapter 12) and greater cravings for sweets has been noted with PCOS. This may be related to impaired release of the satiety factor, cholecystokinin (Hirschberg et al., 2004). As discussed previously, an increased intake of unsaturated fats is a positive goal in the management of the metabolic syndrome and can help increase cholecystokinin levels. Individuals who follow very-low–kilocalorie diets may also have episodes of binge eating and crave sweets. Small, frequent meals with low glycemic index can be very helpful in controlling PCOS. FALLACY: Children instinctively know how to make food choices to stay healthy. FACT: Children need the guidance of adults in selecting foods. The insulin resistance syndrome includes many chronic diseases, such as obesity, heart disease, and high blood pressure, that can start in childhood as a result of poor food choices. Using the MyPyramid to teach children to eat more high-ﬁber plant foods, such as vegetables, fruits, and legumes (beans), is appropriate. ■ 162 SECTION 2 Chronic and Acute Illness WHAT ARE MEDICATION CONCERNS IN MANAGING INSULIN RESISTANCE? There are multiple factors that can influence risk for the metabolic syndrome. It has been noted that persons with schizophrenia who take the medications clozapine or olanzapine are at increased risk for insulin resistance and should be monitored (Henderson et al., 2005). Medications that are known to cause weight gain, such as some antipsychotics, need to be used cautiously in persons at risk for the metabolic syndrome. Medications that serve a positive role include insulin sensitizers such as metformin, sold under the brand name of Glucophage. For PCOS, antiandrogen medications in combination with estrogen can restore regular menstrual cycles and reduce acne and hirsutism found with this syndrome (Homburg, 2005). Other medications exist to control insulin resistance, and more are expected to be developed. The insulin-sensitizing medication rosiglitazone was studied with severely insulin-resistant obese women who had PCOS. It was found that this medication improved insulin resistance and glucose tolerance, decreased ovarian androgen production, normalized insulin levels, and helped restore spontaneous ovulation (Sepilian and Nagamani, 2005). WHAT IS THE ROLE OF THE NURSE OR OTHER HEALTH PROFESSIONAL IN THE PREVENTION AND MANAGEMENT OF THE INSULIN RESISTANCE SYNDROME? The nurse or other health professional should be aware of the common occurrence and risk factors of the metabolic syndrome. The nurse can help identify at-risk individuals through review of family history and health correlates of insulin resistance. Prompt identiﬁcation can help to prevent early heart disease and diabetes. The nurse or other health care professional can provide lifestyle guidance. This might entail encouraging low-sugar beverages, such as seltzer water or iced tea, or recommending that a pitcher of water with lemon slices be kept in the refrigerator to increase its appeal. To encourage intake of vegetables and ﬁber, use of mayonnaise-based dressings or using olive oil to sauté vegetables can be suggested. To lower glycemic index of meals, it can be advised to “Eat fruit; don’t drink it.” It should be clariﬁed, however, that 4 oz of juice (15 g of carbohydrates) is generally well tolerated; advice might be to drink juice the “European way” (mixed with seltzer water). Reviewing food labels for ﬁber content is a practical strategy that can empower individuals to reduce their risk of the metabolic syndrome. Increased physical activity should be promoted; walking, dancing, or other forms of exercise can be encouraged. For individuals with mobility issues, even chair exercises can be of help. Adolescents might be encouraged to play basketball or skip rope to help stem the epidemic of obesity and diabetes in our youth. 1. If you are working with an individual who has central obesity and hypertension, is this individual at risk of diabetes? What laboratory values can help determine this risk? Insulin Resistance and the Metabolic Syndrome CHAPTER 5 163 2. Ask students to raise their hands if they have experienced symptoms of hypoglycemia, such as feeling weak, shaky, or irritable, that are resolved with food. 3. Have students volunteer, as desired, their family history of insulin resistance correlates. Estimate the percentage of students in class who are at risk for the metabolic syndrome. 4. Assess the following menu for the questions that follow: BREAKFAST LUNCH DINNER Banana Hot dog on roll Cheeseburger Corn flakes Mustard and relish French fries Whole milk Chocolate chip cookies Coleslaw Sugar Coke Milkshake Toast, butter, and jelly Judge these meals based on a typical adult’s needs according to the new MyPyramid. Identify the foods or beverages high in sugar and saturated fat. What suggestions would you make to change this menu to lower the risk of developing the metabolic syndrome? Royce had been on a very-low–fat diet since his open heart surgery 2 years before. He was now being advised by the nurse practitioner that he had prediabetes and should include more fat and ﬁber with moderate amounts of carbohydrate. It was a bit confusing, but it seemed to make sense. He had said he would be delighted to put real olive oil on his salads, instead of the fat-free dressings he had been using. He certainly loved nuts and was willing to try natural peanut butter on his toast. He had been getting hungry right after breakfast when he just used jam. And being advised to eat sardines was particularly easy; that took him back to his childhood when he sat on his grandfather Sean’s lap while the two of them ate sardines together. The advice to eat beans wasn’t new to him, either. He’d been eating his grandmother’s baked beans for years, and even now his wife’s cooking included beans. He and Nellie loved pinto beans and collards, and her mother had taught them to like adzuki beans, along with her specialty of succotash. Thinking about all this food made him hungry. He didn’t like to cook, so he got out the can of kidney beans and prepared to add the vinegar and pinch of sugar. He loved eating cold beans from the can. Then he was going for a walk, he told himself. He was motivated, since he’d learned he had prediabetes. And he was very thankful for being able to walk, since his car accident had put him in the hospital a number of years back. Yes, life was okay. Critical Thinking Applications 1. What laboratory value(s) must Royce have to diagnose prediabetes? 2. What is known about the prevention of diabetes? How does this relate to the advice given by the nurse practitioner? 3. What factors in Royce’s diet help meet the nutritional guidelines to manage the metabolic syndrome and help prevent diabetes? 164 SECTION 2 Chronic and Acute Illness 4. Why would the nurse practitioner advise eating more monounsaturated fats and fewer carbohydrates? 5. What is in sardines, and how might they help Royce? 6. If Royce needs 2000 kcal, how many grams of carbohydrate would be advised? How many grams of fat? 7. In doing a diet history, what foods and nutrients are important to assess? REFERENCES Aguilera AA, Diaz GH, Barcelata ML, Guerrero OA, Ros RM: Effects of ﬁsh oil on hypertension, plasma lipids, and tumor necrosis factor-alpha in rats with sucrose-induced metabolic syndrome, J Nutr Biochem 15(6):350-357, 2004. Armitage JA, Taylor PD, Poston L: Experimental models of developmental programming: consequences of exposure to an energy rich diet during development, J Physiol 565(pt1):3-8, 2005. Arslanian SA: Metabolic differences between Caucasian and African-American children and the relationship to type 2 diabetes mellitus, J Pediatr Endocrinol Metab 15(suppl 1):509- 517, 2002. Basciano H, Federico L, Adeli K: Fructose, insulin resistance, and metabolic dyslipidemia, Nutr Metab (Lond) 2(1):5, 2005. Boney CM, Verma A, Tucker R, Vohr BR: Metabolic syndrome in childhood: association with birth weight, maternal obesity, and gestational diabetes mellitus, Pediatrics 115(3):e290-e296, 2005. Brady LM, Lovegrove SS, Lesauvage SV, Gower BA, Minihane AM, Williams CM, Lovegrove JA: Increased n-6 polyunsaturated fatty acids do not attenuate the effects of long-chain n-3 polyunsaturated fatty acids on insulin sensitivity or triacylglycerol reduction in Indian Asians, Am J Clin Nutr 79(6):983-991, 2004. Brea A, Mosquera D, Martin E, Arizti A, Cordero JL, Ros E: Nonalcoholic fatty liver disease is associated with carotid atherosclerosis: a case-control study, Arterioscler Thromb Vasc Biol 25(5):1045-1050, 2005. Carnethon MR, Loria CM, Hill JO, Sidney S, Savage PJ, Liu K: Risk factors for the metabolic syndrome: the Coronary Artery Risk Development in Young Adults (CARDIA) study, 1985-2001, Diabetes Care 27(11):2707-2715, 2004. Carson JA: Nutrition therapy for dyslipidemia, Curr Diab Rep 3(5):397-403, 2003. Choi HK, Liu S, Curhan G: Intake of purine-rich foods, protein, and dairy products and relationship to serum levels of uric acid: the Third National Health and Nutrition Examination Survey, Arthritis Rheum 52(1):283-289, 2005. Choi KM, Lee J, Kim YH, Kim KB, Kim DL, Kim SG, Shin DH, Kim NH, Park IB, Choi DS, Baik SH; Koreans-Southwest Seoul (SWS) Study: Relation between insulin resistance and hematological parameters in elderly Koreans, Diabetes Res Clin Pract 60(3):205-212, 2003. Cohn GS, Kittleson MM, Blumenthal RS: Toward an improved diagnosis of the metabolic syndrome: other clues to the presence of insulin resistance, Am J Hypertens 18(8):1099-1103, 2005. Davy BM, Melby CL: The effect of ﬁber-rich carbohydrates on features of Syndrome X, J Am Diet Assoc 103(1):86-96, 2003. Dessein PH, Joffe BI, Stanwix AE: Subclinical hypothyroidism is associated with insulin resistance in rheumatoid arthritis, Thyroid 14(6):443-446, 2004. Djousse L, Arnett DK, Eckfeldt JH, Province MA, Singer MR, Ellison RC: Alcohol consumption and metabolic syndrome: does the type of beverage matter? Obes Res 12(9):1375-1385, 2004. Esposito K, Marfella R, Ciotola M, Di Palo C, Giugliano F, Giugliano G, D’Armiento M, D’Andrea F, Giugliano D: Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial, JAMA 292(12):1440-1446, 2004. Insulin Resistance and the Metabolic Syndrome CHAPTER 5 165 Farshchi HR, Taylor MA, Macdonald IA: Beneﬁcial metabolic effects of regular meal frequency on dietary thermogenesis, insulin sensitivity, and fasting lipid proﬁles in healthy obese women, Am J Clin Nutr 81(1):16-24, 2005. Ford ES, Ajani UA, Mokdad AH: The metabolic syndrome and concentrations of C-reactive protein among U.S. youth, Diabetes Care 28(4):878-881, 2005. Fredrikson GN, Hedblad B, Nilsson JA, Alm R, Berglund G, Nilsson J: Association between diet, lifestyle, metabolic cardiovascular risk factors, and plasma C-reactive protein levels, Metabolism 53(11):1436-1442, 2004. Furberg AS, Jasienska G, Bjurstam N, Torjesen PA, Emaus A, Lipson SF, Ellison PT, Thune I: Metabolic and hormonal proﬁles: HDL cholesterol as a plausible biomarker of breast cancer risk. The Norwegian EBBA Study, Cancer Epidemiol Biomarkers Prev 14(1):33-40, 2005. Henderson DC, Cagliero E, Copeland PM, Borba CP, Evins E, Hayden D, Weber MT, Anderson EJ, Allison DB, Daley TB, Schoenfeld D, Goff DC: Glucose metabolism in patients with schizophrenia treated with atypical antipsychotic agents: a frequently sampled intravenous glucose tolerance test and minimal model analysis, Arch Gen Psychiatry 62(1):19-28, 2005. Higashiura K, Shimamoto K: Magnesium and insulin resistance, Clin Calcium 15(2):251-254, 2005. Hirschberg AL, Naessen S, Stridsberg M, Bystrom B, Holtet J: Impaired cholecystokinin secretion and disturbed appetite regulation in women with polycystic ovary syndrome, Gynecol Endocrinol 19(2):79-87, 2004. Homburg R: Polycystic ovary syndrome in adolescence. New insights in pathophysiology and treatment, Endocr Dev 8:137-149, 2005. Hulbert AJ, Turner N, Storlien LH, Else PL: Dietary fats and membrane function: implications for metabolism and disease, Biol Rev Camb Philos Soc 80(1):155-169, 2005. Ilanne-Parikka P, Eriksson JG, Lindstrom J, Hamalainen H, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Mannelin M, Rastas M, Salminen V, Aunola S, Sundvall J, Valle T, Lahtela J, Uusitupa M, Tuomilehto J; Finnish Diabetes Prevention Study Group: Prevalence of the metabolic syndrome and its components: ﬁndings from a Finnish general population sample and the Diabetes Prevention Study cohort, Diabetes Care 27(9):2135-2140, 2004. Jehn M, Clark JM, Guallar E: Serum ferritin and risk of the metabolic syndrome in U.S. adults, Diabetes Care 27(10):2422-2428, 2004. Jiang R, Ma J, Ascherio A, Stampfer MJ, Willett WC, Hu FB: Dietary iron intake and blood donations in relation to risk of type 2 diabetes in men: a prospective cohort study, Am J Clin Nutr 79(1):70-75, 2004. Johnson RJ, Titte S, Cade JR, Rideout BA, Oliver WJ: Uric acid, evolution and primitive cultures, Semin Nephrol 25(1):3-8, 2005. Kelly AS, Wetzsteon RJ, Kaiser DR, Steinberger J, Bank AJ, Dengel DR: Inflammation, insulin, and endothelial function in overweight children and adolescents: the role of exercise, J Pediatr 145(6):731-736, 2004. Kelly CC, Lyall H, Petrie JR, Gould GW, Connell JM, Sattar N: Low-grade chronic inflammation in women with polycystic ovarian syndrome, J Clin Endocrinol Metab 86(6):2453-2455, 2001. Kopp W: Pathogenesis and etiology of essential hypertension: role of dietary carbohydrate, Med Hypotheses 64(4):782-787, 2005. Kuriki K, Tokudome S, Tajima K: Association between type II diabetes and colon cancer among Japanese with reference to changes in food intake, Asian Pac J Cancer Prev 5(1):28-35, 2004. Laaksonen DE, Lindstrom J, Lakka TA, Eriksson JG, Niskanen L, Wikstrom K, Aunola S, Keinanen-Kiukaanniemi S, Laakso M, Valle TT, Ilanne-Parikka P, Louheranta A, Hamalainen H, Rastas M, Salminen V, Cepaitis Z, Hakumaki M, Kaikkonen H, Harkonen P, Sundvall J, Tuomilehto J, Uusitupa M; Finnish diabetes prevention study: Physical activity in the prevention of type 2 diabetes: the Finnish diabetes prevention study, Diabetes 54(1):158-165, 2005. 166 SECTION 2 Chronic and Acute Illness Laukkanen JA, Laaksonen DE, Niskanen L, Pukkala E, Hakkarainen A, Salonen JT: Metabolic syndrome and the risk of prostate cancer in Finnish men: a population-based study, Cancer Epidemiol Biomarkers Prev 13(10):1646-1650, 2004. Maumus S, Marie B, Siest G, Visvikis-Siest S: A prospective study on the prevalence of metabolic syndrome among healthy French families: two cardiovascular risk factors (HDL cholesterol and tumor necrosis factor-α) are revealed in the offspring of parents with metabolic syndrome, Diabetes Care 28(3):675-682, 2005. McCarty MF: Magnesium may mediate the favorable impact of whole grains on insulin sensitivity by acting as a mild calcium antagonist, Med Hypotheses 64(3):619-627, 2005. McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW, Jacques PF: Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort, Diabetes Care 27(2):538-546, 2004. Miller JL, Silverstein JH: The management of type 2 diabetes mellitus in children and adolescents, J Pediatr Endocrinol Metab 18(2):111-123, 2005. Musso G, Gambino R, De Michieli F, Cassader M, Rizzetto M, Durazzo M, Faga E, Silli B, Pagano G: Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis, Hepatology 37(4):909-916, 2003. Omar HA, Logsdon S, Richards J: Clinical proﬁles, occurrence, and management of adolescent patients with HAIR-AN syndrome, ScientiﬁcWorldJournal 4:507-511, 2004. Orchard TJ, Temprosa M, Goldberg R, Haffner S, Ratner R, Marcovina S, Fowler S; Diabetes Prevention Program Research Group: The effect of metformin and intensive lifestyle intervention on the metabolic syndrome: the Diabetes Prevention Program randomized trial, Ann Intern Med 142(8):611-619, 2005. Piperno A, Vergani A, Salvioni A, Trombini P, Vigano M, Riva A, Zoppo A, Boari G, Mancia G: Effects of venesections and restricted diet in patients with the insulin-resistance hepatic iron overload syndrome, Liver Int 24(5):471-476, 2004. Pontiroli AE: Type 2 diabetes mellitus is becoming the most common type of diabetes in school children, Acta Diabetol 41(3):85-90, 2004. Rakugi H, Ogihara T: The metabolic syndrome in the Asian population, Curr Hypertens Rep 7(2):103-109, 2005. Rayssiguier Y, Mazur A: Magnesium and inflammation: lessons from animal models, Clin Calcium 245-248, 2005. Reinehr T, Kiess W, Andler W: Insulin sensitivity indices of glucose and free fatty acid metabolism in obese children and adolescents in relation to serum lipids, Metabolism 54(3):397-402, 2005. Richardson MR: Current perspectives in polycystic ovary syndrome, Am Fam Physician 68(4):697-704, 2003. Sanchez-Castillo CP, Pichardo-Ontiveros E, Lopez-RP: The epidemiology of obesity, Gac Med Mex 140(suppl 2):S3-S20, 2004. Schulze M, Hu FB: Primary prevention of diabetes: what can be done and how much can be prevented? Annu Rev Public Health 26:445-467, 2005. Schulze MB, Manson JE, Ludwig DS, Colditz GA, Stampfer MJ, Willett WC, Hu FB: Sugar- sweetened beverages, weight gain, and incidence of type 2 diabetes in young and middle-aged women, JAMA 292(8):927-934, 2004. Sepilian V, Nagamani M: Effects of rosiglitazone in obese women with polycystic ovary syndrome and severe insulin resistance, J Clin Endocrinol Metab 90(1):60-65, 2005. Setola E, Monti LD, Galluccio E, Palloshi A, Fragasso G, Paroni R, Magni F, Sandoli EP, Lucotti P, Costa S, Fermo I, Galli-Kienle M, Origgi A, Margonato A, Piatti P: Insulin resistance and endothelial function are improved after folate and vitamin B12 therapy in patients with metabolic syndrome: relationship between homocysteine levels and hyperinsulinemia, Eur J Endocrinol 151(4):483-489. Silfen ME, Manibo AM, McMahon DJ, Levine LS, Murphy AR, Oberﬁeld SE: Comparison of simple measures of insulin sensitivity in young girls with premature adrenarche: the fasting glucose-to-insulin ratio may be a simple and useful measure, J Clin Endocrinol Metab 86(6):2863-2868, 2001. Insulin Resistance and the Metabolic Syndrome CHAPTER 5 167 Smith SM, Holohan J, McAuliffe A, Firth RG: Irish diabetes detection programme in general practice, Diabet Med 20(9):717-722, 2003. Souter I, Sanchez LA, Perez M, Bartolucci AA, Azziz R: The prevalence of androgen excess among patients with minimal unwanted hair growth, Am J Obstet Gynecol 191(6):1914-1920, 2004. St-Onge MP, Janssen I, Heymsﬁeld SB: Metabolic syndrome in normal-weight Americans: new deﬁnition of the metabolically obese, normal-weight individual, Diabetes Care 27(9):2222-2228, 2004. Valencia ME, Weil EJ, Nelson RG, Esparza J, Schulz LO, Ravussin E, Bennett PH: Impact of lifestyle on prevalence of kidney disease in Pima Indians in Mexico and the United States, Kidney Int Suppl 97:S141-S144, 2005. Viner RM, Segal TY, Lichtarowicz-Krynska E, Hindmarsh P: Prevalence of the insulin resistance syndrome in obesity, Arch Dis Child 90(1):10-14, 2005. Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R: Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population, J Rheumatol 31(8):1582-1587, 2004. Yoo S, Nicklas T, Baranowski T, Zakeri IF, Yang SJ, Srinivasan SR, Berenson GS: Comparison of dietary intakes associated with metabolic syndrome risk factors in young adults: the Bogalusa Heart Study, Am J Clin Nutr 80(4):841-848, 2004. Zhu S, St-Onge MP, Heshka S, Heymsﬁeld SB: Lifestyle behaviors associated with lower risk of having the metabolic syndrome, Metabolism 53(11):1503-1511, 2004.
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