WORK A Journal of Prevention, Assessment & Rehabilitation

ELSEVIER

Work 9 (1997) 97-109

Diabetes mellitus: medical aspects and rehabilitation implications Phillip D. Rumrill, Jr. a,*, Candace A. Holmanb , Edwina J. Harris a , James A. Mullins, Jr.c aKent State University, 405-P White Hall, PO Box 5190, Kent, OH 44242-0001, USA b University of Wisconsin, Milwaukee, W1, USA C University of California, Berkeley, CA, USA

Abstract This article examines the etiologies, incidence and prevalence of diabetes mellitus - a chronic, systemic disease of the endocrine system. It presents current information for rehabilitation professionals concerning diagnosis, treatment, and physiological effects of this, most common of all endocrine disorders. © 1997 Elsevier Science Ireland Ltd.

Keywords: Diabetes; Medical aspects; Incidence; Prevalence

1. Introduction Diabetes mellitus is a chronic, systemic disease of the endocrine system. The endocrine system works in conjunction with the nervous system to keep bodily organs and response mechanisms working together in a balanced manner. Diabetes mellitus is characterized by an imbalance in the body's supply of and/or demand for insulin that results in abnormally high levels of glucose in the blood (hyperglycemia). Insulin, the hormone necessary for metabolizing carbohydrates, fats and proteins, is normally produced by beta cells in the

* Corresponding author.

pancreas [National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), Undated]. Insulin serves three major functions. First, it binds to insulin receptors of the cells that compose muscle, fat and liver tissue, thereby allowing glucose to be transported from the blood into the cells where it is used as energy. Second, once inside the cells, insulin allows excess glucose to be stored as fat, excess protein to be stored as muscle tissue and excess fat to be stored as adipose tissue. Third, it prevents the breakdown of these energy sources from the storage sites [Miller, 1981; US Department of Health and Human Services (DHHS), 1994a]. In diabetes mellitus, body cells are unable to use the glucose in the blood for energy because

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either the pancreas is not able to make enough insulin or the available insulin is not effective. Defective insulin secretion may be due to: (1) the destruction of endogenous insulin produced before it can be utilized; or (2) the inability of the body to use the insulin that is produced. The result of the body's inability to convert glucose into energy is often first observed as excessive thirst. The kidney, which normally returns glucose to the blood as filtered blood, is unable to return the excessive amount of glucose to the blood. This results in the 'spillover' of glucose into the urine (glycosuria). The high concentration of glucose in the urine, in tum, causes the kidneys to release large amounts of water (polyuria). Excessive thirst necessitates consumption of large volumes of water, which serve to replace the excess fluid loss (polydipsia). Additionally, because the glucose ingested is not metabolized, there is an inadequate supply of energy available to body tissues. Hence, food intake may increase (polyphasia) yet weight may decrease because the body begins to metabolize its own stores of fats and proteins for energy (Falvo, 1991). There are two main clinical classifications of diabetes mellitus; Type I, or insulin-dependent diabetes mellitus (IDDM), and Type II, or non-insulin-dependant diabetes mellitus (NIDDM). However, controversy exists over these classifications for two reasons. First, both forms are heterogeneous in terms of etiology, symptomatology, and treatment (Zimmet, 1995). Second, hyperglycemia exists on a continuum of severity. Hence, cutoff values for diagnosis are arbitrary (Davidson et aI., 1995); what represents Type I diabetes to one diagnostician may represent Type II to another. Additionally, other forms of the disease are currently recognized and will be discussed in the section to follow. The common thread connecting all forms of diabetes mellitus is that of glucose intolerance. 2. Forms and symptoms of diabetes mellitus

2.1. Insulin-dependent diabetes mellitus (IDDM) IDDM is an autoimmune disease characterized

by the production of little or no insulin by the beta cells of the pancreas. Persons with this disorder must receive insulin from an external source to survive. Onset of IDDM usually occurs abruptly (over a period of days or weeks) during childhood or adolescence, although it can appear at any age (Miller, 1981; Zimmet, 1995). The classic symptoms of diabetes - including weight loss, an excessive intake and output of water and hunger - may be extreme. This form of diabetes has also been called ketosis-prone diabetes. When blood sugar levels rise too high and the condition is not treated, the body begins to break down proteins and fatty acids for energy because glucose cannot be metabolized. The by-products of this metabolic process, ketones, are normally broken down and excreted. However, in people with IDDM, the body's capacity to excrete the ketones is exceeded, resulting in toxic levels of ketones in the blood and an imbalance in the body's acid-base balance. This condition is known as ketoacidosis and may result from infection, taking too little insulin, or getting too little excercise. Initial symptoms include nausea and vomiting, which often lead to dehydration, stomach pain, deep/rapid breathing, fruity breath odor, and low blood pressure (US Department of Health and Human Services, 1994a). When fluids and insulin are not supplied right away, ketoacidosis becomes a medical emergency that can lead to coma or death (Falvo, 1991; Miller, 1981). In fact, 10% of all deaths attributed to diabetes occur in conjunction with ketoacidosis.

2.2. Non-insulin-dependent diabetes mellitus (NIDDM) In NIDDM, the more common form of diabetes mellitus, the pancreas produces insulin, sometimes in excess, but the body is unable to use the insulin effectively (NIDDK, 1995a). Approximately 40% of people with this disorder require exogeneous insulin to survive. The remaining 60% maintain acceptable blood-glucose levels via oral medications, diet and/or exercise (NIDDK, Undated). NIDDM usually occurs in adults over the age of 40, but it occasionally occurs in young

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persons. Onset occurs gradually (over a period of weeks to months), and individuals sometimes remain asymptomatic for years. During advanced stages, the individual may experience the classic symptoms discussed above, as well as blurred vision, feeling tired or ill, frequent infections, and slowed healing processes (Miller, 1981; NIDDK, 1995a). NIDDM is subdivided according to the presence or absence of obesity. Approximately 80% of people diagnosed with NIDDM diabetes are overweight (Waife, 1980) - defined as having greater than 20% extra body fat for one's age, sex, height and bone structure. NIDDM in obese patients is often characterized by insulin resistance and hyperglycemia. Insulin resistance refers to a reduced response by the body tissues to the action of insulin. Excess fat cells, which work against the action of insulin, and the aging process impair the body's ability to respond to insulin. Hyperinsulimia, the production of too much insulin, occurs to overcome insulin resistance. Blood glucose levels then rise, because beta cells are unable to sustain this level of insulin production (Zimmet, 1995; NIDDK, Undated), and, eventually, become exhausted. The three conditions just discussed (i.e. obesity, hyperinsulinemia and hyperglycemia), in addition to a fourth condition frequently associated with NIDDM; hypertension, constitute a condition known as Syndrome X, or the Deadly Quartet (Zimmet, 1995). Syndrome X is so named because each of its constituents alone conveys an increased risk for cardiovascular disease (CVD). Moreover, when one or more of the conditions are combined, as they frequently are in NIDDM, they become a medical 'time bomb' (Zimmet, 1993). Therefore, it is not surprising that twothirds of NIDDM patients die from cardiovascular disease.

2.3. Maturity-onset diabetes of the young Maturity-onset diabetes of the young (MODy) is a familial condition often associated with a mutation in the gene responsible for the enzyme glucokinase. This enzyme helps regulate the body's secretion of insulin in response to bloo~

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glucose levels. Although similar to NIDDM, this form of diabetes mellitus generally occurs in patients younger than 25. Symptoms tend to be mild and, in most cases, can be controlled without insulin injections. MODY progresses very slowly if at all, and the cardiovascular problems associated with NIDDM are rarely seen.

2.4. Latent onset diabetes in adults Latent onset diabetes in adults (WDA), like IDDM, is characterized by the destruction of insulin-producing beta cells by the immune system. However, WDA generally occurs in persons aged 35 years or older. This form of diabetes mellitus is often misdiagnosed as NIDDM because onet is gradual. Within months or years, however, metabolic control fails and the individual progresses to insulin dependency (Zimmet, 1995). Between 10 and 20% of adult-onset diabetic patients have WDA. 25. Gestational diabetes mellitus Gestational diabetes mellitus (GDM) affects women in whom the onset of glucose intolerance occurs during pregnancy. The disorder then disappears almost immediately after delivery in most (95%) cases (US Department of Health and Human Services, 1994a). Yet, it substantially increases the risk of developing adult-onset diabetes within 5-10 years after bearing a child (National Diabetes Data Group, 1979). Women who experience GDM are also at a higher risk for developing complications throughout the pregnancy and are five times more likely than non-diabetic women to experience a cardiovascular event at some time in their life (NIDDK, undated). 3. Causes

A major obstacle to the complete understanding of diabetes mellitus is the fact that it is not one disease but, rather, a group of disorders that appears to be heterogeneous in terms of both symptomatology and etiology (Zimmet, 1995). Certain populations are more likely to develop the disease than are others (see Incidence and

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Prevalence sections of this article), and some populations are more prone to develop one form of the disease than others. Furthermore, IDDM occurs equally often among males and females, whereas NIDDM occurs approximately 20% more frequently in females than in males (Everhart et al. 1985; NIDDK, 1995a). Although the precise cause of each form of diabetes remains unknown, it is thought to be the result of a combination of genetic, immunologic, environmental (lifestyle) and, perhaps, viral factors. 3.1. Insulin-dependent diabetes mellitus (JDDM) As was noted in the previous section, IDDM (Type I) has an autoimmune basis; that is, the

immune system directs itself against the insulinproducing beta cells of the pancreas. Accumulating evidence indicates that the antigens to which immune cells are directed may be particular types of Human Leukocyte Antigens (HLAs). HLAs are histocompatibility genes (genetic markers) present on the surfaces of most human cell membranes. Precisely which types are present in any given individual is determined by four pairs of genetic material located on chromosome 6. Individuals with certain HlA types or patterns, such as HlA-B8, appear to run a significantly increased risk for the development of IDDM (Laporte and Cruickshanks, 1985). Autoantibodies against a number of beta-cell constituents have been identified, some of which can be detected up to 10 years before a clinical diagnosis is made. One such antibody, antiglutamatic acid decarboxylase (anti-GAD), is found in the majority of newly diagnosed IDDM patients. A recent study conducted with Finnish women indicates that a test for anti-GAD may predict the future development of IDDM with 82% sensitivity and 100% specificity (Zimmet, 1995). However, genetic susceptibility alone probably does not result in the destruction of beta cells. Although relatives of IDDM patients appear to be at a greatly increased risk for developing IDDM, no consistant mode of inheritance has been established. The occurrence of IDDM in

one monozygotic twin does not uniformly predict the disorder in the other (Waife, 1980). Researchers suspect that genetic susceptibility interacts with unknown environmental agents, resulting in the destruction of beta cells. The most actively investigated of the environmental factors possibly associated with IDDM are viruses. Atkinson and Maclaren (1994) suggested that the protein of the coxsackie virus B mimics the action of the enzyme GAD, thereby initiating events that lead to beta-cell destruction. Other viruses that have been implicated in the development of IDDM include mumps and rubella (Waife, 1980). 3.2. Non-insulin-dependentdiabetes mellitus (NIDDM)

NIDDM is thought to have a stronger genetic basis than IDDM and appears to have a more consistent mode of inheritance. The genetic occurrence of NIDDM is directly related to parental diabetes status. For example, the rate of NIDDM in the offspring of two diabetic parents is close to twice that of the rate when only one parent is diabetic. Additionally, monozygotic (identical) twins have a higher concordance rate for NIDDM than do dizygotic (fraternal) twins. Barnett et al. (1981) found that, among identical twins in whom NIDDM had been diagnosed in one twin, 91% of the cotwins had NIDDM. A similar study of identical twins with IDDM resulted in a concordance rate of approximately 58% (LaPorte and Cruickshanks, 1985). Hyperinsulinemia and insulin resistance, the hallmarks of NIDDM, have been associated with various genetic abnormalities including mutations in mitochondrial DNA, of insulin, and of insulin receptors. MODY has been linked to mutation of the gene for the enzyme glucokinase, which helps regulate the body's secretion of insulin (Zimmet, 1995). Although researchers believe that this strong genetic component is a prerequisite for the development of NIDDM, the genetic suseptibility is thought to be significantly heightened by lifestyle factors. In fact, 80% of people diagnosed with NIDDM are overweight. Additionally, high corre-

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lations have been found between the mean weight of a country's population and the prevalence of NIDDM within that country. The concept of a 'thrifty gene' is the most commonly provided explaination for this association. Theoretically, such a gene, at one time among certain populations, provided a selective advantage by storing calories during times when food was plentiful to be used during periods of food shortages and starvation. Today, as the result of such markers as urbanization, modernization, and improved socioeconomic status, caloric intake is higher than it once was, energy expenditure is lower, and the selective advantage is thus lost. Some postulate that the gene may now actually accentuate insulin resistance, thereby leading to a high prevalence of obesity in communities where it exists within the gene pool. Zimmet (1995) contends that both obesity and physical inactivity independently associated with IGT and NIDDM, and that they probably affect insulin sensitivity or action thus causing insulin resistance. The combination of obesity and a family history of diabetes appears to be the strongest risk factor for NIDDM, although interactions among other risk factors probably occur. Elevated blood-glucose concentrations are also among the strongest predictors for the development of NIDDM. Other metabolic risk factors, including serum cholesterol levels (plasma lipids), hypertension, and exposure to specific drugs (e.g. steroids and thiazine diuretics), have also been implicated. Age is another strong risk factor. Most incidence and prevalence research demonstrates an increasing risk of NIDDM with age for both men and women (Everhart et aI., 1985). It has been estimated that 40-50% of persons over the age of 65 have either NIDDM or impaired glucose tolerance (IGT). 4. Diagnosis It is estimated that diabetes now affects more than 100 million people worldwide. In the United States, the National Institute of Diabetes and Digestive and Kidney Diseases (1995b) estimates that there are 16 million people with diabetes, and that only half of them have been diagnosed.

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Of those who are diagnosed, approximately 90-95% have NIDDM, 5-10% have IDDM, and approximately 2% are diagnosed with diabetes secondary to other conditions. GDM occurs in approximately 2-5% of all pregnancies. In total, approximately 625,000 people are diagnosed as diabetic each year. Although most cases of diabetes mellitus are classified as either IDDM (also traditionally called juvenile-onset diabetes) or NIDDM (adult-onset), the previous sections indicate that a diagnosis based on age of onset is inappropriate. Further complicating the diagnosis and classification process is the fact that, in addition to the forms described in previous sections, other forms of diabetes exist that are associated with pancreatic disease, malnutrition, and some genetic syndromes (Waife, 1980; Zimmet, 1995). Diabetes mellitus comprises a genetically and clinically heterogeneous group of disorders. Yet, it is likely that different genetic and environmental etiologic factors result in similar diabetic phenotypes. For example, although the causes of IDDM and NIDDM remain unknown, both can be accompanied by ketoacidosis, blindness, kidney failure, cardiovascular disease, and amputations (National Diabetes Data Group, 1985). Moreover, all forms of diabetes have in common abnormally high levels of glucose in the blood due to either an insulin deficiency or the impaired effectiveness of insulin. The National Diabetes Data Group and the World Health Organization have both developed criteria for the classification and diagnosis of diabetes and other categories of glucose intolerance. Because it is believed that the pathologic consequences of diabetes are due to glucose levels that exceed certain values over extended periods of time, the criteria for diagnosis recommended by both groups are based on blood (plasma) glucose levels (National Diabetes Data Group, 1985). A normal blood glucose level will range from 60 to 120 mg/ dl (mg of sugar per dl blood) (Biermann and Toohey, 1981). After the consumption of food, blood glucose rises and reaches a peak (almost never above 150 mg/ dO beween 0.5 and 1 h later, before returning to its original level approximately 3 h later. In contrast, after an

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individual with diabetes consumes food, there is an abnormally high and prolonged rise in the blood glucose level. Three types of blood tests frequently used for diagnosing diabetes are the Fasting Plasma Glucose (FPG), Random Plasma Glucose, and the Oral Glucose Tolerance Test (OGTT). For the FPG, a single sample of blood is drawn after an overnight fast (10-16 h). When an individual displays symptoms of diabetes (FPG levels> 140 mg/ dl on two or more occasions), diabetes is diagnosed and no further testing is needed. This is also the case when a random blood sample (given without fasting) reveals a blood glucose level> 200 mg/dl and symptoms are present (Hirsch and Molitch, 1986). When either of these tests does not clearly indicate whether blood glucose levels are normal, an OGTT is performed. For the OGTT, an individual's FPG is tested and then he or she is given 75 g of glucose to drink. Next, blood samples are taken at 30 min, 1 h, 2 h, and 3 h to measure blood glucose. Diabetes is diagnosed when the 2-h sample indicates a blood glucose level of ~ 200 mg/dl, according to World Health Organization criteria. The National Diabetes Data Group requires that one of the other samples taken before the 2-h sample be ~ 200 mg/dl. When glucose levels are intermediate between normal and overt diabetes (FPG < 140 mg/dl with a positive OGTT), a diagnosis of impaired glucose tolerance (IGT) is given. 5. Physiological effects

Because diabetes has the potential to cause damage to virtually every part of the body, one of the most devastating aspects of this disease is the varied long-term complications it can cause. Included among these are heart disease, blindness, nerve damage, lower extremity amputations, and kidney disease. Generally, the longer the duration of the illness, the greater the risk of developing such complications. Furthermore, babies born to mothers who have the disease at conception are at increased risk for birth defects.

5.1. Eye disease Diabetes is the leading cause of new cases of blindness among adults 20-74 years of age in the United States (NIDDK, 1995b). Eye diseases associated with diabetes include cataract formation, glaucoma, corneal disease, and retinopathy. Retinopathy, a term used to describe ruptures in the small blood vessels that supply the retina with blood, appears to be the most common of these complications. It is estimated that 97% of insulin-dependent and 80% of non-insulin-dependent people who have had diabetes for 15 or more years have retinopathy. This condition frequently does not impair vision during its early stages and may go unnoticed for a long period of time. Therefore, the increased risk of retinopathy necessitates the careful surveillance of people with diabetes by an opthalmologist. Early treatment through the use of lasers and surgical procedures may prevent visual loss (Klein and Klein, 1985).

5.2. Kidney diseases (nephropathy) Diabetes is also the leading cause of end-stage renal disease (ESRD) in the United States (NIDDK, 1995b). Approximately one-third of people with IDDM and one-fifth of those with NIDDM eventually develop nephropathy. Nephropathy develops when small blood vessels in the kidney that normally filter waste products from the blood are damaged or ruptured. Among people with IDDM, the disease follows a well known and predictatable course. Proteinuria, the continuous excretion of protein through the urine, typically develops between 14 and 19 years after the onset of diabetes. This condition is thought to be attributable to renal microvascular disease. Four to 5 years later, azotemia, an increase in the serum creatinine level, occurs; ESRD and/or death typically follow 1 year later (Herman and Teutsch, 1985). In people with NIDDM, proteinuria occurs after a shorter duration of the illness but does not always result in progressive renal insufficiency.

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However, when it does, the amount of time between the onset of proteinuria and the development of ESRD appears to be about the same as that observed in people with IDDM and nephropathy. Most people who develop ESRD are initially treated with dialysis, although some have successfully received kidney transplants. Recent studies indicate that anti-hypertensive drugs called ACE-inhibitors may delay or prevent kidney failure in people with diabetes (US Department of Health and Human Services, 1994b).

5.3. Nerve diseases (neuropathies) Approximately 60-70% of people with diabetes have some form of associated nerve damage. Researchers disagree as to whether this damage results from metabolic or vascular problems. Three types of neuropathy commonly occur in conjunction with diabetes. The most frequently seen form, peripheral neuropathy, results in numbness, burning and/or pain in the lower extremities and fingertips. The loss of feeling associated with this form of neuropathy threatens well-being when lacerations or sores go undetected, leading to infection, gangrene and, eventually, amputation. Autonomic or visceral neuropathy affects nerves that are not under conscious control. Most often affected nerves are those that control the bladder muscles, cardiovascular system, digestive tract, and genital organs. Autonomic neuropathy often results in incontinence, tachycardia, diarrhea and delayed gastric emptying, and sexual impotence (Waife, 1980; US Department of Health and Human Services, 1994a). The third type of neuropathy, mononeuropathy, occurs most often in the elderly and may be very painful. This form usually affects a single nerve, usually in the leg, torso or head. The eye is a frequently affected organ, resulting in an aching feeling, an inability to focus the eye or double vision. However, nerve damage located in the head region may also cause facial paralysis or hearing problems. When a nerve within the torso is affected, lower back, chest, or abdominal pain

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results. In the leg, nerve damage is manifested through pain in the front of one thigh. Fortunately, the pain generally subsides within weeks or months without causing long-term damage. As noted, evidence indicates that proper nutrition and intensive control over diabetes may help prevent neuropathy. Once it occurs, those with the peripheral form must carefully examine extremities for cuts, bruises, or sores regularly and notify their physicians if anything is unusual. Physicians may prescribe pain relievers, anti-depressants, or other medications to help reduce symptoms associated with autonomic and mononeuropathy (US Department of Health and Human Services, 1994b).

5.4. Hypertension People with diabetes are two to three times more likely to have high blood pressure than are people without diabetes. Particularly, systolic hypertension occurs at a higher frequency and may be due to a higher prevalence of atherosclerosis among people with diabetes, which leads to decreased vascular distensibility (Horan, 1985). The National Heart, Lung, and Blood Institute (NHLBI) estimates that between 2.5 and 3 million Americans have both NIDDM and high blood pressure. It is possible that in many of these individuals an abnormal response to insulin, resulting in hyperinsulinemia, has an impact upon sodium reabsorbtion by the kidneys, thereby increasing the likelihood of high blood pressure (NIDDK, Undated). Others, however, have speculated that medications used to treat high blood pressure are precipitants of NIDDM. Bengtsson et al. (1992) observed a fourfold increased risk of diabetes in Swedish women taking antihypertensive drugs. Treatment of hypertension in people with diabetes generally involves decreasing dietary salt and caloric intake, as well as the use of thiazine diuretics and beta blockers. The NHLBI has discovered that one drug used to treat NIDDM, Metformin, may increase sensitivity to insulin, thereby reducing blood sugar while reducing blood pressure.

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5.5. Heart (cardiovascular) disease A greater risk for atherosclerotic coronary heart disease is associated with both IDDM and NIDDM. Relative to non-diabetics, heart disease in people with diabetes appears earlier in life, affects women as often as men, and tends to be more fatal. As noted in a previous section, people with diabetes are more likely to have characteristics associated with an increased risk of heart disease such as high blood pressure, lipid abnormalities, and higher cholesterol levels (BarretConnor and Orchard, 1985). Despite these differences, heart disease is usually of the same type as is seen in non-diabetics, and occlusion of the coronary arteries tends to be more extensive and severe; that is, people with diabetes tend to have more fat and cholesterol in their arteries, thereby forcing the heart to work harder. To reduce the risk of heart disease, the NIDDK (1994) suggests: (1) establishing a diet low in fat and high in fruits and vegetables; (2) having blood pressure and cholesterol checked regularly; and (3) avoiding smoking.

5.6. Peripheral vascular disease (PVD) Peripheral vascular disease in people with diabetes is most frequently manifested in the form of arteriosclerosis obliterans (ASO), which refers to the blockage of major blood vessels in the feet, legs, or arms. This condition, like peripheral neuropathy, can lead to ulcers, gangrene, and amputation as a result of the reduced blood supply to the extremities (Palumbo and Melton, 1985). The coincidence of ASO and diabetes is about 20% greater among men than among women but is elevated for both in relation to people without diabetes. Lehto et al. (1996) found that the strongest predictors of amputation in patients with NIDDM are poor glycemic control and the duration of diabetes. 5. Z Cerebrovascular disease

Studies on the incidence and prevalence of diabetes and stroke indicate that the occurrence rate for cerebrovascular accidents is two to six

times higher among diabetics than among non-diabetics. A high level of glucose in the blood appears to not only be important as a precursor for this disease, but also as a metabolic determinant that increases mortality following stroke (Kuller et aI., 1985). As with cardiovascular diseases, high blood pressure is a major risk factor for cerebrovascular accidents. Therefore, researchers speculate that the relationship between diabetes and stroke may be due to the increased prevalence of hypertension among people with diabetes. 6. Treatment Although there is no cure for diabetes, the discovery of insulin in 1921 significantly reduced the mortality rate associated with the disease. Before that time, all people with IDDM died within a few years after symptoms appeared (NIDDK, 1995a). Presently, treatment of all forms of diabetes emphasizes control over blood glucose levels through self-monitoring, regular physical activity, and meal planning. The goal of any form of treatment is to keep blood glucose levels as close to the normal range as is safely possible.

6.1. Blood glucose control All individuals with IDDM, by definition, require insulin injections in order to survive. Of those with NIDDM, approximately 40% use insulin, 49% use glucose lowering (hypoglycemic) oral agents, and 10% use a combination of both (NIDDK, 1995a). Self-management and care is extremely important for anyone engaged in insulin therapy due to the possibility of ketoacidosis or, its opposite, an insulin reaction. An insulin reaction occurs when there is too low a level of glucose in the blood (hypoglycemia). This reaction may occur as the result of injecting too much insulin, eating too little food, or exercising in excess. Symptoms include hunger, nausea, weakness, shaking, confusion, and perspiration. Consuming small amounts of sugar (e.g. 4-6 Lifesavers) when this happens often reduces symptoms within 10-15 min. When an insulin reaction is left untreated, in-

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sulin shock may result. In addition to the previous symptoms, double vision, convultions, and loss of consciousness occur. Insulin shock is a potentially life-threatening reaction that requires the assistance of another person immediately. It is treated either by an injection of glucose directly into a vein or with an injection of glucagon, an insulin antagonist, into muscle tissue (Kahn, 1981; US Dept. of Health and Human Services, 1994b). Kahn (1981) contends that a regimen of three or four equally spaced injections of insulin with equally spaced meal/snack patterns results in an insulin program most closely approximating the non-diabetic state. In the Diabetes Control and Complications Trial (DCCT), a study conducted by the Institute of Diabetes and Digestive and Kidney Diseases between 1983 and 1993, Kahn's assertions were confirmed. Findings from the DCCT indicate that keeping blood sugar levels as close to normal as possible, through intensive treatment, slows the onset of eye, kidney, and nerve diseases caused by diabetes (NIDDK, 1994). Intensive treatment involves the following: 1. testing blood sugar levels four or more times per day; 2. four insulin injections/day or use of an insulin pump; 3. adjusting insulin doses according to food intake and exercise; 4. maintaining a diet and exercise plan; and 5. monthly visits to a healthcare team composed of a physician, nurse educator, dietitian and behavioral therapist. Self-monitoring of blood glucose involves taking a drop of blood from the fingertip and placing it on a specially coated strip. The strip is then read, either visually or with a glucose meter that provides a digital reading of the blood sugar level within minutes. The blood glucose level serves as a guidepost for making decisions about food intake, insulin doses, and exercise (US Dept. of Health and Human Services, 1994b). Intensive treatment allows for greater flexibility in when and what individuals eat. Several insulin delivery systems are currently

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available for outpatient use. Insulin may be injected using a needle and syringe or an insulin pen into tissue under the skin. An insulin pen is a device the size of a pen that includes a needle and holds a vial of insulin. The insulin pump is also available and is a device worn outside the body on a belt or in a pocket. The insulin flows from the pump through a plastic tube that is connected to a needle taped into place under the skin (US Dept. of Health and Human Services, 1994b). Oral hypoglycemic agents are administered in the form of pills or capsules. They belong to a class of drugs known as sulfonylureas. Six types of these agents are sold in the United States (US Department of Health and Human ServIces, 1994a). This sort of treatment is most appropriate for those who are not prone to experience ketoacidosis, and whose diabetes had its onset after adolescence. The primary advantage of oral agents is that they are easy for the individual to administer and accept. They also naturally stimulate the secretion of insulin from the beta cells instead of simply replacing the hormone. However, the ease and convenience of this type of treatment can also lead individuals to fail to maintain a proper regard for the dangers of diabetes and the importance of self-management (Waife, 1980).

6.2. Physical activity Exercise is important for people with diabetes for the same reasons as it is for people without the disease. It tones the body and is healthy for the heart and lungs. However, because exercise can lower blood sugar levels quickly, people with diabetes must take precautions and, whenever possible, plan their activities so as to avoid ketoacidosis and/or insulin shock. Blood sugar should be checked before beginning exercise. When it is low, a snack should be eaten before initiating activity. If it is high, it should be brought under control prior to exerting oneself. Some will need to lower the usual dose of insulin before planned exercise. Allied health professionals and physicians can assist in developing an exercise program that maintains a balance between calo-

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ries (amount of glucose in the blood) and the amount of activity to be performed (US Department of Health and Human Services, 1994b). 6.3. Meal planning

Historically in the treatment of diabetes, there has been a strong belief that, because sugars are more rapidly absorbed than other carbohydrates, they are more likely to produce high blood sugar levels; other carbohydrates must be converted into glucose before absorbtion, which, theoretically, makes associated increases in blood sugar levels more gradual. Hence, people with diabetes were often required to replace sugars with such carbohydrates as cereals and potatoes. However, in 1994, the American Diabetes Association (ADA) broke away from this notion. New guidelines released in 1994 state that there is little scientific evidence to support this theory. As a result, there are fewer restrictions on sugar and other sweetners. Instead, the ADA considers the critical factor affecting post-meal blood sugar levels to be the total amount of carbohydrates in the diet. In other words, sucrose containing foods can be substituted for other carbohydrates and the focus is on the total amount of carbohydrates consumed as opposed to the sources of them (Franz and Miller, 1994). The ADA also broke away from the notion of a standard 'diabetic diet' for all people with diabetes. Today it is recognized that meal plans must be tailored to the type of diabetes present; other types of treatment being used; other health concerns such as obesity and the person's tastes (to improve motivation to comply); and other lifestyle factors. Accordingly, the new guidelines recommend consultation with a registered dietition for all people with diabetes to ensure the individualization of healthy meal plans. These plans should be prescribed based on the individual's treatment goals in terms of blood glucose levels, weight, and lipid levels. Although less restrictive, the new guidelines also recognize that traditional dietary strategies (based on the percentage of fats, proteins, and carbohydrates taken in) have not been effective in achieving long-term weight loss for the majority

of people with NIDDM who are overweight. Therefore, they recommend that the focus be placed on achieving desired blood sugar and lipid levels instead of pressuring overweight individuals to achieve unrealistic goals. However, they also note that a reduction in dietary fat is an effecient way to reduce weight, particularly when combined with exercise (Franz and Miller, 1994). Despite the liberalization of the ADAs guidelines, people with diabetes should follow a healthy eating plan that is low in fat and cholesteral, because such ingredients have been linked to heart disease which, as previously noted, is a common complication of diabetes. Children and pregnant women may have additional nutritional needs to be addressed. Also, all people with diabetes need to be educated about the different effects that different foods will have on blood sugar. Maintaining consistent food choices and eating times is also important for all with diabetes, particularly for those engaging in insulin therapy. Alcohol can be consumed in moderation, i.e. one or two occasional drinks - but it should always be taken with food. Drinking on an empty stomach can cause blood sugar levels to drop quickly, and symptoms of hypoglycemia may be mistaken for intoxication (US Department of Health and Human Services, 1994a). 7. Incidence and prevalence Medical historians estimate that diabetes mellitus was recognized as early as 2000 Be. However, the vast majority of progress toward a significant understanding of the disease has been made since the discovery of insulin in 1921 (Miller, 1981). Banting and Best are credited with this discovery, although, shortly thereafter, improved and more purified forms of the hormone were developed by others (Kahn, 1981). Less than a century later, diabetes was firmly established as the most common of the endocrine disorders (Subak-Sharpe, 1985). The NIDDK (1995b) estimates the prevalence of diabetes in the United States to be about 8 million diagnosed cases, and another 8 million that have yet to be diagnosed. Diagnosed cases consist of approximately 800000 cases of IDDM and between 7 and

P.D. Rumrill, Jr. et at.

7.5 million cases of NIDDM. Diabetes is currently the sixth leading cause of death by disease in the US. The incidence and prevalence of diabetes across the countries of the world vary widely, providing evidence that genetic and environmental factors play a major role in the development of diabetes. 7.1. Insulin-dependent diabetes mellitus (NIDDM)

There are clear geographic and/or racial differences in the risk of developing IDDM. Incidence rates (the number of people who acquire a condition in a given year) in the United States are lower than those reported in Scandanavian countries, but they are considerably higher than those reported in Asian countries. Yet, the US also has one of the highest prevalence rates (the total number of cases within a population) in the world (Laporte and Tajima, 1985). Across the world incidence rates range from less than 0.8 pe; 100000 people in Japan, to over 34 times that rate in Finland. Interestingly, prevalence rates of diabetes among Japanese migrants to the US have been found to be higher than the prevalence rates among Japanese people living in Japan. Data concerning prevalence rates within the United States are limited due to the fact that no national registry exists for cases of IDDM. However, the prevalence of IDDM is low within Asian Hispanic, and Native American populations withi~ the US relative to non-Hispanic whites (Stem, 1985; NIDDK, 1995a). Zimmet (1995) suggests that this variability may be tied to antibodies for the enzyme glutamatic acid decarboxylase (GAD), the beta-cell constituent discussed in a previous section. Studies indicate that the frequency of these anti-bodies is lower in people from Asian countries and higher among people from European countries. 7.2. Non-insulin-dependent diabetes mellitus (NIDDM)

NIDDM is a 'life-style disorder' (Zimmet, 1995, p. 1050) with the highest prevalence rates occuring in populations with heightened genetic susceptibility and environmental factors that unmask the disease. Consistent with the thrifty genotype

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theory, high incidence and prevalence rates appear in newly industrialized nations, where changes in diet and caloric expenditure have occured rapidly. Furthermore, they vary by urban or rural habitation, degree of modernization, and socioeconomic status. Incidence rates for NIDDM increase with age for both sexes, but they are higher for females in some age groups and higher for males in others. The highest prevalence of NIDDM in the world (for adults age 25 and older) occurs among the Pima Indian population i~ Arizona. Almost half (42.2%) of this populatIon have NIDDM, despite the fact that, at the tum of the century, when the Pima indians still maintained a traditional lifestyle, very few had the disease. IDDM, in contrast, is almost non-existant among these peoples (Everhart et al. 1985). The lowest prevalence rates of NIDDM are found among those in the United Kingdom (approx. 2%), Former Soviet Union (approx. 2%), and in rural Bantu (approx. 1%). NIDDMs prevalence rate in the United States is currently approximatly 8% (Zimmet, 1995). Within the United States, people of color are at a higher risk of developing NIDDM than are non-Hispanic whites. NIDDM is more prevalent in African-Americans (10.2%), Mexican-Americans (13%), and Puerto Ricans (13.4%) than it is in non-Hispanic whites (6.2%). As noted Native . . ' Amencans have. the highest prevalence rates in the world, approximating 50% of the entire population (NIDDK, 1995a). Exactly why incidence and prevalence rates among people of color are so high relative to white popUlations remains unknown. However, several potentially important genetic markers in blacks with NIDDM have been identified, as well as several variants of gentically determined traits (polymorphisms) in the region of the insulin gene in Blacks with NIDDM. Researchers also speculate that the gene for glucokinase (the gene that may be linked to the development of MODY), may also be linked to the development of diabetes in minority populations. 8. Conclusion

Diabetes mellitus is the most prevalent disease

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of the endocrine system and the sixth leading cause of death by disease in the United States. Diabetes is thought to result from some combination of genetic, immunologic, environmental, and, perhaps, viral factors, and it produces a wide range of potentially life threatening medical effects. Although stress management, diet, and selfmonitoring of blood-glucose levels enable many people with diabetes to control their symptoms and lead active lives, regular medical check-ups and responsive allied health services must supplement patients' self-care regimens. By understanding the various types and manifestations of diabetes mellitus, its pervasive psychomedical impact, and the importance of patient-directed treatment - allied health and other rehabilitation professionals can address the needs of people diagnosed with this chronic illness in a manner that both· activates the consumer's role in maintaining wellness and complements the efforts of medical professionals. References Atkinson MA, Maclaren NK. The pathogensis of insulin-dependent diabetes mellitus. N Engl J Med 1994;331: 1428-1436. Barnett AH, Eff C, Leslie RDG, Pyke DA. Diabetes in identical twins. Diabetologia 1981;70:87-93. Barrett-Connor E., Orchard T. Diabetes and heart disease. Diabetes in America, XVIl-41. Washington: National Institutes of Health, 1985. Bengtsson C, Blohme G, Lapidus L, Lissner L, Lundgren H. Diabetes incidence in users and non-users of antihypertensive drugs in relation to serum insulin, glucose tolerance and degree of adiposity: a 12-year prospective population study. J Intern Med 1992;231(6):583-588. Biermann J, Toohey B. The diabetic's book. Los Angeles, CA: JP Tarcher, 1981:39-40. Davidson MB, Peters AL, Schriger DL. An alternative approach to the diagnosis of diabetes with a review of the literature. Diabetes Care 1995;18(7):1065-1071. Everhart J, Knowler WC, Bennett PH. Incidence and risk factors for non-insulin-dependent diabetes. Diabetes in America, IV. Washington: National Institutes of Health, 1985:1-35. Falvo DR. Medical and psychosocial aspects of chronic illness and disability. Gaithersburg, MD: Aspen, 1991. Franz J, Miller E. New nutrition guidelines issue by American Diabetes Association. Alexandria, VA: American Diabetes Association, 1994.

Herman WH, Teutsch SM. Kidney diseases associated with diabetes. Diabetes in America, XIV. Washington: National Institutes of Health. 1985:1-31. Hirsch U, Molitch ME. Diagnosis: diabetes. Diabetes Forecast, 1986:315-317. Horan MJ. Diabetes and Hypertension. Diabetes in America, XVII. Washington: National Institutes of Health, 1985:1-22. Kahn CB. Advances in insulin therapy of diabetes mellitus. In: Brownlee M, editor. Diabetes mellitus, vol. 5. Current and future therapies. New York: Garland STPM Press, 1981:75-94. Klein R, Klein BE. Vision disorders in diabetes. Diabetes in America, XIII. Washington: National Institutes of Health, 1985:1-36. Kuller LH, Dorman JS, Wolf PA. Cerebrovascular disease and diabetes. Diabetes in America, XVIII. Washington: National Institutes of Health, 1985:1-18. Laporte RE, Cruickshanks R. Incidence and risk factors for insulin dependent diabetes. Diabetes in America, III. Washington: National Institutes of Health, 1985:1-12. LaPorte RE, Tajima N. Prevalence of insulin dependent diabetes. Diabetes in America, V. Washington, DC: National Institutes of Health, 1985:1-8. Lehto S, Ronnemaa T, Pyorala K, Laakso M. Risk factors predicting lower extremity amputations in patients with NIDDM. Diabetes Care 1996;19(6):607-612. Miller LV. Diabetes mellitus. In: Stolov WC, Clowers MR, editors. Handbook of severe disability. Washington: US Department of Education, 1981:321-328. National Diabetes Data Group. Summary. Diabetes in America, I. Washington, DC: National Institutes of Health, 1985:1-8. National Diabetes Data Group. Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes 1979;28:1039-1057. National Institute of Diabetes and Digestive and Kidney Diseases. Diabetes Special Report (NIH PUB. No. 943422). Washington, DC: National Institutes of Health, undated. National Institute of Diabetes and Digestive and Kidney Diseases. Diabetes Control and Complications Trial (DCCT) (NIH Publication No. 94-3874). Washington, DC: National Institutes of Health, 1994. National Institute of Diabetes and Digestive and Kidney Diseases. Diabetes overview (NIH Publication No. 94 3873). Washington, DC: National Institutes of Health, 1995a. National Institute of Diabetes and Digestive and Kidney Diseases. Diabetes statistics (NIH Publication No. 963926). Washington, DC: National Institutes of Health, 1995b. National Institute of Diabetes and Digestive and Kidney Diseases. Diabetic neuropathy: the nerve damage of diabetes (NIH Pub. No. 95-3185). Washington, DC: National Institutes of Health, 1995c. Palumbo PJ, Melton U. Peripheral vascular disease and diabetes. Diabetes in America, XV. Washington: National Institutes of Health, 1985:1-21.

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Subak-Sharpe GJ. The basics of diabetes. In: Subak-Sharpe GJ, editor. Living with diabetes. New York: Doubleday, 1985:3-8. Stern MP. Diabetes in Hispanic Americans. Diabetes in America, IX. Washington: National Institutes of Health, 1985:1-11. US Department of Health and Human Services. The diabetes dictionary (NIH Publication No. 94-3016). Washington, DC: National Institutes of Health, 1994a.

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US Department of Health and Human Services. Insulin-dependent diabetes (NIH Publication No. 95- 2098). Washington, DC: National Institutes of Health, 1994b. Waife SO, editor. Diabetes mellitus. 8th ed. Indianapolis, Indiana: Eli Lilly, 1980. Zimmet PZ. Hyperinsulinemia - how innocent a bystander. Diabetes Care 1993;16 Suppl 3:56-70. Zimmet PZ. The pathogenesis and prevention of diabetes in adults. Diabetes Care 1995;18(7):1050-1064.