Nutritional management of obesity and diabetes

Nutrition Research, Vol. 14, No. 3~ pp. 465-483, 1994 Copyright 9 1994 Elsevier Science Ltd Printed in the USA. All rights reserved 0271-5317/94 $6.00 + .00

Pergamon

NUTRITIONAL MANAGEMENT OF OBESITY AND DIABETES Kay Griver, R.D. t and Robert R. Henry, M.D. *t Department of Medicine, University of California, San Diego* and Veterans Affairs Medical Center, San Diego, California t

ABSTRACT Diet therapy and especially weight loss are cornerstones in the management of obese NIDDM. Dietary treatment of diabetes remains a controversial area and the ideal diet remains to be defined. General recommendations include reductions in total and saturated fat and limited protein intake with replacement by complex carbohydrates and/or monounsaturated fatty acids. The need to individualize the diet must be recognized and should follow the recommendations of the American Diabetes Association, as much as possible. These recommendations are primarily intended to improve metabolic control in diabetes and reduce the risk of cardiovascular disease and other chronic complications. Caloric restriction and weight loss need to be considered in all obese NIDDM and can have dramatic benefits on glucose, lipid and other metabolic abnormalities as well as hypertension. A multidisciplinary health care team is beneficial in initiating and re-enforcing weight loss and a combination of diet, exercise, and behavior modification are needed to ensure long-term compliance and weight maintenance. The specific diet and approach chosen will depend on the patient, the degree of obesity and the extent of metabolic decompensation and complications present. Key words: Nutrition; obesity; diabetic diet; weight loss; diabetes mellitus; NIDDM INTRODUCTION Obesity and diabetes are common metabolic disorders that frequently co-exist. Of the two major forms of diabetes, the non-insulin dependent (NIDDM or Type II) type is far more common and is often associated with obesity. NIDDM occurs in approximately 8090% of the estimated 5-10 million Americans diagnosed with diabetes and 70-80% of these individuals are obese (1-3). NIDDM occurs more frequently in certain ethnic populations including Blacks, Hispanics, and Native Americans (4) and is usually diagnosed after the onset of the fourth decade. Both obesity and NIDDM have strong genetic patterns of inheritance (1,2,5). Moreover, obesity increases the likelihood that NIDDM will develop in individuals who are genetically prone to the disease (2). In many cases, it is believed that obesity and NIDDM are co-inherited. Total body weight, distribution of body fat, as well as the amount and rate of weight gain are all important aspects of obesity that need to be considered as potential risk factors for the development of NIDDM. Diet modification is a key factor in treating obese NIDDM (6). The major objective of diet therapy in this group of individuals is weight reduction followed by maintenance of 465

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desirable body weight. Additional considerations include changes in the form, composition and distribution of meals as well as avoidance of certain items. For the most part, the earlier diet therapy is initiated, the greater are the potential benefits. Moreover, diet manipulation alone may reduce or eliminate the need for pharmacologic therapy of diabetes (7). In this review, we will focus on these various forms of dietary therapy and discuss their implementation as well as potential benefits and limitations. The role of exercise and behavior modification combined with diet therapy will also be considered in the overall promotion of a program designed to optimize metabolic control and the well-being of those with NIDDM. In turn, the provision of appropriate diet therapy in NIDDM may reduce or retard the development of numerous end-organ complications of this disease. PATHOPHYSIOLOGY OF NIDDM There are three basic pathophysiologic abnormalities which characterize NIDDM (8). These include impaired pancreatic insulin secretion, peripheral insulin resistance primarily at liver and muscle tissue, and excessive hepatic glucose production. Each individual with NIDDM may have different degrees of severity of these abnormalities which result in a wide range of fasting and postprandial hyperglycemia as well as other metabolic derangements. Obese and non-obese varieties of NIDDM have the same basic pathophysiologic abnormalities, but their pattern of expression and contribution to the development of hyperglycemia differ. It is important to recognize these pathophysiologic variants of NIDDM because the strategies used to achieve the goals of nutrition management can be influenced by the different patterns of clinical expression. Obese NIDDM tend to exhibit severe insulin resistance (in both muscle and liver) and have hyperinsulinemia (9). Hyperglycemia develops because the large quantity of insulin produced by the pancreas is insufficient to overcome the insulin resistance that is present (8,9). In NIDDM, the abnormalities of insulin resistance and hyperinsullnemia have both been shown to be aggravated by obesity (10-12). Obesity per se does not cause hyperglycemia but contributes to its development in those individuals with the genetic predisposition to develop NIDDM. Thus, a major thrust of diet therapy in obese NIDDM includes a plan for weight reduction which serves as a tool for controlling hyperglycemia (7). Caloric restriction and weight loss improve both glucose and lipid abnormalities through a variety of mechanisms (13). Lean or non-obese NIDDM have less insulin resistance, often mild to moderate in severity, with relative or absolute hypoinsullnemia due to deficient pancreatic insulin secretion as the predominant abnormality. Therefore in lean NIDDM individuals, diet therapy is directed primarily at optimal composition, form, content, and timing of food intake rather than emphasis on reduction of caloric intake. In this paper we will concentrate on the approaches to diet therapy of obese NIDDM. APPROACH TO THERAPY Overview The nutritional recommendations and requirements for obese NIDDM are similar to those of obese non-diabetic individuals (3,6). Diet manipulation in NIDDM can be a major factor used to control the various metabolic abnormalities in this disorder. In obese NIDDM, weight loss is the key to major metabolic changes but is a goal that is often difficult to achieve and maintain. In this situation, a variety of diet plans can be initiated and modified to include greater individualization and flexibility in meal planning that are intended to improve compliance. The objectives in the management of NIDDM are to strive for a normal metabolic state in order to prevent or delay development of the micro- and macrovascular complications that frequently occur (3). The foundation of sound management is nutrition modification combined with exercise and oral hypoglycemic agents

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or insulin as needed. A consistent and individualized meal plan is needed to be successful in meeting the objectives stated above. However, the optimal diet for individuals with NIDDM remains elusive. It is unlikely that there will ever be one diet plan applicable to all NIDDM patients. Despite extensive research efforts, there continues to be much controversy about the content and types of carbohydrates, protein, and fat that should be used, the role of dietary fiber, the need for micronutrient supplementation, diet form, hypocaloric diet therapy, timing of food intake, and meal planning methods. Our opinions and approach to these management issues in the nutritional therapy of NIDDM will be discussed in this chapter. IMPLEMENTATION OF DIET A co-ordinated team approach with active participation by the physician, registered dietitian, diabetes nurse educator, person with NIDDM, and family members provides the most effective nutrition management (6). Encouragement to stay on diet therapy by all team members improves short and long-term compliance. The meal plan or weight loss plan needs to be realistic and flexible. An appropriate diet plan should consider factors such as age, sex, activity level, degree of obesity, presence of complications, medications, and current nutritional status of the patient. Other factors such as cultural, ethnic, and socio-economic status must also be considered in meeting the individual's requirements (14). Discussion of the benefits of diet therapy should begin at the initial visit to the physician. The physician can discuss the importance of adhering to the diet prescription and the potential benefits of diet on metabolic parameters as glucose, lipids, and blood pressure. It is at this early stage that a referral should be made to the dietitian. The dietitian can complete a diet history including lifestyle and eating habits, review basic principles of diet therapy, and develop a meal plan. Education on the meal plan must be realistic with active involvement of the patient in setting small increment goals. The meal plan and goals need to be tailored so that the individual will be able to comply long-term to the diet. The dietary intervention planned will also depend on whether the patient is lean or obese and the current pharmacologic treatment (oral hypoglycemic agents or insulin). Goals of nutrition education for long term weight loss must include discussions with patients and family members on such topics as the purchasing of food, reading of food labels, preparation of food, and types of foods to consume. Patients should be taught to read and understand package labels to enable them to make food choices based not only on the content of the food but on the amounts of sugar, calories, sodium, and fat in food items as well. Patients do not need to purchase special foods but must understand the importance of portion sizes and the need to include a variety of foods for their individual meal plan. The most important aspect to ensure successful diet therapy is long-term compliance by the patient. Nutrition monitoring by the dietitian and follow-up is needed on a regular basis to continue to reinforce the needed changes. Each member of the health care team can encourage adherence to diet at every opportunity. Old eating habits are difficult to change unless new lifestyle behaviors are encouraged and re-enforced. There are different education methods available to counsel individuals with NIDDM about meal planning. The Food Guide Pyramid recently developed by the United States Department of Agriculture provides nutritional advice on healthy eating that can be applied to those with NIDDM. Healthy Food Choices (pamphlets available from the American Dietetic Association, and American Diabetes Association, Inc.) is a simplified version of food grouping that categorizes the six food groups by calories. The six food groups include

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bread/starch, vegetables, milk, meat, fruit, and fat. A simplified meal plan can be developed by using the food groups to include a variety of foods at each meal. The meal plan can also be used to count calories and lower fat intake. The format includes guidelines to assist in changing dietary habits in order to lower fat, salt, and sugar intake, and increase fiber intake. The pamphlet can serve as an important resource to assist obese NIDDM patients in achieving the nutritional goals of lowering fat intake and weight loss. Nutrition education should focus on the individual being able to make the appropriate changes to achieve weight loss and improve metabolic control. The recording of daily food intake and self monitoring of blood glucose are additional tools utilized by the dietitian as well as the physician to follow up and assess individual problem areas. Group classes are appropriate to discuss food choices, healthy snacks, and dining out guidelines. It is important to first identify the major problems in the dietary meal plan and then make gradual changes in eating habits to achieve the desired results. Actual food records can be used to identify priority areas and then recommend the changes needed. Food records can be used to point out calorie-dense foods and high fat snacks which can be major contributors to excessive caloric intake. The dietitian can also aid in identifying problem areas and offer solutions to modify the problems. Self monitoring of blood glucose records enable the dietitian to assess the relationship of food intake and glucose control. Suggestions to decrease portion sizes of meals, distribute calories throughout the day, eliminate problem foods, and increase physical activity can result in improved metabolic control of parameters such as glucose and lipid levels. Diet therapy should be initiated as close to the time of diagnosis as possible to emphasize the pivotal role of diet in the management of obese NIDDM. If the fasting glucose is <200 mg/dl, diet manipulation by itself is often sufficient and may obviate the need for additional drug therapy. Above this level (>200 mg/dl), patients tend to be symptomatic and diet therapy is usually initiated along with pharmacologic agents. Glucose toxicity, which may develop from marked hyperglycemia over a prolonged period (15) may be the reason for the failure to respond to dietary therapy alone. Initial treatment with oral hypoglycemic agents or insulin to reduce hyperglycemia may reverse the glucose toxicity and make diet therapy more efficacious (15). Nutritional efforts in obese NIDDM should be directed primarily at weight loss strategies. A desirable body weight defined as the ideal body weight may be unrealistic and is not necessary to achieve substantial metabolic benefits. Even a weight loss of 10 pounds of initial body weight may be beneficial to control the multiple metabolic derangements and enhance the efficacy of drug therapy. Patients need to discuss their individual weight goal with the health care team members to avoid later frustration and guilt. We aim for weight loss of 10-20% of initial body weight since we believe patients can often achieve and maintain this goal. Even with this degree of weight loss, patients may still be obese but metabolic parameters are improved and sometimes dramatically.

DISTRIBUTION OF CALORIES An important component of glycemic control in NIDDM is distributing the calories throughout the day (3,6). Large caloric loads at any one time tend to produce large glycemic excursions. Distributing calories more uniformly throughout the day allows time for a more optimal response with less insulin required to achieve glycemic control. Spacing meals every 4-5 hours allows sufficient time for insulin to act before the next meal. An even distribution and consistency of caloric intake is needed in all patients and especially those that are insulin-treated. Missing meals at breakfast or lunch and then overeating

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at the dinner meal may be a major contributor to development of obesity as well as poor glycemic control in NIDDM and can result in both hypoglycemia and hyperglycemia. DIET COMPOSITION There is still considerable controversy about the optimal composition of the diabetic diet in the treatment of NIDDM. There continues to be a wide range of opinions about the most efficacious carbohydrate, fat, and protein content of the diet. While group guidelines for those with diabetes have general applicability, it should be emphasized that recommendations for diet need to be individualized and based upon clinical characteristics and metabolic parameters such as glucose and lipid levels. In the sections below, we will discuss the guidelines advocated by the American Diabetes Association and American Dietetic Association including the specific areas of controversy and our opinion in these matters (Table 1). (~ARBOHYDRATES Current recommendations for dietary management emphasize reduction oftotai and saturated fat and replacement with complex carbohydrate (3,6). This advice is based on the assumption that altering the diet composition in such a manner will have a favorable effect on both glycemia and lipid levels, therefore reducing the risks of cardiovascular disease and possibly other complications. Support for the inclusion of increased complex carbohydrate in the diabetic diet is derived from several lines of scientific evidence. Complex carbohydrates tend to be fiber-rich and research has shown that, in certain circumstances, when carbohydrates containing little or no fiber are included in the diet, deterioration in blood glucose control and triglyceride levels can occur (16-18). Furthermore, increasing high fiber complex carbohydrates in the diabetic diet is reported to improve glycemic control and lower LDL cholesterol levels (16-18). On the other hand, these diets may produce adverse effects and have been reported to increase VLDLtriglyceride and cholesterol levels and possibly lower HDL levels when used in NIDDM (1618). Thus, it appears that increasing the content of complex carbohydrates in the diabetic diet may not always be beneficial. In addition, most patients find it difficult to adhere to the current recommendation of 55-60% of total calories as carbohydrate with emphasis on complex high fiber foods. Until this contentious area is sorted out, we believe that it is important to individualize the diet and aim to increase the complex carbohydrate content to the level the patient can readily achieve by encouraging foods high in water-soluble fiber such as fruits, vegetables and legumes. We utilize high fiber carbohydrate intake primarily to reduce the cholesterol and saturated fat intake. Such diets may also be beneficial as an aid in weight loss by means of lowering fat intake. As patients follow a high fiber, high carbohydrate diet their glucose and lipid levels should be monitored periodically to evaluate individual metabolic responses. It is apparent that a given glycemic response to a carbohydrate cannot be predicted simply on the basis of whether it is a complex or simple sugar. The glycemic index is a method that has been used to indicate the expected glycemic response to ingestion of individual carbohydrate-containing foods (19). It is determined by expressing the glucose response to a given carbohydrate-containing food as a percentage of the response elicited by an equivalent amount of a standard food such as glucose or white bread. The glycemic index clearly illustrates that the glucose response to carbohydrate is highly variable. For example, the glycemic index of complex carbohydrate containing foods such as bread, rice, and pasta is 80 while the simple sugars vary widely with sucrose at 86 and fructose at 30. Moreover, a variety of other factors influence blood glucose response to food including such variables as the rate, timing of food ingestion, form, extent of cooking, percent of fat and protein in the diet and effects of previous meals. As one might expect, there may also be

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a large degree of individual variability in the glycemic response to various foods. Glycemic response studies have provided no evidence that sucrose causes a greater rise in postprandial glucose levels than other starchy carbohydrates (20). The influence of dietary sucrose on lipid levels in NIDDM has been conflicting with adverse effects in some but not all studies (20). Aside from the contribution of sucrose consumption to dental caries, there is no convincing evidence that sucrose produces adverse effects in NIDDM. Our goal for sucrose and other simple sugars is to keep their combined consumption to 510% of total calories and to include them as part of a mixed meal. Adverse effects on glycemia or lipidemia have not been demonstrated when sucrose and other simple sugars were used in this manner. Fructose is a naturally occurring monosaccharide with taste, sweetness and caloric content similar to sucrose. It has a lower glycemic index than sucrose and most starches (21) and thus has been advocated as an alternate sweetener in the diabetic diet. Numerous studies have documented that replacement of other carbohydrates by fructose in the diabetic diet reduces glycemia (21) but some evidence exists that fructose may have adverse effects on serum lipids in NIDDM (21). Fructose present naturally in fruits, vegetables and honey does not need to be restricted but should be used in moderation as an added sweetener due to its potential for adverse effect on serum lipids. FATS The major nutritional recommendations for NIDDM include reducing saturated fat and cholesterol intake in the diet due to the high incidence and prevalence of cardiovascular disease (3,6). Amongst other factors, the incidence of cardiovascular disease in NIDDM has been directly related to abnormal lipid levels. Lipid abnormalities are 2-3 times more prevalent in NIDDM compared with non-diabetic individuals and usually involve increases in VLDL-triglyceride and cholesterol and decreases in HDL cholesterol concentrations (22,23). The composition of lipoproteins may also be abnormal in NIDDM with increased concentrations of small, dense LDL and IDL particles (22,23). This abnormality in lipid composition has been termed the phenotype B pattern and may be associated with an increase in cardiovascular disease. One of the most effective ways to treat abnormalities in lipid metabolism is by reducing the saturated fat content of the diet. However, there is considerable controversy as to how saturated fats should be replaced. Current research indicates that replacement of saturated fat with monounsaturates (as oleic acid) rather than complex carbohydrates may be a more efficacious alternative due to the propensity for high carbohydrate diets to elevate triglyceride and reduce HDL cholesterol levels (23). Furthermore, high carbohydrate, low fat diets are reported to increase postprandial glucose and insulin levels in NIDDM which together with increased triglycerides and low HDL are associated with increased cardiovascular risk (23,24). It is recommended that total saturated fatty acids be kept below 10% of total calories (23). Small increment goals may be used in NIDDM patients to achieve the desired degree of fat modification. A realistic approach to reduce saturated fat intake requires a marked decrease in red meats, organ meats, high fat dairy products, and tropical oils (eg. palm, palm kernal, coconut oil, etc). Complex carbohydrates, lean meat, fish, and low fat dairy products as well as mono-unsaturated fats can be used to replace saturated fat. As indicated above, recent research in the dietary management of NIDDM indicates that monounsaturates (oleic acid) may be a satisfactory replacement for saturated fatty acids in the diet (23). Until recently, most studies supporting such advice, however, have been short-term in nature, usually several weeks or less in duration and in limited number of subjects (25). Preliminary results from a more long-term multi-center trial (3-5 months duration) have now been reported (26) which compare high carbohydrate diets (55% carbohydrate, 30% fat) to high-monounsaturated-fat diets (40% carbohydrates and 45%

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fats). The amounts of other nutrients such as saturated fats, polyunsaturated fats, cholesterol, sucrose, and protein were kept similar in both diets. The high carbohydrate diet increased day long plasma glucose and insulin values, and raised fasting plasma triglycerides and very-low-density lipoprotein levels. The high monounsaturated diet was well tolerated and there was no tendency for its beneficial effects to wane over time. These studies strongly support a role for monounsaturate replacement of saturated fats in the diabetic diet and add credence to earlier evidence that high carbohydrate diets may have undesirable consequences in some patients with NIDDM. Monounsaturated fatty acids have been used in large amounts in Mediterranean countries for centuries and appear to be safe. Common oils such as olive, canola, and peanut which are high in monounsaturated fatty acids may be added to the diet in a palatable manner. Oils may be added to salads and in gravies and baked products, Each diet needs to be tailored to the individual but a diet higher in monounsaturate rather than just complex carbohydrate may be indicated especially when triglycerides are elevated or a history of hypertriglyceridemia exists. Patients often find it easier to follow this type of diet but need to be specific in their choice of oils. If weight loss is needed, it can still be achieved by decreasing the total caloric intake while keeping the composition unaltered. A diet with a composition of 45-50% carbohydrate (-40% complex, -5-10% simple), with 1520% monounsaturates, -10% polyunsaturates, a n d 5-10% saturated fats is what we currently strive for. It is our opinion that such a diet is well-tolerated over the long term and may have favorable effects on glycemia as well as lipid levels in NIDDM. The consumption of polyunsaturated fatty acids can lower cholesterol levels and may have other potential benefits for NIDDM, but there is concern over using these compounds in large amounts and for prolonged periods. No population has ever consumed these compounds in large amounts over extended periods of time. Potential adverse effects, such as lowering high density lipoprotein (HDL) cholesterol especially when consumed in large quantities, have been reported with polyunsaturates (22,25). We recommend replacing saturated fatty acids with polyunsaturates but limiting the intake to 5-10% of total calories. Fish oil (W-3 fatty acids) enrichment of the diabetic diet could have a number of potential benefits on plasma triglycerides, platelet aggregation and blood pressure (27). However, fish-oils have also been documented to have adverse effects on glycemic control in NIDDM and a tendency to elevate LDL cholesterol (27). We encourage the consumption of natural occuring W-3 fatty acids in the form of fish and other marine sources to reduce saturated fat intake and do not recommend fish oil supplements. PROTEIN The optimal protein content of the diabetic diet is not currently well-defined due to the potential for protein to exert both beneficial and adverse effects in diabetes. The majority of research regarding protein intake has been conducted in IDDM rather than NIDDM. In NIDDM, protein can have favorable properties on carbohydrate metabolism, stimulating insulin secretion and reducing glycemic excursions (29-33). In contrast, excess dietary protein in persons with NIDDM may lead to problems by increasing the workload of the kidney and hastening the onset of diabetic nephropathy (29). Approximately 20% of persons with NIDDM develop diabetic nephropathy within 20 years of diagnosis (34) and recent research has shown that restricting protein may aid by delaying progression of diabetic nephropathy (35-38). The extent to which protein should be restricted and when it should be initiated remains to be determined however. Additionally, it remains unclear whether the source of dietary protein (eg. animal versus vegetable sources) influences renal workload and subsequent progression of diabetic nephropathy. Preliminary reports suggest that the origin of the protein source (e.g. animal or vegetable) may be just as important as the total quantity of protein consumed in affecting the progression of renal disease (39-42).

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These studies suggest that animal but not vegetable protein influence the progression of renal disease. If the potential benefits of vegetable protein are borne out, supplementing or substituting animal with vegetable protein might allow for more liberal total protein intake in NIDDM without the potential for adverse renal effects. There are also other issues which need to be considered before recommendations of protein intake in diabetic nephropathy can be made. Several recent studies have indicated t h a t the short term beneficial effects of low protein diet therapy on diabetic nephropathy may not persist during chronic therapy. Thus, long term follow-up and evaluation of low protein diets in diabetic nephropathy are needed. It is also unclear whether the quantity of protein required for potential renal benefits can be achieved without protein-calorie malnutrition. In addition to protein content, the role of phosphorus in the progression of diabetic renal disease needs to be more fully addressed. There is some evidence that the limitation of phosphorus intake may have benefits that are synergistic when combined with protein restriction (43,44). Before any specific recommendation can be made, it needs to be recognized that changes in protein intake invariably alter the intake of other macronutrients which, by themselves, may result in independent metabolic effects and consequences in diabetes. Furthermore, in many cases of NIDDM, there is limited scientific data upon which to establish firm recommendations. The current recommendation of the American Diabetes Association for protein is 1220% of total calories (3,6). This amount is similar to recent national surveys which indicate that the average protein intake for all ages is 14-18% of the total dally energy requirement (45). These amounts are substantially greater than the recommended dietary allowance (RDA) of protein for healthy adults of both sexes which is 0.Sg/kg body weight per day or approximately 10% of total energy (45). There is no evidence currently available that adults with uncomplicated NIDDM have protein requirements greater than non-diabetic individuals. Thus, current reported intakes and recommendations for protein actually exceed that required to meet known nutritional needs. In light of the potential risks and benefits of both low and high protein diets, our goal at present is to strive for intakes that approximate the RDA for non-diabetic adults ensuring that 65-75% of this amount is composed of protein of high biologic value. When viewed in the context of current protein consumption patterns, this amount of protein translates into a significant reduction of intake. Although low protein diets are difficult to adhere to for any prolonged period, the RDA is a level of protein intake that is both tolerable and readily achievable. Currently, there is insufficient scientific evidence to support either higher or lower protein intakes in NIDDM. DIETARY FIBER Dietary fiber is generally categorized according to its water solubility into the insoluble non-carbohydrate forms such as cellulose and lignin and the soluble pectins, gums and mucilages. Recommendations about dietary fiber generally refer to the total of insoluble and soluble types. Current estimates of total dietary intake for American adults average 10-15g per day which is low in comparison to the current American Diabetes Association recommendation for total daily dietary fiber intake of approximately 25g per 1000 calories with emphasis on soluble fibers (6). Increased dietary fiber intake appears to have multiple metabolic benefits including improved glucose tolerance, lower insulin requirements, lower levels of atherogenic lipids, blood pressure reduction and possibly weight reduction through enhanced satiety (16). Dietary fiber comes in various forms that vary widely in their ability to affect post prandial glucose response. Fiber content, especially the soluble varieties, as well as the physical form of foods may delay or prolong

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digestion and absorption. Insoluble fiber such as whole wheat breads and cereals are poorly metabolized and have little influence on acute glucose response to carbohydrate loads. Water soluble fibers such as guar gum reduce the rate of glucose absorption and the rate of plasma glucose rise (16). Legumes, vegetables, and fruits are also rich in watersoluble fiber. We recommend that the fiber content of the diet be increased through consumption of natural foods that are rich in total and, in particular, soluble fiber. We strive for a total daily intake of at least 20-30g and do not use concentrated fiber preparations to assist with improving glucose or lipid control in NIDDM. The increase in dietary fiber content also needs to be gradual over a period of weeks to months. Problems that can occur with rapid increase in fiber intake include diarrhea, abdominal cramping and flatulence. Because soluble fibers delay the absorption of foodstuff from the gut, the possibility exists that chronic ingestion may produce nutritional deficiencies or alter the pharmacokinetics of certain drugs. Fiber should come from a variety of sources and be relatively consistent in amount from day-to-day. High fiber diets also require adequate fluid intake to assist in passage through the intestines. Patients with significant abdominal disorders or autonomic neuropathy leading to impaired gastric motility may be at increased risk of bezoar formation and should not undertake a high fiber diet (46). ALCOHOL Excess alcohol (ethanol) consumption can adversely affect the metabolic status of people with diabetes. Alcohol influences glycemic control, lipid levels and contributes to excess caloric intake. If used, alcohol ingestion should be curtailed as suggested by the American Diabetes Association (6). The current guidelines suggest that alcohol should be consumed in moderation of not more than 2 equivalents of alcoholic beverage once or twice a week. One equivalent is equal to approximately 1 ounce of alcohol and is found in a 1.5 ounce shot of distilled spirits, 4-5 ounces of wine or 12 ounces of beer. Hepatic metabolism of alcohol involves oxidative reactions with generation of excess NADH reducing equivalents. Formation of NADH alters the NADH/NAD ratio and the redox state favoring biochemical reactions that can lead to hypoglycemia, hyperlipidemia and hyperuricemia in NIDDM (47). In the fed state, alcohol may produce hyperglycemia by stimulating glycogenolysis and increasing peripheral insulin resistance (47). In people with NIDDM, alcohol should be taken with a meal to prevent hypoglycemia. If patients have a history of hypertriglyceridemia, pancreatitis, gastritis or other conditions affected by alcohol, its use should be actively discouraged. When alcohol is consumed regularly, the calories provided should be counted in the meal plan. In the exchange system, alcohol should be substituted for fat as it is high in calories (-7 kcal/g) and is metabolized in a similar fashion (48). Moderate and occasional use of alcohol when consumed with meals does not alter blood glucose levels in well-controlled NIDDM. SODIUM The average daily sodium intake in the U.S. is reported to be 4-6 g which is far greater than needed to replenish losses. The excessive consumption of sodium in the American diet is derived in large part, from processed and fast foods. As a principal regulator of fluid balance and blood pressure sodium intake is of particular importance in diabetes. The frequent development of hypertension and nephropathy in persons with NIDDM requires that sodium intake be limited in the diet. People with NIDDM are more susceptible to the development of hypertension and its presence can exacerbate the progression of cardiovascular complications and diabetic nephropathy (3,49). The recommended intake of the American Heart Association of 1000 mg sodium per 1000 kcal ingested, not to exceed 3000 rag/day seems prudent and is the approach we use. When hypertension is present in NIDDM, additional sodium restriction to 2500rag or less per day is warranted. The above goal is achieved by avoiding the addition of excess salt, limiting

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intake of high sodium foods, replacing salt with herbs and spices and decreasing the amount of convenience and fast foods. Anti-hypertensive medication may need to be tapered with institution of a limited sodium intake diet.

ALTERNATIVE S W E E T E N E R S

Alternative sweeteners are categorized as caloric (or nutritive) versus non-caloric (or non-nutritive). Caloric sweeteners include fructose and the sugar alcohols (eg. sorbitol, mannitol) and the non-caloric sweeteners include aspartame, acesulfame K and saccharin. The use of alternate sweeteners in the management of diabetes is considered acceptable and safe (50). We recommend use of sweeteners in moderation without excessive use due to lack of research on possible long-term adverse effects. Sweeteners should be tailored in the diet plan on an individual basis after consideration of the meal plan, lifestyle and influence on glycemic control. TREATMENT OF OBESITY IN NIDDM

lY_~ight]~Lm~ As indicated earlier in this chapter, obesity may exacerbate many of the metabolic abnormalities and complications which occur in NIDDM and the majority of patients with NIDDM are obese. Table 2 outlines three indices commonly used to indicate whether treatment of obesity is indicated. Many individuals may be minimally obese or non-obese by weight standards but have increased intra-abdominal adipose accumulation which will be reflected by an increased waist-to-hip ratio. Upper body segment obesity, defined by an increased waist-to-hip ratio, has been associated with a greater risk of cardiovascular disease and other metabolic abnormalities. In all patients, we determine their weight and height, waist-to-hip ratio, and other anthropometric measurements including triceps and abdominal skin-fold thickness. In order to record waist-to-hip ratios, the abdominal circumference is measured at the level of the umbilicus. A measuring tape is wrapped around the patient's abdomen at the umbilicus to obtain the maximum circumference recorded in centimeters. The hip circumference is measured by wrapping a measuring tape around the hip area while the patient is standing. The waist-hip ratio is then calculated by dividing the waist circumference in centimeters by the hip circumference in centimeters. Skin-fold measurements are obtained using calipers while following standardized procedures. The triceps skin-fold thickness is measured at the midline on the back of the right arm over the triceps muscle midway between the acromial process of the scapula and olecranon process of the ulna. Abdominal skinfold thickness measures the subcutaneous fat at the waist between the last rib and iliac crest in the mid-axillary line. We complete all of the above measurements both pre and post weight loss in order to assess the extent and location of fat mass lost during dieting. Changes in fat mass and body composition before and after weight loss can also be correlated to changes in a variety of metabolic parameters. Weight loss can show dramatic improvements in metabolic abnormalities associated with NIDDM but require that weight loss be sustained. Thus, a major goal of diet therapy in obese NIDDM must be to not only achieve but maintain a reasonable weight. Due to the high rates of recidivism, there is often a lack of enthusiasm on the part of both patients and health care personnel for diet therapy in the control of glucose and lipid levels in NIDDM and a greater reliance on pharmacologic therapy. Patients tend to have difficulty adhering to calorie-restricted diets especially long-term so that pharmacologic therapy may be started at an earlier phase of the disease. There is often a failure on the part of health care

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professionals to appreciate the potential and dramatic therapeutic benefits that can result from dietary modification alone. In our diabetes clinics, we constantly stress the use and benefits of weight loss therapy in the treatment of NIDDM. Initial diet therapy and weight loss can often greatly improve glucose control without the need for pharmacologic therapy. Dietary therapy and weight loss is most efficacious in those who have had diabetes for a short duration, usually less than 5 or 10 years (51). In these individuals, insulin secretory capacity is still sufficient to control hyperglycemia as hepatic and peripheral insulin resistance improve with weight loss (51). Although the sustained metabolic benefits of weight loss in obese NIDDM require a prolonged period of weight reduction (7), rapid improvement, often within days, can occur in glucose and lipid levels as well as hypertension. The fact that these benefits occur before substantial weight loss has resulted indicates that caloric restriction per se mediates a large part of these effects (7). There are a number of potentially harmful aspects of weight loss in obese individuals including those with NIDDM that need to be considered. One of the major significant dangers is the excessive loss of lean, rather than fat mass, especially during rapid weight loss. This tends to occur more commonly in those with minimal or mild obesity who use severe calorie and protein restricted diets. Men, particularly those with upper body segment obesity but minimal excessive total body weight are most prone to excessive loss of lean body mass. Reducing the caloric deficit and increasing the protein content of the diet slows both the rate of total body weight lost and the contribution of lean body mass. There are several different approaches used to achieve the goals of weight loss based primarily upon the caloric content and composition of the diet desired. Two types of weight loss plans commonly used by us are shown in Table 3. The caloric recommendations range from 400-600 kcal/day using very low calorie diets (VLCD) to 1200-1800 kcal/day for conventional diet plans. In cases where weight loss is too rapid, calories are added back in 100-150 kcal increments primarily in the form of complex carbohydrate or high quality protein. The two major obstacles that need to be overcome for a successful weight loss program involve initiating and achieving weight reduction and then maintaining the reduced weight. Initiating weight reduction is often more difficult with the smaller caloric deficits of conventional diet plans than with the larger deficits resulting from use of VLCD's. VLCD's are a more structured program of limited food choices that are associated with less temptation to overeat food outside the diet plan. Patients often find this diet more convenient and thus easier to follow. While on a VLCD, it is important for patients to begin to introduce other lifestyle changes which they will use to maintain the weight lost. Weight maintenance is the most difficult component of a diet program and new lifestyle changes need to be instituted and continually re-enforced. A multidisciplinary team approach is helpful in this difficult time of weight maintenance. Exercise and behavioral modification combined with a diet program and constant re-enforcement will enhance the success of weight maintenance (7,52). Obese NIDDM patients need to be provided with the opportunity to achieve some weight loss and the plan chosen must be individually structured. As discussed earlier, even modest weight loss of as little as ten pounds or 5-10% of initial body weight can significantly impact glucose tolerance, lipid profiles and blood pressure (7). In many patients, this degree of weight loss is both realistic and maintainable in the long-term. In others, the aim for greater weight loss of 10-20% of initial body weight can be achieved and maintained with additional benefits on metabolic parameters. We do not strive to achieve ideal or even desirable body weight but focus on an acceptable weight that both the patient and the health care team believe can be sustained.

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With both VLCD and conventional diets plans, the goals of therapy and logistics of the treatment plan need to be extensively reviewed with the patient and his or her family in the prediet sessions. A target goal weight is set and discussed with each patient and the time frame to complete the goal is negotiated. A thorough medical and dietary history is obtained tAldng into consideration important aspects unique to each individual. Therapy goals may need to be adjusted due to the person's age, lifestyle, exercise, culture, medications, and other medical problems. Gradual step-by-step increment goals are set with each patient and monitored by frequent follow-up. Patients may be seen weekly in the initial phase and food records evaluated to monitor compliance to VLCD or to monitor calorie and fat intake and caloric distribution in conventional diets. Records of exercise and blood glucose levels are also beneficial to monitor diet therapy. Weekly visits should continue until the first weight goal is achieved. Most VLCD's provide 400-800 kcal/day and consist primarily of high-quality protein with micronutrient supplements. Most VLCD's are commercially available preparations that are provided as a powder that is reconstituted to liquid with water or skim milk. VLCD's provide a daily average intake of 50-100 g of high quality protein from milk, eggs, or soybeans; 50-100 g of carbohydrate is mainly as sucrose, fructose, or maltodextrins; and small quantities of fat (usually < 5 or 10g) are provided to ensure adequate intake of essential fatty acids. Some products also include up to 15 g soluble fiber/day. We often use a 600 kcal VLCD consisting of-400 kcal of powdered formula drinks with -200 kcal of fresh fruit and vegetables for additional fiber. During hypocaloric diet therapy, urinary volume losses can be substantial and lead to severe dehydration and hypotension. Thus, it is important to stress adequate water intake of at least two liters of water or other non-caloric liquids per day. Vitamin and mineral supplementation is usually not necessary unless the products have not been aggressively supplemented and do not meet the RDA minimum for essential vitamins and minerals. We have extensive experience with VLCD therapy of obese NIDDM and find that it is well tolerated and safe when used for short periods of time ranging from 6-12 weeks. VLCD therapy is now recognized as an effective alternative form of therapy for obese NIDDM when weight loss and metabolic control cannot be achieved with conventional diet therapy (3,6). Patients are often unable to adhere to conventional diet therapy for prolonged periods of time because weight loss is slow and food choices are not limited. VLCD's may be particularly useful to achieve rapid short-term weight loss without the plateau often associated with traditional diets. We often use this form of diet therapy to improve insulin sensitivity to enable glycemic control to be re-established with oral hypoglycemic agents or insulin. When VLCD's are instituted, these pharmacologic agents often need to be rapidly tapered or discontinued to prevent severe hypoglycemia. Conventional diets that provide 1200-1800 kcal/day result in caloric deficits of approximately 500-1000 kcal/day and weight loss of 1-2 lb/week. The caloric deficit during VLCD is 1000-1500 kcaYday which lead to rapid weight loss during the first few weeks followed by a steady loss of 3-5 lb/week. Both conventional and VLCD diet therapy require close medical supervision and constant interaction and follow up with the multidisciplinary team. When the target weight is achieved the weight maintenance phase is initiated. A three week refeeding program (Table 4) is used to allow patients to adjust to gradual increases in food during this time. Unfortunately, patients often regress to old eating habits unless new lifestyle changes are re-enforced. Weight regain and a tendency to increase fat intake are problems often encountered by patients. Frequent visits and contacts with the multidisciplinary team are required. Food record, exercise and blood glucose records, and behavior modification sessions are essential during the weight

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maintenance period. In general, the weight maintenance diet should be calculated to meet the diet recommendations of the American Diabetes Association and American Dietetic Association. Frequent follow-up visits also need to be scheduled with the physician and registered dietitian to monitor weight, calorie and fat intake, and effect on metabolic parameters such as glucose and lipids. A combination of diet, exercise, and behavior modification is needed for long term success in weight maintenance. EXERCISE Exercise, unless contraindicated, should be included as part of the treatment program for obese individuals with NIDDM (3,53,54). Exercise alone reduces glucose intolerance, improves insulin sensitivity, and lowers cardiac risk factors (53,54). In fact, several recent studies have demonstrated that regular exercise can prevent or delay development of NIDDM (54). Exercise also increases energy expenditure which aids dietary therapy to reduce and maintain body weight. One of the important lifestyle changes needed to maintain weight is a scheduled regular exercise program. Individuals need to incorporate exercise into their overall therapy plan. Exercise is an important adjunct to diet therapy in the management of obese NIDDM, and must be individually planned to account for the physical capabilities of each person. Most individuals with NIDDM are sedentary and therefore deconditioned. As a result, each individual must gradually increase exercise sessions and be aware of the potential for adverse effects. There may be physical injury, cardiac problems, or problems with hypoglycemia in diabetic patients treated with insulin or oral hypoglycemic agents. If concern exists about cardiac problems, a cardiac thallium stress test should be performed before initiating an exercise schedule. Hypoglycemia in persons with NIDDM may be immediate in onset or delayed for up to 24 hours after a bout of exercise. Thus, individuals need to self-monitor blood glucose levels frequently both pre- and post-exercise and consume appropriate snacks as necessary to prevent hypoglycemia. One of the most effective methods to prevent or minimize exercise induced hypoglycemia is to institute a regular routine of exercise activities. Self-monitoring of capillary blood glucose measurements just before and after each exercise session assists in preventing hypoglycemia and reinforces the benefits of exercise on glycemic control. A regular program is required to obtain the more chronic beneficial effects on glucose and lipid metabolism. Exercise should be initiated by beginning at a low level of intensity with gradual increments. Walking, stationary cycling, and lap swimming three to four times per week for 20-30 minutes (100-200 kcal expended per session) are safe and effective forms of exercise advocated for patients with NIDDM. Increasing exercise intensity needs to be closely monitored so that diet and medications can be adjusted as needed. Individuals requesting a more intensive exercise program need to be referred to a physical therapy fitness program that specializes in the treatment of medical disorders. Communication needs to be maintained between the exercise program personnel and the diabetes multidisciplinary team. Gratifying results often result when a regular exercise program is initiated and maintained. SPECIAL CONSIDERATIONS Elderlv Elderly individuals with NIDDM may develop nutritional deficiencies. Diet therapy needs to be tailored to account for individual food preferences, ethnic background, and the presence of associated medical conditions requiring dietary restriction. When weight loss is required or if major changes in diet are needed it is often more difficult to change long-

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standing existing habits. Compliance with dietary advice may be influenced by physical limitations, problems with purchase and cooking of food, and functional disabilities. Elderly NIDDM patients require nutritional advice that is individualized to their specific abilities and unique needs yet aids in control of metabolic disorders. Close follow-up by the multidisciplinary team with the individual and family members will aid in achieving dietary goals of diabetes. MINORITY PATIENTS The incidence and prevalence of NIDDM in minority populations is rapidly increasing (14). Diet therapy needs to look at the culture and economic status of each person and strive to individualize the goals of diet. The information must be presented in a manner that is understandable and enables the individual to implement the recommendations within their cultural and educational background. Nutrition educators dealing with minority patients need to be resourceful, using a variety of tools and techniques to make changes that will favorably impact the treatment of NIDDM. CONCLUSION In conclusion, diet therapy and especially weight loss in obese NIDDM is a key factor in control of metabolic disorders. As much as possible, the diet should meet the current recommendations of the American Diabetes Association. Conventional or very low calorie diets may be used in the short-term treatment of obesity. Initiation of diet and close follow-up should be carried out by a multidisciplinary nutritional team including physician, dietitian, and nurse. Most importantly, each diet should be individualized to meet not only the goals of therapy but the ability of patients to comply over the long-term. The combination of diet, exercise, and behavior modification are all mandatory to ensure the long term compliance and success of nutritional advice.

TABLE 1 Macronutrient Composition of Diet for NIDDM Qption 1 Carbohydrate Complex Sucrose t Fiber

Option 2

55-60%* 45-50% 50-55% 40-45% ........................... 5-10% ......................... 25g/1000kcal or 40g/day

Protein .... 0.8 g/kg B.W./day ....

Fats Saturated Polyunsaturated Monounsaturated

<30% < 10% 210% 10-15%

B.W. = body weight; * - expressed as % of total calories 9 Sucrose and other sugars such as lactose and fructose

35-40% < 10% ~ 10% 15-20%

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TABLE 2 Common Treatment Indices of Obesity in NIDDM

Men

WQmCn

1) Ideal Body Weight*

>120%

>120%

2) Body Mass Index [Wt(kg)/Ht(mZ)]

>25

> 27

>1,0

_>0.8

Waist-Hip RatiosJ" *

Based on medium frame, Metropolitan Life Tables, 1983.

t

Abdominal circumference (cm) divided by hip circumference (cm)

TABLE 3 Weight Loss Plans for Obese NIDDM DIET PLAN a) Conventional kcaYday 1200-1800 % of total calories CHO 50-55 PRO 15-20 FAT 25-30 Fiber 25 gin/1000 kcal b) Very Low Calorie kcaYdav 400-800 % of total calories CHO 30-50 PRO 35-50 FAT 5-15 Fiber < 15 gin/1000 keal

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TABLE 4 Refeeding Schedule Following Weight Loss Therapy WEIGHT MAINTENANCE Pre-Diet 25-30 kcal/kgB.W.

Refeedin~ Week 1 = 10 kcal/kgB.W. Week 2 = 15 kcal/kgB.W. Week 3 = 20-25 kcal/kgB.W.

Post-Diet 25-35 kca]]kgB.W.

B.W. = Body Weight

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Accepted for publication December 12, 1993.