Historically, nutrition principles and recommendations for diabetes and related complications have been based on scientific evidence and diabetes knowledge when available and, when evidence was not available, on clinical experience and expert consensus. Often it has been difficult to discern the level of evidence used to construct the nutrition principles and recommendations. Furthermore, in clinical practice, many nutrition recommendations that have no scientific supporting evidence have been and are still being given to individuals with diabetes. To address these problems and to incorporate the research done in the past 8 years, this 2002 technical review provides principles and recommendations classified according to the level of evidence available. It reviews the evidence from randomized, controlled trials; cohort and case-controlled studies; and observational studies, which can also provide valuable evidence (1,2), and takes into account the number of studies that have provided consistent outcomes of support. In this review, nutrition principles are graded into four categories based on the available evidence: those with strong supporting evidence, those with some supporting evidence, those with limited supporting evidence and those based on expert consensus.

Evidence-based nutrition recommendations attempt to translate research data and clinically applicable evidence into nutrition care. However, the best available evidence must still be moderated by individual circumstances and preferences. The goal of evidence-based recommendations is to improve the quality of clinical judgments and facilitate cost-effective care by increasing the awareness of clinicians and patients with diabetes of the evidence supporting nutrition services and the strength of that evidence, both in quality and quantity.

Before 1994, the American Diabetes Association’s (ADA’s) nutrition principles and recommendations attempted to define an “ideal” nutrition prescription that would apply to everyone with diabetes (3,4,5). Although individualization was a major principle of all recommendations, it was usually done within defined limits for recommended energy intake and macronutrient composition. The 1994 nutrition recommendations shifted this focus to one that emphasized effects of nutrition therapy on metabolic control (6,7). The nutrition prescription is determined considering treatment goals and lifestyle changes the diabetic patient is willing and able to make, rather than predetermined energy levels and percentages of carbohydrate, protein, and fat. The goal of nutrition intervention is to assist and facilitate individual lifestyle and behavior changes that will lead to improved metabolic control. This focus continues with the 2002 nutrition principles and recommendations.

Medical nutrition therapy (MNT) is an integral component of diabetes management (8,9) and diabetes self-management education (10). (Medical nutrition therapy is the preferred term and should replace other terms, such as diet, diet therapy, and dietary management.) MNT for diabetes includes the process and the system by which nutrition care is provided for diabetic individuals and the specific lifestyle recommendations for that care. However, recommendations should not only be based on scientific evidence but should also take into consideration lifestyle changes the individual can make and maintain. Cultural and ethnic preferences should be taken into account, and the person with diabetes should be involved in the decision-making process.

Results from the Diabetes Control and Complications Trial (DCCT) and the U.K. Prospective Diabetes Study (UKPDS) convincingly demonstrated the importance of glycemic control in preventing the microvascular complications of diabetes (11,12). In both trials, MNT was important in achieving treatment goals (13,14). MNT in diabetes addresses not only glycemic control but other aspects of metabolic status as well, including dyslipidemia and hypertension—major risk factors for cardiovascular disease. This is important, as macrovascular complications are the major contributors to the morbidity and mortality associated with diabetes (15).

The current nutrition principles and recommendations for diabetes focus on lifestyle goals and strategies for the treatment of diabetes. Now, for the first time, the 2002 recommendations specifically address lifestyle approaches to diabetes prevention; they distinguish MNT for treating and managing diabetes from MNT for preventing or delaying the onset of diabetes, as the two may not necessarily be the same.

Whether for management or prevention of diabetes and its complications, basic to the nutrition recommendations is the underlying concern for optimal nutrition through healthy food choices and an active lifestyle. The ADA supports and incorporates the nutrition recommendations from major organizations, such as the U.S. Department of Agriculture (Dietary Guidelines for Americans) (16), American Heart Association (17), National Cholesterol Education Program (18), American Institute for Cancer Research (19), and Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (20).

Although many studies have focused on the role of single nutrients, food, or food groups in disease prevention or promotion, emerging research suggests there are health benefits from food patterns that include mixtures of food containing multiple nutrients and nonnutrients (21,22,23,24,25,26,27). Although this approach makes it difficult to elucidate mechanisms through which the diet composition affects a particular health outcome, it does represent a practical approach to making realistic nutrition recommendations for improving health.

The health professional with the greatest expertise in providing MNT for diabetes is the registered dietitian (RD) knowledgeable and skilled in diabetes management (8,9,10,28). Outcome studies (13,29,30,31,32,33,34) have demonstrated that MNT provided by RDs results in a 1.0% decrease in HbA1c in patients with newly diagnosed type 1 diabetes (29), a 2.0% decrease in HbA1c in patients with newly diagnosed type 2 diabetes (14), and a 1.0% decrease in HbA1c in patients with an average 4-year duration of type 2 diabetes (30). The effectiveness of dietitian-delivered MNT in improving dyslipidemia has also been demonstrated (35,36,37,38,39,40,41). However, it is essential that all team members involved in diabetes treatment and management be knowledgeable about MNT and supportive of the patient’s need to make lifestyle changes (42,43,44,45).

Goals of MNT that apply to all persons with diabetes are as follows:

  1. To attain and maintain optimal metabolic outcomes, including

  2.  a. blood glucose levels in the normal range or as close to normal as is safely possible to prevent or reduce the risk for complications of diabetes

  3.  b. a lipid and lipoprotein profile that reduces the risk for macrovascular disease

  4.  c. blood pressure levels that reduce the risk for vascular disease

  5. To prevent and treat the chronic complications of diabetes; modify nutrient intake and lifestyle as appropriate for prevention and treatment of obesity, dyslipidemia, cardiovascular disease, hypertension, and nephropathy

  6. To improve health through healthy food choices and physical activity

  7. To address individual nutritional needs, taking into consideration personal and cultural preferences and lifestyle while respecting the individual’s wishes and willingness to change

The goals of MNT that apply to specific situations include the following:

  1. For youth with type 1 diabetes, to provide adequate energy to ensure normal growth and development, and to integrate insulin regimens into usual eating and physical activity habits

  2. For youth with type 2 diabetes, to facilitate changes in eating and physical activity habits that reduce insulin resistance and improve metabolic status

  3. For pregnant or lactating women, to provide adequate energy and nutrients needed for optimal outcomes

  4. For older adults, to provide for the nutritional and psychosocial needs of an aging individual

  5. For individuals being treated with insulin or insulin secretagogues, to provide self-management education for treatment (and prevention) of hypoglycemia, acute illnesses, and exercise-related blood glucose problems

  6. For individuals at risk for diabetes, to decrease the risk by encouraging physical activity and promoting food choices that facilitate moderate weight loss or at least prevent weight gain

The next sections of this technical review paper focus on MNT for the management of diabetes. The first section includes nutrition recommendations for type 1 and type 2 diabetes—intake of carbohydrate, sweeteners, protein, fat, micronutrients, and alcohol; energy balance and obesity; and special considerations. The second section reviews MNT for special populations—children and adolescents, pregnant and lactating women, and older adults. The third section reviews MNT for acute complications—hypoglycemia and acute illness—and comorbid conditions—hypertension, dyslipidemia, nephropathy, and catabolic illness. The last section reviews lifestyle recommendations for the prevention or delay of diabetes.

Carbohydrate and diabetes

When referring to common food carbohydrates, the following terms are preferred: sugars, starch, and fiber (Table 1). This classification is based on the recommendations of the Food and Agriculture Organization of the United Nations and the World Health Organization in which carbohydrates are classified according to their degree of polymerization and are initially divided into three principal groups—sugars, oligosaccharides, and polysaccharides (46). Terms such as simple sugars, complex carbohydrates, and fast-acting carbohydrates are not well defined; use of these terms should be abandoned.

A number of factors influence glycemic response to food, including the amount of carbohydrate (47), type of sugar (glucose, fructose, sucrose, lactose) (48), nature of the starch (amylose, amylopectin, resistant starch) (49), cooking and food processing (degree of starch gelatinization, particle size, cellular form) (50), and food structure (51), as well as other food components (fat and natural substances that slow digestion—lectins, phytates, tannins, and starch-protein and starch-lipid combinations) (52). Fasting and preprandial glucose concentrations (53,54,55,56), the severity of glucose intolerance (57), and the second meal or lente effect (58) are other factors affecting the glycemic response to food.  

Carbohydrate and type 1 diabetes

In trying to establish nutrition recommendations for the prescription of carbohydrate for patients with type 1 diabetes, there are several problems: the paucity of studies, the small number of subjects studied, and the lack of long-term studies. Although several studies in subjects with type 1 diabetes have been done comparing differing amounts or percentages of calories from carbohydrate (59,60,61), there is no body of evidence to suggest changing the 1994 recommendation that 60–70% of total energy be distributed between carbohydrate and monounsaturated fat based on nutrition assessment and treatment goals (6). A basis for choosing between carbohydrate and monounsaturated fat, other than ethnic or cultural preferences, is not readily available. In some studies (59,60), a high-carbohydrate diet compared to a high−monounsaturated fat diet resulted in a higher glycemic profile, with no differences in the lipid profile; however, insulin may not have been adjusted appropriately to cover the amount of carbohydrate ingested. In another study (61) comparing a high-carbohydrate diet to a high−monounsaturated fat diet, there were no differences in glycemia, but there was an increase in postprandial triglycerides with the high−monounsaturated fat diet.

More information is available regarding the effects of different types of carbohydrate on postprandial glycemia. In type 1 patients with diabetes, the ingestion of a variety of starches or sucrose, both acutely (62,63,64,65,66,67,68) and for up to 6 weeks (69,70,71,72), was shown to produce no significant differences in glycemic response if the total amount of carbohydrate is similar. Studies in controlled settings (62,63,64,65,66,67,68,69) and in free-living subjects (70,71,72) have demonstrated similar results.

Studies show a strong relationship between the premeal insulin dosage and the postprandial response to the carbohydrate content of the meal (73,74,75,76). In individuals receiving intensive insulin therapy, the total amount of carbohydrate in the meal did not influence glycemic response if the premeal insulin was adjusted for the carbohydrate content of the meal (73). The premeal insulin dosage required was not affected by the glycemic index, fiber, fat, or caloric content of the meal. Furthermore, wide variations in meal carbohydrate content did not modify the basal (long-acting) insulin requirement. The concept of total meal carbohydrate determining the premeal insulin dosage is further supported by the DCCT, in which it was shown that individuals who adjusted their premeal insulin dosages based on the carbohydrate content of meals had 0.5% (P < 0.03) lower HbA1c levels than those who did not adjust premeal insulin (13).

For individuals receiving fixed dosages of short- and intermediate-acting insulin, day-to-day consistency in the amount and source of carbohydrate has been associated with lower HbA1c levels (77). Day-to-day variations in energy and protein or fat intakes were not significantly related to HbA1c.

Glycemic index.

The usefulness of low−glycemic index diets in individuals with type 1 diabetes is controversial. Five studies (n = 48; range 12 days to 6 weeks) (78,79,80,81,82) have compared low−glycemic index diets to high−glycemic index diets for longer than 1 day. The results from these studies did not provide convincing evidence of benefit. Four studies (78,80,81,82) measured HbA1c, and none reported differences in HbA1c between low− and high−glycemic index diets. Four studies (78,79,80,81) measured glycated albumin or fructosamine; three of those (78,79,80) reported decreases in glycated albumin or serum fructosamine after the incorporation of low−glycemic index food in the diet, and one reported no differences in serum fructosamine (81). Three studies (78,79,80) measured fasting plasma glucose (FPG) concentrations, and none reported differences in FPG between low− and high−glycemic index diets. Insulin requirements were measured in four studies (79,80,81,82); one (79) reported lower insulin requirements from low− compared to high−glycemic index diets, whereas three (80,81,82) reported no differences in insulin dosages. Therefore, although the use of low−glycemic index food may reduce postprandial glucose levels, there is not sufficient evidence of long-term benefit to recommend general use of low−glycemic index diets in individuals with type 1 diabetes.

In a cross-sectional study of 2,810 people with type 1 diabetes from the EURODIAB IDDM Complications Study (83), the glycemic index calculated from 3-day food records was examined for its relation to HbA1c and serum lipid concentrations. HbA1c levels were lower in the lowest glycemic index quartile compared with the highest quartile. Of the serum lipids, only HDL cholesterol was independently related to the glycemic index. Interestingly, the consumption of bread and pasta had the biggest effect on the overall glycemic index.

The effects on lipids after low− compared to high−glycemic index diets appear to be minimal. Two studies (79,80) measured cholesterol concentrations and three studies (78,79,80) measured HDL cholesterol concentrations, but none reported differences in the low− compared to the high−glycemic index diets. One study (80) reported lower triglyceride levels, but one (78) did not.

Although it is clear that carbohydrates do have differing glycemic responses, the data reveal no clear trend in outcome benefits. If there are long-term effects on glycemia and lipids, these effects appear to be modest. Moreover, the number of studies is limited, and the design and implementation of several of these studies is subject to criticism.

Fiber.

Early short-term studies using large amounts of fiber (>30 g/day) in small numbers of suboptimally controlled type 1 subjects (84,85,86,87) suggested a positive effect of fiber on glycemia. However, in a study of type 1 diabetes subjects on intensive insulin therapy, 56 g of fiber had no beneficial effect on glycemic control (81). A recent study (88) randomized subjects being treated with two or more injections of insulin per day and HbA1c levels of 7–10% to either a high-fiber (50 g/day), low−glycemic index diet or a low-fiber (15 g/day), high−glycemic index diet for 24 weeks. The high-fiber diet significantly reduced mean daily blood glucose concentration (P < 0.05), the number of hypoglycemic events (P < 0.01), and, in the subgroup of patients compliant to diet, HbA1c (P < 0.05), but had no beneficial effect on cholesterol, HDL cholesterol, or triglyceride concentrations. Conversely, a cross-sectional analysis of dietary fiber in type 1 diabetes patients enrolled in the EURODIAB IDDM Complications Study revealed that a higher intake of total fiber (grams per day) was independently associated with higher levels of HDL cholesterol in both men and women, and lower LDL cholesterol levels in men but not women (89). No substantial differences were observed between soluble and insoluble fiber intakes. Mean total fiber intake was 18.5 g/day in men and 16.2 g/day in women.

The Dietary Guidelines for Americans (16) recommends that all Americans choose a variety of fiber-containing food, such as whole grains, fruits, and vegetables, because they provide vitamins, minerals, fiber, and other substances important for good health. This is an appropriate recommendation for people with type 1 diabetes as well.

There is strong evidence for the following statements:

  • Studies in healthy subjects support the importance of including food containing carbohydrate from whole grains, fruits, vegetables, and low-fat milk in the diet.

  • With regard to the glycemic effects of carbohydrates, the total amount of carbohydrate in meals and snacks is more important than the source or type.

  • Individuals receiving intensive insulin therapy should adjust their premeal insulin dosages based on the carbohydrate content of meals.

There is some evidence for the following statements:

  • Individuals receiving fixed daily insulin dosages should try to be consistent in day-to-day carbohydrate intake.

  • Although the use of low−glycemic index food may reduce postprandial hyperglycemia, there is not sufficient evidence of long-term benefit to recommend use of low−glycemic index diets as a primary strategy in food/meal planning for individuals with type 1 diabetes.

  • As for the general public, consumption of fiber is to be encouraged; however, there is no reason to recommend that people with type 1 diabetes consume a greater amount of fiber than other Americans.

  • Percentages of carbohydrate should be based on individual nutrition assessment.

The following statement is based on expert consensus:

  • Carbohydrate and monounsaturated fat together should provide 60–70% of energy intake.

Carbohydrate and type 2 diabetes

As is the case for type 1 diabetes, there is no body of evidence relating to people with type 2 diabetes to suggest changing the 1994 recommendation that 60–70% of total energy be divided between carbohydrate and monounsaturated fat. In weight-maintaining diets for type 2 patients with diabetes, replacing carbohydrate with monounsaturated fat reduces postprandial glycemia and triglyceridemia (90,91), but there is concern that increased fat intake in ad libitum diets may promote weight gain and potentially contribute to insulin resistance (92,93,94,95,96,97,98,99,100). Thus the contributions of carbohydrate and monounsaturated fat to energy intake should be individualized based on nutrition assessment, metabolic profiles, and weight and treatment goals.

In individuals with type 2 diabetes, postprandial glucose levels and insulin responses to a variety of starches and sucrose are similar if the amount of carbohydrate is constant (69,71,101,102,103,104,105,106). This has been demonstrated in both controlled (69,101,102,103,104) and in free-living subjects (71,105,106). When studied, the effects of starches and sucrose on plasma lipids were similar and no adverse effects were observed (103,104,105,106).

Glycemic index.

There have been nine studies (80,82,107,108,109,110,111,112,113) involving type 2 diabetes subjects (n = 129) that have compared low−glycemic index and high−glycemic index diets for longer than 1 day. One study (107) reported lower HbA1c levels in low− compared to high−glycemic index diets, whereas four studies (80,82,108,109) reported no differences in HbA1c levels. Three studies (110,111,112) reported significantly lower fructosamine levels in low− compared to high−glycemic index diets, whereas three other studies (108,109,113) reported no significant differences in fructosamine. No differences in fasting plasma glucose concentrations were reported in eight studies (80,107,108,109,110,111,112,113), and no differences in insulin levels were found in two studies (107,109).

In studies that also assessed the effects of low− and high−glycemic index diets on plasma lipids, there were no consistent results. One study (112) reported positive differences on cholesterol levels, whereas four (80,107,108,113) reported no differences. One study reported positive differences in HDL cholesterol levels (109), whereas five (80,108,110,112,113) reported no differences. Four studies (108,109,110,112) reported no differences in LDL cholesterol levels. One study (80) reported positive differences in triglyceride levels; five studies (107,108,110,111,112) reported no differences.

Although studies in type 2 diabetes subjects have not consistently reported a relation between glycemic index and insulin and lipid levels, studies in other populations have reported an association between either lower glycemic index diets or lower glycemic loads with lipids, in particular HDL cholesterol, and insulin levels. In a cross-sectional study of middle-aged adults, the glycemic index of the diet was the only dietary variable significantly related to serum HDL cholesterol concentration (114), and a recent analysis (115) of the Third National Health and Nutrition Examination Survey (NHANES III) reported a change in HDL concentration of –2.3 mg/dl per 15-unit increase in glycemic index. In a study of 32 patients with advanced coronary heart disease, 4 weeks of a low−glycemic index diet improved glucose tolerance and insulin sensitivity compared to a high−glycemic index diet over the same period (116). The same group reported that a low− compared to a high−glycemic index diet improved adipocyte insulin sensitivity in women at risk for coronary heart disease (117).

The glycemic load, defined as the product of the glycemic index value of a food and its carbohydrate content, has been reported to be positively associated with the risk of developing type 2 diabetes in men and women (118,119) and coronary heart disease in women (120). In a cross-sectional study of healthy postmenopausal women, dietary glycemic load was inversely related to plasma HDL cholesterol and positively related to fasting triglycerides (121). In the analysis of the NHANES III results, a high glycemic load was associated with a lower concentration of plasma HDL cholesterol (115).

Fiber.

Early studies of the effects of fiber on glycemia showed promising results, but may have suffered from methodological errors (i.e., poor control of confounding variables such as weight loss, differences in energy consumed, different food sources with potential differences in starch digestibility, and differences in dietary fat content) (122). In a study in which dietary variables were controlled for, increasing the fiber content of the diet from 11 to 27 g/1,000 kcal did not lead to improvements in glycemia, insulinemia, or lipemia (123).

In contrast, a diet supplemented with large amounts of water-soluble, gel-forming fiber, such as guar gum, reduced postprandial glycemia (124). In support of this finding, another study comparing a diet containing 24 g fiber per day (high usual intake) to a diet containing 50 g fiber per day found that the intake of food high in dietary fiber improved glycemic control, reduced hyperinsulinemia, and decreased plasma lipids (125). It thus appears that ingestion of large amounts of fiber is necessary to confer metabolic benefit. It is not clear whether the palatability and gastrointestinal side effects of fiber in this amount would be acceptable to most people.

A meta-analysis of 67 controlled clinical trials indicated that diets high in soluble fiber decrease total and LDL cholesterol, but had a small HDL-lowering effect and did not affect triglyceride concentrations (126). Patients with hypercholesterolemia were not more responsive to dietary fiber than healthy individuals. However, the authors concluded that the effect of soluble fiber within practical ranges on cholesterol was modest (daily intake of 3 g soluble fiber, e.g., 3 apples or 3 bowls [29-g servings] oatmeal can decrease total cholesterol by ∼5 mg/dl, an ∼2% reduction), and on risk of heart disease may be only small.

Newer fiber supplements such as psyllium (127) and β-glucan (128,129) have mixed short-term effects on glycemia and lipemia and require further study.

There is strong evidence for the following statements:

  • Studies in healthy subjects and those at risk for type 2 diabetes support the importance of including food containing carbohydrate from whole grains, fruits, vegetables, and low-fat milk in the diet.

  • With regard to the glycemic effect of carbohydrates, the total amount of carbohydrate in meals or snacks is more important than the source or type.

There is some evidence for the following statements:

  • Although the use of low−glycemic index food may reduce postprandial hyperglycemia, there is not sufficient evidence of long-term benefit to recommend general use of low−glycemic index diets in type 2 diabetes patients.

  • As for the general population, consumption of fiber is to be encouraged. Although large amounts of dietary fiber (∼50 g per day) may have beneficial effects on glycemia, insulinemia, and lipemia, it is not known if such high levels of fiber intake can be maintained long-term.

The following statement is based on expert consensus:

  • Carbohydrate and monounsaturated fat should together provide 60–70% of energy intake. However, the individual’s metabolic profile and need for weight loss should be considered when determining the monounsaturated fat content of the diet. Increasing fat intake may result in increased energy intake.

Nutritive sweeteners

Sucrose.

Sucrose is a common, naturally occurring disaccharide composed of a glucose and a fructose molecule. Average per capita consumption of sucrose and other sugars in the U.S. is estimated to be 94 g/day, accounting for 22% of energy intake (130). Historically, the most widely held belief about nutrition and diabetes was that added sugars should be avoided and naturally occurring sugars restricted. This belief was based on the assumption that sucrose and other sugars were more rapidly digested and absorbed then starch-containing food and thereby aggravated hyperglycemia. However, scientific evidence does not support this assumption.

The available evidence from clinical studies demonstrates that dietary sucrose does not increase glycemia more than isocaloric amounts of starch (67,69,101,103,104,106,131,132). Thus the intake of sucrose and sucrose-containing food in diabetic individuals need not be restricted because of a concern about aggravating hyperglycemia. If sucrose is part of the food/meal plan, it should be substituted for other carbohydrate sources or, if added, should be adequately covered with insulin or other glucose-lowering medication. In addition, the intake of other nutrients (such as fat) often ingested with sucrose-containing food should be taken into account. In one study, when individuals with type 2 diabetes included sucrose in their daily meal plan, no negative impact on dietary habits or metabolic control was observed (133).

Fructose.

Fructose is a common, naturally occurring monosaccharide that accounts for ∼9% of average energy intake in the U.S. (134). Fructose is somewhat sweeter than sucrose. It has been reported that ∼33% of dietary fructose comes from fruits, vegetables, and other natural sources in the diet and ∼67% comes from food and beverages to which fructose has been added (135).

In several studies in diabetic subjects, fructose produced a reduction in postprandial glycemia when it replaced sucrose or starch as a carbohydrate source (69,106,136,137). Thus fructose might be a good sweetening agent in the diabetic diet. However, this potential benefit is tempered by the concern that fructose may have adverse effects on plasma lipids. Consumption of large amounts of fructose (15–20% of daily energy intake [90th percentile of usual intake]) has been shown to increase fasting total and LDL cholesterol in subjects with diabetes (137) and fasting total and LDL cholesterol and triglycerides in nondiabetic subjects (138,139,140,141).

Sugar alcohols (polyols).

Sugar alcohols are classified as hydrogenated monosaccharides (e.g., sorbitol, mannitol, xylitol), hydrogenated disaccharides (e.g., isomalt, maltitol, lactitol), and mixtures of hydrogenated mono- (sorbitol), di- (maltitol), and oligosaccharides (e.g., hydrogenated starch hydrolysates) (46). They are used in food as sweeteners and bulking agents. Sugar alcohols have been designated by the U.S. Food and Drug Administration (FDA) as safe for use as food additives or as Generally Recognized as Safe (GRAS) by affirmation petitions accepted for filing by the FDA (Table 2). The FDA has not indicated a need to designate an acceptable daily intake. Food prepared with sugar alcohols may claim on the label that there is an association between sugar alcohols and reduced risk of dental caries. Because sugar alcohols are only partially absorbed from the small intestine, the claim of reduced energy values per gram is allowed. However, if certain polyols are used in food, a warning concerning excess consumption and laxative effects of polyols is required on the food label (Table 2).

In some studies, ingestion of sugar alcohols (∼50 g) by healthy and diabetic individuals has produced lower postprandial glucose responses than after ingestion of fructose, sucrose, or glucose (142,143,144,145,146,147). Because of the reduced available energy of sugar alcohols, the possibility exists that they could be used to reduce energy intake (as with fat replacers and nonnutritive sweeteners). However, no studies have been published showing this to be the case, and the small energy savings do not appear to result in a significant reduction in total daily energy intake. Intake of food containing sugar alcohols such as sorbitol has been reported to cause diarrhea in children with diabetes (148) and adults (149).

There is strong evidence for the following statements:

  • Sucrose does not increase glycemia to a greater extent than isocaloric amounts of starch.

  • Sucrose and sucrose-containing food do not need to be restricted by people with diabetes based on a concern about aggravating hyperglycemia. However, if sucrose is included in the food/meal plan, it should be substituted for other carbohydrate sources or, if added, be adequately covered with insulin or other glucose-lowering medication.

There is some evidence for the following statements:

  • Fructose reduces postprandial glycemia when it replaces sucrose or starch in the diabetic diet.

  • Consumption of fructose in large amounts may have adverse effects on plasma lipids.

  • The use of sugar alcohols as sweetening agents appears to be safe.

  • Sugar alcohols may cause diarrhea, especially in children.

There is limited evidence for the following statement:

  • The use of added fructose as a sweetening agent is not recommended.

The following statements are based on expert consensus:

  • Sucrose and sucrose-containing food should be eaten in the context of a healthy diet, and the intake of other nutrients ingested with sucrose, such as fat, should be taken into account.

  • There is no reason to recommend that diabetic individuals avoid naturally occurring fructose in fruits, vegetables, and other food.

  • It is unlikely that sugar alcohols in the amounts likely to be ingested in individual food servings or meals will contribute to a significant reduction in total energy or carbohydrate intake, although no studies have been conducted to support this.

Resistant starch.

Resistant starch (nondigestible oligosaccharides and the starch amylose) (Table 1) is not digested and therefore not absorbed as glucose in the small intestine. It is, however, almost completely fermented in the colon and produces about 2 kcal/g of energy (46). It is estimated that resistant starch and unabsorbed starch represent ∼2–5% (usually <10 g/day) of the total starch ingested in the average Western diet (150). Legumes are the major food source of resistant starch in the diet, containing 2–3 g resistant starch per 100 g cooked legumes. Uncooked cornstarch contains about 6 g resistant starch per 100 g dry weight (151). It has been suggested that ingestion of resistant starch produces a lesser increase in postprandial glucose than digestible starch and correspondingly lower insulin levels. As a result, it has been proposed that food containing naturally occurring resistant starch (cornstarch) or food modified to contain more resistant starch (high amylose cornstarch) may modify postprandial glycemic response, prevent hypoglycemia, and reduce hyperglycemia; these effects may explain differences in the glycemic indexes of some food.

There have been several one-meal (152,153,154) and second-meal studies (155,156,157) in nondiabetic subjects, comparing subjects’ physical response to food high in resistant starch and their response to food with an equivalent amount of digestible starch. All studies found some reduction in postprandial glucose and insulin responses to the first meal, but observed mixed results after the second meal. Long-term studies have not consistently confirmed these results (155,158,159,160,161).

Published studies involving people with diabetes have focused on uncooked cornstarch and its potential to prevent nighttime hypoglycemia (162,163,164,165). In uncontrolled studies, evening cornstarch in specific dosages or dosages based on g/kg body weight resulted in less hypoglycemia around 0200 h in all groups (166,167). Longer term studies of evening cornstarch snacks in adults with type 1 diabetes reported less hypoglycemia at 0300 h (168). In subjects with type 2 diabetes, evening cornstarch snacks increased nocturnal glucose and insulin (165). It has not been established that bedtime cornstarch snacks are more effective in preventing nocturnal hypoglycemia than other types of carbohydrate.

The is limited evidence for the following statement:

  • Resistant starches have no established benefit for people with diabetes.

Nonnutritive sweeteners.

There are presently four nonnutritive sweeteners (also referred to as high-intensity sugar alternatives, low calorie, or alternative sweeteners) approved for use in the U.S.: saccharin, aspartame, acesulfame potassium (acesulfame K), and sucralose. Saccharin, originally linked to human cancer based on a study in rats more than two decades ago, has now been dropped from the FDA list of cancer-causing chemicals (169).

The newest product approved by the FDA is sucralose (made from sucrose through a multistep process in which three hydrogen-oxygen groups are replaced with three chlorine atoms). Sucralose has been shown to have no effect on glucose homeostasis in diabetic subjects (170,171). FDA approval is being sought for three other nonnutritive sweeteners: alitame (formed from the amino acids aspartic acid and alanine), cyclamates (removed from the market in 1970), and neotame (similar to aspartame but 30–60 times sweeter and will not require special labeling for phenylketonuria) (172). A recent trend in the food industry is to blend high-intensity sweeteners. This decreases the total amount of individual sweeteners used and may improve taste.

Nonnutritive sweeteners approved by the FDA must undergo rigorous scrutiny and are not allowed on the market unless they are demonstrated to be safe for the public, including people with diabetes, to consume. For all food additives, including nonnutritive sweeteners, the FDA determines an acceptable daily intake (ADI), defined as the amount of a food additive that can be safely consumed on a daily basis over a person’s lifetime without risk. Actual intake is much less than the ADI. Although the daily ADI for aspartame is 50 mg/kg body wt, the range of actual daily aspartame intake at the 90th percentile is 2–3 mg/kg body wt (173). Table 3 lists ADIs of nonnutritive sweeteners (174).

Studies to determine the effects of nonnutritive sweeteners during pregnancy and lactation have been conducted in animals. No adverse effects have been reported (175).

There is strong evidence for the following statement:

  • Nonnutritive sweeteners are safe for people with diabetes when consumed within the ADI levels established by the FDA.

The following statement is based on expert consensus:

  • It is unknown if use of nonnutritive sweeteners improves long-term glycemic control or assists in weight loss.

Protein and diabetes

In the U.S., protein intake accounts for 15–20% of average adult energy intake, a statistic that has varied little from 1909 to the present. Protein intake is also fairly consistent across all ages, from infancy to older age (176,177), and appears to be similar in individuals with diabetes. Protein intake in subjects with type 2 diabetes in the U.K. Prospective Diabetes Study was 21% of daily energy (32); protein intake in children with type 1 diabetes has been reported to be 17% of daily energy (178).

Protein needs.

It has been assumed that in people with diabetes, abnormalities of protein metabolism are less affected by insulin deficiency and insulin resistance than abnormalities of glucose metabolism (179). However, moderate hyperglycemia may contribute to increased turnover of protein in type 2 diabetic subjects. During moderate hyperglycemia, obese subjects with type 2 diabetes, compared to nondiabetic obese subjects, had an increase in whole-body nitrogen flux and a higher rate of protein synthesis and breakdown (180,181).

A high-quality protein (95 g protein/day), very-low-energy diet capable of maintaining nitrogen balance in obese subjects without diabetes did not prevent negative nitrogen balance in diabetic subjects, despite weight loss and improved glycemic control (181). This increased protein turnover was restored to normal only with oral glucose-lowering agents or exogenous insulin sufficient to achieve euglycemia and with increased protein intake (182,183). These study results suggest that people with type 2 diabetes have an increased need for protein during moderate hyperglycemia and an altered adaptive mechanism for protein sparing during weight loss. Thus with energy restriction, the protein requirements of people with diabetes may be greater than the recommended dietary allowance (RDA) of 0.8 g protein/kg body wt, although not greater than usual intake, which is ∼1.0 g protein/kg body wt or ∼100 g protein/day (32). However, individuals consuming very low energy intakes may have a deficiency in protein intake and require an assessment of protein adequacy.

Protein degradation and conversion of endogenous and exogenous protein to glucose in type 1 diabetes depends on the state of insulinization and corresponding glycemic control. Insulin deficiency increases whole-body protein synthesis, protein breakdown, oxidation of essential amino acids (184), and gluconeogenesis (185). Conversion of excess dietary protein or endogenous protein to glucose may occur and, in turn, adversely influence glycemia.

Short-term kinetic studies have demonstrated increased protein catabolism in type 1 diabetic subjects treated with conventional insulin therapy (186,187,188). In one study, to protect against increased protein catabolism, type 1 subjects required near-normal glycemia and an adequate protein intake (188). Because most adults eat at least 50% more protein than required, people with diabetes appear to be protected against protein malnutrition when consuming a usual diet.

Protein and development of nephropathy.

An association between dietary protein intake and the development of renal disease has been suggested. In seven studies, dietary protein intake was reported to be similar in patients with diabetes with and without nephropathy (189,190,191,192,193,194,195). In all studies, protein intake was in the range of usual intake and rarely exceeded 20% of the energy intake. In a cross-sectional study of 2,500 type 1 diabetic subjects, those who reported protein consumption <20% of total energy had average albumin excretion rates <20 mcg/min (196). Those in whom protein intake was ≥20% of daily energy (22% of patients) had average albumin excretion rates >20 mcg/min (in the range of microalbuminuria). In individuals with macroalbuminuria, 32% consumed >20% of total energy from protein versus 23% for those with microalbuminuria and 20% for those with normal albumin excretion. This suggests that a high-protein intake may have a detrimental effect on renal function.

The long-term effects of consuming >20% of energy as protein on the development of nephropathy has not been determined. However, intake of protein in the usual range does not appear to be associated with the development of diabetic nephropathy.

Glucose responses to protein.

A number of studies in healthy, normal-weight subjects (197) and subjects with controlled type 2 diabetes (blood glucose <200 mg/dl) (198,199,200) have demonstrated that ingested protein does not increase plasma glucose concentration. Gannon et al. (200) reported that during the 8-h period after subjects with type 2 diabetes ingested 50 g protein in the form of very lean beef, ∼20–23 g of protein were deaminated, which in theory could yield ∼11–13 g glucose. However, the amount of glucose appearing in the circulation was only ∼2 g, confirming that ingested protein does not result in a significant increase in glucose concentration. This raises the question that if gluconeogenesis from protein is occurring, why does the glucose produced not appear in the general circulation after the ingestion of protein?

In type 2 diabetic subjects, the peak plasma glucose response to carbohydrate is similar to the response to carbohydrate plus protein (197,198,199), suggesting that protein does not slow the postprandial absorption of carbohydrate.

In individuals capable of secreting insulin, protein ingestion is just as potent as glucose ingestion in stimulating insulin secretion (197,198,199,200). The net effect on glucose output by the liver depends on the ratio of insulin to glucagon. In type 1 or type 2 diabetic subjects, the glucagon response to protein is considerably greater than in nondiabetic subjects (201).

In one study of subjects with well-controlled type 1 diabetes, the addition of protein to a meal did not slow the absorption of carbohydrate or change either the postprandial peak glucose response to the meal or glucose levels at 5 h (202). Furthermore, in type 1 diabetic subjects, the rate of restoration to euglycemia after hypoglycemia did not differ when treatment was given with carbohydrate or carbohydrate plus protein (203). Glucose levels, the time to peak plasma glucose levels, and subsequent rate of glucose fall were similar after both treatments.

Protein’s effect on satiety and/or energy balance.

It has been claimed that high-protein, low-carbohydrate diets produce weight loss and improvements in glycemia. It should be noted that most of these diets tend to be high in fat. In one study of high-protein diets, there was a significant decrease in weight and plasma triglycerides at 12 weeks (204). However, plasma LDL cholesterol levels were increased. There is no research available to document that high-protein diets maintain long-term weight reduction any better than traditional weight-loss diets and that they are safe for long-term use.

The Continuing Survey of Food Intake by Individuals 1994–1996 (177) was used to examine the relationship among prototype popular diets (205). In a comparison of low-carbohydrate diets (≤30% of energy from carbohydrate [high protein diets]) and high-carbohydrate diets (>55% of energy from carbohydrate), diet quality was lower and total and saturated fat intake was higher on the lower carbohydrate diet, whereas energy intake and BMI were approximately similar between the two.

The effects of dietary protein on the regulation of energy intake and satiety have not been adequately studied (206,207). Short-term meal studies suggest that protein does exert a positive effect on satiety (208,209,210,211). However, results from one study demonstrated that although hunger was suppressed to a greater extent after a high-protein than a high-fat or high-carbohydrate breakfast, the changes in hunger were not of sufficient magnitude to change ad libitum lunchtime energy intake 5 h later or energy intake for the rest of the day, which were similar after all three breakfast types (210).

There is strong evidence for the following statement:

  • In individuals with controlled type 2 diabetes, ingested protein does not increase plasma glucose concentrations, although ingested protein is just as potent a stimulant of insulin secretion as carbohydrate.

There is some evidence for the following statements:

  • For diabetic individuals, there is no evidence to suggest that usual protein intake (15–20% of total daily energy) should be modified if renal function is normal.

  • For diabetic individuals, especially those with less-than-optimal glycemic control, the protein requirement may be greater than the RDA, but not greater than usual intake.

  • Contrary to advice often given to patients with diabetes, the available evidence suggests the following: 1) dietary protein does not slow the absorption of carbohydrate and 2) dietary protein and carbohydrate do not raise plasma glucose later than carbohydrate alone and thus do not prevent late-onset hypoglycemia.

There is limited evidence for the following statement:

  • It may be prudent to avoid protein intake >20% of total daily energy.

The following statement is based on expert consensus:

  • The long-term effects of diets high in protein and low in carbohydrate are unknown. Although such diets may produce short-term weight loss and improved glycemia, it has not been established that weight loss is maintained. The long-term effect of such diets on plasma LDL cholesterol is also a concern.

Dietary fat and diabetes

Saturated fats and dietary cholesterol.

The primary goal regarding dietary fat in patients with diabetes is to decrease intake of saturated fat and cholesterol (212,213,214). Saturated fat is the principal dietary determinant of LDL cholesterol (213). Compared to nondiabetic subjects, diabetic subjects have an increased risk of coronary heart disease with higher intakes of dietary cholesterol (215). The ADA (8,212) and the National Cholesterol Education Program’s Adult Treatment Panel III (18) have recommended that the serum LDL cholesterol goal be <100 mg/dl. To assist in achieving this goal, it is recommended that food with a high content of saturated fatty acids and cholesterol be limited (17,18).

In a meta-analysis (216) of 37 dietary intervention studies in free-living subjects, plasma total cholesterol decreased from baseline by 24 mg/dl (10%), LDL cholesterol by 19 mg/dl (12%), and triglycerides by 15 mg/dl (8%) in Step I (10% saturated fat and 300 mg cholesterol) interventions (P < 0.01 for all). In Step II interventions (7% saturated fat and 200 mg cholesterol), total cholesterol decreased by from baseline by 32 mg/dl (13%), LDL cholesterol by 25 mg/dl (16%), and triglycerides by 17 mg/dl (8%) (P < 0.01 for all). HDL cholesterol decreased by 7% (P = 0.05) in response to Step II but not Step I dietary interventions. Positive correlations between changes in dietary total and saturated fatty acids and changes in total, LDL, and HDL cholesterol were observed. Adding exercise resulted in greater decreases in total and LDL cholesterol and triglycerides and prevented the decrease in HDL cholesterol associated with low-fat diets. However, studies in diabetic subjects demonstrating the effects of specific percentages of saturated fatty acids (e.g., 10 vs. 7% of energy) and specific amounts of dietary cholesterol (e.g., 300 vs. 200 mg) are not available. Therefore, the goal for patients with diabetes remains the same as for the general population: to reduce saturated fat intake to <10% of energy intake. Some individuals (i.e., those with LDL cholesterol ≥100 mg/dl) may benefit by reducing saturated fat to <7% of energy intake. The goal for dietary cholesterol intake is <300 mg/day and for individuals with LDL cholesterol ≥100 mg/dl, <200 mg/day.

For patients with diabetes, the debate has focused not on the extent to which saturated fatty acids and cholesterol intake should be limited, but rather on what is the best alternative energy source. Plasma cholesterol reductions of 9–29% have been reported in four studies in which saturated fat was replaced with carbohydrate in diabetic diets (217,218,219,220). Two of these studies also measured plasma LDL and HDL cholesterol and reported that substituting a low-fat (<30% of total daily calories), high-carbohydrate diet for a high−saturated fat diet resulted in reductions in LDL, but not HDL, cholesterol. (217,218) Glycemic control was improved or unchanged as a result of restricting dietary saturated fat and replacing it with carbohydrate (217,219,221,222,223,224). See Table 4 for classification of fatty acids (225).

Monounsaturated fats.

Diets high in cis-monounsaturated fatty acids (hereafter referred to simply as monounsaturated fat) (90,226,227,228,229) or low in fat and high in carbohydrate (216,217,218,219,220,221,222,223) result in improvements in glucose tolerance and lipids compared with diets high in saturated fat. Diets enriched with monounsaturated fat may also reduce insulin resistance (227); however, some studies have reported total dietary fat to be associated with insulin resistance (96,97,98,99,100). Metabolic study diets in which energy intake is maintained and that are high in either carbohydrate or monounsaturated fat lower plasma LDL cholesterol equivalently (90). Low−saturated fat (i.e., 10% of energy), high-carbohydrate diets increase postprandial levels of plasma glucose and insulin, increase plasma triglycerides (90), and, in some studies, were shown to decrease plasma HDL cholesterol when compared in metabolic studies to isocaloric high−monounsaturated fat diets (91,230). However, high−monounsaturated fat diets have not been shown to improve fasting plasma glucose or HbA1c values. Therefore, if saturated fat calories need to be replaced, they can be replaced with carbohydrate or monounsaturated fat, either of which can contribute to a reduction in plasma LDL cholesterol. There is, however, concern that when high−monounsaturated fat diets are eaten ad libitum outside of a controlled setting, they may result in increased energy intake and weight gain (216). Studies comparing diets high in monounsaturated fat with diets high in carbohydrate with ad libitum energy intake are needed to evaluate the efficacy of these diets and determine which dietary intervention is superior for reducing cardiovascular risk. Each individual’s metabolic profile and need to lose weight will determine the MNT recommendations. For example, a diet in which 60–70% of energy is to be derived from carbohydrate and monounsaturated fat may emphasize carbohydrate intake for the patient to achieve weight loss and monounsaturated fat for the patient to improve plasma triglyceride levels or postprandial glycemia. Furthermore, an Asian patient may be more comfortable with a high-carbohydrate diet, whereas a patient of Mediterranean descent may prefer a monounsaturated fat−containing diet. Monounsaturated fats can also be considered for food preparation and substituted for saturated fats in fat spreads and snacks.

Polyunsaturated fats.

Only a few studies have evaluated the effects of polyunsaturated fat on plasma lipid levels and glycemic control in subjects with diabetes. In one study of type 2 subjects with diabetes, a diet high in total and polyunsaturated fat resulted in lower plasma total and LDL cholesterol than a diet high in total and saturated fat, but produced no difference in other plasma lipid levels (231). Another study in type 2 diabetic subjects compared a diet high in polyunsaturated fat with one high in monounsaturated fat and reported higher plasma total and LDL cholesterol, fasting glucose, and insulin levels with the polyunsaturated fat diet (232).

N-3 polyunsaturated fat (omega-3 fatty acids).

Food sources of n-3 polyunsaturated fatty acids include fish, especially fatty fish, as well as plant sources such as flaxseed and flaxseed oil, canola oil, soybean oil, and nuts. N-3 fatty acid supplements have been shown to reduce plasma triglyceride levels, especially in hypertriglyceridemic individuals (233), and to have beneficial effects on platelet aggregation and thrombogenicity (234). Increasing the intake of n-3 polyunsaturated fatty acids has been shown to be beneficial in subjects with diabetes (235,236,237). Although fish oil supplementation may be beneficial in lowering plasma triglyceride levels in type 2 diabetic subjects, the accompanying rise in plasma LDL cholesterol is of concern (238,239). Therefore, if n-3 fatty acid supplements are used, the effects on plasma LDL cholesterol should be monitored. Glucose metabolism is not likely to be adversely affected with the use of n-3 supplements (236,237,240). N-3 supplements may be most beneficial in the treatment of severe hypertriglyceridemia (236,241). Although studies of the effects of n-3 fatty acids in patients with diabetes have primarily used supplements, there is evidence from the general population that food containing n-3 fatty acids, specifically eicosapentaenoic acid and docosahexaenoic acid, has cardioprotective benefits (242,243,244,245,246).

Transunsaturated fatty acids.

Trans fats—unsaturated fatty acids formed when vegetable oils are processed and made more solid (hydrogenation)—are found in some margarines and in food prepared or fried in hydrogenated vegetable oils. Trans fats also occur naturally in small amounts in meats and dairy products. The mean intake of trans fatty acids in the U.S. has been estimated at 2.6% of total caloric intake and 7.4% of total fat intake (247). When studied independently of other fatty acids, the effect of trans fatty acids is similar to that of saturated fats in raising plasma LDL cholesterol. Trans fatty acids also lower plasma HDL cholesterol (248,249,250). Studies in nondiabetic subjects support limiting the intake of trans fatty acids.

Stanols/sterols.

Plant stanols are found in very small amounts in food from plants such as corn and soy and in other vegetable or plant oils. Within plant tissue they are derived from plant phytosterols. They differ from plant sterols in that their ring structure is saturated. Plant stanols are esterified to other vegetable oil fatty acids to enhance their lipid solubility and make them easier to use as an ingredient in food. Plant sterol and stanol esters block the intestinal absorption of dietary and biliary cholesterol (251) by competing with cholesterol for entry into the mixed micelles that must form during digestion for dietary fatty acids, cholesterol, and fat-soluble vitamins to be absorbed. Plant stanols/sterols in the amount of ∼2 g/day have been shown to lower serum total cholesterol by up to 10% and LDL cholesterol by up to 14% (251,252,253,254,255).

Low-fat diets.

There are potential benefits from low-fat diets. Low-fat diets are usually associated with modest loss of weight, which can be maintained as long as the diet is continued (230,256) and if combined with aerobic exercise (216,257,258). In studies evaluating the effect of ad libitum energy intake as a function of dietary fat content, low-fat, high-carbohydrate intake is associated with a transient decrease in caloric intake and modest weight loss, leading to a new equilibrium body weight (221,259,260,261,262,263,264,265,266,267,268). With this modest weight loss, a decrease in total cholesterol and plasma triglycerides and an increase in HDL cholesterol occur. Consistent with this, low-fat, high-carbohydrate diets over long periods of time have been shown to not increase plasma triglycerides and, when reported, have led to modest weight loss (230,269,270). Although the significance of the effects of reduced dietary fat intake are controversial (256,271,272,273,274,275,276,277,278,279), reduced-fat diets have been shown to maintain weight loss better than other types of reduced energy diets (216,257,280,281,282,283).

In type 2 diabetic subjects, restrained eating behaviors combined with dietary fat restriction have been shown to have beneficial effects on glycemia, plasma lipids, and/or weight (284,285,286). A higher intake of total dietary fat is associated with higher levels of plasma LDL cholesterol, and the adverse effect of a higher carbohydrate intake on triglycerides has been found in individuals who have undiagnosed diabetes or have gained weight during the previous year (287).

Fat replacers/substitutes.

Dietary fat intake can be decreased by reducing the amount of high-fat food in the diet. Another option is to provide lower fat or fat-free versions of food and beverages. This can be accomplished by removing some fat or by using fat replacers (ingredients that mimic the properties of fat with significantly fewer calories than fat) in food formulations. The FDA has approved the majority of the fat replacers as GRAS because the substances’ ingredients have a long history of safe use in food. A few replacers (notably olestra) have been approved as food additives; approval of these requires both demonstration of safety and premarket approval (288,289,290). Although olestra has no effect on water-soluble nutrients, it can lead to a loss of fat-soluble vitamins.

Two recent studies involving diabetic subjects and food made with fat replacers have been reported (291,292). One of these, a short-term study (292), provided correctly labeled regular or fat-free food to free-living subjects with and without diabetes. Use of fat substitutes/replacers in reasonable amounts (five low-fat or no-fat products per day) produced a small decrease in dietary fat, saturated fat, and cholesterol intake with little or no decrease in total energy intake or weight. When fat replacers are used in larger amounts (293,294), there can be a significant decrease in energy intake. Long-term studies are needed to assess the effect of food containing fat replacers/substitutes on the macronutrient content of the diets patients with diabetes and their utility in achieving treatment goals.

Studies in nondiabetic subjects provide strong evidence for the following statements:

  • In all, <10% of energy intake should be derived from saturated fats. Some individuals (i.e., those with LDL cholesterol ≥100 mg/dl) may benefit from lowering saturated fat intake to <7% of energy intake.

  • Dietary cholesterol intake should be <300 mg/day. Some individuals (i.e., those with LDL cholesterol ≥100 mg/dl) may benefit from lowering dietary cholesterol to <200 mg/day.

  • Intake of transunsaturated fatty acids should be minimized.

  • Current fat replacers/substitutes approved by the FDA are safe for use in food.

Studies in diabetic subjects provide strong evidence for the following statement:

  • To lower plasma LDL cholesterol, energy derived from saturated fat can be reduced if concurrent weight loss is desirable or replaced with carbohydrate or monounsaturated fat if weight loss is not a goal.

There is some evidence for the following statements:

  • Polyunsaturated fat intake should be ∼10% of energy intake.

  • In weight-maintaining diets, when monounsaturated fat replaces carbohydrate, it may beneficially affect postprandial glycemia and plasma triglycerides but not necessarily fasting plasma glucose or HbA1c.

  • Incorporation of two to three servings of plant stanols/sterols (∼2 g) food per day, substituted for similar food, will lower total and LDL cholesterol.

  • Reduced-fat diets when maintained long term contribute to modest loss of weight and improvement in dyslipidemia.

There is limited evidence for the following statement:

  • Two or more servings of fish per week provide dietary n-3 polyunsaturated fat and can be recommended.

The following statements are based on expert consensus:

  • Monounsaturated fat and carbohydrate together should provide ∼60–70% of energy intake. However, increasing fat intake may result in increased energy intake.

  • Fat intake should be individualized and designed to fit ethnic and cultural backgrounds.

  • Use of low fat food and fat replacers/substitutes by patients with diabetes may reduce total fat and energy intake and thereby facilitate weight loss.

Energy balance and obesity

Many individuals with type 2 diabetes are overweight, with ∼36% having a BMI ≥30 kg/m2, which would classify them as obese (295). The prevalence of obesity is higher in women and members of minority populations with type 2 diabetes (295). As body adiposity increases, so does insulin resistance (296,297,298). Obesity may also aggravate hyperlipidemia and hypertension in type 2 patients with diabetes (299).

Because of the effects of obesity on insulin resistance, weight loss is an important therapeutic objective for obese individuals with type 2 diabetes. Short-term studies lasting 6 months or less have demonstrated that weight loss in type 2 diabetic subjects is associated with decreased insulin resistance, improved measures of glycemia, reduced serum lipids, and reduced blood pressure (300,301,302). Long-term data assessing the extent to which these improvements can be maintained in people with type 2 diabetes are not available.

Data from the general public suggest that long-term maintenance of weight loss is challenging. In two observational studies on weight maintenance after weight loss in nondiabetic subjects, one study (303) reported that only 6% in the final study group maintained a 5% weight loss over 9–15 years, while in a random telephone survey (304), 21% of 228 overweight subjects reported that they had intentionally lost weight and maintained a weight loss of 10% for at least ≥5 years. However, long-term data assessing the extent to which weight loss is maintained in patients with diabetes are not available. In studies of weight loss in type 2 diabetic subjects (305,306,307), the most successful long-term weight loss from diet was reported in the Diabetes Treatment Study (307), with weight loss of 9 kg maintained over the 6-year study period. To accomplish this required long-term access to therapeutic contact.

The reason that long-term weight loss is difficult for most people to accomplish is probably because energy intake and energy expenditure, and thereby body weight, are controlled and regulated by the central nervous system (308,309,310). Although our understanding of central nervous system regulation of energy balance is incomplete, it is thought that the hypothalamus may be the center of control. Neuropeptide Y, leptin, insulin, and a variety of other neural, endocrine, and gastrointestinal signals also appear to be involved. Individual characteristics of central nervous system control of energy balance may be genetically determined. For example, in a study of Danish adoptees, there was a strong relation between BMI of the adoptees and their biological parents, and no relation whatsoever between the BMI of the adoptees and their adoptive parents (311). These study results suggest that genetic factors have an important role in determining body weight. Other data support this conclusion (312,313). Furthermore, environmental factors often make losing weight difficult for those genetically predisposed to obesity.

The National Weight Control Registry has enrolled over 3,000 subjects successful at long-term maintenance of weight loss (314). A group of ∼800 people who lost an average of 30 kg and maintained a minimum weight loss of 13.6 kg (30 lb) for 5 years were identified from the registry (315). Slightly more than half lost weight through formal programs, and the remainder lost weight with a program of their own. Average energy consumption was ∼1,400 kcal/day, with 24% of energy derived from fat. Average energy expenditure through added physical activity was 2,800 kcal/week. Importantly, nearly 77% of this sample of people who were successful in achieving and maintaining weight loss reported a triggering event that preceded the weight loss. The most common triggering events were acute medical conditions and emotional problems. Thus a new diagnosis of type 2 diabetes could trigger lifestyle changes that result in reduced fat and energy intake, increased physical activity, and associated weight loss.

Structured programs to produce lifestyle change.

The recently completed Diabetes Prevention Program (DPP) demonstrated long-term benefit in people with glucose intolerance from structured, intensive lifestyle programs (316,317). In the DPP, participants randomly assigned to an intensive lifestyle intervention that included a low-fat diet, increased physical activity, educational sessions, and frequent follow-up were able to lose 7% of body weight in the first year and sustain a 5% weight loss over an average follow-up period of 3 years. DPP program participants received training in diet, exercise, and behavior modification from case managers who met with them for at least 16 sessions in the first 24 weeks and monthly thereafter. With intensive lifestyle intervention, the risk of developing diabetes was reduced by 58% relative to standard care. Wing et al. (318) demonstrated a 2.5-kg weight loss and Tuomilehto et al. (319) documented a 3.5-kg weight loss at 2 years with such programs, and also demonstrated that lifestyle changes reduce the risk of developing diabetes. A recently initiated clinical trial called Look AHEAD (Action for Health in Diabetes) will assess the long-term effects of diet and exercise in type 2 patients with diabetes.

For weight loss, dietary fat is probably the most important nutrient to be restricted. Spontaneous food consumption and total energy intake are increased when the diet is high in fat and decreased when the diet is low in fat (259,260). Moreover, epidemiological studies have demonstrated that dietary fat intake is positively associated with adiposity and BMI (320,321). In healthy individuals, simply reducing the fat content of the diet can result in reduced energy intake and weight loss of 2–3 kg (260,322,323). Toubro and Astrup (283) compared the efficacy of an ad libitum, low-fat, high-carbohydrate diet with that of a fixed−energy intake diet for long-term maintenance of weight loss. Both treatment groups attended reinforcement sessions 2–3 times weekly. At 1-year follow up, the ad libitum group had maintained a greater weight loss than the fixed−energy intake group.

Exercise improves insulin sensitivity, can acutely lower blood glucose in patients with diabetes, and may also improve cardiovascular status. Exercise by itself has only a modest effect on weight (324). Exercise is to be encouraged, but like behavioral therapies, may be most useful as an adjunct to other weight-loss strategies, such as dietary fat reduction. Exercise is, however, important in long-term maintenance of weight loss (325,326).

Behavioral approaches to weight loss include strategies such as self-monitoring of food intake and exercise, nutrition education, stimulus control, preplanning of food intake, and self-reinforcement. Weight loss with behavioral therapy alone has been modest (327,328); behavioral approaches may be most useful as an adjunct to other weight-loss strategies.

Other nutrition interventions.

Standard weight-reduction diets, meal replacements, and very-low-calorie diets (VLCDs) are other nutrition options. Standard weight-reduction diets provide 500–1,000 fewer calories than are estimated to be necessary for weight maintenance. An ADA technical review paper on the prevention and treatment of obesity (326) concluded when such diets are used alone in patients with type 2 diabetes as well as in the general population, participants generally lose ∼10% of initial body weight (329). However, an average of 33% of the lost weight is usually regained in the year after treatment, and almost all of the lost weight may be regained within 5 years (330). Nevertheless, standard weight-reduction diets may still be recommended for overweight patients with type 2 diabetes as some people can lose weight with them and maintain the weight loss, particularly if they increase their physical activity.

Structured meal replacements provide a defined amount of energy (usually 200–300 calories), often as a prepackaged meal, snack bar, or formula product. Most of the energy is derived from protein and carbohydrate. Vitamins, minerals, and fiber may also be included. Use of meal replacements once or twice daily to replace a usual meal can result in significant weight loss (331,332,333,334,335). Presumably the meal replacement causes a reduction in energy intake by eliminating the choice of type and amount of food. Weight loss can be as much as 11% of starting weight at 2 years, but meal replacement therapy must be continued if weight loss is to be maintained; attrition may occur in about 33% of patients (331).

VLCDs provide 800 or fewer calories daily, primarily from protein and carbohydrate, with mineral and vitamin supplementation. These diets can produce substantial weight loss and rapid improvements in glycemia and lipemia in patients with type 2 diabetes (301,336). Of note, reductions in glycemia occur before significant weight loss, suggesting that caloric restriction plays an important role in correcting hyperglycemia. Unfortunately, when VLCDs are stopped and self-selected meals are reintroduced, weight gain is common (337,338). Most people treated with VLCDs are not able to maintain long-term weight loss. Thus VLCDs appear to have limited utility in the treatment of type 2 diabetes and should be considered only in conjunction with a structured weight-maintenance program.

Pharmacological therapy.

If energy balance is regulated by a hypothalamic control center that produces and responds to biochemical signals, it might be possible to influence the control center pharmacologically. This possibility first received attention with the publication of a landmark study by Weintraub, who described the effects of fenfluramine and phentermine to induce weight loss (339). When the study was published in 1992, it initiated widespread increased use of fenfluramine and phentermine (fen-phen) for weight loss and maintenance (340). Before the withdrawal of fenfluramine because of cardiac effects, the combination of fenfluramine and phentermine was demonstrated to have beneficial weight-loss effects in type 2 diabetic subjects (341).

Since the withdrawal of fenfluramine and its dextroenantiomer dexfenfluramine, only a limited number of weight-loss medications remain available in the U.S. Some are listed in Table 5. Phentermine continues to be available, but appears to have limited efficacy when used as a single agent. Sibutramine suppresses the appetite by inhibiting reuptake of serotonin and norepinephrine in the central nervous system. A 24-week, placebo-controlled study compared sibutramine and diet to placebo and diet in type 2 diabetic subjects (342). Subjects treated with sibutramine lost 4.0 kg more weight, but did not have a significant improvement in HbA1c levels when compared to subjects treated with placebo. Orlistat is a medication that inhibits pancreatic lipase and causes malabsorption of a portion of ingested fat. In a 1-year, placebo-controlled study comparing orlistat and diet to placebo and diet in type 2 diabetic subjects, the orlistat group lost 6.2% of initial body weight as compared to 4.3% weight loss in the placebo group (343). In the orlistat group, HbA1c decreased by 0.2%, whereas in the placebo group it increased by 0.3%. In a second 1-year, placebo-controlled study of orlistat, a diabetic subgroup experienced a reduction in HbA1c that was 0.5% more with orlistat than with placebo (344).

The available data suggest that weight loss medications may be useful in the treatment of overweight patients with type 2 diabetes. However, the effect of these medications is modest. The data also suggest that these drugs work best in conjunction with lifestyle strategies. In addition, like antihypertensive and antihyperlipidemic medications, these medications must be continued to maintain any beneficial effect. As more is learned about the regulation of energy balance, new weight-loss drugs should become available.

Gastric reduction surgery.

Gastric reduction surgery can be an effective weight loss treatment for severely obese patients (including those with type 2 diabetes) (345,346,347). A National Institute of Health Consensus Development Panel has recommended that such surgery be considered in patients with type 2 diabetes and with a BMI ≥35 kg/m2 (348). The two surgical procedures most widely used are vertical banded gastroplasty and gastric bypass. Both procedures involve creation of a small (25–50 ml) gastric pouch to receive food. This small pouch permits consumption of small meals without epigastric pain or vomiting. Larger meals or large fluid intakes cause pain and vomiting.

In a series of 70 obese patients treated with vertical banded gastroplasty, median weight losses 1 and 3 years after surgery were 37 and 32 kg, respectively (345). In a large series of 515 obese patients treated with gastric bypass, mean weight losses at 1 and 3 years were 50 and 45 kg, respectively, and weight loss was well maintained in 44 patients who achieved 10 years of follow-up (346). Within the subgroup of 137 patients in this study who had type 2 diabetes, 107 (78%) experienced clinical remission of diabetes. From a group of 500 patients consecutively treated with laparoscopic adjustable gastric band surgery, 50 patients with type 2 diabetes were studied preoperatively and again 1 year after surgery (347). Their postoperative mean weight loss was 27 kg, with significant improvement in all measures of glucose metabolism and remission of diabetes in 32 (64%) patients, major improvement in control of diabetes in 13 (26%), and no change in 5 (10%).

Potential adverse effects of gastric reduction surgery include perioperative mortality in 1–2% of patients, wound dehiscence, vitamin and mineral deficiencies, cholelithiasis, inability to eat certain types of food (particularly meat, untoasted bread, and raw fruit), and persistent vomiting (345,346,347,348). Prophylactic treatment with ursodiol may prevent gallstone formation (349).

It is unfortunate that there are no data comparing medical and surgical approaches to weight loss in obese patients with type 2 diabetes; thus the relative benefits and risks of surgical approaches are uncertain. In the absence of data defining benefits and risks, gastric reduction surgery probably should be considered unproven in treating diabetes.

There is strong evidence for the following statements:

  • In insulin-resistant individuals, reduced energy intake and modest weight loss improve insulin resistance and glycemia in the short term.

  • Structured programs that emphasize lifestyle changes, including education, reduced fat (<30% of daily energy) and energy intake, regular physical activity, and regular participant contact can produce long-term weight loss of 5–7% of starting weight.

  • Exercise and behavior modification are most useful as adjuncts to other weight-loss strategies. Exercise is helpful in maintaining weight loss.

  • Nutrition interventions, such as standard weight-reduction diets, when used alone are unlikely to produce long-term weight loss. Structured, intensive lifestyle programs are necessary.

  • Optimal strategies for preventing and treating obesity long-term have yet to be defined.

There is some evidence for the following statement:

  • Currently available weight-loss drugs have modest beneficial effects in patients with diabetes. These drugs should be used only in people with BMI >27.0 kg/m2.

There is limited evidence for the following statement:

  • Gastric reduction surgery can be considered for patients with diabetes and a BMI >35.0 kg/m2. Long-term data comparing the benefits and risks of gastric reduction surgery to those of medical therapy are not available.

Micronutrients and diabetes

Adequate intake of micronutrients within the range of Dietary Reference Intake (DRI) prevents deficiency diseases and is important in maintaining the health and well-being of patients with diabetes. Nutrient recommendations for adults, adolescents, and children with type 1 or type 2 diabetes and for women with diabetes during pregnancy and lactation are similar for people with or without diabetes (350,351,352,353,354,355). However, uncontrolled diabetes is often associated with micronutrient deficiencies (356,357).

Individuals with diabetes should be educated about the importance of acquiring daily vitamin and mineral requirements from natural food sources, and about the potential toxicity of megadoses of vitamin and mineral supplements. In select groups, such as elderly individuals, pregnant or lactating women, strict vegetarians, or individuals on calorie-restricted diets, supplementation with a multivitamin preparation is advisable (16). However, vitamin and mineral supplementation in pharmacological dosages should be viewed as a therapeutic intervention and, as with medications, be subjected to placebo-controlled trials to demonstrate its safety and efficacy.

To determine how much of a specific micronutrient an individual needs on a daily basis, four estimates of DRIs have been made by the Institute of Medicine’s Food and Nutrition Board: Estimated Average Requirement (EAR), the Recommended Dietary Allowance (RDA), the Adequate Intake (AI), and the Tolerable Upper Intake Level (UL). The RDA is a daily intake level that is sufficient to meet the nutrient requirement of nearly all (97–98%) healthy individuals within a specific age, sex, life stage, and physiological state; the UL is the largest amount of a nutrient that is likely to pose no risk of adverse health effects for almost all the general population (350,351,352,353). Table 6 provides RDAs for certain vitamins and minerals and upper limits for those deemed harmful at high dosages.

Evaluation of the micronutrient status of patients with diabetes begins with a careful clinical history and should include a food/nutrition history to document use of “health food”; over-the-counter vitamin, mineral, and herbal supplements; food supplements; and methods of preparing food. Laboratory evaluation of micronutrient status is confounded by methodological problems and, as a result, does not always define micronutrient deficiencies. For example, wide seasonal variations for vitamin D occur in some parts of the country, and serum measurements of intracellular cat ions poorly reflect body stores. However, measurements of serum folate, vitamin B12, vitamin D, calcium, potassium, magnesium, and iron concentrations may be clinically useful.

Antioxidants and vitamins.

An Institute of Medicine report concluded that consuming megadoses of dietary antioxidants—vitamin C, vitamin E, selenium, beta carotene, and other carotenoids—has not been demonstrated to protect against cardiovascular disease, diabetes, or various forms of cancer, nor does megavitamin use necessarily prevent basic nutritional deficiencies. In fact, the opposite may be true. High dosages of antioxidants may lead to health problems, including diarrhea, bleeding, and toxic reactions (350). Although results from a large number of population-based studies have suggested a link between antioxidants and a lower incidence of certain chronic diseases, the Institute of Medicine’s comprehensive review of the scientific evidence concluded it was not certain that antioxidants were responsible for any benefit.

Antioxidants.

Because diabetes may be a state of increased oxidative stress, there has been interest in prescribing antioxidant vitamins to patients with diabetes. Large observational studies have shown a correlation between dietary or supplemental consumption of antioxidants and a variety of clinical outcomes, such as prevention of disease states (358,359,360,361,362,363,364,365,366,367,368,369,370,371,372,373,374,375,376,377). However, large, placebo-controlled clinical trials have failed to show a benefit from antioxidants and, in some instances, have suggested adverse effects (378,379,380,381,382,383). Of particular interest is the Heart Outcomes Prevention Evaluation Trial, which included 9,541 subjects, 38% of whom had diabetes (378). Supplementation with vitamin E (400 IU/day) for 4.5 years did not result in any significant benefit.

Several placebo-controlled studies of small numbers of subjects have found beneficial effects of antioxidants on physiological and biochemical end points (384,385,386,387,388). However, most of these findings have not been confirmed. In addition, concern remains about potential long-term toxicity of antioxidants. Two trials with beta carotene found an unexpected increase in the incidence of lung cancer in those randomized to beta carotene (380,382).

Folate.

The role of folate in preventing birth defects is widely accepted and has been the impetus for folate fortification of wheat and grain products in the U.S. (351). Because of the association between elevated serum homocysteine levels and cardiovascular disease, there has been increasing interest in folate supplementation to lower homocysteine (389). However, the role of folate supplementation in reducing cardiovascular events is far from settled. It is noteworthy that there are no health concerns with folate supplementation, except for aggravating vitamin B12 deficiency and occasionally causing seizures in people with epilepsy and marginal folate status who are receiving anticonvulsants. Folate supplementation trials are currently ongoing and are likely to yield important information.

B vitamins.

The role of vitamins B1, B6, and B12 in the treatment of diabetic neuropathy has not been established; therefore, supplementing diet with B vitamins cannot be recommended as a standard or routine therapeutic option (356,357). It has been suggested from some studies that nicotinamide might preserve β-cell mass in newly diagnosed type 1 diabetic subjects, but the number of subjects enrolled in these studies has not been large enough and the treatment effect was not clear enough to warrant application of the findings (390,391).

Minerals.

Deficiencies of certain minerals, such as potassium and magnesium, and possibly zinc and chromium, may predispose a person to carbohydrate intolerance. Whereas the need for potassium or magnesium replacement is relatively easy to detect based on low serum levels of these minerals, the need for zinc or chromium supplementation is more difficult to detect (356,357).

Chromium.

There have been two randomized, placebo-controlled studies in Chinese diabetic subjects where chromium supplementation has had beneficial effects on glycemia (392,393). However, the study populations may have had marginal baseline chromium status. In the first study (392), the chromium status was not evaluated either at baseline or after supplementation. Other smaller studies have also suggested a role for chromium supplementation in the management of diabetes (394), glucose intolerance (395), gestational diabetes (396), and corticosteroid-induced diabetes (397). Results from these studies indicate that the dosage and formulation of chromium used significantly influences the outcome. In one study of patients with diabetes (392), 1,000 μg/day of chromium picolinate was more effective than 200 μg/day. Similarly, in gestational diabetes, 8 μg · kg−1 · day−1 of chromium was more effective than 4 μg · kg−1 · day−1 (396). In contrast, two well-designed studies in the U.S. (398,399) and two in Finland (400,401) failed to demonstrate any significant benefit of chromium supplementation in patients with diabetes. The latter studies used chromium chloride, which may not be as bioavailable as chromium picolinate. At the present time, benefit from chromium supplementation in diabetic individuals has not been conclusively demonstrated.

The Institute of Medicine Food and Nutrition Board’s DRIs found insufficient evidence to set an estimated average requirement for chromium. An adequate intake was determined based on estimated mean intakes. The adequate intake for adult men >51 years is 30 μg/day and for women >51 years is 20 μg/day. However, few serious adverse effects have been associated with excess intake of chromium from food, and therefore a tolerable upper intake level has not been established (352).

Zinc.

Another area of current interest in micronutrient supplementation is the role of zinc in diabetic individuals. Small studies in older subjects with diabetes have suggested some benefit from zinc supplementation in healing skin ulcerations (356,357). A more recent placebo-controlled trial with a formulation of zinc and rabbit prostatic extracts found a significant reduction in HbA1c in subjects randomized to the active treatment arm (402). However, in that study, those randomized to the active treatment had higher baseline HbA1c levels than those randomized to placebo.

Calcium.

The rationale for recommending daily intakes of 1,000–1,500 mg of calcium, especially in older subjects with diabetes (403), is based on the recommendations of the Institute of Medicine Food and Nutrition Board (353) and the National Institutes of Health Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy (404). This recommendation appears to be safe and likely to reduce the incidence of osteoporosis in older individuals. Vitamin D is also required for optimal calcium absorption, and a recommended vitamin D intake of 400–600 IU/day has been established for adults (353,404). The uncertainty of the value of calcium supplementation in younger individuals and potential long-term benefits have been discussed in a critical review by Kanis (405).

Vanadium.

The role of vanadium salts in diabetes has been explored in several small studies. There is no clear evidence of efficacy and there is a potential for toxicity (406,407,408,409).

Herbal preparations.

A full review of herbal preparations and issues is outside the scope of this technical review paper. A variety of herbal preparations have been shown to have modest short-term beneficial effects on glycemia. Of these, the best studied is American ginseng (410,411). Many herbal supplements used to treat obesity also have caffeine and ephedrine-containing herbs in them. Commercially available products are not well standardized, varying greatly in content of active ingredients. In addition, some herbal preparations have been found to surreptitiously include pharmaceutical agents that produce hypoglycemia. Herbal preparations also have the potential to interact with other medications. Therefore, it is important that health care providers know when their patients with diabetes are using these products.

There is some evidence for the following statements:

  • There is no clear evidence of benefit from vitamin or mineral supplementation in patients with diabetes who do not have underlying deficiencies. Exceptions include folate for prevention of birth defects (strong evidence) and calcium for prevention of bone disease (some evidence).

  • Although difficult to ascertain, if deficiencies of vitamins and minerals are identified, supplementation can be beneficial.

  • Routine supplementation of the diet with antioxidants is not advised because of uncertainties related to long-term efficacy and safety.

The following statements are based on expert consensus:

  • Select populations, such as elderly individuals, pregnant or lactating women, strict vegetarians, and people on calorie-restricted diets, may benefit from supplementation with a multivitamin preparation.

  • In individuals with diabetes, there is no evidence to suggest long-term benefit from herbal preparations.

Alcohol and diabetes

According to data for the period 1989–1991, alcohol accounts for ∼2.5% of energy intake in U.S. adults (412) compared with the previous ∼5% based on NHANES II data (1976–1980) (413). It is not clear whether this change is attributable to decreased intake or to methodological differences in the measurement of alcohol intake. Nearly 67% of the adult U.S. population are reported to drink alcoholic beverages, whereas 33% claim to abstain from them (414). People with diabetes undoubtedly fall into both categories.

The alcohol in distilled spirits (hard liquor), wine, and beer is ethanol (ethyl alcohol, C2H5OH). It is the by-product of the oxidation of sugars by yeast enzymes (fermentation). One drink or alcoholic beverage is commonly defined as 12-oz beer, 5-oz glass of wine, or 1.5-oz glass of distilled spirits, each of which contains ∼15 g of alcohol. The cardioprotective effects of alcohol are not determined by the type of alcoholic beverage (415,416). A summary of ecological, case-control, and cohort studies concluded that all alcoholic drinks are linked with lower risk of coronary heart disease, so that much of the benefit is from the alcohol itself rather than other components of each type of drink (415).

The same precautions that apply to the general population regarding the use of alcohol apply to individuals with diabetes. Abstention from alcohol should be advised for women during pregnancy and for people with medical problems such as pancreatitis, advanced neuropathy, severe hypertriglyceridemia (417), or alcohol abuse. The Dietary Guidelines for Americans (16) recommends no more than two drinks per day for adult men and no more than one drink per day for adult women. After consuming comparable amounts of alcohol, women have higher blood ethanol concentrations than men, even with allowances for size differences. Women, compared to men, have an increased bioavailability of alcohol resulting from decreased gastric first-pass metabolism and decreased gastric alcohol dehydrogenase activity; this may contribute to the enhanced susceptibility of women to the effects of alcohol (418).

Alcohol and blood glucose levels.

Alcoholic beverages can have both hypo- and hyperglycemic effects in patients with diabetes, depending on the amount of alcohol acutely ingested, if alcohol is consumed with or without food, and if alcohol use is chronic or excessive. Moderate (419) or severe hypoglycemia (420), no hypoglycemia (421,422), and hyperglycemia (423,424) have all been reported in patients with diabetes after alcohol ingestion. Ingestion of moderate amounts of alcohol has also been shown to blunt the awareness of hypoglycemia in type 1 diabetic subjects (425).

Moderate amounts of alcohol can enhance the glucose-lowering action of exogenous insulin and certain oral glucose-lowering agents. Although alcohol does not affect the rate and degree of decline in plasma glucose, it appears to alter the phase of glucose recovery by interfering with hepatic gluconeogenesis. The hypoglycemia induced by alcohol is not ameliorated by glucagon because it is caused by indirect impairment of gluconeogenesis and is not associated with excessive insulin secretion (420).

In type 1 and type 2 diabetic subjects, it has been shown that ingesting moderate amounts of alcohol with food has no acute effect on blood glucose or insulin levels (419,421,422,426,427,428,429,430,431,432,433,434). The risk of alcohol-induced hypoglycemia during fasting is modest for type 2 diabetic individuals, and is probably present only if they are being treated with insulin or insulin secretagogues.

Relationship of alcohol to other health risks.

Heavy or excessive alcohol consumption is a leading, avoidable cause of death in the U.S. There may be additional specific adverse effects of chronic alcohol consumption for patients with diabetes. In people with type 2 diabetes, chronic alcohol ingestion (customary intake of ∼45 g/day) causes deterioration in long- and short-term glucose metabolism (423). Therefore metabolic control should be carefully monitored if alcohol is an important component of a patient’s diet. The effects induced by excess alcohol are reversed after abstinence from alcohol for 3 days (423,424).

Epidemiological evidence in nondiabetic individuals suggests that light-to-moderate alcohol ingestion in adults is associated with decreased risk of type 2 diabetes (435,436,437) and stroke (438) and increased insulin sensitivity (439,440,441), although insulin sensitivity may be attenuated by central adiposity (441). In adults with diabetes, chronic intake of light-to-moderate amounts of alcohol (5,6,7,8,9,10,11,12,13,14,15 g/day) is associated with a decreased risk for coronary heart disease, perhaps because of the concomitant increase in HDL cholesterol (442,443,444). Prospective, long-term studies are needed to confirm these observations.

Alcohol ingestion increases the capacity for lipoprotein synthesis, especially of VLDL particles. This increase in synthesis is enhanced by a genetic predisposition, high-fat diet, and diabetes (445). Increased lipoprotein synthesis may be more an effect of chronic or excessive alcohol intake, as nondiabetic subjects with fasting hypertriglyceridemia who, in one study, consumed the equivalent of two alcoholic beverages did not demonstrate an acute increase in triglycerides (417). This suggests that even people with hypertriglyceridemia may occasionally use alcohol in moderation.

There appears to be a U- or J-shaped relationship between alcohol intake and blood pressure. Light-to-moderate amounts of alcohol do not raise blood pressure (446,447,448,449,450,451). However, a strong association exists between chronic, excessive intake of alcohol (>30–60 g/day) and blood pressure elevation in men and women. Each additional 10-g increment of alcohol intake above 30 g/day increases systolic blood pressure by an average of 1–2 mmHg and diastolic blood pressure by 1 mmHg (452). In addition to being a risk factor for hypertension, alcohol may interfere with antihypertensive therapy and may be a risk factor for stroke (446,452).

There is strong evidence for the following statements:

  • If individuals choose to drink alcohol, daily intake should be limited to one drink for adult women and two drinks for adult men. One drink is defined as a 12-oz beer, 5-oz glass of wine, or 1.5-oz glass of distilled spirits.

  • The type of alcoholic beverage consumed does not make a difference.

  • When moderate amounts of alcohol are consumed with food, blood glucose levels are not affected.

  • To reduce risk of hypoglycemia, alcohol should be consumed with food.

  • Ingestion of light-to-moderate amounts of alcohol does not raise blood pressure; excessive, chronic ingestion of alcohol raises blood pressure and may be a risk factor for stroke.

  • Pregnant women and people with medical problems such as pancreatitis, advanced neuropathy, severe hypertriglyceridemia, or alcohol abuse should be advised to not ingest alcohol.

There is some evidence for the following statement:

  • There are potential benefits from the ingestion of moderate amounts of alcohol, such as decreased risk of type 2 diabetes, coronary heart disease, and stroke.

The following statement is based on expert consensus:

  • Alcoholic beverages should be considered an addition to the regular food/meal plan for all patients with diabetes. No food should be omitted.

Special considerations

Type 1 diabetes.

Nutrition recommendations for a healthy lifestyle for the general public are also appropriate for individuals with type 1 diabetes. What differs for individuals requiring insulin is the integration of an insulin regimen into their lifestyle. With the many insulin options available, if an individual’s preferred meal routine and food choices are known, an appropriate insulin regimen can usually be developed. The food/meal plan should be based on an assessment of the individual’s appetite, preferred types of food, and usual eating and exercise schedule, and should reflect cultural and ethnic preferences. The food/meal plan should be shared with the entire health professional team so that insulin therapy can be integrated into the individual’s preferred food and physical activity patterns (4,5,6).

As discussed in the Carbohydrate and Diabetes section, above, for individuals requiring insulin, the total carbohydrate content of meals and snacks is the first priority and determines the premeal insulin dosage and postprandial glucose response (62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,81). Glycemic index and usual fiber content of meals and snacks do not affect the premeal insulin dosage (73,81). Subjects in the DCCT who reported following their meal plan at least 90% of the time and adjusted their premeal insulin based on changes in usual carbohydrate intake had HbA1c levels 1.0% lower than those who reported following their meal plan less often (13). For individuals who are on fixed insulin regimens and do not adjust premeal insulin dosages, consistency of carbohydrate intake is the first priority (77).

Improved glycemic control with intensive insulin therapy is often associated with an increase in body weight (453,454,455). In DCCT subjects, a BMI >30 kg/m2 has been associated with increases in lipids and blood pressure (456). In the Pittsburgh Epidemiology of Diabetes Complications study, moderate weight gain did not adversely affect lipid profiles if glycemic control was improved (457). Given the potential for weight gain to adversely affect glycemia, lipemia, blood pressure, and general health, the prevention of weight gain is desirable. Because strategies effective in preventing weight gain have not been defined, treatment of the adverse metabolic effects of weight gain is indicated (456).

For individuals with type 1 diabetes, attention also must be paid to nutrition therapy for improving lipids and blood pressure control, and, if present, reducing microalbuminuria. (See medical nutrition therapy for the Treatment/Prevention of Acute Complications of Diabetes and Comorbid Complications, below, for the conditions comorbid with diabetes).

Hypoglycemia is more frequent in individuals with type 1 diabetes as blood glucose levels and HbA1c are reduced (458), and needs to be treated appropriately to prevent cognitive changes, rebound hyperglycemia, and weight gain. With hypoglycemia, 10 g of oral glucose can raise blood glucose levels by ∼40 mg/dl (2.2 mmol/l) over 30 min, and 20 g of oral glucose can raise blood glucose levels by ∼60 mg/dl (3.3 mmol/) over 45 min (459). With both treatments, however, glucose levels begin to fall 60 min after glucose ingestion. Although glucose may be the preferred treatment choice, any form of carbohydrate will raise blood glucose (460). In one study, adding protein to the treatment of hypoglycemia did not affect the response to carbohydrate treatment or prevent later-onset hypoglycemia (203). (See medical nutrition therapy for the Treatment/Prevention of Acute Complications of Diabetes and Comorbid Complications, below, for more details on the treatment/prevention of acute complications of diabetes.)

Additional carbohydrate may be needed for unplanned exercise. Carbohydrate supplementation is based on the blood glucose level before exercise, previous experience with the particular form of exercise, and the individual’s insulin regimen (461). Exercise of moderate intensity increases glucose uptake by 2–3 mg · kg−1 · min−1 above usual requirements (e.g., a 70-kg person would need 8.4–12.6 g of carbohydrate per hour of exercise) (10,11,12,13,14,15 g). During high-intensity exercise, glucose uptake increases by 5–6 mg · kg−1 · min−1; however, exercise of this intensity usually cannot be sustained for long intervals (462). For planned exercise, reduction in the insulin dosage may be the preferred choice to prevent hypoglycemia (463). Regardless, carbohydrate-containing food should be readily available during and after exercise (461,464).

Carbohydrate is needed during exercise lasting longer than 60–90 min (465,466) as well as after such exercise to replenish muscle glycogen stores (467). Fluid intake is also essential. It has been found that 6–8% carbohydrate solutions are absorbed better and cause less gastric upset than regular soft drinks and fruit juices, which are 13–14% carbohydrate solutions (464).

Type 2 diabetes.

Nutrition recommendations for a healthy lifestyle for the general public are also appropriate for individuals with type 2 diabetes. Because most type 2 patients with diabetes are overweight and resistant to insulin, MNT should emphasize lifestyle strategies that result in reduced energy intake (468,469,470), usually through reducing the fat content of the diet, and increased energy expenditure through exercise (471). Most patients with diabetes also have dyslipidemia and hypertension, making reductions in dietary intake of saturated fat, cholesterol, and sodium desirable. Therefore, the emphasis of nutrition therapy for type 2 diabetes is on lifestyle strategies to reduce glycemia, dyslipidemia, and blood pressure. These strategies should be implemented as soon as the diagnosis of diabetes is made (472).

Moderate amounts of short-term weight loss improve metabolic abnormalities in many individuals with type 2 diabetes (473), but not in all (474). Moderate amounts of weight loss, especially of intra-abdominal fat, reduce insulin resistance and help correct dyslipidemia (475,476). Intentional weight loss is also associated with reductions in mortality in overweight individuals with diabetes (477). However, the best strategy for accomplishing and maintaining weight loss is unclear and may vary from person to person.

In the UKPDS, before being randomized into study groups, subjects received 3 months of intensive nutrition therapy, which resulted in an ∼2% reduction in HbA1c and a mean 5% weight loss (14). The initial glucose response was reported to be more related to the decreased energy intake, with the decrease in body weight being a secondary response. Fasting plasma glucose levels of 100 mg/dl (5.6 mmol/l) were maintained only in individuals who continued a restricted energy intake; once caloric intake was increased, fasting plasma glucose levels increased, even when weight loss was maintained.

Increased physical activity is important for the maintenance of weight loss. Furthermore, increased physical activity can improve glycemia (478), decrease insulin resistance (479,480), and reduce cardiovascular risk factors in women with diabetes (481) and may independently reduce the risk of mortality in men with type 2 diabetes (482). A minimum cumulative total of 1,000 kcal/week from physical activities is recommended (471).

Food intake frequency—three meals or smaller meals and snacks—is not associated with long-term differences in glucose, lipid, or insulin responses (483,484). Therefore, division of food intake should be based on individual preferences.

Food containing carbohydrate is an important component of a healthy diet. Individuals with type 2 diabetes may benefit by knowing what types of food contain carbohydrate (starches, fruits, starchy vegetables, milk, sweets), portion sizes, and the number of servings for meals and, if desired, for snacks. The effect of carbohydrate on blood glucose and plasma lipids may depend on the severity of glucose intolerance (57). With the use of pre- and postmeal blood glucose monitoring data, it can be determined if adjustments in food/meal planning will be helpful or if medication(s) need to be combined with nutrition therapy.

When individuals with type 2 diabetes require insulin, consistency in the timing of meals and carbohydrate content becomes important. As with type 1 diabetes, flexible insulin dosing regimens allow for variations in food intake and a more flexible lifestyle. Treatment with sulfonylureas and other insulin secretagogues also requires consistency in timing and carbohydrate content of meals. Short-acting insulin secretagogues may allow for greater flexibility in mealtimes. People with type 2 diabetes are more resistant to hypoglycemia than people with type 1 diabetes; nevertheless, when type 2 patients with diabetes being treated with insulin or insulin secretagogues may need to reduce medication dosages if they are not able to eat.

Children and adolescents with diabetes

Most diabetes cases diagnosed in children are type 1 diabetes, although the prevalence of type 2 diabetes in youth is increasing (485,486,487,488). Nutrition recommendations for children and adolescents with type 1 diabetes should focus on achieving blood glucose goals without excessive hypoglycemia (489,490,491,492). This can be accomplished through individualized food and meal planning, flexible insulin regimens and algorithms, self-blood glucose monitoring, and education promoting decision making based on outcomes (493). Nutrition recommendations for youth with type 2 diabetes focus on a healthy lifestyle and treatment goals to normalize glycemia (494).

There is no research on the nutrient requirements for children and adolescents with diabetes; therefore, nutrient recommendations are based on requirements for all healthy children and adolescents (350,351,352,353,495). Children and adolescents should achieve healthful eating habits to ensure adequate intake of essential vitamins and minerals. In general, U.S. children are not eating the recommended amounts of fruits and vegetables (496), although children with diabetes may be doing somewhat better than the general population in some areas. A 1996 report (178) on dietary intake of children with type 1 diabetes, ages 4–9 years, found that their energy, vitamin, and mineral intakes were adequate, whereas fiber intake was less than recommended. Of concern was a reported mean saturated fat intake that exceeded the National Cholesterol Education Program (NCEP) recommendations (497). Many children consumed levels of saturated fat well above recommendations. The Food Guide Pyramid, which is a broad tool encompassing food preferences and differences in food choices among various segments of the population, can be used to increase selection of fruits, vegetables, whole grains, and nuts and reduce intake of total and saturated fat (498).

Energy.

Many children with type 1 diabetes present at diagnosis with weight loss that must be restored through insulin initiation, hydration, and adequate energy intake. The best method for estimating a child or adolescent’s energy needs is a food/nutrition history of a typical daily intake as obtained from a 24-h recall or 3-day food record, provided that growth and development are within normal limits. The typical daily energy intake can be compared to reference intakes for normal growth and development. An evaluation of weight gain and growth begins at diagnosis by recording height and weight on the Centers for Disease Control pediatric growth charts (499). Adequacy of energy intake can be evaluated by following weight gain and growth patterns on a regular basis.

Consideration of a child’s appetite must be given when determining energy requirements and the nutrition prescription. Because energy requirements change with age, physical activity, and growth rate, an evaluation of height, weight, and energy intake is recommended every 3–6 months (29). Achieving good metabolic control is essential to normal growth and development (489). However, the practice of withholding food or having the child eat consistently without an appetite for food in an effort to control blood glucose is discouraged.

Macronutrients.

Macronutrient composition of the nutrition prescription is individualized according to blood glucose and plasma lipid goals and requirements for growth and development. Children and adolescents with type 1 diabetes are not at high risk for developing lipid abnormalities, but should be screened and monitored according to guidelines issued by the NCEP in the report of its Expert Panel on Blood Cholesterol Levels in Children and Adolescents (497) and by the American Academy of Pediatrics (500). The stepwise approach to dietary management of lipid abnormalities suggested by the NCEP recommends a reduction in total fat, saturated fat, and cholesterol for children over age 2 years.

Fiber.

Dietary fiber recommendations for children with diabetes are the same as for nondiabetic children. It has been recommended that children older than age 2 years increase their intake of dietary fiber to an amount equal to or greater than their age plus 5 g/day (501).

Physical activity.

Physical inactivity is associated with adverse health effects (502). Intervention strategies for the entire family that promote lifelong physical activity may help children overcome these adverse effects. Physical activity may also provide a lipid-lowering effect in adolescents with diabetes (503).

Type 2 diabetes in youth.

Successful treatment of type 2 diabetes in children and adolescents with nutrition therapy and exercise is comprised of the cessation of excessive weight gain with normal linear growth and the achievement of blood glucose and HbA1c goals (494). Nutrition recommendations for children and adolescents with type 2 diabetes should also address comorbidities, such as hypertension and dyslipidemia (494). Behavior modification strategies to decrease intake of high-calorie, high-fat food while encouraging healthy eating habits and regular physical activity for the entire family should be considered. Regular exercise in obese children, without dietary intervention, has been shown to lead to favorable changes in plasma triglycerides, serum insulin concentrations, and percent body fat (504). However, the benefits of exercise were lost when the children became less active. Intervention strategies should be culturally appropriate, sensitive to family resources, provided to all caregivers, and followed consistently by all health care providers.

Adolescents whose parents have type 2 diabetes have more risk factors—higher BMI, plasma cholesterol, plasma triglycerides, serum insulin, plasma glucose, and insulin-resistance index and lower plasma HDL cholesterol—compared with adolescents whose parents do not have diabetes (505). These risk factors can be detected early and provide incentive for interventions, such as control of weight gain and increased exercise.

There is some evidence for the following statements:

  • Individualized food/meal plans, insulin regimens using basal and bolus insulins, and insulin algorithms can provide flexibility for children with type 1 diabetes and their families to accommodate irregular meal times and schedules, varying appetite, and varying activity levels.

  • Blood glucose monitoring data can be used to integrate an insulin regimen into the meal/snack and exercise schedules.

  • Nutrient requirements for children and adolescents with type 1 or type 2 diabetes appear to be similar to those for same-age nondiabetic children and adolescents.

  • In obese children, increased physical activity improves plasma lipids and insulin sensitivity.

The following statement is based on expert consensus:

  • Successful lifestyle treatment regimens for youth with type 2 diabetes have not been defined.

Pregnant and lactating women

During pregnancy, the goals of nutrition are similar for women with and without diabetes. MNT goals are to provide adequate maternal and fetal nutrition, energy intake for appropriate maternal weight gain (506), and any necessary vitamin and mineral supplements. For pregnancy complicated by diabetes, nutrition therapy should also attempt to achieve and sustain optimal maternal blood glucose control. A favorable pregnancy outcome is defined as gestational duration of 39–41 weeks and live birth of an infant weighing 6.6–8.8 lb. (3–4 kg) (355).

Weight gain/energy requirements.

Infant birth weight is related to maternal size and weight gain during pregnancy. Recommended weight gain goals are based on pregravid BMI and should be steady and progressive (355). For obese women (BMI >30 kg/m2), a relatively small weight gain of ∼7 kg is recommended during pregnancy (507). For underweight women (BMI <19.8 kg/m2), greater weight gain (up to 18 kg) is recommended. A normal-weight woman should gain 1.4–2.3 kg/month during the first trimester and 0.5–0.9 kg/week during the rest of her pregnancy. Overweight women should gain weight at <50% of these rates (355).

Energy intake should be sufficient to promote appropriate weight gain. Unless a woman begins pregnancy with depleted body reserves, energy needs do not increase in the first trimester. An additional 300 kcal/day are suggested during the second and third trimesters for increases in maternal blood volume and breast, uterus, and adipose tissue; placental growth; fetal growth; and amniotic fluids (508). Obese women with ample body fat stores may require fewer calories. Studies have reported successful pregnancy outcomes for women with energy intake of only 100 kcal/day above prepregnancy intake during the second and third trimesters (509). Energy estimates must be individualized based on a food/nutrition assessment, physical activity, and weight gain patterns during pregnancy.

Protein requirements and vitamin and mineral supplementation.

In addition to adequate energy intake, pregnant women need to eat a balanced diet with adequate protein. Protein requirements for women with diabetes during pregnancy are the same as for nondiabetic women during pregnancy—0.75 g · kg−1 · day−1 plus an additional 10 g/day (508).

A balanced diet resulting in appropriate weight gain generally supplies all the vitamins and minerals needed for pregnancy. However, assessment of the pregnant woman’s eating patterns may yield specific individual needs. Although abnormal folate metabolism does not appear to occur in pregnant women with diabetes (510), 400 μg/day of folic acid from fortified food and/or as a supplement as well as food folate from a varied diet is recommended for all women of childbearing age who are capable of becoming pregnant for the prevention of neural tube defects and other congenital abnormalities (351,511,512,513,514). Low-dosage iron supplementation (30 mg/day) during the second and third trimesters is often recommended (508). The average zinc intake of pregnant women is 11 mg/day, whereas the RDA is 15 mg/day (515). Zinc supplementation for women with low pregravid weight and low plasma zinc levels leads to infants with a higher birth weight (516). Food is considered the optimal vehicle for nutrient intake. However, prenatal vitamin and mineral supplements are often prescribed because of uncertainty of nutritional status and intake.

Nonnutritive sweeteners.

The FDA has approved four nonnutritive sweeteners for general use: saccharin, aspartame, acesulfame-K, and sucralose. These sweeteners appear to be safe for use during pregnancy. However, moderation is often recommended (517,518).

Although saccharin can cross the placenta and remain in fetal tissues because of slow fetal clearance (519), there is no evidence that saccharin causes ill effects. If a woman chooses to use saccharin during pregnancy, the evidence suggests it is safe.

In animal studies, aspartame use has shown no risk to the fetus when ingested in amounts three times the ADI (520,521). Phenylalanine, aspartate, and methanol are dietary components of aspartame. Maximum maternal plasma phenylalanine concentrations occurring after ingestion of aspartame would be less than those after ingestion of protein food, making it highly unlikely that customary intakes of aspartame would raise fetal levels to a toxic range. Clinical trials with single and repeated doses of aspartame have shown that aspartame has minimal impact on serum concentrations of aspartate, phenylalanine, and methanol, and no clinical effects in healthy women and women heterozygous for phenylketonuria (520). Aspartate does not cross the placenta at any intake level less than enormous amounts (100 times normal) (521,522). Plasma methanol does not increase significantly after an aspartame load. Thus, if placental transport of these compounds occurs, the amount is not clinically significant (523).

Multigenerational studies of rats that received acesulfame-K and sucralose have shown no adverse effects on fertility, number of offspring, birth weight, mortality, or fetal development (169,524). Acesulfame-K and sucralose are thus considered safe during pregnancy.

Pregnancy with prior onset of type 1 or type 2 diabetes.

For women with type 1 (525) or type 2 diabetes, achieving optimal glycemic control before and after conception has been shown to lower the incidence of birth defects and spontaneous abortion (526). Prepregnancy nutrition therapy includes an individual prenatal food/meal plan to optimize blood glucose control. During pregnancy, the distribution of calories and carbohydrates in the meal plan should be based on the woman’s food and eating habits, blood glucose records, and the expected physiological effects of pregnancy on her body. Regular meals and snacks are important to avoid hypoglycemia made more likely by the continuous fetal draw of glucose from the mother. Moreover, the accelerated starvation of pregnancy leads to fat catabolism, ketonemia, and ketonuria after only 12–14 h of fasting. This ketonemia has been associated with lower intelligence scores in offspring at ages 2–5 years (527,528).

An evening snack is usually necessary for pregnant women with diabetes to decrease the potential for overnight hypoglycemia and fasting ketosis. Blood glucose monitoring and daily food records provide valuable information for insulin and meal plan adjustments.

Gestational diabetes.

Prevention of adverse perinatal outcomes is the primary focus of antepartum management of gestational diabetes (526). Women who fail to achieve or maintain glycemic goals or who show signs of excessive fetal growth with nutrition therapy should be considered for pharmacological therapy with insulin (529,530,531). Results from a single study have suggested that glyburide may be an alternative strategy that merits future consideration (532). Intensive treatment of hyperglycemia in women with gestational diabetes can reduce the risk of infants having excessive fetal size for gestational age. However, the perinatal outcomes of small-for-gestational-age neonates in pregnancies with gestational diabetes may be worse with intensive therapy than for appropriate size and large-for-gestational-age neonates (533).

The goal of nutrition therapy for women with gestational diabetes is to promote nutrition necessary for maternal and fetal health, with adequate energy levels for appropriate gestational weight gain, achievement and maintenance of normoglycemia, and absence of ketones. Carbohydrate is distributed throughout the day among three small-to-moderate-size meals and two to four snacks. An evening snack may be needed to prevent accelerated ketosis overnight. Specific nutrition/food recommendations are determined and modified based on individual assessment and self−blood glucose monitoring data (518).

Diets containing 40–45% of total energy intake from carbohydrate have been shown to reduce postprandial glucose levels (534,535,536), with carbohydrate being less well tolerated at breakfast than at other meals (534). Nutrition management should include evaluation of the individual glycemic response to food at different times of the day (537,538). If insulin therapy is added to nutrition therapy, a primary goal must be to maintain carbohydrate consistency at meals and snacks to facilitate insulin adjustments.

Several research studies have focused on use of energy-restricted diets during pregnancy. Hypocaloric diets (<1,200 calories per day) in obese women with gestational diabetes have been shown to result in ketonemia and ketonuria (539). In one study, a modest energy reduction (33% calorie restriction of estimated energy needs or ∼1,600–1,800 kcal/day) resulted in reduced mean blood glucose levels without elevations in plasma free fatty acids or ketonuria, whereas a more severe energy reduction (50% calorie restriction) increased ketonuria by about twofold (540). Energy intake should maintain desirable weight gain during pregnancy. Daily food records, weekly weight checks, and ketone testing can be used to determine individual energy recommendations and if a woman is undereating to avoid insulin therapy (541,542).

Regular aerobic exercise has been shown to lower fasting and postprandial glucose concentrations and may be used as an adjunct to nutritional therapy to improve maternal glycemia (529). Other benefits of exercise during pregnancy include cardiovascular fitness (543) and reduced discomfort in later pregnancy. The optimal frequency and intensity of exercise for lowering maternal glucose concentrations have not been determined, but it appears that a minimum of three episodes of exercise per week, each >15 min, is required to modify maternal glucose levels. In addition, 2–4 weeks of regular exercise may be required before a lowering of glycemia is seen (529). Insufficient evidence exists to recommend any specific type of exercise as being superior to another in the management of gestational diabetes.

Blood glucose data allow evaluation of the effectiveness of nutrition therapy and the need for pharmacological therapy. Postprandial glucose levels may be more closely related to fetal risks than are fasting levels (544,545). Pre-breakfast ketone measurements are recommended for patients receiving hypocaloric or carbohydrate-restricted diets to allow the detection and treatment of ketones. However, the effectiveness of ketone monitoring in improving fetal outcomes has not been demonstrated (529).

Although most women with gestational diabetes return to normal glucose tolerance postpartum, they are at increased risk of developing gestational diabetes in subsequent pregnancies and type 2 diabetes later in life. Evidence suggests that a single birth results in a 2–3 kg higher average body weight for the mother, and thus increases the risk of becoming overweight after delivery. Body weight changes during the postpartum period are likely to be a combination of retention of gestational weight gain and weight changes caused by the lifestyle alterations associated with child rearing (546). Lifestyle behaviors aimed at reducing weight and increasing physical activity may be beneficial to reduce the subsequent risk of developing diabetes.

Lactation.

Breastfeeding is recommended for women with preexisting diabetes or gestational diabetes (547,548), although achieving desired metabolic control during lactation may be difficult for women with type 1 diabetes. Breastfeeding lowers blood glucose, often requiring insulin-treated women to eat a snack containing carbohydrate either before or during breastfeeding. Evening or late night snacks may also be necessary (547). Energy requirements during the first 6 months of lactation require an additional ∼200 calories above the pregnancy meal plan. However, an energy intake of 1,800 kcal/day usually meets the nutritional requirements for lactation and may allow a slow weight loss of 1–2 lb/month (549). Although not all women lose weight while breastfeeding, it is normal for weight loss to occur as maternal fat stores are mobilized. Overweight women may lose up to 2 kg/month without affecting milk volume.

There is strong evidence for the following statements:

  • Nutrient requirements during pregnancy and lactation are similar for women with and without diabetes. For all women of childbearing age who are capable of becoming pregnant, 400 μg/day of folic acid from fortified food and/or a supplement as well as folate from a variety of types of food is recommended for the prevention of neural tube defects and other congenital abnormalities in any potential offspring.

  • Because previous gestational diabetes is a risk factor for subsequent development of impaired glucose tolerance and type 2 diabetes, lifestyle modifications aimed at reducing weight or preventing weight gain and increasing physical activity after pregnancy is recommended.

  • Use of nonnutritive sweeteners is safe during pregnancy.

  • As with nondiabetic women, diabetic women should avoid alcoholic beverages during pregnancy.

There is some evidence for the following statements:

  • In women with type 1 or type 2 diabetes, MNT is important in achieving and maintaining optimal glycemic control during pregnancy.

  • MNT for gestational diabetes focuses on food choices for appropriate weight gain, normoglycemia, and absence of ketones. For some women, modest energy and carbohydrate restriction may be appropriate.

  • To prevent ketosis, adequate energy intake and appropriate distribution of meals and snacks is important. An evening snack may be needed to prevent accelerated ketosis overnight.

  • Although regular exercise has been shown to lower fasting and postprandial glucose concentrations, there is insufficient evidence to recommend any specific type of exercise in the management of gestational diabetes.

  • Successful lactation requires planning and coordination of care following delivery.

The following statement is based on expert consensus:

  • There is inadequate evidence to support the benefit of prenatal vitamin-mineral supplementation; however, these supplements are often prescribed because of uncertainty about nutritional status and intake.

Older adults with diabetes

Aging is associated with many biological changes that may predispose the older adult to nutritional deficiencies (550,551). These include alterations in taste, smell, mastication and salivary flow, gastric acidity, hepatic function, and renal function. In addition, difficulty in preparing food, polypharmacy, and alcoholism are common problems in elderly individuals and may interfere with adequate nutrition. Given these concerns, it is prudent that any nutritional intervention start with a thorough assessment that includes a clinical and nutritional history and a psychosocial and environmental evaluation (552).

There is limited research on the changing nutritional needs with aging and virtually none in aging diabetic subjects. Therefore, nutritional recommendations for older adults with diabetes must be extrapolated from what is known for the general population. The most reliable indicator of poor nutritional status in an elderly individual is probably change in body weight. In general, involuntary gain or loss of >10 pounds or 10% of body weight in less than 6 months should be evaluated to determine if the reason is nutrition related (552).

Energy intake/nutrient requirements.

Because of the changes in body composition (i.e., loss of lean body mass) and exercise patterns, the energy requirements of older adults are 20–30% lower than those of younger adults (553). However, it has been suggested that the current RDA for energy may underestimate the energy needs of healthy elderly individuals (554). Nevertheless, in one cross-sectional study, the resting metabolic rate was lower in elderly subjects, even after adjustment for body composition (555).

The need for weight loss in overweight older adults should be carefully evaluated. Older patients with diabetes, especially those in nursing homes, tend to be under- rather than overweight (556). Low body weight has been associated with greater morbidity and mortality in this age group (557). Aging does not appear to alter the synthesis or breakdown rate of proteins when results are adjusted for fat-free mass (553,558). Similarly, the age-related changes in appearance of free fatty acids and fat oxidation can be attributed to reduced lean body mass (559). Finally, older men do not demonstrate an impairment in energy conservation or disposition during experimental conditions of underfeeding or overfeeding (560,561).

In long-term care settings, malnutrition and dehydration may develop because of lack of food choices, poor quality of food, and unnecessary restrictions. Specialized diabetic diets do not appear to be superior to standard (regular) diets in such settings (562). Therefore, it is recommended that residents be served the regular menu with consistent amounts of carbohydrate (+/−15 g) for meals and snacks (563,564). It may often be preferable to make medication changes to control blood glucose than to implement food restrictions.

The recommended macronutrient composition of the diet and the individualization of carbohydrate and fat components for older adults do not differ from the general recommendations for patients with diabetes. However, any increase in dietary fiber should be done cautiously in elderly individuals, especially in those who are not ambulatory or are likely to become dehydrated (552). Because of reduced alcohol tolerance with age, alcohol ingestion by elderly patients should be looked at carefully.

Micronutrients.

Restricting sodium intake to <2,400 mg/day (the current limit recommended for the management of hypertension and congestive heart failure) may predispose older subjects who enjoy salty food to further limit their caloric intake and increase their risk of nutritional deficiencies. Older subjects are more likely to have deficiencies in micronutrients such as thiamine, vitamin B12, folate, vitamin C, and vitamin D (565,566,567,568,569,570). Calcium, zinc, and magnesium deficiencies are also common (571,572,573). All older adults should be advised to have a calcium intake of at least 1,200 mg/day. The Baltimore Longitudinal Study of Aging found that daily intake and plasma levels of certain antioxidants, such as vitamin A and vitamin E, were suboptimal in the elderly population (574). In the Framingham Study, poor intake of folate, vitamin B6, and vitamin B12 was related to higher plasma homocysteine concentrations and increased prevalence of carotid artery stenosis (569,575). In a study in healthy elderly subjects supplemented with chromium picolinate (1,000 μg/day), chromium did not alter insulin sensitivity, serum lipid profile, or body composition (576).

Vitamin D deficiency has been found in 8% of nursing home residents; 17% of those had evidence of secondary hyperparathyroidism (571). Minority populations, such as elderly Hispanic adults, may have low serum vitamin B12, vitamin C, and folate levels compared to elderly white adults (568).

Use of nutritional supplements is appropriate when the patient cannot achieve nutritional needs through food. Daily supplementation with 1,000–1,500 mg of elemental calcium is probably safe and may reduce the risk of osteoporosis (352).

Physical activity.

Exercise training can significantly reduce the decline in maximal aerobic capacity (VO2) that occurs with age (577), improve risk factors for atherosclerosis (578), slow the decline in age-related lean body mass, decrease central adiposity (579), and improve insulin sensitivity, all of which are beneficial for the older adult with diabetes. However, because of the potential risks of exercise (cardiac ischemia, musculoskeletal and foot injuries, and hypoglycemia in patients treated with insulin or insulin secretagogues), an evaluation and education session should be undertaken before initiating an exercise training program. Physical activity should increase gradually, and appropriate stretching, warm-up, and cool-down periods should accompany all exercise (579).

There is strong evidence for the following statements:

  • Energy requirements for older adults are less than those for younger adults.

  • All older adults should be advised to have a calcium intake of at least 1,200 mg/day.

  • Physical activity should be encouraged in elderly individuals.

  • Undernutrition is more likely than overnutrition in older adults, and therefore caution should be exercised when prescribing weight-loss diets.

There is some evidence for the following statements:

  • A daily multivitamin supplement may be appropriate for elderly individuals, especially for those with reduced energy intake.

  • The imposition of dietary restrictions on elderly, diabetic residents in long-term care health facilities is not warranted. Residents with diabetes should be served regular (unrestricted) menus, with consistency in the amount and timing of carbohydrate.

The following statement is based on expert consensus:

  • There is no evidence to support the prescribing of diets such as “no concentrated sweets” or “no sugar added,” which are often served to elderly individuals in long-term care facilities.

Acute complications

Hypoglycemia.

Hypoglycemia is primarily an issue for individuals taking injected insulin, although those taking insulin secretagogues can also be affected. Changes in food intake, physical activity, and medication(s) can contribute to the development of hypoglycemia. Two treatment modalities are the ingestion of carbohydrate and an adjustment in medication(s). A logistic regression analysis of 6,425 self-monitored blood glucose events in 93 adults with type 1 diabetes showed that more insulin, less food, or more exercise predicted 61% of all blood glucose values <70 mg/dl (<3.9 mmol/l), but did not predict severe hypoglycemia (580).

Although rigid definitions of hypoglycemia are useful for epidemiological studies, more flexible definitions are needed in the management of diabetes. In general, a glucose level ≤50 mg/dl (≤2.8 mmol/l) should be treated promptly (459). However, even a level of 60–80 mg/dl (3.3–4.4 mmol/l) may require a management decision (e.g., carbohydrate ingestion, deferral of exercise, change in insulin dosage) (459).

Treatment of hypoglycemia requires ingestion of glucose or carbohydrate-containing food. The glycemic response correlates better with the glucose content than with the carbohydrate content of the food (581). Although any carbohydrate will raise glucose levels, glucose is preferred (460,581). Treatment of insulin-induced hypoglycemia with 20 g glucose has been shown to produce a greater rise in plasma glucose than treatment with 20 g carbohydrate from orange juice or milk (581), a difference presumably attributable to the fact that some of the carbohydrate in juice is fructose and some of the carbohydrate in milk is galactose, and neither is as effective as glucose in raising plasma glucose levels. In another study (460), type 1 diabetic subjects with induced hypoglycemia who were treated with 15 g carbohydrate from glucose solution or tablets, sucrose solution or tablets, or corn syrup had alleviation of symptoms in 10 min. Treatment with 15 g carbohydrate from glucose gel or orange juice was less effective in alleviating their symptoms. Although pure glucose may be the preferred treatment, any form of carbohydrate that contains glucose will raise blood glucose levels.

In a study of insulin-induced hypoglycemia (582), 10 g oral glucose raised plasma glucose from 60 mg/dl (3.3 mmol/l) to 97 mg/dl (5.4 mmol/l) over 30 min, with the glucose level starting to decline after 60 min; 20 g oral glucose raised plasma glucose from 58 mg/dl (3.2 mmol/l) to 122 mg/dl (6.8 mmol/l) over 45 min, with the glucose level again starting to decline after 60 min. Although 10–20 g glucose may be an effective treatment for adults (0.3 g/kg body wt in children), these amounts of glucose are only temporarily effective. If glucagon is required, a standard dosage of 1.0 mg (15 μg/kg in children) produces rapid and substantial hyperglycemia, with glucose levels beginning to fall after ∼1.5 h (459). Treatment with glucagon is also a temporary measure. Treatment of hypoglycemia requires continued evaluation of glycemia to determine if additional carbohydrate is needed to prevent recurrent hypoglycemia.

Adding protein to carbohydrate in the treatment of hypoglycemia does not accelerate the treatment response to carbohydrate and does not prevent subsequent hypoglycemia (201). Adding fat, however, may retard the acute glycemic response. Furthermore, during hypoglycemia, gastric emptying rates are twice as high as during euglycemia (56,583), and are similar for liquids and solid food (56).

Treatment of sulfonylurea-induced hypoglycemia in type 2 patients with diabetes differs from insulin-induced hypoglycemia. Sulfonylurea-induced hypoglycemia can be prolonged and recur and therefore requires more persistent treatment. However, type 2 diabetic subjects, compared to type 1 diabetic subjects, release counterregulatory hormones at higher plasma glucose levels and maintain glucagon response to hypoglycemia, reducing their risk of severe hypoglycemia (584).

There is strong evidence for the following statements:

  • Glucose is the preferred treatment for hypoglycemia, although any form of carbohydrate that contains glucose may be used.

  • Ingestion of 15–20 g of glucose is effective treatment for hypoglycemia, but blood glucose may be only temporarily corrected.

There is some evidence for the following statements:

  • The form of the carbohydrate—liquid or solid—used to treat hypoglycemia does not make a difference.

  • Adding protein to the carbohydrate does not assist in the treatment of hypoglycemia or prevent subsequent hypoglycemia.

The following statement is based on expert consensus:

  • Initial response to treatment for hypoglycemia should be seen in ∼10–20 min; however, blood glucose should be evaluated again in ∼60 min, as additional treatment may be necessary.

Acute illness.

Acute illness in individuals with type 1 diabetes can result in diabetic ketoacidosis. To prevent ketoacidosis, individuals with type 1 diabetes need to know how to handle illnesses appropriately. During acute illnesses, with the accompanying increases in counterregulatory hormones, the need for insulin continues and additional insulin is often required. Testing blood glucose and blood or urine for ketones, drinking adequate amounts of fluids, and ingesting carbohydrate, especially if blood glucose level is <100 mg/dl (<5.5 mmol/l) are important actions during an acute illness.

Fluid intake should be increased to prevent dehydration. To avoid depletion of intravascular volume, replacement fluids containing sodium, such as broth, tomato juice and sports drinks, are helpful.

In adults, ingestion of 150–200 g carbohydrate daily (45–50 g or three or four carbohydrate choices every 3–4 h) will reduce or prevent starvation ketosis (585,586,587,588). If regular food is not tolerated, liquid or soft carbohydrate-containing food, such as sugar-sweetened soft drinks, juices, soups, and ice cream, should be eaten. However, if nausea, vomiting, or obtundation prevents fluid and carbohydrate intake, prompt consultation with a health care professional is advisable. Most importantly, individuals with type 1 diabetes should not omit insulin. Supplemental insulin may also be required.

There is strong evidence for the following statements:

  • During acute illnesses, individuals with type 1 diabetes should continue insulin.

  • During acute illnesses, testing blood glucose and blood or urine ketones, drinking adequate amount of fluids, and ingesting carbohydrate are important.

There is some evidence for the following statement:

  • During acute illness, oral ingestion of ∼150–200 g of carbohydrate per day should be sufficient, along with medication adjustments, to keep glucose in the goal range and to prevent starvation ketosis.

Hypertension

MNT for the management of hypertension has focused on reducing weight (589,590,591) and sodium intake (592,593,594). Other variables that have been considered include alcohol intake (595), potassium (592,596) and calcium levels (597,598,599), and diet composition (total fat, saturated fat, cholesterol) (600). Few studies have been done exclusively in diabetic subjects. However, there is no compelling reason to believe that differences exist between diabetic and nondiabetic individuals with regard to the benefits of weight reduction. The response to sodium reduction may be greater in subjects who are salt sensitive, a factor that may apply to many individuals with diabetes (601,602). Currently there is no available routine clinical measure to identify individuals who may be salt sensitive.

Sodium.

Several meta-analyses and reviews have examined the relationship between sodium intake and blood pressure (603,604,605). A review of 32 trials covering 2,635 subjects concluded that moderate reduction of dietary sodium lowers systolic and diastolic blood pressure (603). The mean effect was modest, with a reduction of 5 mmHg systolic and 2 mmHg diastolic in hypertensive subjects and a reduction of 3 mmHg systolic and 1 mmHg diastolic in normotensive subjects. It should be noted that there was a wide variation in the blood pressure responses to alterations in sodium intakes. A similar conclusion was reached in a meta-analysis of 56 trials (26 studies in hypertensive and 28 in normotensive subjects) (604). Mean reduction in daily urinary sodium excretion was 95 mmol/day in 1,131 hypertensive subjects and 125 mmol/day in 2,374 normotensive subjects. In hypertensive subjects, the mean decrease in blood pressure per each 100 mmol decrease in sodium intake per day was 4 mmHg systolic and 1 mmHg diastolic. In the normotensive subjects, the mean decrease was 1 mmHg systolic and only negligible for diastolic.

The Dietary Approaches to Stop Hypertension (DASH) study evaluated the effect of three dietary patterns on blood pressure: 1) a control diet that was similar to a traditional American diet, 2) a diet high in fruit and vegetables, and 3) the DASH diet, which was higher in fruits, vegetables, and low-fat dairy products, and lower in total fat, saturated fat, and cholesterol (606,607,608,609). Sodium intake, physical activity, and body weight remained constant. Compared to the control diet, both of the other diets were associated with lower systolic and diastolic blood pressure over the 8-week study periods. The DASH diet lowered systolic and diastolic blood pressure by 6 and 3 mmHg more, respectively, than the control diet. Although the DASH diet was effective in all subgroups, systolic blood pressure in blacks and hypertensive individuals decreased more than in whites and nonhypertensive individuals. In another study, the effects of three levels of sodium intake were compared in 412 subjects randomly assigned to the control or DASH diet (610). Within the assigned diet, subjects ate food with high (150 mmol/day Na [3.6 g Na or 8.7 g NaCl]), intermediate (100 mmol/day Na [2.4 g Na or 6 g Na]), and low (50 mmol/day Na) levels of sodium for 30 days each. Weight remained stable in all subjects. Reducing the sodium intake from the high to the intermediate level reduced systolic blood pressure by 2.1 mmHg (P < 0.001) during the control diet and by 1.3 mmHg (P = 0.03) during the DASH diet. Reducing the sodium intake from the intermediate to the low level caused additional reductions of 4.6 mmHg during the control diet (P < 0.001) and 1.7 mmHg during the DASH diet (P < 0.01). Therefore, the lower the sodium intake, the greater the lowering of blood pressure. The effects of sodium reduction were greater in hypertensive participants, blacks, and women.

Weight.

In patients with diabetes, there is a general association between weight reduction and a reduction in blood pressure, but there is a great deal of variability in the response. Reductions in blood pressure occur before (and without) desirable body weight is achieved. In a meta-analysis of 11 weight loss trials, the average systolic and diastolic blood pressure reductions per kilogram of weight loss were 2 and 1 mmHg, respectively (611).

Alcohol.

An association between high alcohol intake (more than three drinks per day) and elevated blood pressure has been reported in a number of observational studies (612,613). However, large studies do not show much difference in blood pressure among people who consume less than three drinks per day compared to nondrinkers (614).

Potassium, magnesium, and calcium.

Clinical trials have reported a beneficial effect of potassium supplementation on blood pressure (596,615). Evidence for a beneficial effect from calcium and magnesium supplementation is not consistent (615). Because a high dietary intake of potassium, magnesium, and calcium can be achieved from food sources, it is recommended that appropriate types of food rather than supplements be used to increase the intake of these minerals (20).

There is strong evidence for the following statements:

  • In both normotensive and hypertensive individuals, a reduction in sodium intake lowers blood pressure. The goal should be to reduce sodium intake to 2,400 mg sodium (100 mmol sodium) or 6,000 mg sodium chloride (salt) per day. In nondiabetic subjects, this reduction in sodium intake lowered systolic blood pressure by 4–5 mmHg.

  • A modest amount of weight loss beneficially affects blood pressure.

  • Drinking small-to-moderate amounts of alcohol will not adversely affect blood pressure levels.

There is some evidence for the following statement:

  • A low-fat diet that includes fruits and vegetables (five to nine servings per day) and low-fat dairy products (two to four servings per day) will be rich in potassium, magnesium, and calcium and will modestly reduce blood pressure and body weight.

Dyslipidemia

Dyslipidemia (abnormal lipid levels, lipoprotein composition, or both) is often found in individuals with type 1 or type 2 diabetes before the initiation of therapy for hyperglycemia. For most individuals with type 1 diabetes, effective insulin therapy returns lipid serum levels to normal and usually lowers plasma triglycerides; LDL cholesterol may decrease modestly as well (212).

For all individuals with diabetes, elevated LDL cholesterol is identified as the primary target of cholesterol-lowering therapy (8,212). Therapy begins with a multifaceted lifestyle approach. In adult individuals with elevated LDL cholesterol levels, saturated and trans fatty acids should be limited to <10% and preferably to <7% of energy intake (17,18), cholesterol intake should be limited to <200 mg/day, and modest weight loss and physical activity should be encouraged. The LDL cholesterol response should be evaluated after 6 weeks (18). If the LDL cholesterol goal is not achieved, LDL cholesterol−lowering therapy should be intensified by reinforcing the need for dietary reduction in saturated fat and cholesterol. Adding plant stanols/sterols (2 g/day) has been reported to lower total cholesterol by 10–32 mg/dl and LDL cholesterol by 8–29 mg/dl (251,253,255). Increasing soluble fiber intake (10–25 g/day) can also be suggested (18). A recent meta-analysis concluded that for every gram of increase in soluble fiber, LDL cholesterol would be expected to decrease by an average of 2.2 mg/dl—an effect that is small within the practical range of soluble fiber intake (126). The LDL cholesterol response should be monitored again after 6 weeks, and if the LDL goal is not achieved, weight management and physical activity should be intensified and drug therapy considered. It is recommended that adherence to therapeutic lifestyle changes be monitored every 4–6 months (18).

Obese individuals with type 1 diabetes (456) and many individuals with type 2 diabetes (616,617,618,619,620,621) manifest a dyslipidemia consisting of increased plasma triglycerides, reduced serum HDL cholesterol levels, and small, dense serum LDL cholesterol particles that persist despite improved glycemic control. This dyslipidemia is strongly associated with increased body adiposity that is abdominal (visceral) in distribution (622,623). Dietary fat restriction and weight loss will lead to decreased plasma triglycerides and a modest lowering of LDL cholesterol (300,326,475). Regular physical activity also reduces plasma triglycerides (461,471,481) and improves insulin sensitivity (624). However, with one exception (624), most studies have not shown improvements in HDL cholesterol from exercise in individuals with type 2 diabetes. This may be because of the relatively modest exercise intensities used (461).

In type 2 diabetic subjects with mild-to-moderate elevations of plasma triglycerides and low HDL cholesterol, replacing saturated fat with carbohydrate has been shown by most (217,219,625,626,627,628), but not all (629,630), studies to result in improvements in LDL cholesterol, with beneficial or neutral effects on plasma triglycerides and HDL cholesterol. Monounsaturated fat can also be substituted for saturated fat (90,227,228,229). However, increased dietary fat may cause weight gain and, although controversial, also cause insulin resistance (96,97,98,99,100).

If goals for serum lipid levels are not achieved with lifestyle improvement, including MNT and exercise, lipid-lowering medications should be added (18,212). Maximal changes in nutrition typically reduce LDL cholesterol 15–25 mg/dl (0.40–0.65 mmol/l) (631). Therefore, if LDL cholesterol exceeds the goal by >25 mg/dl (0.65 mmol/l), pharmacological therapy is likely to be necessary (632,633,634).

For patients with persistently elevated plasma triglycerides despite the addition of medication, supplementation with fish oils that include n-3 fatty acids may be recommended. However, fish oils may increase LDL cholesterol, the levels of which should then be monitored (236,237). Patients with plasma triglycerides >1,000 mg/dl are at increased risk for chylomicronemia syndrome and pancreatitis and should restrict all types of dietary fat (635,636) and institute lipid-lowering medication, such as a fibric acid derivative or perhaps niacin (637).

There is strong evidence for the following statements:

  • For individuals with diabetes and elevated LDL cholesterol, saturated fatty acids and transunsaturated fatty acids should be limited to <10% and perhaps to <7% of energy, and if replaced, can be substituted by carbohydrates or monounsaturated fats.

  • For individuals with diabetes and elevated plasma triglycerides, reduced HDL cholesterol, and small dense LDL cholesterol (the metabolic syndrome), improved glycemic control, modest weight loss, restricted intake of saturated fats, increased physical activity, and incorporation of monounsaturated fats may be beneficial.

  • LDL cholesterol lowering can be enhanced by the addition of plant stanols/sterols and by an increase in soluble (viscous) fiber.

  • Individuals with plasma triglycerides >1,000 mg/dl should restrict all types of dietary fat (except for n-3 fatty acids) and be treated with medication to reduce plasma triglycerides.

There is limited evidence for the following statement:

  • Supplementation with fish oils containing n-3 fatty acids may benefit those with resistant hypertriglyceridemia.

Nephropathy

In individuals with type 1 or type 2 diabetes, microalbuminuria predicts the later development of macroalbuminuria and overt nephropathy. Once clinical nephropathy has developed, end-stage renal disease is almost always the consequence. Recommended treatments focus on reversing or at least retarding the progression of proteinuria and preventing nephropathy. Improved glycemic control, reduction of blood pressure—particularly by the use of ACE inhibitors and MNT—all are important in this regard (638).

Several dietary factors have been identified as having a role in the prevention of nephropathy. Animal studies have suggested a beneficial effect from energy (639,640) and sodium (641) restriction and supplementation with vitamin C (642) and vitamin E (642,643). Human studies have identified associations between urinary microalbumin and dietary saturated fat (193) and between glomerular filtration rate (GFR) and total fat (644). However, the majority of human studies have focused on dietary protein.

Several studies have attempted to reduce protein intake in people with type 1 or type 2 diabetes and microalbuminuria. The achieved protein reductions (measured by urine urea nitrogen) were 1.2 g (645), 1.1 (646), 0.8 (647), and 0.8 · kg−1 · day−1 (achieved by only half of subjects) (648). Even with small reductions in protein intake, the GFR improved significantly in all four studies and the albumin excretion rate was reduced significantly in three. In a dosage-response analysis (645), a 0.1 g · kg−1 body wt · day−1 change in intake of animal protein was related to an 11.1% change in albuminuria.

Many studies have been conducted in type 1 diabetic subjects with macroalbuminuria (overt nephropathy). The achieved protein reductions were 0.8 (647), 0.9 (649), 0.7 (650), 0.7 (651), and 0.7 g · kg−1 · day−1 (652). In the latter two studies, reduced protein intake slowed the rate of decline in the GFR significantly over 33–35 months (P < 0.05 and P < 0.001, respectively). However, in one of the studies (652), antihypertensive treatment might have been responsible for part of the beneficial effect on the GFR.

A few studies have explored the potential beneficial effects of plant protein rather than animal protein. When predominantly plant protein replaced animal protein in three studies of type 1 diabetic subjects, the amount of protein consumed was also reduced significantly (653,654,655). Any beneficial effects may have been from reduction in the amount or change in the protein source. In the only published study (656) comparing approximately equivalent amounts of animal and plant protein, type 1 diabetic subjects were normoalbuminuric, normotensive, and not hyperfiltering, so that renal benefits may not have been expected. Long-term clinical trials are needed to determine whether reductions in certain types of protein (plant versus animal) or changes in various plant proteins such as soy or various animal proteins will have a beneficial effect on diabetic nephropathy.

Because of the small number of clinical studies and their methodological problems (e.g., food intake not closely controlled, lack of success in reducing protein to prescribed levels), there is insufficient evidence to make definite recommendations for patients with diabetes and microalbuminuria or clinical nephropathy. There is, however, suggestive evidence that even small reductions in dietary protein intake from usual amounts (e.g., achieved reduction of 0.8–1.0 g · kg−1 body wt · day−1 in people with microalbuminuria, 0.8 g · kg−1 body wt · day−1 or lower for people with clinical nephropathy) will retard the progression of renal disease. However, reduction of protein intake should be done in the context of overall good nutrition. A dietitian familiar with MNT for both diabetes and renal diseases should be involved in developing the reduced-protein diet.

There is some evidence for the following statements:

  • In patients with diabetic nephropathy, reduction of dietary protein to 0.8–1.0 g · kg−1 body wt · day−1 for people with microalbuminuria and 0.8 g · kg−1 body wt · day−1 for people with overt nephropathy may slow the progression of nephropathy.

There is limited evidence for the following statement:

  • There is insufficient evidence to make recommendations regarding the source of dietary protein (animal versus plant).

Catabolic illness

The catabolic state induced by injury, inflammation, or severe illness is associated with special nutrition considerations. Most studies of nutrient needs are in nondiabetic subjects, but the results are likely applicable to patients with diabetes. Many of the changes in nutrient requirements appear to be cytokine mediated. Cytokines reduce albumin production, decrease plasma levels of some trace proteins through tissue redistribution, induce negative nitrogen balance, and alter intermediary metabolism in such a way as to increase glucose levels through the actions of the counterregulatory hormones (657). These changes, as well as altered fluid balance, make nutritional assessment difficult during times of critical illness. Overall, catabolic disease states result in a change in body compartments that may be characterized by an increased extracellular fluid compartment (frequently with an actual increase in body weight) and an associated shrinkage of body fat and body cell mass (body cell mass is defined as the actively functioning protein-rich tissue and associated intracellular fluid) (658).

The magnitude of recent weight loss, taking into account the presence of excess fluid that is often present in critically ill patients, along with the presence or absence of clinical markers of stress and the amount of time the patient will be unable to eat should determine the need for nutritional intervention (657). A recent weight loss of >10% of usual weight necessitates a thorough nutritional assessment; an unintentional loss of 10–20% suggests moderate protein-calorie malnutrition, and a loss of >20% usually indicates severe malnutrition (659). Numerous studies have shown that the needs of most hospitalized patients can be met by providing 25–35 kcal/kg body wt (657). Care should be taken not to overfeed the patient, as this can exacerbate hyperglycemia, cause abnormal liver function, and increase oxygen consumption and carbon dioxide production (657).

Protein needs are ∼1.0 g/kg body wt for mildly stressed patients and 1.5 g/kg body wt for moderately to severely stressed patients with normal hepatic and renal function. This intake of protein will not decrease protein catabolism, but will result in an increase in protein synthesis. At least 30% of total energy should be given as lipids (659).

For the hospitalized patient with diabetes who requires parenteral or enteral nutrition, the goal is to provide adequate nutrition while avoiding extremes of hyper- and hypoglycemia. For stressed hospitalized patients, a reasonable aim is to maintain glucose levels at 100–200 mg/dl (5.6–11.1 mmol/l) (659). As with solid food, the total grams of carbohydrate in the feeding will have the greatest impact on the blood glucose response (660). The enteral route is preferred if the gastrointestinal tract is functional. A standard enteral formula (50% carbohydrate) or a lower carbohydrate (33–40% carbohydrate) formula may be used in individuals with diabetes (660). Careful monitoring of vital signs, hemodynamic data, weight, fluid balance, plasma glucose and electrolytes, and acid-based status is essential (659). Medications, usually insulin, may need to be adjusted to maintain glycemic control.

There is limited evidence for the following statements:

  • Careful monitoring of nutritional status indicators (e.g., change in body weight) and glycemia are necessary to ensure that nutrient needs are being met and hyperglycemia is prevented. The energy needs of most hospitalized patients can be met by providing 25–35 kcal/kg body wt.

  • Protein needs are 1.0–1.5 g/kg body wt, with the higher end of the range being for more stressed patients.

The importance of preventing diabetes in high-risk individuals is highlighted by the substantial increase in the prevalence of diabetes in the U.S. over an 11-year period (661,662). From the most recent data available, the increase in the prevalence of diabetes continued unabated well through the late 1990s (663) and, most likely, continues to the present day.

Genetic susceptibility appears to play a powerful role in the occurrence of type 2 diabetes in certain populations; however, given that population gene pools shift quite slowly, the current epidemic likely reflects marked changes in lifestyle. Lifestyle changes that are characterized by decreased physical activity and increased energy consumption have together promoted obesity, which is a remarkably strong risk factor for diabetes that itself is influenced by both genes and behavior.

Weight loss

Excess body fat is perhaps the most notable modifiable risk factor for the development of type 2 diabetes (664). It is estimated that the risk of type 2 diabetes attributable to obesity is as much as 75% (92). A striking increase in the prevalence of obesity, as well as diabetes, was reported between NHANES II and III. As of the early 1990s, over 50% of the U.S. adult population was overweight (665). If the prevalence of obesity continues to increase, it is expected that the prevalence of diabetes in the population will also increase.

Numerous interventions focusing on weight loss through hypocaloric, low-fat diets, increased physical activity, and a variety of behavior change strategies have emerged (316,318,327,338,666,667). It is unfortunate that preventing obesity and effectively reducing body weight have proven difficult to accomplish and particularly challenging to maintain over the long term. Accordingly, pharmacological agents to enhance weight reduction and maintenance of weight loss have recently been recommended for individuals at high risk for obesity-related conditions when other weight-loss methods have failed (668,669,670,671).

Despite these difficulties, several recent studies have demonstrated the potential for moderate, sustained weight loss to substantially reduce risk for type 2 diabetes (672,673,674,675,676,677). Wannamethee and Shaper (678) reported increased risk for diabetes in men who gained weight over a 12-year period of follow-up. Overweight men who lost weight had a reduced risk of diabetes. In the Framingham Study cohort, sustained weight loss over two consecutive 8-year periods led to a 37% lower risk of diabetes; however, those who regained the lost weight failed to experience any reduction in diabetes incidence (677).

Clinical trial data also support the potential for weight loss to reduce risk for diabetes. In the Malmo Feasibility Study (673), both weight reduction and increased fitness were associated with reduced incidence of diabetes in a lifestyle intervention group when compared to a control group. In the Da Qing Study, diet, exercise, and diet plus exercise all reduced the incidence of diabetes compared to the control condition (672). In the Swedish Obese Subjects Study, obese individuals with sustained weight loss 2 years after bariatric surgery demonstrated substantially lower risk of type 2 diabetes and hyperinsulinemia compared to control subjects (676). Results from a 2-year clinical trial showed reduced risk for progression from impaired glucose tolerance to diabetes among individuals randomized to orlistat compared to those randomized to behavioral therapy (675).

The Finnish Diabetes Prevention Study (319) included 522 overweight individuals with impaired glucose tolerance randomized to control or intensive lifestyle intervention, which included weight reduction (5% or more), reduction of total (<30% of energy intake) and saturated fat (<10% of energy intake), increased fiber (>15 g/1,000 kcal), and increased physical activity (>4 h/week). The subjects in the intervention group were more likely to report changes in dietary and exercise habits than subjects in the control group. Success in achieving goals in the intervention group varied from 25% (fiber intake) to 86% (exercise). The cumulative incidence of diabetes after 4 years was 11% in the intervention group and 23% in the control group. The risk of diabetes was reduced by 58% in the intervention group, an outcome directly associated with changes in lifestyle.

In the U.S., the DPP study tested the safety and efficacy of pharmacological therapy and lifestyle modification of weight management and physical activity (316). The study was recently completed, approximately 1 year earlier than planned, because of the remarkable success of both interventions (317). The DPP study included 3,234 individuals of diverse ethnic backgrounds (45% minority inclusion), all of whom had impaired glucose tolerance at study entry. Participants randomly assigned to intensive lifestyle reduced their risk of developing type 2 diabetes by 58% over nearly 3 years of follow-up. Significant risk reduction was observed across subgroups of ethnicity, age, gender, BMI, and fasting glucose. Among individuals over age 60 years, the risk reduction was 71%. On average, individuals in the lifestyle intervention group reduced their percent calories from fat from ∼34 to ∼27.5%; maintained their physical activity at ∼30 min/day, usually with walking or other moderate intensity physical activity; and lost 5–7% of their baseline body weight. Of interest was the finding that the pharmacological agent tested, metformin, reduced diabetes risk by 31%, which was less than the risk reduction observed for the lifestyle intervention. However, unlike lifestyle, metformin was not uniformly successful. Although effective in men and women and in all ethnic groups, metformin was relatively ineffective in the older volunteers and in those who were less overweight.

The consistency of beneficial effects of lifestyle interventions used in the Finnish Diabetes Study and the DPP is further supported by an analysis of data from the Nurses’ Health Study (679) in which individuals categorized as low risk based on a BMI <25 and a set of related lifestyle variables experienced reduced risk for diabetes incidence over 16 years of follow-up. Thus there is clearly strong evidence that comprehensive lifestyle interventions reduce the incidence of type 2 diabetes. Additional work in the area of increasing adherence and long-term success of intervention strategies for sustained lifestyle change is needed (680).

Exercise

Although obesity is generally regarded as the salient modifiable risk factor for type 2 diabetes, decreased physical activity also has been identified as a diabetes risk factor, independent of its impact on energy balance. A relationship between physical activity and type 2 diabetes was suggested by studies in societies that had abandoned traditional lifestyles typically involving large amounts of habitual physical activity and subsequently experienced major increases in rates of type 2 diabetes. More recently, the fact that an active lifestyle may prevent or delay the development of type 2 diabetes has been demonstrated in a number of prospective studies (681,682,683,684,685). Protection from diabetes appears to occur from moderate intensity activities, such as brisk walking, as well as from participation in vigorous physical activity. Moreover, physical activity may provide some protection against mortality at all levels of glucose tolerance, as has been demonstrated in middle-aged men (686). Of interest in this regard is a large prospective observational study demonstrating that cardiorespiratory fitness levels in men influence the effects of obesity on health (687). No elevated mortality risk in obese men was observed if they were physically fit, and lean men had increased longevity only if they were physically fit. Thus moderate-to-high cardiorespiratory fitness may reduce mortality risk across all categories of body composition.

Dietary fat

Dietary fat intake appears to be an important determinant of diabetes risk, independent of total caloric intake. Using a case-control design, increased intake of dietary fat was associated with occurrence of diabetes among second-generation Japanese-American men (688). After adjustment for total caloric intake and obesity, Marshall et al. (93) reported increased incidence of diabetes with increased intake of dietary fat. However, three large prospective studies that relied on patient-report of physician-diagnosed diabetes did not detect an effect of dietary fat on diabetes incidence, or else suggested differential effects of various subtypes of dietary fat (118,119,689). Results from two recent studies (690,691) suggest that increased intake of polyunsaturated fat may be associated with reduced risk of type 2 diabetes, independent of BMI, total energy intake, physical activity, and other potential confounders. Potential mechanisms underlying these findings are unclear.

Several studies have identified dietary fat as a contributor to insulin resistance independent of obesity (92,93,94,95,96,97,98,99,100), but other studies do not support this (690,691,692). Nevertheless, it appears that all types of dietary fat, except n-3 fatty acids, may have an adverse effect on insulin sensitivity. Results are most consistent for an adverse effect of saturated fats. These effects may be enhanced among individuals with obesity (99) or low levels of physical activity (98,99).

Although early animal studies suggested a potential deleterious effect of dietary fat on insulin secretion (693), recent studies in human populations have failed to demonstrate either clinically or statistically significant effects (694,695).

In total, the impact of dietary fat on diabetes risk appears to lie primarily in the impact of high-fat diets on long-term energy balance. Other specific metabolic effects of dietary fat may occur, but seem likely to play only a minor role in overall diabetes risk.

Whole grains/fiber

Recent studies have provided preliminary evidence for reduced risk of diabetes with increased intake of whole grains and dietary fiber (27,696,697). In both the Nurses’ Health Study (27) and the Iowa Women’s Health Study (697), increased intake of whole grain food was associated with significant reductions in incidence of type 2 diabetes. A higher glycemic load, calculated and applied to food frequency data, was related to increased incidence of diabetes in men (118) and women (119). The glycemic load is defined as the product of the glycemic index value of a food and its carbohydrate content in an average serving. It incorporates both the quality and quantity of carbohydrate consumed. However, glycemic load or glycemic index was not related to diabetes incidence in the Iowa Women’s Health Study (697).

Micronutrients

Selected micronutrients may affect glucose and insulin metabolism, but the data are scarce or inconsistent. Within the range that can be obtained from food intake, men with higher plasma concentrations of α-tocopherol experienced reduced risk for diabetes compared to men with lower concentrations of α-tocopherol (374). Results of studies that evaluated effects of vitamin E on insulin sensitivity have been equivocal (363,698,699). Insufficient intake of magnesium, zinc, and chromium have been implicated as possible risk factors for the development of diabetes (118,697,700,701,702,703); however, neither the efficacy nor the safety of supplemented intake has been established.

Alcohol

When compared to abstinence and heavy drinking, moderate alcohol intake has been related to improved insulin sensitivity (439,440,441) and reduced risk for diabetes (437) However, insufficient data exist to support a specific recommendation for moderate alcohol intake for prevention of type 2 diabetes, and potential adverse effects of heavy drinking must be carefully considered.

Cow’s milk

Type 1 diabetes accounts for ∼10% of all diabetes and, like type 2 diabetes, has both genetic and environmental determinants. Early introduction of cow’s milk in infants may be an environmental factor contributing to the development of childhood diabetes, but the research evidence has been equivocal (704,705,706,707,708,709,710). Currently there are no clear dietary determinants of type 1 diabetes.

Youth onset type 2 diabetes

Although most of the diabetes diagnosed in children is type 1 diabetes, recently non−type 1 phenotypes, particularly among minority youth, have been reported. As such, youth-onset type 2 diabetes is a relatively new area of research. Obesity and physical inactivity seem likely to play an important role in development of this condition; however, no sufficient data have been collected from youth to justify any clear recommendations for the prevention of diabetes in youth at this time.

There is strong evidence for the following statements:

  • Sustained, modest weight loss of ∼5–7% of body weight through reduced energy intake, reduced intake of dietary fat, and increased physical activity will reduce the risk for developing type 2 diabetes.

  • Structured programs that emphasize lifestyle changes are necessary to accomplish these objectives.

  • All individuals, especially family member of individuals with type 2 diabetes, should be encouraged to engage in regular physical activity to decrease the risk of developing type 2 diabetes. Both moderate and vigorous exercise decrease the risk of impaired glucose tolerance and type 2 diabetes.

There is some evidence for the following statements:

  • Increased intake of whole grains and dietary fiber may reduce diabetes risk.

  • Reduced intake of total fat, particularly saturated fat, may improve insulin sensitivity and reduce risk for diabetes, independent of weight loss.

There is limited evidence for the following statement:

  • Increased intake of polyunsaturated fat, in the context of appropriate total energy intake for weight management, may reduce the risk for type 2 diabetes.

The following statements are based on expert consensus:

  • No nutritional recommendations can be made for the prevention of type 1 diabetes. Breastfeeding may be beneficial.

  • Although increasing obesity in youth may be related to an increase in the prevalence of type 2 diabetes, particularly in minority adolescents, there is insufficient data at present to warrant any specific recommendation for the prevention of type 2 diabetes in youth. Increased physical activity, reduced energy and fat intake, and resultant weight management may prove to be beneficial.

Major nutrition recommendations are listed in Table 7. The major nutrition recommendations listed in Table 7 are classified according to the level of evidence using the American Diabetes Association evidence grading system. The principles reviewed in the above technical review paper are the basis for the recommendations. MNT for people with diabetes should be individualized, with consideration given to each individual’s usual food and eating habits, metabolic profile, treatment goals, and desired outcomes. Monitoring of metabolic parameters, including glucose, HbA1c, lipids, blood pressure, body weight, and renal function, when appropriate, as well as quality of life is essential to assess the need for changes in therapy and to ensure successful outcomes. Ongoing nutrition self-management education and care need to be available for individuals with diabetes. Finally, many areas of nutrition and diabetes require additional research.

Table 1—

Carbohydrate classification and terminology

Major dietary carbohydrate classes based on degree of polymerization and subgroupsComponentsU.S. food labeling designation
Sugars* (1–2 molecules)   
 Monosaccharides Glucose, galactose, fructose Sugars 
 Disaccharides Sucrose, lactose Sugars 
 Polyols (sugar alcohols) Sorbitol, mannitol, xylitol, isomalt, malitol, lactitol, hydrogenated starch hydrolysates Sugar alcohol 
Oligosaccharides (3–9 molecules)   
 Malto-oligosaccharides Maltodextrins Other carbohydrate 
 Other oligosaccharides Raffinose, stachyose, fructo-oligosaccharides Other carbohydrate 
Polysaccharides (>9 molecules)   
 Starch* Amylose, amylopectin, modified starches Other carbohydrate 
 Fiber* (non-starch polysaccharides) Cellulose, hemicellulose, pectins, hydrocolloids Dietary fiber 
Major dietary carbohydrate classes based on degree of polymerization and subgroupsComponentsU.S. food labeling designation
Sugars* (1–2 molecules)   
 Monosaccharides Glucose, galactose, fructose Sugars 
 Disaccharides Sucrose, lactose Sugars 
 Polyols (sugar alcohols) Sorbitol, mannitol, xylitol, isomalt, malitol, lactitol, hydrogenated starch hydrolysates Sugar alcohol 
Oligosaccharides (3–9 molecules)   
 Malto-oligosaccharides Maltodextrins Other carbohydrate 
 Other oligosaccharides Raffinose, stachyose, fructo-oligosaccharides Other carbohydrate 
Polysaccharides (>9 molecules)   
 Starch* Amylose, amylopectin, modified starches Other carbohydrate 
 Fiber* (non-starch polysaccharides) Cellulose, hemicellulose, pectins, hydrocolloids Dietary fiber 

All U.S. food labeling designations are in total grams of carbohydrate.

*

Preferred terminology. Adapted from World Health Organization and Food and Agriculture Organization of the United Nations: Carbohydrates in Human Nutrition. Food and Agriculture Organization of the United Nations, Rome, 1998.

Table 2—

Sugar alcohols: caloric content and regulatory status

Sugar alcoholCaloric content (kcal/g)FDA designation
Erythritol 0.2 GRAS affirmation petition accepted for filing 
Hydrogenated starch hydrolysates 3.0 GRAS affirmation petitions accepted for filing 
Isomalt 2.0 GRAS affirmation petition accepted for filing 
Lactitol 2.0 GRAS affirmation petition accepted for filing 
Maltitol 3.0 GRAS affirmation petition accepted for filing 
Mannitol* 1.6 Food additive permitted in food or in contact with food on an interim basis pending additional study 
Sorbitol* 2.6 Affirmed as GRAS 
Xylitol 2.4 Food additive permitted for direct addition to food for human consumption 
Sugar alcoholCaloric content (kcal/g)FDA designation
Erythritol 0.2 GRAS affirmation petition accepted for filing 
Hydrogenated starch hydrolysates 3.0 GRAS affirmation petitions accepted for filing 
Isomalt 2.0 GRAS affirmation petition accepted for filing 
Lactitol 2.0 GRAS affirmation petition accepted for filing 
Maltitol 3.0 GRAS affirmation petition accepted for filing 
Mannitol* 1.6 Food additive permitted in food or in contact with food on an interim basis pending additional study 
Sorbitol* 2.6 Affirmed as GRAS 
Xylitol 2.4 Food additive permitted for direct addition to food for human consumption 

Caloric content based on Federation of American Societies for Experimental Biology, “The evaluation of the energy of certain polyols used as food ingredients,” June 1994, (unpublished), and Life Sciences Research Office: “Evaluation of the net energy value of maltitol,” April 1999 (unpublished).

*

“Excess consumption may have a laxative effect” must be on label for foods whose reasonably foreseeable consumption may result in the daily ingestion of 20 g mannitol or 50 g sorbitol.

Table 3—

ADI of nonnutritive sweeteners

ADI (mg/kg body wt)Average amount in 12-oz can of soda* (mg)Cans of soda to reach ADI for 60-kg (132-lb) person (n)Amount in packet of sweetener (mg)Packets to reach ADI for 60-kg (132-lb) person (n)
Acesulfame K 15 40 25 50 18 
Aspartame 50 200 15 35 86 
Saccharin 5 140 40 7.5 
Sucralose 70 4.5 60 
ADI (mg/kg body wt)Average amount in 12-oz can of soda* (mg)Cans of soda to reach ADI for 60-kg (132-lb) person (n)Amount in packet of sweetener (mg)Packets to reach ADI for 60-kg (132-lb) person (n)
Acesulfame K 15 40 25 50 18 
Aspartame 50 200 15 35 86 
Saccharin 5 140 40 7.5 
Sucralose 70 4.5 60 
*

Fountain drinks may have different amounts and may contain a sweetener blend.

based on most typical blend with 90 mg aspartame. ADIs are independent. With this sweetener blend, it takes 35 cans to reach the ADI of aspartame.

set by Joint Expert Committee of Food Additives of World Health Organization (175). Adapted from Powers M: Sugar alternatives and fat replacers. In American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Franz MJ, Bantle JP, Eds. Alexandria, VA, American Diabetes Association, 1999.

Table 4—

Composition of some common dietary fatty acids and typical food sources

Fatty acid (common name)Chemical notationAmount found in U.S. diet (g/day)
Food sources
MenWomen
Polyunsaturated fatty acids    
 Linoleic acids 18:2, n-6 14.7 10.4 Vegetable oil, nuts, seeds 
 α-linolenic acid 18:3, n-3 1.6 1.1 Flaxseed oil (linseed oil), canola oil, soybean oil, walnuts 
 Eicosapentaenoic acid (EPA)* 20:5, n-3  0.1 (based on EPA and DHA together)
 
Fish and fish oil, plankton 
 Docosahexaenoic acid (DHA)* 22:6, n-3   Fish and fish oil, oceanic algae, plankton 
Monounsaturated fatty acids     
 Oleic acid 18:1, n-9 (cis form) 31.0 20.8 Olive oil, soybean oil, canola oil, safflower oil, peanut oil, almonds, cashews, pecans, avocado, peanuts, peanut butter 
 Elaidic acid 18:1 n-9 (trans form) 4.2 1.8 Solid margarines, shortenings, salad dressing, processed food containing partially hydrogenated oil 
Saturated fatty acids     
 Lauric acid 12:0 0.9 0.7 Meats, poultry, butterfat in butter, nonskim milk or yogurt, cheese, ice cream, egg yolks 
 Myristic acid 14:0 2.7 1.9 Dairy products, food made with coconut oil 
 Palmitic acid 16:0 1.7 11.6 Dairy products, meat, processed grain products 
 Stearic acid 18:0 8.1 5.4 Dairy products, meat, processed grain products, chocolate 
Fatty acid (common name)Chemical notationAmount found in U.S. diet (g/day)
Food sources
MenWomen
Polyunsaturated fatty acids    
 Linoleic acids 18:2, n-6 14.7 10.4 Vegetable oil, nuts, seeds 
 α-linolenic acid 18:3, n-3 1.6 1.1 Flaxseed oil (linseed oil), canola oil, soybean oil, walnuts 
 Eicosapentaenoic acid (EPA)* 20:5, n-3  0.1 (based on EPA and DHA together)
 
Fish and fish oil, plankton 
 Docosahexaenoic acid (DHA)* 22:6, n-3   Fish and fish oil, oceanic algae, plankton 
Monounsaturated fatty acids     
 Oleic acid 18:1, n-9 (cis form) 31.0 20.8 Olive oil, soybean oil, canola oil, safflower oil, peanut oil, almonds, cashews, pecans, avocado, peanuts, peanut butter 
 Elaidic acid 18:1 n-9 (trans form) 4.2 1.8 Solid margarines, shortenings, salad dressing, processed food containing partially hydrogenated oil 
Saturated fatty acids     
 Lauric acid 12:0 0.9 0.7 Meats, poultry, butterfat in butter, nonskim milk or yogurt, cheese, ice cream, egg yolks 
 Myristic acid 14:0 2.7 1.9 Dairy products, food made with coconut oil 
 Palmitic acid 16:0 1.7 11.6 Dairy products, meat, processed grain products 
 Stearic acid 18:0 8.1 5.4 Dairy products, meat, processed grain products, chocolate 
*

Both DHA and EPA can be synthesized from α-linolenic acid. Adapted from Sega-Isaacson CJ, Carello E, Wylie-Rosett J: Dietary fats and diabetes mellitus. Is there a food fat? Current Diabetes Reports 1:161–169, 2001

Table 5—

Selected weight-loss drugs available in the U.S.

DrugMechanism of actionFA Labeling
Phentermine Nonadrenergic; appetite suppression and/or stimulation of metabolic rate Short-term usage 
Sibutramine Serotonin and norepinephrine reuptake inhibition; appetite suppression Safety and effectiveness beyond 1 year not determined 
Orlistat Inhibition of pancreatic lipase; partial malabsorption of fat Safety and effectiveness beyond 2 years not determined 
DrugMechanism of actionFA Labeling
Phentermine Nonadrenergic; appetite suppression and/or stimulation of metabolic rate Short-term usage 
Sibutramine Serotonin and norepinephrine reuptake inhibition; appetite suppression Safety and effectiveness beyond 1 year not determined 
Orlistat Inhibition of pancreatic lipase; partial malabsorption of fat Safety and effectiveness beyond 2 years not determined 
Table 6—

Adult DRIs for select vitamins and minerals

RDATolerable upper intake levelAdverse effects upon which upper intake level is based
Vitamin A 700 μg/day for women 900 μg/day for men 3,000 μg/day  
Vitamin B6 1.3 mg/day 100 mg/day Sensory neuropathy 
Vitamin B12 2.4 μg/day Insufficient data to set upper intake level  
Folic acid 400 μg/day of dietary folate equivalents 1,000 μg/day from fortified food and supplement intake (exclusive of food intake)  
Niacin 14 mg/day niacin equivalents for women, 16 mg/day niacin equivalents for men 35 mg/day niacin equivalents Flushing 
Riboflavin 1.1 mg/day for women, 1.3 mg/day  for men Insufficient data to set upper intake level  
Thiamin 1.1 mg/day for women, 1.3 mg/day  for men Insufficient data to set upper intake level  
Vitamin C 75 mg/day for women, 90 mg/day  for men 2,000 mg/day Diarrhea and other  gastrointestinal disturbances 
Vitamin E 15 mg/day α-tocopherol 1,000 mg/day Hemorrhage 
Calcium 1,000 mg/day for adults <age 50 years, 1,200 mg/day for adults >age 50 years 2,500 mg/day  
Chromium Insufficient data to set RDA; adequate intake is 25 μg/day for women and 35 μg/day for men Not established  
Iron 8 mg/day for men and postmenopausal women, 18 mg/day for premenopausal women 45 mg/day Gastrointestinal disturbances 
Magnesium 320 mg/day for women, 420 mg/day for men 350 mg/day from supplements  (exclusive of intake from food and  water)  
Selenium 55 μg/day 400 μg/day Selenosis 
Vanadium Insufficient data to set RDA or adequate intake 1.8 mg/day  
Zinc 8 mg/day for women, 11 mg/day for men 40 mg/day Interference with the absorption of copper 
RDATolerable upper intake levelAdverse effects upon which upper intake level is based
Vitamin A 700 μg/day for women 900 μg/day for men 3,000 μg/day  
Vitamin B6 1.3 mg/day 100 mg/day Sensory neuropathy 
Vitamin B12 2.4 μg/day Insufficient data to set upper intake level  
Folic acid 400 μg/day of dietary folate equivalents 1,000 μg/day from fortified food and supplement intake (exclusive of food intake)  
Niacin 14 mg/day niacin equivalents for women, 16 mg/day niacin equivalents for men 35 mg/day niacin equivalents Flushing 
Riboflavin 1.1 mg/day for women, 1.3 mg/day  for men Insufficient data to set upper intake level  
Thiamin 1.1 mg/day for women, 1.3 mg/day  for men Insufficient data to set upper intake level  
Vitamin C 75 mg/day for women, 90 mg/day  for men 2,000 mg/day Diarrhea and other  gastrointestinal disturbances 
Vitamin E 15 mg/day α-tocopherol 1,000 mg/day Hemorrhage 
Calcium 1,000 mg/day for adults <age 50 years, 1,200 mg/day for adults >age 50 years 2,500 mg/day  
Chromium Insufficient data to set RDA; adequate intake is 25 μg/day for women and 35 μg/day for men Not established  
Iron 8 mg/day for men and postmenopausal women, 18 mg/day for premenopausal women 45 mg/day Gastrointestinal disturbances 
Magnesium 320 mg/day for women, 420 mg/day for men 350 mg/day from supplements  (exclusive of intake from food and  water)  
Selenium 55 μg/day 400 μg/day Selenosis 
Vanadium Insufficient data to set RDA or adequate intake 1.8 mg/day  
Zinc 8 mg/day for women, 11 mg/day for men 40 mg/day Interference with the absorption of copper 

From the Institute of Medicine Food and Nutrition Board.  

Table 7—

Major nutrition recommendations

Nutrition RecommendationsGrading
Carbohydrate  
• Foods containing carbohydrate from whole grains, fruits, vegetables, and low-fat milk are important components and should be included in a healthy diet. 
• With regard to the glycemic effects of carbohydrates, the total amount of carbohydrate in meals or snacks is more important than the source or type. 
• Because sucrose does not increase glycemia to a greater extent than isocaloric amounts of starch, sucrose and sucrose-containing foods do not need to be restricted by people with diabetes, however, they should be substituted for other carbohydrate sources or, if added, be covered with insulin or other glucose-lowering medication. 
• Nonnutritive sweeteners are safe when consumed within the ADI levels established by the FDA. 
• Individuals receiving intensive insulin therapy should adjust their premeal insulin dosages based on the carbohydrate content of meals. 
• Although the use of low–glycemic index foods may reduce postprandial hyperglycemic, there is not sufficient evidence of long-term benefit to recommend use of low-glycemic index diets as a primary strategy in food/meal planning. 
• As far the general public, consumption of dietary fiber is to be encouraged; however, there is no reason to recommend that people with diabetes consume a greater amount of fiber than other Americans. 
• Individuals receiving fixed daily insulin dosages should try to be consistent in day-to-day carbohydrate intake. 
• Carbohydrate and monounsaturated fat should together provide 60–70% of energy intake. However, the individual’s metabolic profile and need for weight loss should be considered when determining the monounsaturated fat content of the diet. 
• Sucrose and sucrose-containing foods should be eaten in the context of a healthy diet. 
Protein  
• In individuals with controlled type 2 diabetes, ingested protein does not increase plasma glucose concentrations, although ingested protein is just as potent a stimulant of insulin secretion as carbohydrate. 
• For persons with diabetes, especially those not with less-than-optimal glucose control, the protein requirements may be greater than the RDA, but not greater than usual intake. 
• For individuals with diabetes, there is no evidence to suggest that usual protein intake (15–20% of total daily energy) should be modified if renal function is normal. 
• The long-term effects of diets high in protein and low in carbohydrate are unknown. Although such diets may produce short-term weight loss and improved glycemia, it has not been established that weight loss is maintained long-term. The long-term effect of such diets on LDL cholesterol is also a concern. 
Fat  
• In all, <10% of energy intake should be derived from saturated fats. Some individuals (i.e., those with LDL cholesterol ≥100 mg/dl) may benefit from lowering saturated fat intake to <70% of energy intake. 
• Dietary cholesterol intake should be <300 mg/day. Some individuals (i.e., those with LDL cholesterol ≥100 mg/dl) may benefit from lowering dietary cholesterol to <200 mg per day. 
• To lower LDL cholesterol, energy derived from saturated fat can be reduced if weight loss is desirable or replaced with either carbohydrate or monounsaturated fat if weight loss is not a goal. 
• Intake of transunsaturated fatty acids should be minimized. 
• Reduced-fat diets when maintained long term contribute to modest loss of weight and improvement in dyslipidemia. 
• Polyunsaturated fat intake should be ∼10% of energy intake. 
Energy balance and obesity  
• In insulin-resistant individuals, reduced energy intake and modest weight loss improve insulin resistance and glycemia in the short-term. 
• Structured programs that emphasize lifestyle changes including education, reduced fat (<30% of daily energy) and energy intake, regular physical activity, and regular participant contact, can produce long-term weight loss on the order of 5 to 7% of starting weight. 
• Exercise and behavior modification are most useful as adjuncts to other weight-loss strategies. Exercise is helpful in maintenance of weight loss. 
• Standard weight-reduction diets, when used alone, are unlikely to produce long-term weight loss. Structured, intensive lifestyle programs are necessary. 
Micronutrients  
• There is no clear evidence of benefit from vitamin or mineral supplementation in people with diabetes who do not have underlying deficiencies. Exceptions include folate for prevention of birth defects and calcium for prevention of bone disease. 
• Routine supplementation of the diet with antioxidants is not advised because of uncertainties related to long-term efficacy and safety. 
Nutrition Recommendations Grading 
Alcohol  
• If individuals choose to drink alcohol, daily intake should be limited to one drink for adult women and two drinks for adult men. One drink is defined as a 12-oz beer, a 5-oz glass of wine, or 1.5-oz glass of distilled spirits. 
• To reduce risk of hypoglycemia, alcohol should be consumed with food. 
Children and adolescents with diabetes  
• Individualized food/meal plans and intensive insulin regimens can provide flexibility for children and adolescents with diabetes to accommodate irregular meal times and schedules, varying appetite, and varying activity levels. 
• Nutrient requirements for children and adolescents with type 1 or type 2 diabetes appear to be similar to requirements for same age nondiabetic children and adolescents. 
Pregnancy and lactation  
• Nutrition requirements during pregnancy and lactation are similar for women with and without diabetes. 
• Medical nutrition therapy for gestational diabetes focuses on food choices for appropriate weight gain, normoglycemia, and absence of ketones. 
• For some women with gestational diabetes, modest energy and carbohydrate restriction may be appropriate. 
Older adults  
• Energy requirements for older adults are less than for younger adults. 
• Physical activity should be encouraged 
• In the elderly, undernutrition is more likely than overnutrition and therefore caution should be exercised when prescribing weight-loss diets. 
Acute complications  
• Glucose is the preferred treatment for hypoglycemia, although any form of carbohydrate that contains glucose may be used. 
• Ingestion of 15–20 g of glucose is an effective treatment for hypoglycemia, but blood glucose may be only temporarily corrected. 
• During acute illnesses, testing blood glucose and blood or urine for ketones, drinking adequate amounts of fluids, and ingesting carbohydrate are important. 
• Initial response to treatment for hypoglycemia should be seen in ∼10–20 min; however, blood glucose should be evaluated in ∼60 min, as additional treatment may be necessary. 
Hypertension  
• In both normotensive and hypertensive individuals, a reduction in sodium intake lowers blood pressure. 
• A modest amount of weight loss beneficially affects blood pressure. 
•  The goal should be to reduce sodium intake 2,400 mg (100 mmol) or sodium chloride to 6,000 mg per day. 
Dyslipidemia  
• For persons with elevated LDL cholesterol, saturated fatty acids and transsaturated fatty acids should be limited to <10% and perhaps to <7% of energy. 
• Energy derived from saturated fat can be reduced if weight loss is desirable or replaced with either carbohydrates or monounsaturated fats if weight loss is not a goal. 
• For individuals with elevated plasma triglycerides, reduced HDL cholesterol, and small dense LDL cholesterol (the metabolic syndrome), improved glycemic control, modest weight loss, dietary saturated fat restriction, increased physical activity, and incorporation of monounsaturated fats may be beneficial. 
Nephropathy  
• In individuals with microalbuminuria, reduction of protein to 0.8–1.0 g · kg1 · body weight per day and in individuals with overt nephropathy, reduction to 0.8 g · kg1 · body wt per day, may slow the progression of nephropathy. 
Catabolic illness  
• The energy needs of most hospitalized patients can be met by providing 25–35 kcal/kg body wt. 
• Protein needs are between 1.0 and 1.5 g/kg body wt, with the higher end of the range being for more stressed patients. 
Prevention of diabetes  
• Structured programs that emphasize lifestyle changes including education, reduced fat and energy intake, regular physical activity, and regular participant contact can produce long-term weight loss of 5–7% of starting weight and reduce the risk for developing diabetes. 
• All individuals, especially family members of individuals with type 2 diabetes, should be encouraged to engage in regular physical activity to decrease risk of developing type 2 diabetes. 
Nutrition RecommendationsGrading
Carbohydrate  
• Foods containing carbohydrate from whole grains, fruits, vegetables, and low-fat milk are important components and should be included in a healthy diet. 
• With regard to the glycemic effects of carbohydrates, the total amount of carbohydrate in meals or snacks is more important than the source or type. 
• Because sucrose does not increase glycemia to a greater extent than isocaloric amounts of starch, sucrose and sucrose-containing foods do not need to be restricted by people with diabetes, however, they should be substituted for other carbohydrate sources or, if added, be covered with insulin or other glucose-lowering medication. 
• Nonnutritive sweeteners are safe when consumed within the ADI levels established by the FDA. 
• Individuals receiving intensive insulin therapy should adjust their premeal insulin dosages based on the carbohydrate content of meals. 
• Although the use of low–glycemic index foods may reduce postprandial hyperglycemic, there is not sufficient evidence of long-term benefit to recommend use of low-glycemic index diets as a primary strategy in food/meal planning. 
• As far the general public, consumption of dietary fiber is to be encouraged; however, there is no reason to recommend that people with diabetes consume a greater amount of fiber than other Americans. 
• Individuals receiving fixed daily insulin dosages should try to be consistent in day-to-day carbohydrate intake. 
• Carbohydrate and monounsaturated fat should together provide 60–70% of energy intake. However, the individual’s metabolic profile and need for weight loss should be considered when determining the monounsaturated fat content of the diet. 
• Sucrose and sucrose-containing foods should be eaten in the context of a healthy diet. 
Protein  
• In individuals with controlled type 2 diabetes, ingested protein does not increase plasma glucose concentrations, although ingested protein is just as potent a stimulant of insulin secretion as carbohydrate. 
• For persons with diabetes, especially those not with less-than-optimal glucose control, the protein requirements may be greater than the RDA, but not greater than usual intake. 
• For individuals with diabetes, there is no evidence to suggest that usual protein intake (15–20% of total daily energy) should be modified if renal function is normal. 
• The long-term effects of diets high in protein and low in carbohydrate are unknown. Although such diets may produce short-term weight loss and improved glycemia, it has not been established that weight loss is maintained long-term. The long-term effect of such diets on LDL cholesterol is also a concern. 
Fat  
• In all, <10% of energy intake should be derived from saturated fats. Some individuals (i.e., those with LDL cholesterol ≥100 mg/dl) may benefit from lowering saturated fat intake to <70% of energy intake. 
• Dietary cholesterol intake should be <300 mg/day. Some individuals (i.e., those with LDL cholesterol ≥100 mg/dl) may benefit from lowering dietary cholesterol to <200 mg per day. 
• To lower LDL cholesterol, energy derived from saturated fat can be reduced if weight loss is desirable or replaced with either carbohydrate or monounsaturated fat if weight loss is not a goal. 
• Intake of transunsaturated fatty acids should be minimized. 
• Reduced-fat diets when maintained long term contribute to modest loss of weight and improvement in dyslipidemia. 
• Polyunsaturated fat intake should be ∼10% of energy intake. 
Energy balance and obesity  
• In insulin-resistant individuals, reduced energy intake and modest weight loss improve insulin resistance and glycemia in the short-term. 
• Structured programs that emphasize lifestyle changes including education, reduced fat (<30% of daily energy) and energy intake, regular physical activity, and regular participant contact, can produce long-term weight loss on the order of 5 to 7% of starting weight. 
• Exercise and behavior modification are most useful as adjuncts to other weight-loss strategies. Exercise is helpful in maintenance of weight loss. 
• Standard weight-reduction diets, when used alone, are unlikely to produce long-term weight loss. Structured, intensive lifestyle programs are necessary. 
Micronutrients  
• There is no clear evidence of benefit from vitamin or mineral supplementation in people with diabetes who do not have underlying deficiencies. Exceptions include folate for prevention of birth defects and calcium for prevention of bone disease. 
• Routine supplementation of the diet with antioxidants is not advised because of uncertainties related to long-term efficacy and safety. 
Nutrition Recommendations Grading 
Alcohol  
• If individuals choose to drink alcohol, daily intake should be limited to one drink for adult women and two drinks for adult men. One drink is defined as a 12-oz beer, a 5-oz glass of wine, or 1.5-oz glass of distilled spirits. 
• To reduce risk of hypoglycemia, alcohol should be consumed with food. 
Children and adolescents with diabetes  
• Individualized food/meal plans and intensive insulin regimens can provide flexibility for children and adolescents with diabetes to accommodate irregular meal times and schedules, varying appetite, and varying activity levels. 
• Nutrient requirements for children and adolescents with type 1 or type 2 diabetes appear to be similar to requirements for same age nondiabetic children and adolescents. 
Pregnancy and lactation  
• Nutrition requirements during pregnancy and lactation are similar for women with and without diabetes. 
• Medical nutrition therapy for gestational diabetes focuses on food choices for appropriate weight gain, normoglycemia, and absence of ketones. 
• For some women with gestational diabetes, modest energy and carbohydrate restriction may be appropriate. 
Older adults  
• Energy requirements for older adults are less than for younger adults. 
• Physical activity should be encouraged 
• In the elderly, undernutrition is more likely than overnutrition and therefore caution should be exercised when prescribing weight-loss diets. 
Acute complications  
• Glucose is the preferred treatment for hypoglycemia, although any form of carbohydrate that contains glucose may be used. 
• Ingestion of 15–20 g of glucose is an effective treatment for hypoglycemia, but blood glucose may be only temporarily corrected. 
• During acute illnesses, testing blood glucose and blood or urine for ketones, drinking adequate amounts of fluids, and ingesting carbohydrate are important. 
• Initial response to treatment for hypoglycemia should be seen in ∼10–20 min; however, blood glucose should be evaluated in ∼60 min, as additional treatment may be necessary. 
Hypertension  
• In both normotensive and hypertensive individuals, a reduction in sodium intake lowers blood pressure. 
• A modest amount of weight loss beneficially affects blood pressure. 
•  The goal should be to reduce sodium intake 2,400 mg (100 mmol) or sodium chloride to 6,000 mg per day. 
Dyslipidemia  
• For persons with elevated LDL cholesterol, saturated fatty acids and transsaturated fatty acids should be limited to <10% and perhaps to <7% of energy. 
• Energy derived from saturated fat can be reduced if weight loss is desirable or replaced with either carbohydrates or monounsaturated fats if weight loss is not a goal. 
• For individuals with elevated plasma triglycerides, reduced HDL cholesterol, and small dense LDL cholesterol (the metabolic syndrome), improved glycemic control, modest weight loss, dietary saturated fat restriction, increased physical activity, and incorporation of monounsaturated fats may be beneficial. 
Nephropathy  
• In individuals with microalbuminuria, reduction of protein to 0.8–1.0 g · kg1 · body weight per day and in individuals with overt nephropathy, reduction to 0.8 g · kg1 · body wt per day, may slow the progression of nephropathy. 
Catabolic illness  
• The energy needs of most hospitalized patients can be met by providing 25–35 kcal/kg body wt. 
• Protein needs are between 1.0 and 1.5 g/kg body wt, with the higher end of the range being for more stressed patients. 
Prevention of diabetes  
• Structured programs that emphasize lifestyle changes including education, reduced fat and energy intake, regular physical activity, and regular participant contact can produce long-term weight loss of 5–7% of starting weight and reduce the risk for developing diabetes. 
• All individuals, especially family members of individuals with type 2 diabetes, should be encouraged to engage in regular physical activity to decrease risk of developing type 2 diabetes. 

Scientific principles ranked based on the American Diabetes Association grading system. The highest ranking, A, is assigned when there is supportive evidence from multiple, well-conducted studies; B is an intermediate rating; C is a lower ranking; and E represents recommendations based on expert consensus.

1
Benson K, Hartz AJ: A comparison of observational studies and randomized, controlled trials.
N Engl J Med
342
:
1878
–1886,
2000
2
Concato J, Sihah N, Horwitz RI: Randomized, controlled trials, observational studies, and the hierarchy of research designs.
N Engl J Med
342
:
1887
–1892,
2000
3
American Diabetes Association Special Report: Principles of nutrition and dietary recommendations for patients with diabetes mellitus:
1971
. Diabetes
20
:
633
–634,
1971
4
American Diabetes Association Special Report: Principles of nutrition and dietary recommendations for individuals with diabetes mellitus:
1979
. Diabetes
28
:
1027
–1030,
1979
5
American Diabetes Association: Nutrition recommendations and principles for individuals with diabetes mellitus:
1986
. Diabetes Care
10
:
126
–132,
1987
6
American Diabetes Association: Nutrition recommendations and principles for people with diabetes mellitus (Position Statement).
Diabetes Care
17
:
519
–522,
1994
7
Franz MJ, Horton ES, Bantle JP, Beebe CA, Brunzell JD, Coulston AM, Henry RR, Hoogwerf BJ, Stacpoole PW: Nutrition principles for the management of diabetes and related complications.
Diabetes Care
17
:
490
–518,
1994
8
American Diabetes Association: Standards of medical care for patients with diabetes mellitus (Position Statement).
Diabetes Care
25(Suppl. 1): S33–S49, 2002
9
American Diabetes Association Provider Recognition Program: Available from http:/www.diabetes.org/recognition/Provider. Accessed January 2001
10
Mensing C, Boucher J, Cypress M, Weinger K, Mulcahy K, Barta P, Hosey G, Kopher W, Lasichak A, Lamb B, Mangan M, Norman J, Tanja J, Yauk L, Wisdom K, Adams C: National standards for diabetes self-management education (Standards and Review Criteria).
Diabetes Care
23
:
682
–689,
2000
11
Diabetes Control and Complications Trial Research Group: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus.
N Engl J Med
329
:
977
–986,
1993
12
U.K. Prospective Diabetes Study (UKPDS) Group: Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33).
Lancet
352
:
837
–853,
1998
13
Delahanty LM, Halford BH: The role of diet behaviors in achieving improved glycemic control in intensively treated patients in the Diabetes Control and Complications Trial.
Diabetes Care
16
:
1453
–1458,
1993
14
UKPDS Group: UK Prospective Diabetes Study 7: Response of fasting plasma glucose to diet therapy in newly presenting type II patients with diabetes.
Metabolism
39
:
905
–912,
1990
15
Haffner SM: Management of dyslipidemia in adults with diabetes (Technical Review).
Diabetes Care
21
:
160
–178,
1998
16
U.S. Department of Agriculture, U.S. Department of Health and Human Services: Nutrition and Your Health: Dietary Guidelines for Americans. 5th ed. Home and Garden Bulletin No. 232, 2000
17
Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, Erdman JW, Kris-Etherton P, Goldberg IJ, Kotchen TA, Lichtenstein AH, Mitch WE, Mullis R, Robinson K, Wylie-Rosett J, St. Jeor S, Suttie J, Tribble DL, Bazzarre TL: AHA Dietary Guidelines Revision 2000: a statement for health care professionals from the Nutrition Committee of the American Heart Association.
Circulation
102
:
2284
–2299,
2000
18
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III).
JAMA
285
:
2486
–2497,
2001
19
de Chavez M, Chavez A: Diet that prevents cancer: recommendations from the American Institute for Cancer Research.
Int J Cancer Suppl
11
:
85
–89,
1998
20
The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
Arch Intern Med
157
:
2412
–2446,
1997
21
Kant AK, Schatzkin A, Graubard BI, Schairer C: A prospective study of diet quality and mortality in women.
JAMA
283
:
2109
–2115,
2000
22
Hu FB, Rimm EB, Stampfer MJ, Ascherio A, Spiegelman D, Willett WC: Prospective study of major dietary patterns and risk of coronary heart disease in men.
Am J Clin Nutr
72
:
912
–921,
2000
23
Huijbregts P, Feskens E, Rasanen L, Fidanza F, Nissinen A, Menotti A, Kromhout D: Dietary patterns and 20 year mortality in elderly men in Finland, Italy, and The Netherlands: longitudinal cohort study.
BMJ
315
:
13
–17,
1997
24
Appel LJ, Moore TJ, Obarzanek E, Vollmer VW, Svetkey LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N: A clinical trial of the effects of dietary patterns on blood pressure.
N Engl J Med
336
:
1117
–1124,
1997
25
Anderson JW, Hanna TJ, Peng X, Kryscio RJ: Whole grain food and heart disease risk.
J Am Coll Nutr
19
:
291S
–299S,
2000
26
Liu S, Manson JE, Lee I-M, Cole SR, Hennekens CH, Willett WC, Buring JE: Fruit and vegetable intake and risk of cardiovascular disease: the Women’s Health Study.
Am J Clin Nutr
72
:
922
–928,
2000
27
Liu S, Manson JE, Stampfer MJ, Hu FB, Giovannucci E, Colditz GA, Hennekens CH, Willett WC: A prospective study of whole-grain intake and risk of type 2 diabetes mellitus in U.S. women.
Am J Public Health
90
:
1409
–1415,
2000
28
Institute of Medicine:
The Role of Nutrition in Maintaining Health in the Nation’s Elderly: Evaluating Coverage of Nutrition Services for the Medicare Population
. Washington, DC, National Academy Press, 2000
29
Kulkarni K, Castle G, Gregory R, Holmes A, Leontos C, Power M, Snetselar L, Splett P, Wylie-Rosett J, for the Diabetes Care and Education Dietetic Practice Group: Nutrition practice guidelines for type 1 diabetes mellitus positively affect dietitian practices and patient outcomes.
J Am Diet Assoc
98
:
62
–70,
1998
30
Franz MJ, Monk A, Barry B, McLain K, Weaver T, Cooper N, Upham P, Bergenstal R, Mazze R: Effectiveness of medical nutrition therapy provided by dietitians in the management of non-insulin-dependent diabetes mellitus: a randomized, controlled clinical trial.
J Am Diet Assoc
95
:
1009
–1017,
1995
31
Christensen NK, Steiner J, Whalen J, Pfister R: Contribution of medical nutrition therapy and diabetes self-management education to diabetes control as assessed by hemoglobin A1c.
Diabetes Spectrum
13
:
72
–75,
2000
32
Eely EA, Stratton IM, Haddon DR, Turner RC, Holman RR, on behalf of the U.K. Prospective Diabetes Study Group: UKPDS 18: estimated dietary intake in type 2 patients with diabetes randomly allocated to diet, sulphonylurea or insulin therapy.
Diabet Med
13
:
656
–662,
1996
33
Franz MJ, Splett PL, Monk A, Barry B, McLain K, Weaver T, Upham P, Bergenstal R, Mazze RS: Cost effectiveness of medical nutrition therapy provided by dietitians for persons with non-insulin-dependent diabetes.
J Am Diet Assoc
95
:
1018
–1024,
1995
34
Johnson EQ, Valera S: Medical nutrition therapy in non-insulin-dependent diabetes mellitus improves clinical outcomes.
J Am Diet Assoc
95
:
700
–701,
1995
35
Hebert JR, Ebbeling CB, Ockene IS, Ma Y, Rider L, Merriam PA, Ockene JK, Saperia GM: A dietitian-delivered group nutrition program leads to reductions in dietary fat, serum cholesterol, and body weight: the Worcester Area Trial for Counseling in Hyperlipidemia (WATCH).
J Am Diet Assoc
99
:
544
–552,
1999
36
Delahanty LM, Sonnenberg LM, Hayden D, Nathan DM: Clinical and cost outcomes of medical nutrition therapy for hypercholesterolemia: a controlled trial.
J Am Diet Assoc
101
:
1012
–1023,
2001
37
Rhodes KS, Bookstein LC, Aaronson LS, Mercer NM, Orringer CE: Intensive nutrition counseling enhances outcomes of National Cholesterol Education Program dietary therapy.
J Am Diet Assoc
96
:
1003
–1010,
1996
38
Caggiula AW, Watson JE, Kuller LH, Olson MB, Milas NC, Berry M, Germanowski J: Cholesterol-Lowering Intervention Program: effect of the step I diet in community office practices.
Arch Intern Med
156
:
1205
–1213,
1996
39
Henkin Y, Shai I, Zuk R, Brickner D, Avilli I, Neuman L, Shany S: Dietary treatment of hypercholesterolemia: Do dietitians do it better? a randomized, controlled trial.
Am J Med
109
:
549
–555,
2000
40
Sikand G, Kashyap ML, Yang I: Medical nutrition therapy lowers serum cholesterol and saves medication costs in men with hypercholesterolemia.
J Am Diet Assoc
98
:
889
–894,
1998
41
Sikand G, Kashyap ML, Wong ND, Hsu JC: Dietitian intervention improves lipid values and saves medication costs in men with combined hyperlipidemia and a history of niacin noncompliance.
J Am Diet Assoc
100
:
218
–222,
2000
42
Diabetes Control and Complications Trial Research Group: Expanded role of the dietitian in the Diabetes Control and Complications Trial: implications for practice.
J Am Diet Assoc
93
:
758
–767,
1993
43
Diabetes Control and Complications Trial Research Group: Implementation protocols in the Diabetes Control and Complications Trial.
Diabetes Care
18
:
361
–376,
1995
44
Glasgow RE, Toobert DJ, Hampson SE, Brown JE, Lewinsohn PM, Donnelly J: Improving self-care among older patients with type II diabetes: the “Sixty Something. . .” study.
Patient Educ Couns
19
:
61
–74,
1992
45
Sadur CN, Moline N, Costa M, Michalik D, Mendlowitz D, Roller S, Watson R, Swain BE, Selby JV, Javorski WC: Diabetes management in a health maintenance organization.
Diabetes Care
22
:
2011
–2017,
1999
46
Report of a Joint FAO/WHO Expert Consultation: Carbohydrates in Human Nutrition. Rome, Italy, Food and Agriculture Organization of the United Nations and World Health Organization, 1998
47
Gannon MC, Nuttall FQ, Westphal SA, Fang D, Ercan-Fang N: Acute metabolic response to high-carbohydrate, high-starch meals compared with moderate-carbohydrate, low-starch meals in subjects with type 2 diabetes.
Diabetes Care
21
:
1619
–1626,
1998
48
Wolever TMS, Nguyen P-M, Chiasson J-L: Determinants of diet glycemic index calculated retrospectively from diet records of 342 individuals with non-insulin-dependent diabetes mellitus.
Am J Clin Nutr
59
:
1265
–1269,
1994
49
O’Dea K, Snow P, Nestel P: Rate of starch hydrolysis in vitro as a predictor of metabolic responses to complex carbohydrate in vivo.
Am J Clin Nutr
34
:
1991
–1993,
1981
50
Snow P, O’Dea K: Factors affecting the rate of hydrolysis of starch in food.
Am J Clin Nutr
34
:
2721
–2727,
1981
51
Jarvi A, Karlstrom B, Granfeldt Y, Bjorck I, Vessby B: The influence of food structure on postprandial metabolism in patients with NIDDM.
Am J Clin Nutr
61
:
837
–842,
1995
52
Hughes TA, Atchison J, Hazelrig JB, Boshell BR: Glycemic responses in insulin-dependent patients with diabetes: effect of food composition.
Am J Clin Nutr
49
:
658
–666,
1989
53
Nielsen PH, Nielsen GL: Preprandial blood glucose values: influence on glycemic response studies.
Am J Clin Nutr
53
:
1243
–1246,
1989
54
Rasmussen I, Hermansen K: Preprandial blood glucose values and glycemic responses in insulin-dependent diabetes mellitus at constant insulinemia.
Am J Clin Nutr
53
:
520
–523,
1991
55
Fraser RJ, Horowitz M, Maddox AF, Harding PE, Chatterton BE, Dent J: Hyperglycemia slows gastric emptying in type 1 (insulin-dependent) diabetes mellitus.
Diabetologia
33
:
675
–680,
1990
56
Schvarcz E, Palmer M, Aman J, Lindkvist B, Beckman K-W: Hypoglycaemia increases gastric emptying rate in patients with type 1 diabetes mellitus.
Diabet Med
10
:
660
–663,
1993
57
Parillo M, Giacco R, Ciardullo AV, Rivellese AA, Riccardi G: Does a high-carbohydrate diet have different effects in NIDDM patients treated with diet alone or hypoglycemic drugs?
Diabetes Care
19
:
498
–500,
1996
58
Jenkins DHA, Wolever TMS, Taylor RH, Griffiths C, Krzeminska K, Lawrie JA, Bennett CM, Goff DV, Sarson DL, Bloom SR: Slow release carbohydrate improves second meal tolerance.
Am J Clin Nutr
35
:
1339
–1346,
1982
59
Perrotti N, Santoro D, Genovese S, Giacco A, Rivellese A, Riccardi G: Effect of digestible carbohydrates on glucose control in insulin-dependent patients with diabetes.
Diabetes Care
7
:
354
–359,
1984
60
Strychar IM, Blain E, Rivard M, Gélinas MD, Radwan F, Crawhall JC: Association between dietary adherence measures and glycemic control in outpatients with type 1 diabetes mellitus and normal serum lipid levels.
J Am Diet Assoc
98
:
76
–79,
1998
61
Georgopoulous A, Bantle JP, Noutsou M, Swaim WR, Parker SJ: Differences in the metabolism of postprandial lipoproteins after a high-monounsaturated-fat versus a high-carbohydrate diet in patients with type 1 diabetes mellitus.
Arterioscler Thromb Vasc Biol
18
:
773
–782,
1998
62
Forlani G, Galuppi V, Santacroce G, Braione AF, Giangiulio S, Ciavarella A, Vannini P: Hyperglycemic effect of sucrose ingestion in IDDM patients controlled by artificial pancreas.
Diabetes Care
12
:
296
–298,
1989
63
Hassinger W, Sauer G, Cordes U, Krause U, Beyer J, Baessler KH: The effects of equal caloric amounts of xylitol, sucrose and starch on insulin requirements and blood glucose levels in insulin-dependent diabetics.
Diabetologia
21
:
37
–40,
1981
64
Loghmani E, Rickard K, Washburne L, Vandagriff J, Fineberg N, Golden M: Glycemic response to sucrose-containing mixed meals in diets of children with insulin-dependent diabetes mellitus.
J Pediatr
119
:
531
–537,
1991
65
Steel JM, Mitchell D, Prescott RL: Comparison of the glycaemic effect of fructose, sucrose and starch-containing mid-morning snacks in insulin-dependent diabetics.
Hum Nutr Appl Nutr
37
:
3
–8,
1983
66
Wheeler ML, Fineberg E, Gibson R, Fineberg N: Controlled portions of presweetened cereals present no glycemic penalty in persons with insulin-dependent diabetes mellitus.
J Am Diet Assoc
96
:
458
–463,
1996
67
Slama G, Haardt MJ, Jean-Joseph P, Costagliola D, Goicolea I, Bornet F, Elgrably F, Tchobroutsky G: Sucrose taken during mixed meal has no additional hyperglycemic action over isocaloric amounts of starch in well-controlled diabetics.
Lancet
i 
i
:
122
–125,
1984
68
Rickard KA, Loghmani E, Cleveland JL, Fineberg NS, Greidenberg GR: Lower glycemic response to sucrose in the diets of children with type 1 diabetes.
J Pediatr
133
:
429
–432,
1998
69
Bantle JP, Laine DC, Thomas JW: Metabolic effects of dietary fructose and sucrose in type I and II diabetic subjects.
JAMA
256
:
3241
–3246,
1986
70
Venhaus A, Chanteleau E: Self-selected unrefined and refined carbohydrate diets do not affect metabolic control in pump-treated patients with diabetes.
Diabetologia
31
:
153
–157,
1988
71
Peterson DB, Lambert J, Gerring S, Darling P, Carter RD, Jelfs R, Mann JI: Sucrose in the diet of patients with diabetes–just another carbohydrate?
Diabetologia
29
:
216
–220,
1986
72
Wise JE, Keim KS, Huisinga JL, Willmann PA: Effect of sucrose-containing snacks on blood-glucose control.
Diabetes Care
12
:
423
–426,
1989
73
Rabasa-Lhoret R, Garon J, Langelier H, Poisson D, Chiasson J-L: The effects of meal carbohydrate content on insulin requirements in type 1 patients with diabetes treated intensively with the basal bolus (ultralente-regular) insulin regimen.
Diabetes Care
22
:
667
–673,
1999
74
Hamet P, Abarca G, Lopez D, Hamet M, Bourque M, Peyronnard J-M, Charron L, Larochelle P: Patient self-management of continuous subcutaneous insulin infusion.
Diabetes Care
5
:
485
–491,
1982
75
Heinemann L, Heise T, Wahl LC, Trautmann ME, Ampudia J, Starke AAR, Berger M: Prandial glycaemia after a carbohydrate-rich meal in type 1 patients with diabetes: using the rapid acting insulin analogue [Lys(B28),Pro(B29)] human insulin.
Diabet Med
13
:
625
–629,
1996
76
Slama G, Klein JC, Delage A, Ardila E, Lemaignen H, Papoz L, Tchobroutsky G: Correlation between the nature and amount of carbohydrate in meal intake and insulin delivery by the artificial pancreas in 24 insulin-dependent diabetics.
Diabetes
30
:
101
–105,
1981
77
Wolever TMS, Hamad S, Chiasson J-L, Josse RG, Leiter LA, Rodger NW, Ross SA, Ryan EA: Day-to-day consistency in amount and source of carbohydrate intake associated with improved glucose control in type 1 diabetes.
J Am Coll Nutr
18
:
242
–247,
1999
78
Collier GR, Giudici S, Kalmusky J, Wolever TMS, Helman G, Wesson V, Ehrlich RM, Jenkins DJA: Low glycaemic index starchy food improve glucose control and lower serum cholesterol in diabetic children.
Diabetes Nutr Metab
1
:
11
–19,
1988
79
Fontvieille AM, Acosta M, Rizkalla SW, Bornet F, David P, Letanoux M, Tchobroutsky G, Slama G: A moderate switch from high to low glycaemic-index food for 3 weeks improves the metabolic control of type I (IDDM) diabetic subjects.
Diabetes Nutr Metab
1
:
139
–143,
1988
80
Fontvieille AM, Rizkalla SW, Penfornis A, Acosta M, Bornet FR, Slama G: The use of low glycaemic index food improves metabolic control of patients with diabetes over five weeks.
Diabet Med
9
:
444
–450,
1992
81
Lafrance L, Rabasa-Lhoret R, Poisson D, Ducros F, Chiasson J-L: The effects of different glycaemic index food and dietary fibre intake on glycaemic control in type 1 patients with diabetes on intensive insulin therapy.
Diabet Med
15
:
972
–978,
1998
82
Calle-Pascual AL, Gomez V, Leon E, Bordiu E: Food with a low glycemic index do not improve glycemic control of both type 1 and type 2 patients with diabetes after one month of therapy.
Diabetes Metab
14
:
629
–633,
1988
83
Buyken AE, Toeller M, Heitkamp G, Karamanos B, Rottiers R, Muggeo M, Fuller JH, EURODIAB IDDM Complications Study Group: Glycemic index in the diet of European outpatients with type 1 diabetes: relations to glycated hemoglobin and serum lipids.
Am J Clin Nutr
73
:
574
–581,
2001
84
Vaaler S, Hanssen KF, Aagenaes O: Effect of different kinds of fibre on postprandial blood glucose in insulin-dependent diabetics.
Acta Med Scand
208
:
389
–391,
1980
85
Chenon D, Mbumba P, Monnier LH, Colette C, Orsetti A, Mirouze J: Effects of dietary fiber on postprandial glycemic profiles in patients with diabetes submitted to continuous programmed insulin infusion.
Am J Clin Nutr
40
:
58
–65,
1984
86
Riccardi G, Rivellese A, Pacioni D, Genovese S, Mastranzo P, Mancini M: Separate influence of dietary carbohydrate and fibre on the metabolic control in diabetes.
Diabetologia
26
:
116
–121,
1984
87
Nygren C, Hallmans G, Lithner F: Effects of high-bran bread on blood glucose control in insulin-dependent patients with diabetes.
Diabetes Metab
10
:
39
–43,
1984
88
Giacco R, Parillo M, Rivellese AA, Lasorellla G, Giacco A, D’Episcopo L, Riccardi G: Long-term dietary treatment with increased amounts of fiber-rich low-glycemic index natural food improves blood glucose control and reduces the number of hypoglycemic events in type 1 patients with diabetes.
Diabetes Care
23
:
1461
–1466,
2000
89
Toeller M, Buyken AE, Heitkamp G, de Pergola G, Giorgino F, Fuller JH, The EURODIAB IDDM Complications Study Group: Fiber intake, serum cholesterol levels, and cardiovascular disease in European individuals with type 1 diabetes.
Diabetes Care
22(Suppl. 2)
:
B21
–B28,
1999
90
Garg A, Bantle JP, Henry RR, Coulston AM, Griver KA, Raatz SK, Brinkley L, Chen Y-D I, Grundy SM, Huet BA, Reaven GM: Effects of varying carbohydrate content of diet in patients with non-insulin dependent diabetes mellitus.
JAMA
271
:
1421
–1428,
1994
91
Garg A: High-monounsaturated fat diets for patients with diabetes mellitus: a meta-analysis.
Am J Clin Nutr
67
:
577S
–582S,
1998
92
Manson JE, Spelsberg A: Primary prevention of non-insulin-dependent diabetes mellitus.
Am J Prev Med
10
:
172
–184,
1994
93
Marshall JA, Bessesen DH, Hamman RF: High saturated fat and low starch and fiber are associated with hyperinsulinaemia in a non-diabetic population: the San Luis Valley Diabetes Study.
Diabetologia
40
:
430
–438,
1997
94
Feskens EJ, Loeber JG, Kromhout D: Diet and physical activity as determinants of hyperinsulinemia: the Zutphen Elderly Study.
Am J Epidemiol
140
:
350
–360,
1994
95
Folsom AR, Ma J, McGovern PG, Eckfeldt H: Relation between plasma phospholipid saturated fatty acids and hyperinsulinemia.
Metabolism
45
:
223
–228,
1996
96
Lovejoy JC, DiGirolamo M: Habitual dietary intake and insulin sensitivity in lean and obese adults.
Am J Clin Nutr
55
:
1174
–1179,
1992
97
Lovejoy JC, Windhauser MM, Rood JC, de la Bretonne JA: Effect of a controlled high-fat versus low-fat diet on insulin sensitivity and leptin levels in African-American and Caucasian women.
Metabolism
47
:
1520
–1524,
1998
98
Mayer EJ, Newman B, Quesenberry CP Jr, Selby JV: Usual dietary fat intake and insulin concentrations in healthy women twins.
Diabetes Care
16
:
1459
–1469,
1993
99
Mayer-Davis EJ, Monaco JH, Hoen HM, Carmichael S, Vitolins MZ, Rewers MJ, Haffner SM, Ayad MF, Bergman RN, Karter AJ: Dietary fat and insulin sensitivity in a triethnic population: the role of obesity. The Insulin Resistance Atherosclerosis Study.
Am J Clin Nutr
65
:
79
–87,
1997
100
Maron DJ, Fair JM, Haskell WL: Saturated fat intake and insulin resistance in men with coronary artery disease.
Circulation
84
:
2070
–2074,
1991
101
Bantle JP, Laine DC, Castle GW, Thomas JW, Hoogwerf BJ, Goetz FG: Postprandial glucose and insulin responses to meals containing different carbohydrates in normal and diabetic subjects.
N Engl J Med
309
:
7
–12,
1983
102
Hollenbeck CB, Coulston AM, Donner CC, Williams RA, Reaven GM: The effects of variations in percent of naturally occurring complex and simple carbohydrates on plasma glucose and insulin response in individuals with non-insulin-dependent diabetes mellitus.
Diabetes
34
:
151
–155,
1985
103
Abraira C, Derler J: Large variations of sucrose in constant carbohydrate diets in type II diabetes.
Am J Med
84
:
193
–200,
1988
104
Bantle JP, Swanson JE, Thomas W, Laine DC: Metabolic effects of dietary sucrose in type II diabetic subjects.
Diabetes Care
16
:
1301
–1305,
1993
105
Colagiuir S, Miller JJ, Edwards RA: Metabolic effects of adding sucrose and aspartame to the diet of subjects with non-insulin-dependent diabetes mellitus.
Am J Clin Nutr
50
:
474
–478,
1989
106
Malerbi DA, Paiva ES, Duarte AL, Wajchenberg BL: Metabolic effects of dietary sucrose and fructose in type 2 diabetic subjects.
Diabetes Care
19
:
1249
–1256,
1996
107
Brand JC, Colagiuri S, Crossman S, Allen A, Roberts DCK, Truswell AS: Low glycemic index food improve long-term glycemic control in NIDDM.
Diabetes Care
14
:
95
–101,
1991
108
Jenkins DJA, Wolever TMS, Buckley G, Lam KY, Giudici S, Kalmusky J, Jenkins AL, Patten RL, Bird J, Wong GS, Josse RG: Low-glycemic index starchy food in the diabetic diet.
Am J Clin Nutr
48
:
248
–254,
1988
109
Luscombe ND, Noakes M, Clifton PM: Diets high and low in glycemic index versus high monounsaturated fat diets: effects on glucose and lipid metabolism in NIDDM.
Eur J Clin Nutr
53
:
473
–478,
1999
110
Wolever TMS, Jenkins DJA, Vuksan V, Jenkins AL, Wong GS, Josse RG: Beneficial effects of low-glycemic index diet in overweight NIDDM.
Diabetes Care
15
:
562
–564,
1992
111
Wolever TMS, Jenkins DJA, Vuksan V, Jenkins AL, Buckley GC, Wong GS, Josse RG: Beneficial effect of low-glycaemic index diet in type 2 diabetes.
Diabet Med
9
:
451
–458,
1992
112
Jarvi A, Karlstrom B, Granfeldt Y, Bjorck I, Asp NG, Vessby B: Improved glycemic control and lipid profile and normalized fibrinolytic activity on a low glycemic index diet in type 2 patients with diabetes.
Diabetes Care
22
:
10
–18,
1999
113
Frost G, Wilding S, Beecham J: Dietary advice based on the glycaemic index improves dietary profiles and metabolic control in type 2 patients with diabetes.
Diabet Med
11
:
397
–401,
1994
114
Frost G, Leeds AA, Doré CJ, Madeiros S, Brading S, Domhorst A: Glycaemic index as a determinant of serum HDL cholesterol concentration.
Lancet
353
:
1045
–1048,
1999
115
Ford ES, Liu S: Glycemic index and serum high-density lipoprotein cholesterol concentration among US adults.
Arch Intern Med
161
:
572
–576,
2001
116
Frost G, Leeds A, Trew G, Margara R, Dornhorst A: Insulin sensitivity in women at risk of coronary heart disease and effect of a low glycemic index diet.
Metabolism
47
:
1245
–1251,
1998
117
Frost G, Keogh B, Smith D, Akinsanya K, Leeds A: The effect of low-glycemic carbohydrate on insulin and glucose response in vivo and in vitro in patients with coronary heart disease.
Metabolism
45
:
669
–672,
1996
118
Salmeron J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ, Stampfer MJ, Wing AL, Willett WC: Dietary fiber, glycemic load, and risk of NIDDM in men.
Diabetes Care
20
:
545
–550,
1997
119
Salmeron J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC: Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women.
JAMA
277
:
472
–477,
1997
120
Liu S, Willett WC, Stampfer MJ, Hu FB, Franz M, Sampson L, Hennekens CH, Manson JE: A prospective study of dietary glycemic load, carbohydrate intake and risk of coronary heart disease in US women.
Am J Clin Nutr
71
:
1455
–1461,
2000
121
Liu S, Manson JE, Stampfer MJ, Holmes MD, Hu FB, Hankinson SE, Willett WC: Dietary glycemic load assessed by food-frequency questionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women.
Am J Clin Nutr
73
:
560
–566,
2001
122
Nuttall FQ: Dietary fiber in the management of diabetes.
Diabetes
42
:
503
–508,
1993
123
Hollenbeck CB, Coulston AM, Reaven GM: To what extent does increased dietary fiber improve glucose and lipid metabolism in patients with noninsulin-dependent diabetes mellitus (NIDDM)?
Am J Clin Nutr
43
:
16
–24,
1986
124
Jenkins DJA, Leeds AR, Gassull MA, Wolever TMS, Goff DV, Alberti KGMM, Hockaday TDR: Unabsorbable carbohydrates and diabetes: decreased postprandial hyperglycemia.
Lancet
i 
i
:
172
–174,
1976
125
Chandalia M, Garg A, Luthohann D, von Bergmann K, Grundy SM, Brinkley LJ: Beneficial effects of a high dietary fiber intake in patients with type 2 diabetes.
N Engl J Med
342
:
1392
–1398,
2000
126
Brown L, Rosner B, Willett WW, Sacks FM: Cholesterol-lowering effects of dietary fiber: a meta-analysis.
Am J Clin Nutr
69
:
30
–42,
1999
127
Anderson JW, Allgood LD, Turner J, Oeltgen PR, Daggy BP: Effects of psyllium on glucose and serum lipid responses in men with type 2 diabetes and hypercholesterolemia.
Am J Clin Nutr
70
:
466
–473,
1999
128
Tappy L, Gugolz E, Wursch P: Effects of breakfast cereals containing various amounts of B-glucan fibers on plasma glucose and insulin responses in NIDDM subjects.
Diabetes Care
19
:
831
–834,
1996
129
Bourdon I, Yokoyama W, Davis P, Hudson C, Backus R, Richter D, Knuckles B: Postprandial lipid, glucose, insulin, and cholecystokinin responses in men fed barley pasta enriched with B-glucan.
Am J Clin Nutr
69
:
55
–63,
1999
130
Gibney M, Sigman-Grant M, Stanton JL, Keast DR: Consumption of sugars.
Am J Clin Nutr
62 (Suppl.):178S−194S, 1995
131
Bornet F, Haardt MJ, Costagliola D, Blayo A, Slama G: Sucrose or honey at breakfast have no additional acute hyperglycaemic effect over an isoglucidic amount of bread in type 2 diabetes patients.
Diabetologia
28
:
213
–217,
1985
132
Rickard KA, Cleveland JL, Loghmani EB, Fineberg NS, Freidenberg GR: Similar glycemic responses to high versus moderate sucrose-containing food in test meals for adolescents with type 1 diabetes and fasting euglycemia.
J Am Diet Assoc
101
:
1202
–1205,
2001
133
Nadeau J, Koski KG, Strychar I, Yale J-F: Teaching subjects with type 2 diabetes how to incorporate sugar choices into their daily meal plan promotes dietary compliance and does not deteriorate metabolic profile.
Diabetes Care
24
:
222
–227,
2001
134
Sigman-Grant M, Keast DR: Addendum to Am J Clin Nutr 62 (Suppl.):178S−194S,
1995
. Am J Clin Nutr
65
:
1572
–1574,
1997
135
Park YK, Yetley EA: Intakes and food sources of fructose in the United States.
Am J Clin Nutr
58 (Suppl):737S−747S, 1993
136
Crapo PA, Kolterman OG, Henry RR: Metabolic consequence to two-week fructose feeding in diabetic subjects.
Diabetes Care
9
:
111
–119,
1986
137
Bantle JP, Swanson JE, Thomas W, Laine DC: Metabolic effects of dietary fructose in diabetic subjects.
Diabetes Care
15
:
1468
–1476,
1992
138
Hallfrisch J, Reiser S, Prather ES: Blood lipid distribution of hyperinsulinemic men consuming three levels of fructose.
Am J Clin Nutr
37
:
740
–748,
1983
139
Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ: Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch.
Am J Clin Nutr
49
:
832
–839,
1989
140
Swanson JE, Laine DC, Thomas W, Bantle JP: Metabolic effects of dietary fructose in healthy subjects.
Am J Clin Nutr
55
:
851
–856,
1992
141
Bantle JP, Raatz SK, Thomas W, Georgopoulos A: Effects of dietary fructose on plasma lipids in healthy subjects.
Am J Clin Nutr
72
:
1128
–1134,
2000
142
Natah SS, Hussien KR, Tuominen JA, Koivisto VA: Metabolic response to lactitol and xylitol in healthy men.
Am J Clin Nutr
65
:
947
–950,
1997
143
Ishikawa M, Miyashita M, Kawashima Y, Nakamura T, Saitou N, Modderman J: Effects of oral administration of erythritol on patients with diabetes.
Regul Toxicol Pharmacol
24
:
S303
–S308,
1996
144
Vernia P, Frandina C, Bolotta T, Ricciardi MR, Vollotti G, Fallucca F: Sorbitol malabsorption and nonspecific abdominal symptoms in type II diabetes.
Metabolism
44
:
796
–799,
1995
145
Wheeler ML, Fineberg SE, Gibson R, Fineberg N: Metabolic response to oral challenge of hydrogenated starch hydrolysates versus glucose in diabetes.
Diabetes Care
13
:
733
–740,
1990
146
Vaaler S, Bjorneklett A, Jelling I, Skrede G, Hanssen KG, Fausa O, Aagenaes O: Sorbitol as a sweetener in the diet of insulin-dependent diabetes.
Acta Med Scand
221
:
165
–170,
1987
147
Akgun S, Ertel NH: A comparison of carbohydrate metabolism after sucrose, sorbitol, and fructose meals in normal and diabetic subjects.
Diabetes Care
3
:
582
–585,
1980
148
Payne ML, Craig WJ, Williams AC: Sorbitol is a possible risk factor for diarrhea in young children.
J Am Diet Assoc
97
:
532
–534,
1997
149
Jain NK, Rosenberg DB, Ulahannan MJ, Glasser MJ, Pitchumoni CS: Sorbitol intolerance in adults.
J Gastroenterol
80
:
678
–681,
1985
150
Würsch P: Starch in human nutrition.
World Rev Nutr Diet
60
:
199
–256,
1989
151
Englyst HN, Veenstra J, Hudson GJ: Measurement of rapidly available glucose (RAG) in plant food: a potential in vitro predictor of the glycemic response.
Br J Nutr
75
:
327
–337,
1996
152
Hoebler C, Karinthi A, Chiron H, Champ M, Barry J-L: Bioavailability of starch in bread rich in amylose: metabolic responses in healthy subjects and starch structure.
Eur J Clin Nutr
53
:
360
–366,
1999
153
Granfeldt Y, Drews A, Björck I: Arepas made from high amylose starch corn flour produce favorably low glucose and insulin responses in healthy humans.
J Nutr
125
:
459
–465,
1995
154
Raben A, Tagliabue A, Christensen NJ, Madsen J, Holst JJ, Astrup A: Resistant starch: the effect on postprandial glycemia, hormonal response, and satiety.
Am J Clin Nutr
60
:
544
–551,
1994
155
Liljebert HGM, Åkerberg KE, Björck IME: Effect of the glycemic index and content of indigestible carbohydrates of cereal-based breakfast meals on glucose tolerance at lunch in healthy subjects.
Am J Clin Nutr
69
:
647
–655,
1999
156
Heijnen MLA, van Amelsvoort JMM, Weststrate JA: Interaction between physical structure and amylose: amylopectin ratio of food on postprandial glucose and insulin responses in healthy subjects.
Eur J Clin Nutr
49
:
446
–457,
1995
157
Achour L, Flourié B, Briet F, Franchisseur C, Bornet F, Champ M, Rambaud JC, Messing B: Metabolic effects of digestible and partially indigestible cornstarch: a study in the absorptive and postabsorptive periods in healthy humans.
Am J Clin Nutr
66
:
1151
–1159,
1997
158
Noakes M, Clifton PM, Nestel PJ, LeLeu R, McIntosh G: Effect of high-amylose starch and oat bran on metabolic variables and bowel function in subjects with hypertriglyceridemia.
Am J Clin Nutr
64
:
944
–951,
1996
159
Behall KM, Howe JC: Effect of long-term amylose vs amylopectin starch on metabolic variables in human subjects.
Am J Clin Nutr
61
:
334
–340,
1995
160
Luo J, Rizkalla W, Alamowitch C, Boussairi A, Blayo A, Barry JL, Lafitte A, Guyon F, Bornet F, Slama G: Chronic consumption of short-chain fructooligosaccharides by healthy subjects decreased basal hepatic glucose production but had no effect on insulin-stimulated glucose metabolism.
Am J Clin Nutr
63
:
939
–945,
1996
161
Jenkins DJA, Vuksan V, Kendall CWC, Würsch P, Jeffcoat R, Waring S, Mehling CC, Vidgen E, Augustin LSA, Wong E: Physiological effects of resistant starches on fecal bulk, short chain fatty acids, blood lipids and glycemic index.
J Am Coll Nutr
17
:
609
–661,
1998
162
Axelsen M, Arvidsson-Lenner R, Lönnroth P, Smith U: Breakfast glycaemic response in patients with type 2 diabetes: effects of bedtime dietary carbohydrates.
Eur J Clin Nutr
53
:
706
–710,
1999
163
Alles MS, Roos N, Boks J, Van de Lisdonk E, Zock P, Hautvast J: Consumption of fructooligosaccharides does not favorably affect blood glucose and serum lipid concentrations in patients with type 2 diabetes.
Am J Clin Nutr
69
:
64
–69,
1999
164
Axelsen M, Lönnroth P, Arvidsson LR, Smith U: Suppression of the nocturnal free fatty acid levels by bedtime cornstarch in NIDDM.
Euro J Clin Invest
27
:
157
–163,
1997
165
Axelsen M, Lönnroth P, Arvidsson LR, Taskinen M, Smith U: Suppression of nocturnal free fatty acid concentrations by bedtime carbohydrate supplement in type 2 diabetes: effects on insulin sensitivity, lipids, and glycemic control.
Am J Clin Nutr
71
:
1108
–1114,
2000
166
Detlofson I, Kroon M, Åman J: Oral bedtime cornstarch supplementation reduces the risk of nocturnal hypoglycemia in young children with type 1 diabetes.
Acta Paediatr
88
:
596
–597,
1999
167
Kaufman FR, Halvorson M, Kaufman ND: A randomized blinded trial of uncooked cornstarch to diminish nocturnal hypoglycemia at diabetes camp.
Diabetes Res Clin Pract
30
:
205
–209,
1995
168
Axelsen M, Wesslau C, Lönnroth P, Arvidsson LR, Smith U: Bedtime uncooked cornstarch supplement prevents nocturnal hypoglycaemia in intensively treated type I diabetic subjects.
J Intern Med
245
:
229
–236,
1999
169
National Institutes of Environmental Health Sciences: 9th National Toxicology Report on Carcinogens. Washington, DC, DHHS, NIH, May 2000
170
Borzelleca JF, Verhagen H (Eds): Sucralose safety assessment.
Food Chem Toxicol
38(Suppl. 2)
:
S1
–S129,
2000
171
Mezitis NH, Maggio CA, Koch P, Quuddoos A, Allison DB, Pi-Sunyer FX: Glycemic effect of a single high oral dose of the novel sweetener sucralose in patients with diabetes.
Diabetes Care
19
:
1004
–1005,
1996
172
Stargel WW, Mayhew DA, Comer P, Andress SE, Butchko HH: Neotame. In
Alternative Sweeteners
. Nabors LO, Ed. New York, Marcel Dekker, 2001, p. 129–145
173
Butchko HH, Stargel WW: Aspartame: scientific evaluation in the postmarketing period.
Regul Toxicol Pharmacol.
In press
174
Powers M: Sugar alternatives and fat replacers. In American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Franz MJ, Bantle JP, Eds. Alexandria, VA, American Diabetes Association, 1999, p. 148–164
175
World Health Organization Expert Committee on Food Additives:
Toxicological Evaluation of Certain Food Additives and Food Contaminants
. Geneva, World Health Organization, 
16
:
11
–27, 
18
:
12
–14,
1981
, 1983
176
U.S. Department of Agriculture, Center for Nutrition Policy and Promotion: Nutrient content of the US food supply, 1909–94.
Home Economics Research Report No
53: US Government Printing Office, Washington, DC, 1997
177
U.S. Department of Agriculture, Agriculture Research Service: Food and Nutrient Intakes by Individuals in the United States by Sex and Age, 1994–96. Nationwide Food Surveys, Report No. 96–2, 1998
178
Randecker GA, Smiciklas-Wright H, McKenzie JM, Shannon BM, Mitchell DC, Becker DJ, Kieselhorst K: The dietary intake of children with IDDM.
Diabetes Care
19
:
1370
–1374,
1996
179
Henry RR: Protein content of the diabetic diet (Technical Review).
Diabetes Care
17
:
1502
–1513,
1994
180
Gougeon R, Pencharz PB, Marliss EB: Effect of NIDDM on the kinetics of whole-body protein metabolism.
Diabetes
43
:
318
–328,
1994
181
Gougeon R, Pencharz PB, Sigal RJ: Effect of glycemic control on the kinetics of whole-body protein metabolism in obese subjects with non-insulin dependent diabetes mellitus during iso and hypoenergetic feeding.
Am J Clin Nutr
65
:
861
–870,
1997
182
Gougeon R, Marliss EB, Jones PJ, Pencharz PB, Morais JA: Effect of exogenous insulin on protein metabolism with differing non-protein energy intakes in type 2 diabetes.
Int J Obes Relat Metab Disord
22
:
250
–261,
1998
183
Gougeon R, Styhler K, Morais JA, Jones PJH, Marliss EB: Effects of oral hypoglycemic agents and diet on protein metabolism in type 2 diabetes.
Diabetes Care
23
:
1
–8,
2000
184
Nair KS, Garrow JS, Ford C, Mahler RF, Halliday D: Effect of poor diabetic control and obesity on whole protein metabolism in man.
Diabetologia
25
:
400
–403,
1983
185
Felig P, Wahren J, Sherwin R, Palaiologos G: Amino acid and protein metabolism in diabetes mellitus.
Arch Intern Med
137
:
507
–513,
1977
186
Lariviere F, Chiasson J-L, Schiffrin A, Taveroff A, Hoffer LJ: Effects of dietary protein restriction on glucose and insulin metabolism in normal and diabetic humans.
Metabolism
43
:
462
–467,
1994
187
Brodsky IG, Robbins DC, Hiser E, Fuller SP, Fillyaw M, Devlin JT: Effects of low-protein diets on protein metabolism in insulin-dependent diabetes mellitus patients with early nephropathy.
J Clin Endocrinol Metab
75
:
351
–357,
1992
188
Brodsky IG, Devlin JT: Effects of dietary protein restriction on regional amino acid metabolism in insulin-dependent diabetes mellitus.
Am J Physiol
270
:
E148
–E157,
1996
189
Nyberg G. Norden G, Attman P-O, Aurell M, Uddebom G, Lenner RA, Isaksson B: Diabetic nephropathy: is dietary protein harmful?
Diabetic Complications
1
:
37
–40,
1987
190
Watts GF, Gregory L, Naoumova R, Kubal C, Shaw KM: Nutrient intake in insulin-dependent patients with diabetes with incipient nephropathy.
Eur J Clin Nutr
42
:
697
–702,
1988
191
Ekberg G, Sjofors G, Grefberg N, Larsson LO, Vaara I: Protein intake and glomerular hyperfiltration in insulin-treated diabetics without manifest nephropathy.
Scand J Urol Nephrol
27
:
441
–446,
1993
192
Toeller M, Buyken A: Protein intake: new evidence for its role in diabetic nephropathy.
Nephrol Dial Transplant
13
:
1926
–1927,
1998
193
Riley MD, Dwyer T: Microalbuminuria is positively associated with usual dietary saturated fat intake and negatively associated with usual dietary protein intake in people with insulin-dependent diabetes mellitus.
Am J Clin Nutr
67
:
50
–57,
1998
194
Jameel N, Pugh JA, Mitchell BD, Stern MP: Dietary protein intake is not correlated with clinical proteinuria in NIDDM.
Diabetes Care
15
:
178
–183,
1992
195
Skov AR, Toubro S, Bülow J, Krabbe K, Parving H-H, Astrup A: Changes in renal function during weight loss induced by high vs low-protein low-fat diets in overweight subjects.
Int J Obes Relat Metab Disord
23
:
1170
–1177,
1999
196
Toeller M, Buyken A, Heitkamp G, Bramswig S, Mann J, Milne R, Gries FA, Keen H, the EURODIAB IDDM Complications Study: Protein intake and urinary albumin excretion rates in the EURODIAB IDDM Complications Study.
Diabetologia
40
:
1219
–1226,
1997
197
Westphal SA, Gannon MC, Nuttall FQ: Metabolic response to glucose ingested with various amounts of protein.
Am J Clin Nutr
52
:
267
–272,
1990
198
Nuttall FQ, Mooradian AD, Gannon MC, Billington CJ, Krezowski PA: Effect of protein ingestion on the glucose and insulin response to a standardized oral glucose load.
Diabetes Care
7
:
465
–470,
1984
199
Nordt TK, Besenthal I, Eggstein M, Jakober B: Influence of breakfasts with different nutrient contents on glucose, C peptide, insulin, glucagon, triglycerides, and GIP in non-insulin-dependent diabetics.
Am J Clin Nutr
53
:
155
–160,
1991
200
Gannon MC, Nuttall JA, Damberg G, Gupta V, Nuttall FQ: Effect of protein ingestion on the glucose appearance rate in people with type 2 diabetes.
J Clin Endocrinol Metab
86
:
1040
–1047,
2001
201
Gannon MC, Nuttall FQ: Protein and diabetes. In
American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes
. Franz MJ, Bantle JP, Eds. American Diabetes Association, Alexandria, VA, 1999, p. 107–125
202
Peters AL, Davidson MB: Protein and fat effects on glucose responses and insulin requirements in subjects with insulin-dependent diabetes mellitus.
Am J Clin Nutr
58
:
555
–560,
1993
203
Gray RO, Butler PC, Beers TR, Kryshak EJ, Rizza RA: Comparison of the ability of bread versus bread plus meat to treat and prevent subsequent hypoglycemia in patients with insulin-dependent diabetes.
J Clin Endocrinol Metab
81
:
1508
–1511,
1996
204
Larosa JC, Fry AG, Muesing R, Rosing DR: Effects of high-protein, low-carbohydrate dieting on plasma lipoproteins and body weight.
J Am Diet Assoc
77
:
264
–270,
1980
205
Kennedy ET, Bowman SA, Spence JT, Freedman M, King J: Popular diets: correlation to health, nutrition, and obesity.
J Am Diet Assoc
101
:
411
–420,
2001
206
Westerterp KR, Wilson SAJ, Rolland V: Diet induced thermogenesis measured over 24 h in a respiration chamber: effect of diet composition.
Int J Obes Relat Metab Disord
23
:
287
–292,
1999
207
Skov AR, Toubro S, Ronn B, Holm L, Astrup A: Randomized trial on protein vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity.
Int J Obes Relat Metab Disord
23
:
528
–536,
1999
208
Hill AJ, Blundell JE: Macronutrients and satiety: the effects of high-protein or high-carbohydrate meal on subjective motivation to eat and food preferences.
Nutrition and Behavior
3
:
133
–144,
1986
209
Barkeling B, Rossner S, Bjorvell H: Effects of a high-protein meal (meat) and a high-carbohydrate meal (vegetarian) on satiety measured by automated computerized monitoring of subsequent food intake, motivation to eat and food preferences.
Int J Obes Relat Metab Disord
14
:
743
–751,
1990
210
Stubbs RJ, van Wyk MCW, Johnstone AM, Habron CG: Breakfasts high in protein, fat or carbohydrate: effect on within day appetite and energy intake.
Eur J Clin Nutr
50
:
409
–417,
1996
211
Rolls BJ, Hetherington M, Burley VJ: The specificity of satiety: the influence of food of different macronutrient content on the development of satiety.
Physiol Behav
43
:
145
–153,
1988
212
American Diabetes Association: Management of dyslipidemia in adults with diabetes (Position Statement).
Diabetes Care
24(Suppl. 1)
:
S58
–S61,
2001
213
Hegsted DM, Ausman LM, Johnson JA, Dallal GE: Dietary fat and serum lipids: an evaluation of the experimental data. [Published erratum appears in Am J Clin Nutr
58
:
245
,
1993
].
Am J Clin Nutr
57
:
875
–883,
1993
214
Schwab US, Ausman LM, Vogel S, Zhengling L, Lammi-Keefe CJ, Goldin BR, Ordovas JM, Schaefer EJ, Lichtenstein AH: Dietary cholesterol increases the susceptibility of low density lipoprotein to oxidative modification.
Atherosclerosis
149
:
83
–90,
2000
215
Hu FB, Stampfer MJ, Rjimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC: A prospective study of egg consumption and risk of cardiovascular disease in men and women.
JAMA
281
:
1387
–1394,
1999
216
Yu-Poth S, Zhao G, Etherton T, Naglak M, Jonnalagadda S, Kris-Etherton PM: Effects of the National Cholesterol Education Program’s Step I and Step II dietary intervention programs of cardiovascular disease risk factors: a meta-analysis.
Am J Clin Nutr
69
:
632
–646,
1999
217
Stone DB, Connor WE: The prolonged effects of a low cholesterol, high carbohydrate diet upon the serum lipids in patients with diabetes.
Diabetes
12
:
127
–132,
1963
218
Hjolllund E, Pedersen O, Richelsen B, Beck-Nielsen H, Sorensen NS: Increased insulin binding to adipocytes and monocytes and increased insulin sensitivity of glucose transport and metabolism in adipocytes from non-insulin-dependent diabetics after a low fat/high starch/high fiber diet.
Metabolism
32
:
1067
–1074,
1983
219
Simpson RW, Mann JI, Eaton J, Moore RA, Carter R, Hockaday TDR: Improved glucose control in maturity-onset diabetes treated with high-carbohydrate-modified fat diet.
BMJ
1
:
1753
–1756,
1979
220
Abbott WGH, Boyce VL, Grundy SM, Howard BV: Effects of replacing saturated fat with complex carbohydrate in diets of subjects with NIDDM.
Diabetes Care
12
:
102
–107,
1989
221
Brunzell JD, Lerner RL, Hazzard WR, Porte D, Bierman EL: Improved glucose tolerance with high carbohydrate feeding in mild diabetes.
N Engl J Med
284
:
521
–524,
1971
222
Brunzell JD, Lerner RL, Porte D, Bierman EL: Effect of a fat free, high carbohydrate diet on diabetic subjects with fasting hyperglycemia.
Diabetes
23
:
138
–142,
1974
223
Hales CN, Randle PJ: Effects of low-carbohydrate diet and diabetes mellitus on plasma concentrations of glucose, non-esterified fatty acid, and insulin during oral glucose tolerance tests.
Lancet
i
:
790
–794,
1963
224
Kolterman OG, Greenfield M, Reaven GM, Saekow M, Olefsky JM: Effect of a high carbohydrate diet on insulin binding to adipocytes and on insulin action in vivo in man.
Diabetes
28
:
731
–736,
1979
225
Segal-Isaacson CJ, Carello E, Wylie-Rosett J: Dietary fats and diabetes mellitus: Is there a food fat?
Current Diabetes Reports
1
:
161
–169,
2001
226
Walker KZ, O’Dea K, Johnson L, Sinclair AJ, Piers LS, Nicholson GC, Muir JG: Body fat distribution and non-insulin-dependent diabetes: comparison of a fiber-rich, high-carbohydrate, low-fat (23%) and a 35% fat diet high in monounsaturated fat.
Am J Clin Nutr
63
:
254
–260,
1996
227
Parillo M, Rivellese AA, Ciardullo AV, Capaldo B, Giacco A, Genovese S, Ricardi G: A high-monounsaturated fat/low carbohydrate diet improves peripheral insulin sensitivity in non-insulin-dependent patients with diabetes.
Metabolism
41
:
1373
–1378,
1992
228
Rasmussen OW, Thomsen C, Hanson KW, Vesterlund M, Winther E, Hermansen K: Effects on blood pressure, glucose, and lipid levels of a high-monounsaturated fat diet compared with a high-carbohydrate diet in non-insulin-dependent diabetic (NIDDM) subjects.
Diabetes Care
16
:
1565
–1571,
1993
229
Campbell LV, Marmot PE, Dyer JA, Borkman M, Storlien LH: The high-monounsaturated fat diet as a practical alternative for NIDDM.
Diabetes Care
17
:
177
–182,
1994
230
Lichtenstein AH, Ausman LM, Carrasco W, Jenner JL, Ordovas JM, Schaefer EJ: Short-term consumption of a low fat diet beneficially affects plasma lipid concentrations only when accompanied by weight loss.
Arterioscler Thromb Vasc Biol
14
:
1751
–1760,
1994
231
Heine RJ, Mulder C, Popp-Snijders C, van der Meer J, van der Meer EA: Linoleic-acid-enriched diet: long-term effects on serum lipoprotein and apolipoprotein concentrations and insulin sensitivity in noninsulin-dependent diabetic subjects.
Am J Clin Nutr
49
:
448
–456,
1989
232
Madigan C, Ryan M, Owens D, Collins P, Tomkin GH: Dietary unsaturated fatty acids in type 2 diabetes.
Diabetes Care
23
:
1472
–1477,
2000
233
Phillipson BE, Rothrock DW, Connor WE, Harris WS, Illingworth DR: Reduction of plasma lipids, lipoproteins, and apoproteins by dietary fish oils in patients with hypertriglyceridemia.
N Engl J Med
312
:
1210
–1216,
1985
234
Harris WS, Connor WE, Illingworth DR, Rothrock DW, Foster DM: Effects of fish oil on VLDL triglyceride kinetics in humans.
J Lipid Res
31
:
1549
–1558,
1990
235
Sirtori CR, Paoletti R, Mancini M, Crepaldi G, Manzato E, Rivellese A, Pamparana F, Stragliotto E: N-3 fatty acids do not lead to an increased diabetic risk in patients with hyperlipidemia and abnormal glucose tolerance: Italian Fish Oil Multicenter Study.
Am J Clin Nutr
65
:
1874
–1881,
1997
236
Friedberg CE, Janssen MJEM, Heine RJ, Grobbee DE: Fish oil and glycemic control in diabetes: a meta-analysis.
Diabetes Care
21
:
494
–500,
1998
237
Montori VM, Farmer A, Wollan PC, Dinneen SF: Fish oil supplementation in type 2 diabetes: a quantitative systematic review.
Diabetes Care
23
:
1407
–1415,
2000
238
Glauber H, Wallace P, Griver K, Brechtel G: Adverse metabolic effect of omega-3 fatty acids in non-insulin-dependent diabetes mellitus.
Ann Intern Med
108
:
663
–668,
1988
239
Westerveld HT, deGraaf JC, van Breugel HH, Akkerman JWN, Sixma JJ, Erkelens DW, Banga JD: Effects of low-dose EPA-E on glycemic control, lipid profile, lipoprotein (a), platelet aggregation, viscosity, and platelet and vessel wall interaction in NIDDM.
Diabetes Care
16
:
683
–688,
1993
240
Toft I, Bønaa KH, Ingebretsen OC, Nordøy A, Jenssen T: Effects of n-3 polyunsaturated fatty acids on glucose homeostasis and blood pressure in essential hypertension.
Ann Intern Med
123
:
911
–918,
1995
241
Patti L, Maffettone A, Iovine C, Marino LD, Annuzzi G, Riccardi G, Rivellese AA: Long-term effects of fish oil on lipoprotein subfractions and low density lipoprotein size in non-insulin-dependent patients with diabetes with hypertriglyceridemia.
Atherosclerosis
146
:
361
–367,
1999
242
Daviglus ML, Stamler J, Orencia AJ, Dyer AR, Liu K, Greenland P, Walsh MK, Morris D, Shekelle RB: Fish consumption and the 30-year risk of fatal myocardial infarction.
N Engl J Med
336: 1046–1053, 1997
243
Albert CM, Hennekens CH, O’Donnell CJ, Ajani UA, Carey VJ, Willet WC: Fish consumption and risk of sudden cardiac death.
JAMA
279
:
65
–66,
1998
244
Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, Sweetman R, Elwood PC, Deadman NM: Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial (DART).
Lancet
30
:
2
(8666):757–761, 1989
245
de Lorgeril M, Salen P, Martin JL, Monjaud I, Delaye J, Mamelle N: Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final of the Lyon Diet Heart Study.
Circulation
99
:
733
–735,
1999
246
Mori TA, Beilin LJ, Burke V, Morris J, Ritchie J: Interactions between dietary fat, fish, and fish oils and their effect on platelet function in men at risk of cardiovascular disease.
Arterioscler Thromb Vasc Biol
17
:
279
–286,
1997
247
Allison DB, Egan DK, Barraj LM, Caughman C, Infante M, Heimbach JT: Estimated intakes of trans fatty and other fatty acids in the US population.
J Am Diet Assoc
99
:
166
–174,
1999
248
Lichtenstein AH, Ausman LM, Jalbert SM, Schaefer EJ: Effects of different forms of dietary hydrogenated fats on serum lipoprotein cholesterol levels. [Published erratum appears in N Engl J Med 
341
:
856
,
1999
.] N Engl J Med
340
:
1933
–1940,
1999
249
Judd JT, Clevidence BA, Muesing RA, Wittes J, Sunkin ME, Podczasy JJ: Dietary trans fatty acids: effects on plasma lipids and lipoproteins of healthy men and women.
Am J Clin Nutr
59
:
861
–868,
1994
250
Ascherio A, Katan MB, Zock PL, Stampfer MJ, Willett WC: Trans fatty acids and coronary heart disease.
N Engl J Med
340
:
1994
–1998,
1999
251
Miettinen TA, Puska P, Gylling H, Vanhanen H, Vartiainen E: Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population.
N Engl J Med
333
:
1308
–1312,
1995
252
Weststrate JA, Meijer GW: Plant sterol-enriched margarines and reduction of plasma total- and LDL cholesterol concentrations in normocholesterolaemic and mildly hypercholesterolaemic subjects.
Eur J Clin Nutr
52
:
334
–343,
1998
253
Hendriks HFJ, Weststrate JA, van Vliet T, Meijer GW: Spreads enriched with three different levels of vegetable oil sterols and the degree of cholesterol lowering in normocholesterolaemic and mildly hypercholesterolaemic subjects.
Eur J Clin Nutr
53
:
319
–327,
1999
254
Hallikainen MA, Uusitupa MIJ: Effects of two low-fat stanol ester-containing margarines on serum cholesterol concentrations as part of a low-fat diet in hypercholesterolemic subjects.
Am J Clin Nutr
69
:
403
–410,
1999
255
Blair SN, Capuzzi DM, Gottlieb SO, Nguyen T, Morgan JM, Cater NB: Incremental reduction of serum total cholesterol and low-density lipoprotein cholesterol with the addition of plant stanol ester-containing spread to statin therapy.
Am J Cardiol
86
:
46
–52,
2000
256
Purnell JQ, Brunzell JD: Food fats and dyslipidemia. In American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Franz MJ, Bantle JP, Eds. Alexandria, VA, American Diabetes Association, 1999, p. 126–147
257
Carmichael HE, Swinburn BA, Wilson MR: Lower fat intake as a predictor of initial and sustained weight loss in obese subjects consuming an otherwise ad libitum diet.
J Am Diet Assoc
98
:
35
–39,
1998
258
Larson DE, Ferraro RT, Robertson DS, Ravussin E: Energy metabolism in weight-stable postobese individuals.
Am J Clin Nutr
62
:
735
–739,
1995
259
Lissner L, Levitsky DA, Strupp BJ, Kalkwarf HJ, Roe DA: Dietary fat and the regulation of energy intake in human subjects.
Am J Clin Nutr
46
:
886
–892,
1987
260
Kendall A, Levitsky DA, Strupp BJ, Lissner L: Weight loss on a low-fat diet: consequence of the imprecision of the control of food intake in humans.
Am J Clin Nutr
53
:
1124
–1129,
1991
261
Schaefer EJ, Lichtenstein AH, Lamon-Fava S, McNamara JR, Schaefer MM, Rasmussen H, Ordovas JM: Body weight and low-density lipoprotein cholesterol changes after consumption of a low-fat ad libitum diet.
JAMA
274
:
1450
–1455,
1995
262
Doucet E, Alméras N, White MD, Després J-P, Bouchard C, Tremblay A: Dietary fat composition and human adiposity.
Eur J Clin Nutr
52
:
2
–6,
1998
263
Knopp RJ, Walden CE, Retzlaff BM, McCann BS, Dowdy AA, Albers JJ, Gey GO, Cooper MN: Long-term cholesterol-lowering effects of four fat-restricted diets in hypercholesterolemic and combined hyperlipidemic men: the Dietary Alternatives Study.
JAMA
278
:
1509
–1515,
1997
264
Stamler J, Dolecek TA: Relation of food and nutrient intakes to body mass in the special intervention and usual care groups in the Multiple Risk Factor Intervention Trial.
Am J Clin Nutr
65
:
366S
–373S,
1997
265
Tillotson JL, Grandits GA, Bartsch GE, Stamler J: Relation of dietary carbohydrates to blood lipids in the special intervention and usual care groups in the Multiple Risk Factor Intervention Trial.
Am J Clin Nutr
65
:
314S
–326S,
1997
266
Sheppard L, Kristal AR, Kushi LH: Weight loss in women participating in a randomized trial of low-fat diets.
Am J Clin Nutr
54
:
821
–828,
1991
267
Westerterp KR, Verboeket-van de Venne WP, Westerterp-Plantenga MS, Velthuis-te Wierik EJ, de Graaf C, Weststrate JA: Dietary fat and body fat: an intervention study.
Int J Obes Relat Metab Disord
20
:
1022
–1026,
1996
268
Prewitt TE, Schmeisser D, Bowen PE, Aye P, Dolacek TA, Langenberg P, Cole T, Brace L: Changes in body weight, body composition, and energy intake in women fed high- and low-fat diets.
Am J Clin Nutr
54
:
304
–310,
1991
269
Blankenhorn DH, Azen SP, Kramsch DM, Mack WJ, Cashin-Hemphill L, Hodis HN, DeBoer LW, Mahrer PR, Masteller MJ, Vailas LI: Coronary angiographic changes with lovastatin therapy: the Monitored Atherosclerosis Regression Study (MARS).
Ann Intern Med
119
:
969
–976,
1993
270
Turley ML, Skeaff CM, Mann JI, Cox B: The effect of a low-fat, high-carbohydrate diet on serum high density lipoprotein cholesterol and triglyceride.
Eur J Clin Nutr
52
:
728
–732,
1998
271
Watts GF, Lewis B, Brunt JN, Lewis ES, Coltart OJ, Smith LD, Mann JI, Swan AV: Effects on coronary artery disease of lipid-lowering diet or diet plus cholestyramine in the St. Thomas’ Atherosclerosis Regression Study (STARS).
Lancet
339
:
563
–569,
1992
272
Willett WC: Is dietary fat a major determinant of body fat?
Am J Clin Nutr
67
:
556S
–562S,
1998
273
Bray GA, Popkin BM: Dietary fat intake does affect obesity! Am J Clin Nutr
68
:
1157
–1173,
1998
274
Willett WC: Dietary fat and obesity: an unconvincing relation! Am J Clin Nutr
68
:
1149
–1150,
1998
275
Purnell JQ, Knopp RH, Brunzell JD: Dietary fat and obesity.
Am J Clin Nutr
70
:
108
–110,
1999
276
Willett WC: Reply to JQ Purnell, RH Knopp, and JD Brunzell.
Am J Clin Nutr
70
:
108A
−109, 1999
277
Bray GA, Popkin BM: Reply to JQ Purnell, RH Knopp, and JD Brunzell.
Am J Clin Nutr
70
:
109
–110,
1999
278
Purnell JQ, Brunzell JD: The central role of dietary fat, not carbohydrate, in the insulin resistance syndrome.
Curr Opin Lipidol
8
:
17
–22,
1997
279
Reaven GM: Do high carbohydrate diets prevent the development or attenuate the manifestations (or both) of syndrome X? A viewpoint strongly against.
Curr Opin Lipidol
8
:
23
–27,
1997
280
Shah M, Garg A: High-fat and high-carbohydrate diets and energy balance.
Diabetes Care
19
:
1142
–1152,
1996
281
Pasqale R, Wing R, Butler B, Mullen M, Bononi P: Effects of a behavioral weight loss program stressing caloric restriction vs calorie plus fat restriction in obese individuals with NIDDM or a family history of diabetes.
Diabetes Care
18
:
1241
–1248,
1995
282
Astrup A, Ryan L, Grunwald GK, Storgaard M, Saris W, Melanson E, Hill JO: The role of dietary fat in body fatness: evidence from a preliminary meta-analysis of ad libitum low-fat dietary intervention study.
Br J Nutr
83(Suppl. 1)
:
S25
−S32, 2000
283
Toubro S, Astrup A: Randomised comparison of diet for maintaining obese subjects’ weight after major weight loss: ad lib, low fat, high carbohydrate diet vs fixed energy intake.
BMJ
314
:
29
–34,
1997
284
Heilbronn L, Noakes M, Clifton P: Effect of energy restriction, weight loss, and diet composition on plasma lipids and glucose in patients with type 2 diabetes.
Diabetes Care
22
:
889
–895,
1999
285
Walker K, O’Dea K, Nicholson G, Muir J: Dietary composition, body weight, and NIDDM.
Diabetes Care
18
:
401
–403,
1995
286
Storm H, Thomsen C, Pedersen E, Rasmussen O, Christiansen C, Hermansen K: Comparison of a carbohydrate-rich diet and diets rich in stearic or palmitic acid in NIDDM patients.
Diabetes Care
20
:
1807
–1813,
1997
287
Mayer-Davis EJ, Levin S, Marshall JA: Heterogeneity in associations between macronutrient intake and lipoprotein profile in individuals with type 2 diabetes.
Diabetes Care
22
:
1632
–1639,
1999
288
Kelly SM, Shorthouse M, Cotterell JC, Riordan AM, Lee AJ, Thurnham DI, Hanka R, Hunter JO: A 3-month, double-blind, controlled trial of feeding with sucrose polyester in human volunteers.
Br J Nutr
80
:
41
–49,
1998
289
Sandler RS, Zorich NL, Filloon TG, Wiseman HB, Lietz DJ, Brock MH, Royer MG, Miday RK: Gastrointestinal symptoms in 3181 volunteers ingesting snack food containing olestra or triglycerides.
Ann Intern Med
130
:
253
–261,
1999
290
Warshaw H, Franz M, Powers MA, Wheeler M: Fat replacers: their use in food and role in diabetes medical nutrition therapy (Technical Review).
Diabetes Care
19
:
1294
–1301,
1996
291
Slama G, Rossi F, Bellisle F, Casassus P, Fiquet P, Chappuis AS, Desplanque N, Laffitte A: Low-fat (41%) butter consumption decreases total energy and lipid intake in patients with diabetes under acute conditions.
Appetite
25
:
119
–126,
1995
292
Rodriguez LM, Castellanos VH: Use of low-fat food by people with diabetes decreases fat, saturated fat, and cholesterol intakes.
J Am Diet Assoc
100
:
531
–536,
2000
293
DeGraaf C, Hulshof T, Weststrate JA, Hautvast GAJ: Nonabsorbable fat (sucrose polyester) and the regulation of energy intake and body weight.
Am J Physiol
270
:
R1386
–R1393,
1996
294
Cotton JR, Weststrate JA, Blundell JE: Replacement of dietary fat with sucrose polyester: effects on energy intake and appetite control in nonobese males.
Am J Clin Nutr
63
:
891
–896,
1996
295
Cowie CC, Harris MI: Physical and metabolic characteristics of persons with diabetes. In Diabetes in America. 2nd ed. National Diabetes Data Group, Eds. Bethesda, MD, NIH, NIDDK, 1995, p. 117–164 (NIH publ. no. 95–1468)
296
Campbell PJ, Gerich JE: Impact of obesity on insulin action in volunteers with normal glucose tolerance: demonstration of a threshold for adverse effect of obesity.
J Clin Endocrinol Metab
70
:
1114
–1118,
1990
297
Olefsky JM, Kolterman OG, Scarlett JA: Insulin action and resistance in obesity and non insulin-dependent diabetes mellitus.
Am J Physiol
243
:
E15
–E30,
1982
298
Campbell PJ, Carlson MG: Impact of obesity on insulin action in NIDDM.
Diabetes
42
:
405
–410,
1993
299
Albu J, Konnaaarides C, Pi-Sunyer FX: Weight control: metabolic and cardiovascular effects.
Diabetes Rev
3
:
335
–347,
1995
300
Hughes TA, Gwynne JT, Switzer BR, Herbst C, White G: Effects of caloric restriction and weight loss on glycemic control, insulin release and resistance, and atherosclerotic risk in obese patients with type II diabetes mellitus.
Am J Med
77
:
7
–17,
1984
301
Henry RR, Wiest-Kent A, Scheaffer L, Kolterman OG, Olefsky JM: Metabolic consequences of very-low-calorie diet therapy in obese non-insulin-dependent diabetic and nondiabetic subjects.
Diabetes
35
:
155
–164,
1986
302
Amatruda JM, Richeson JF, Welle SL, Brodows RG, Lockwood DH: The safety and efficacy of a controlled low energy (very-low-calorie) diet in the treatment of non-insulin dependent diabetes and obesity.
Arch Intern Med
148
:
873
–877,
1988
303
Sarlio-Lähteenkorva S, Rissanen A, Kapprio J: A descriptive study of weight-loss maintenance: 6 and 15 year follow-up of initially overweight adults.
Int J Obes Relat Metab Disord
24
:
116
–125,
2000
304
McGuire MT, Wing RR, Hill JO: The prevalence of weight loss maintenance among American adults.
Int J Obes
  Relat Metab Disord
23
:
1314
–1319,
1999
305
Hanefeld M, Fischer S, Schmechel H, Rothe G, Schulze J, Dude H, Schwanebeck U, Julius U: Diabetes Intervention Study: multi-intervention trial in newly diagnosed NIDDM.
Diabetes Care
14
:
308
–317,
1991
306
Laitinen JH, Ahola IE, Sarkkinen ES, Winberg RL, Harmaakorpi-Ivonen PA, Uusitupa MI: Impact of intensified dietary therapy on energy and nutrient intakes and fatty acid composition of serum lipids with recently diagnosed non-insulin dependent diabetes mellitus.
J Am Diet Assoc
93
:
276
–283,
1993
307
Hadden DR, Blair ALT, Wilson EZ, Boyle DM, Atkinson B, Kennedy AL, Buchanan KD, Merrett JD, Montgomery DAD, Weaver JA: Natural history of diabetes presenting at age 40–69 years: a prospective study of the influence of intensive dietary therapy.
QJM
59
:
579
–598,
1986
308
Schwartz MW, Seeley RJ: The new biology of body weight regulation.
J Am Diet Assoc
97
:
54
–58,
1997
309
Rosenbaum M, Leibel RL, Hirsch J: Obesity.
N Engl J Med
337
:
396
–407,
1997
310
Porte D Jr, Seeley RJ, Woods SC, Baskin DG, Figlewicz DP, Schwartz MW: Obesity, diabetes and the central nervous system.
Diabetologia
41
:
863
–881,
1998
311
Stunkard AJ, Sorensen TIA, Hanis C, Teasdale TW, Chakraborty R, Schull WJ, Schulsinger F: An adoption study of human obesity.
N Engl J Med
314
:
193
–198,
1986
312
Bouchard C, Tremblay A, Despres JP, Nadeau A, Lupien PJ, Theriault G, Dussault J, Moorjani S, Pinault S, Fournier G: The response to long-term overfeeding in identical twins.
N Engl J Med
322
:
1477
–1482,
1990
313
Stunkard AJ, Harris JR, Pedersen NL, McClearn GE: The body-mass index of twins who have been reared apart.
N Engl J Med
322
:
1483
–1487,
1990
314
Wing RR, Hill JO: Successful weight loss maintenance.
Annu Rev Nutr
21
:
323
–341,
2001
315
Klem ML, Wing RR, McGuire MT, Seagle HM, Hill JO: A descriptive study of individuals successful at long-term maintenance of substantial weight loss.
Am J Clin Nutr
66
:
239
–246,
1997
316
The Diabetes Prevention Program Research Group: The Diabetes Prevention Program: design and methods for a clinical trial in the prevention of type 2 diabetes.
Diabetes Care
22
:
623
–634,
1999
317
DPP. www.preventdiabetes.com. Accessed October 2001
318
Wing RR, Venditti E, Jakicic JM, Polley BA, Lang W: Lifestyle intervention in overweight individuals with a family history of diabetes.
Diabetes Care
21
:
350
–359,
1998
319
Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V, Uusitupa M, Aunola S, Cepaitis Z, Moltchanov V, Hakumaki M, Mannelin M, Martikkala V, Sundvall J: Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.
N Engl J Med
344
:
1343
–1350,
2001
320
Tucker LA, Kano MJ: Dietary fat and body fat: a multivariate study of 205 adult females.
Am J Clin Nutr
56
:
612
–622,
1992
321
Westsrate JA: Fat and obesity.
Int J Obes Relat Metab Disord
19 (Suppl.):S38–S43, 1995
322
Kasim SE, Martino S, Kim PN, Khilnani S, Boomer A, Depper J, Reading BA, Heilbrum LK: Dietary and anthropometric determinates of plasma lipoproteins during a long-term low fat diet in healthy women.
Am J Clin Nutr
57
:
146
–153,
1993
323
Sheppard L, Kristal AR, Kushi LH: Weight loss in women participating in a randomized trial of low fat diets.
Am J Clin Nutr
54
:
821
–828,
1993
324
Bouchard C, Deprés JP, Tremblay A: Exercise and obesity.
Obes Res
1
:
133
–147,
1993
325
Pavlou KN, Krey S, Steffee WP: Exercise as an adjunct to weight loss and maintenance in moderately obese subjects.
Am J Clin Nutr
49
:
1115
–1123,
1989
326
Maggio CA, Pi-Sunyer FX: The prevention and treatment of obesity: application to type 2 diabetes (Technical Review).
Diabetes Care
20
:
1744
–1766,
1997
327
Brown S, Upchurch S, Anding T, Winter M, Ramirez G: Promoting weight loss in type 2 diabetes.
Diabetes Care
19
:
613
–624,
1996
328
Foreyt JP, Goodrick GK: Evidence for success of behavior modification in weight loss and control.
Ann Intern Med
119
:
698
–701,
1993
329
Technology Assessment Conference Panel: Methods for voluntary weight loss and control: Technology Assessment Conference statement.
Ann Intern Med
119
:
764
–770,
1993
330
Wadden TA: Treatment of obesity by moderate and severe caloric restriction: results of clinical trials.
Ann Intern Med
119
:
688
–693,
1993
331
Ditschuneit HH, Flechtner-Mors M, Johnson TD, Adler G: Metabolic and weight-loss effects at a long-term dietary intervention in obese patients.
Am J Clin Nutr
69
:
198
–204,
1999
332
Rothacker DQ: Five year self-management of weight using meal replacements: comparison with matched control in rural Wisconsin.
Nutr
16
:
344
–348,
2000
333
Ashley JM, St. Jeor ST, Schrage JP, Perumean-Chaney SE, Gilbertson MN, McCall NL, Bovee V: Weight control in the physician’s office.
Arch Intern Med
161
:
1599
–1604,
2001
334
Rothacker DQ, Staniszewki BA, Ellis PK: Liquid meal replacement vs traditional food: a potential model for women who cannot maintain eating habit change.
J Am Diet Assoc
101
:
345
–347,
2001
335
Metz JA, Stern JS, Kris-Etherton P, Reusser ME, Morris CD, Hatton D, Oparil S, Haynes RB, Renick LM, Pi-Sunyer FX, Clark S, Chester L, McMahon M, Snyder GW, McCarron DA: A randomized trial of improved weight loss with a prepared meal plan in overweight and obese patients.
Arch Intern Med
160
:
2150
–2158,
2000
336
Wing RR, Marcus MD, Salata R, Epstein LH, Miaskiewicz S, Blair EE: Effects of a very low calorie diet on long-term glycemic control in obese type 2 diabetic subjects.
Arch Intern Med
151
:
1334
–1340,
1991
337
Henry RR, Gumbiner B: Benefits and limitations of very low calorie diet therapy in obese NIDDM.
Diabetes Care
14
:
802
–823,
1991
338
Wing RR: Use of very-low-calorie diets in the treatment of obese persons with non-insulin dependent diabetes mellitus.
J Am Diet Assoc
95
:
569
–572,
1995
339
Weintraub M: Long-term weight control: the National Heart, Lung, and Blood Institute Multimodal Intervention Study.
Clin Pharmacol Ther
51
:
586
–646,
1992
340
Connolly HM, Crary JL, McGoon MD, Hensrud DD, Edwards BS, Edwards WD, Schaff HV: Valvular heart disease associated with fenfluramine-phentermine.
N Engl J Med
337
:
581
–588,
1997
341
Redmon JB, Raatz SK, Kwong CA, Swanson JE, Thomas W, Bantle JP: Pharmacologic induction of weight loss to treat type 2 diabetes.
Diabetes Care
22
:
896
–903,
1999
342
Fujioka K, Seaton TB, Rowe E, Jelinek CA, Raskin P, Lebovitz HE, Weinstein SP, the Sibutramine/Diabetes Clinical Study Group: Weight loss with sibutramine improves glycaemic control and other metabolic parameters in obese patients with type 2 diabetes mellitus.
Diabetes Obes Metab
2
:
175
–187,
2000
343
Hollander PA, Elbein SC, Hirsch IB, Kelley C, McGill J, Taylor T, Weiss SR, Crockett SE, Kaplan RA, Comstock J, Lucas CP, Lodewick PA, Canovatchel W, Chung J, Hauptman J: Role of orlistat in the treatment of obese patients with type 2 diabetes: a randomized double-blind study.
Diabetes Care
21
:
1288
–1294,
1998
344
Lindgarde F, Orlistat Swedish Multimorbidity Study Group: The effect of orlistat on body weight and coronary heart disease risk profile in obese patients: the Swedish Multimorbidity Study.
J Intern Med
248
:
245
–254,
2000
345
Nightengale ML, Sarr MG, Kelly KA, Jensen MD, Zinsmeister AR, Palumbo PJ: Prospective evaluation of vertical banded gastroplasty as the primary operation for morbid obesity.
Mayo Clin Proc
66
:
773
–782,
1991
346
Pories WJ, MacDonald KG, Flickinger EG, Dohm GL, Sinha MK, Barakat HA, May HJ, Khazanie P, Swanson MS, Morgan E, Leggett-Frazier N, Long SD, Brown BM, O’Brien K, Caro JF: Is type II diabetes mellitus (NIDDM) a surgical disease?
Ann Surg
215
:
633
–642,
1992
347
Dixon JB, O’Brien PE: Health outcomes of severely obese type 2 diabetic subjects 1 year after laparoscopic adjustable gastric banding.
Diabetes Care
In press
348
Consensus Development Conference Panel: Gastrointestinal surgery for severe obesity.
Ann Intern Med
115
:
956
–961,
1991
349
Sugerman HJ, Brewer WH, Shiffman ML, Brolin RE, Fobi MAL, Linner JH, MacDonald KG, MacGregor AM, Martin LF, Oram-Smith JC, Popoola D, Schirmer BD, Vickers FF: A multicenter, placebo controlled, randomized, double-blind, prospective trial of prophylactic ursodiol for the prevention of gallstone formation following gastric-bypass-induced rapid weight loss.
Am J Surg
169
:
91
–97,
1995
350
Institute of Medicine Food and Nutrition Board:
Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids
. Washington, DC, National Academy Press, 2000
351
Institute of Medicine Food and Nutrition Board:
Dietary Reference Intakes for Thiamine, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline
. Washington, DC, National Academy Press, 1998
352
Institute of Medicine Food and Nutrition Board:
Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc
. Washington, DC, National Academy Press, 2001
353
Institute of Medicine Food and Nutrition Board:
Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride
. Washington, DC, National Academy Press, 1997
354
Food and Nutrition Board: Recommended Dietary Allowances. 10th ed. Washington, DC, National Academy of Sciences, 1989
355
Food and Nutrition Board:
Nutrition During Pregnancy. Part 1: Weight Gain. Part 2: Nutrient Suppl
. Washington, DC, Institute of Medicine, National Academy of Sciences, 1990
356
Mooradian AD, Failla M, Hoogwerf B, Maryniuk M, Wylie-Rosett: Selected vitamins and minerals in diabetes.
Diabetes Care
17
:
464
–479,
1994
357
Mooradian AD: Micronutrients in diabetes mellitus. In Drugs, Diet and Disease
2
:
183
–200,
1999
358
Klipstein-Grobusch K: Dietary antioxidants and risk of myocardial infarction in the elderly: the Rotterdam Study.
Am J Clin Nutr
69
:
261
–266,
1999
359
Will JC, Ford ES, Bowman BA: Serum vitamin C concentrations and diabetes: findings from the Third National Health and Nutrition Examination Survey 1988–
1994
. Vit C in diabetes. NHANES III.
Am J Clin Nutr
70
:
49
–52,
1999
360
Mayer-Davis EJ, Bell KA, Reboussin BA, Rushing J, Marshall JA, Hamman RF: Antioxidant nutrient intake and diabetic retinopathy: the San Luis Valley Diabetes Study.
Ophthalmology
105
:
2264
–2270,
1998
361
Coudray C, Roussel AM, Mainard F, Arnaud J, Favier A: Lipid peroxidation level and antioxidant micronutrient status in a pre-aging population: correlation with chronic disease prevalence in a French epidemiological study.
J Am Coll Nutr
16
:
584
–591,
1997
362
Mayer-Davis EJ, Monaco JH, Marshall JA, Rushing J, Juhairi J: Vitamin C intake and cardiovascular disease risk factors in persons with non-insulin-dependent diabetes mellitus: from the Insulin Resistance Atherosclerosis Study and the San Luis Valley Diabetes Study.
Prev Med
26
:
277
–283,
1997
363
Sanchez-Lugo L, Mayer-Davis EJ, Howard G, Selby JV, Ayad MF, Rewers M, Haffner S: Insulin sensitivity and intake of vitamins E and C in African American, Hispanic, and non-Hispanic white men and women: the Insulin Resistance and Atherosclerosis Study (IRAS).
Am J Clin Nutr
66
:
1224
–1231,
1997
364
Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, Belanger C, LaMotte F, Gaziano JM, Ridker PM, Willett W, Peto R: Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease.
N Engl J Med
334
:
1145
–1149,
1996
365
Knekt P, Jarvinen R, Reunanen A, Maatela J: Flavenoid intake and coronary mortality in Finland: a cohort study.
BMJ
312
:
478
–481,
1996
366
Kushi LH, Folsom AR, Prineas RJ, Mink PJ, Wu Y, Bostick RM: Dietary antioxidant vitamins and death from coronary in post-menopausal women.
N Engl J Med
334
:
1156
–1162,
1996
367
Losonczy KG, Harris TB, Havlik RS: Vitamin E and vitamin C supplement use and risk of all cause and coronary heart disease mortality in older persons: the Established Population for Epidemiologic Studies of the Elderly.
Am J Clin Nutr
64
:
190
–196,
1996
368
Gaziano JM, Manson JE, Branch LC, Colditz GA, Willett WC, Buring JE: A prospective study of consumption of carotenoids in fruits and vegetables and decreased cardiovascular mortality in the elderly.
Ann Epidemiol
5
:
255
–260,
1995
369
Knekt P, Reunanen A, Jarvinen R, Seppanen R, Heliovaara M, Aromaa A: Antioxidant vitamin intake and coronary mortality in a longitudinal population study.
Am J Epidemiol
139
:
1180
–1189,
1994
370
Rimm EB, Stampfer MJ, Ascherio A, GioVannucci E, Colditz GA, Willett WC: Vitamin E consumption and the risk of coronary heart disease in men.
N Engl J Med
328
:
1450
–1456,
1993
371
Shoff SM, Mares-Pellman JA, Cruickshanks KJ, Klein R, Klein BE, Ritler LL: Glycosylated hemoglobin concentrations and vitamin E, vitamin C, and beta-carotene intake in diabetic and non-diabetic older adults.
Am J Clin Nutr
58
:
412
–416,
1993
372
Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC: Vitamin E consumption and the risk of coronary disease in women.
N Engl J Med
328
:
1444
–1449,
1993
373
Enstrom JE, Kanim LE, Klein MA: Vitamin C intake and mortality among a sample of the United States population.
Epidemiology
3
:
194
–202,
1992
374
Salonen JT, Nyyssonen K, Tuomainen TP, Maenpaa PH, Korpela H, Kaplan GA, Lynch J, Helmrich SP, Salonen R: Increased risk of non-insulin-dependent diabetes mellitus at low plasma vitamin E concentrations: a four year study in men.
BMJ
311
:
1124
–1127,
1995
375
Gey KF, Puska P: Plasma vitamins E and A inversely correlated to mortality from ischemic heart disease in cross-cultural pathology.
Ann N Y Acad Sci
570
:
268
–282,
1989
376
Christen WG, Gaziano JM, Hennekens CH: Design of Physicians’ Health Study II: a randomized trial of beta carotene, vitamins E and C and multivitamins, in prevention of cancer, cardiovascular disease and eye disease and review of results of completed trials.
Ann Epidemiol
10
:
125
–134,
2000
377
Ford ES, Will JC, Bowman BA, Narayan KM: Diabetes mellitus and serum carotenoids: findings from the Third National Health and Nutrition Examination Survey.
Am J Epidemiol
149
:
168
–176,
1999
378
Yusuf S, Dagenais G, Pogue J, Bosch J, Sleight P: Vitamin E supplementation and cardiovascular events in high-risk patients: the Heart Outcomes Prevention Evaluation Study Investigators.
N Engl J Med
342
:
154
–160,
2000
379
GISSI-Prevenzione Investigators: Dietary supplements with n-3 poly unsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevention Trial.
Lancet
354
:
447
–455,
1999
380
Omenn GS, Goodman GE, Thornquist MD, Balmes J, Cullen MR, Glass A, Keogh JP, Meyskens FL Jr, Valanis B, Williams JH Jr, Barnhart S, Cherniak MG, Brodkin CA, Hammar S: Risk factors for lung cancer and for intervention effects in CARET: the Beta Carotene and Retinol Efficacy Trial.
J Natl Cancer Inst
88
:
1550
–1559,
1996
381
Stephens NG, Parsons A, Schofield PM, Kelly F, Cheeseman K, Mitchinson MJ: Randomized, controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study.
Lancet
347
:
781
–786,
1996
382
ATBC (Alpha-Tocopherol, Beta Carotene) Cancer Prevention Study Group: the effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers.
N Engl J Med
330
:
1029
–1035,
1994
383
Blot WJ, Li JY, Taylor PR, Guo W, Dawsey S, Wang GO, Yang CS, Zheng SF, Gail M, Li GY: Nutrition intervention trials in Linxian, China: supplementation with specific vitamin/mineral combination, cancer incidence and disease-specific mortality in general population.
J Natl Cancer Inst
85
:
1483
–1492,
1993
384
Bursell S-E, Clermont AC, Aiello LP, Aiello LM, Schlossman DK, Feener EP, Laffel L, King GL: High-dose vitamin E supplementation normalizes retinal blood flow and creatinine clearance in patients with type 1 diabetes.
Diabetes Care
22
:
1245
–1251,
1999
385
Astley S, Langrish-Smith A, Southon S, Sampson M: Vitamin E supplementation and oxidative damage to DNA and plasma LDL in type 1 diabetes.
Diabetes Care
22
:
1626
–1631,
1999
386
Upritchard JE, Sutherland WHF, Mann JI: Effect of supplementation with tomato juice, vitamin E, and vitamin C on LDL oxidation and products of inflammatory activity in type 2 diabetes.
Diabetes Care
23
:
733
–738,
2000
387
Paolisso G, D’Amore A, Galzerano D, Balbi B, Giugliano D, Varricchio M, D’Onofrio F: Daily vitamin E supplements improve metabolic control but not insulin secretion in elderly type 2 patients with diabetes.
Diabetes Care
16
:
1433
–1437,
1993
388
Reaven PD, Herold DA, Barnett J, Edelman S: Effects of vitamin E on susceptibility of low-density lipoprotein and low-density lipoprotein subfractions to oxidation and on protein glycation in NIDDM.
Diabetes Care
18
:
807
–816,
1995
389
Koehler KM, Pareo-Tubbeh SL, Romero LJ, Baumgartner RN, Garry PJ: Folate nutrition and older adults: challenges and opportunities.
J Am Diet Assoc
97
:
167
–173,
1997
390
Pozzilli P, Visalli N, Signore A, Baroni MG, Buzzetti R, Cavallo MG, Boccuni ML, Fava D, Gragnoli C, Andreani D: Double-blind trial of nicotinamide in recent-onset IDDM (the IMDIAB III study).
Diabetologia
38
:
848
–852,
1995
391
Visalli N, Cavallo MG, Signore A, Baroni MG, Buzzetti R, Fioriti E, Mesturino C, Fiori R, Lucentini L, Matteoli MC, Crino A, Corgbi S, Spera S, Teodonio C, Paci F, Amoretti R, Pisano L, Suraci C, Multari G, Sulli N, Cervoni M, De Mattia G, Faldetta MR, Boscherini B, Pozzilli P: A multi-centre, randomized trial of two different doses of nicotinamide in patients with recent-onset type 1 diabetes (the IMDIAB VI).
Diabetes Metab Res Rev
15
:
181
–185,
1999
392
Anderson RA, Cheng N, Bryden NA, Polansky MM, Cheng N, Chi J, Feng J: Beneficial effects of chromium for people with diabetes.
Diabetes
46
:
1786
–1791,
1997
393
Cheng N, Zhu X, Shi H, Wu W, Chi J, Cheng J, Anderson RA: Follow-up survey of people in China with type 2 diabetes mellitus consuming supplemental chromium.
J Trace Elem Exp Med
12
:
55
–60,
1999
394
Ravina A, Slezak L, Rubal A, Mirsky N: Clinical use of trace element chromium (III) in the treatment of diabetes mellitus.
J Trace Elem Exp Med
8
:
183
–190,
1995
395
Cefalu WT, Bell-Farrow AD, Stegner J, Wang ZQ, King T, Morgan, Terry JG: Effect of chromium picolinate on insulin sensitivity in vivo.
J Trace Elem Exp Med
12
:
71
–83,
1999
396
Jovanovic L, Gutierrez M, Peterson CM: Chromium supplementation for women with gestational diabetes mellitus.
J Trace Elem Exp
  Med
12
:
91
–97,
1999
397
Ravina A, Slezak L, Mirsky N, Bryden NP, Anderson RA: Reversal of corticosteroid-induced diabetes with supplemental chromium.
Diabet Med
16
:
164
–167,
1999
398
Sherman L, Glennon JA, Brech WJ, Klomberg GH, Gordon ES: Failure of trivalent chromium to improve hyperglycemia in diabetes mellitus.
Metabolism
17
:
439
–442,
1968
399
Abraham AS, Brooks BA, Eylat U: The effect of chromium supplementation on serum glucose and lipids in patients with non-insulin-dependent diabetes mellitus.
Metab Clin Exp
41
:
768
–771,
1992
400
Uusitupa M, Kumpulainen J, Voutilainen E, Sarlund H, Hersio K, Pyorala K, Koivistoinen P, Lehto J: The effect of chromium supplementation on glucose tolerance, insulin response and serum lipids in maturity onset diabetes.
Duodecim
100
:
29
–34,
1984
401
Uusitupa MI, Mykkanen L, Siitonen O, Laakso M, Sarlund H, Kolehmainen P, Rasanen T, Kumpulainen J, Pyörälä K: Chromium supplementation in impaired glucose tolerance of elderly: effects on blood glucose, plasma insulin, C-peptide and lipid levels.
Br J Nutr
68
:
209
–216,
1992
402
Song MK, Rosenthal MJ, Naliboff BD, Phanumas L, Kang KW: Effects of bovine prostate powder on zinc, glucose, and insulin metabolism in old patients with non-insulin-dependent diabetes mellitus.
Metabolism
47
:
39
–43,
1998
403
Schwartz AV, Sellmeyer DE, Ensrud KE, Cauley JA, Tabor HK, Schreiner PJ, Jamal SA, Black DM, Cummings SR: Older women with diabetes have an increased risk of fracture: a prospective study.
J Clin Endocrinol Metab
86
:
32
–38,
2001
404
Consensus conference: Osteoporosis prevention, diagnosis, and therapy.
JAMA
285
:
785
–795,
2001
405
Kanis JA: The use of calcium in the management of osteoporosis.
Bone
24
:
279
–290,
1999
406
Cohen N, Halberstam M, Schilmovich P, Chang CJ, Shamoon H, Rosetti L: Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin dependent diabetes mellitus.
J Clin Invest
95
:
2501
–2509,
1995
407
Goldfine A, Simonson D, Folli F, Patti ME, Kahn R: Metabolic effects of sodium metavanadate in humans with insulin-dependent and non-insulin dependent diabetes mellitus in vivo and in vitro studies.
J Clin Endocrinol Metab
80
:
3311
–3320,
1995
408
Verma S, Cam MC, McNeill JH: Nutritional factors which can favorably influence the glucose, insulin system: vanadium.
J Am Coll Nutr
17
:
11
–18,
1998
409
Boden G, Chen X, Ruiz J, vanRossum GD, Turco S: Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus.
Metabolism
45
:
1130
–1135,
1996
410
Vuksan V, Stavro MP, Sievenpiper JL, Beljan-Zdravkovic U, Leiter LA, Josse RG, Xu Z: Similar postprandial glycemic reductions with escalation of dose and administration time of American ginseng in type 2 diabetes.
Diabetes Care
23
:
1221
–1226,
2000
411
Vuksan V, Sievenpiper JL, Koo VY, Francis T, Beljan-Zdravkovic U, Yu Z, Vidgen E: American ginseng (Panax quinquefolius L) reduces postprandial glycemia in non-diabetic subjects and subjects with type 2 diabetes mellitus.
Arch Intern Med
160
:
1009
–1013,
2000
412
Subar AF, Krebs-Smith SM, Cook A, Kahle LL: Dietary sources of nutrients among US adults, 1989 to
1991
. J Am Diet Assoc
98
:
537
–547,
1998
413
Block G, Dresser CM, Hartman AM, Carroll MD: Nutrient sources in the American diet: quantitative data from the NHANES II survey. II. Macronutrients and fats.
Am J Epidemiol
122
:
27
–40,
1985
414
Braum-Baicker C: The health benefits of moderate alcohol consumption: a review of the literature.
Drug Alcohol Depend
15
:
207
–227,
1985
415
Rimm EB, Klatsky A, Grobbee Stumpfer MJ: Review of moderate alcohol consumption and reduced risk of coronary heart disease: is the effects due to beer, wine, or spirits?
BMJ
312
:
731
–736,
1996
416
Wannamethee SG, Shaper AG: Type of alcoholic drink and risk of major coronary heart disease events and all-cause mortality.
Am J Public Health
89
:
685
–690,
1999
417
Pownall HJ, Ballantyne CM, Kimball KT, Simpson SL, Yeshurum D, Grotto AM: Effect of moderate alcohol consumption on hypertriglyceridemia.
Arch Intern Med
159
:
981
–987,
1999
418
Frezza M, di Padova C, Pozzato G, Terpin M, Baraona E, Lieber CS: High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism.
N Engl J Med
322
:
95
–99,
1990
419
Lange J, Arends J, Willms B: Alcohol-induced hypoglycemia in type 1 diabetes.
Med Klin
86
:
551
–554,
1991
420
Arky RA, Veverbrand E, Abramson EA: Irreversible hypoglycemia: a complication of alcohol and insulin.
JAMA
206
:
575
–578,
1968
421
Gin H, Morlat P, Ragnaut JM, Aubertin J: Short-term effect of red wine (consumed during the meals) on insulin requirement and glucose tolerance in diabetic patients.
Diabetes Care
15
:
546
–548,
1992
422
Koivisto VA, Tulokas S, Toivonen M, Haapa E, Pelkonen R: Alcohol with meal has no adverse effects on postprandial glucose homeostasis in patients with diabetes.
Diabetes Care
16
:
1612
–1614,
1993
423
Ben G, Gnidi L, Maran A, Gigante A, Duner E, Iori E, Tiengo A, Avogaro A: Effects of chronic alcohol intake on carbohydrate and lipid metabolism in subjects with type II (non-insulin-dependent) diabetes.
Am J Med
90
:
70
–76,
1991
424
Feingold KR, Siperstein MD: Normalization of fasting blood glucose levels in insulin-requiring diabetes: the role of ethanol abstention.
Diabetes Care
6
:
186
–188,
1983
425
Kerr D, Macdonald IA, Heller SR, Tattersall RB: Alcohol causes hypoglycaemic unawareness in healthy volunteers and patients with type I (insulin-dependent) diabetes.
Diabetologia
33
:
216
–221,
1990
426
Franz MJ: Alcohol and diabetes. In
American Diabetes Association Medical Nutrition Therapy for Diabetes
. Franz MJ, Bantle JP, Eds. Alexandria, VA, American Diabetes Association, 1999, p. 192–208
427
Walsh CH, O’Sullivan DJ: Effect of moderate alcohol intake on control of diabetes.
Diabetes
23
:
440
–442,
1974
428
McMonagle J, Felig P: Effects of ethanol ingestion on glucose tolerance and insulin secretion in normal and diabetic subjects.
Metabolism
24
:
625
–632,
1975
429
Avogaro A, Duner E, Marescotti C, Ferrara D, Del Prato S, Nosadini R, Tiengo A: Metabolic effects of moderate alcohol intake with meals in insulin-dependent diabetics controlled by artificial endocrine pancreas (AEP) and in normal subjects.
Metabolism
32
:
463
–469,
1983
430
Singh SP, Kumar Y, Snyder AK, Ellyin FE, Gilden JL: Effect of alcohol on glucose tolerance in normal and noninsulin-dependent diabetic subjects.
Alcohol Clin Exp Res
12
:
727
–730,
1988
431
Spraul M, Chantelau E, Schonbach A-M, Berger M: Glycemic effects of beer in IDDM patients: studies with constant insulin delivery.
Diabetes Care
11
:
659
–661,
1988
432
Menzel R, Mentel DC, Brunsteil U, Heinke P: Effect of moderate ethanol ingestion on overnight diabetes control and hormone secretion in type I patients with diabetes (Abstract).
Diabetologia
34
:
A188
,
1991
433
Christiansen C, Thomsen C, Rasmussen O, Glerup H, Berthelsen H, Hansen C, Orskov H, Hermansen K: Acute effects of graded alcohol intake on glucose, insulin, and free fatty acid levels in non-insulin-dependent diabetic subjects.
Eur J Clin Nutr
47
:
648
–652,
1993
434
Christiansen C, Thomsen C, Rasmussen O, Balle M, Hauerslev C, Hansen C, Hermansen K: Wine for type 2 patients with diabetes?
Diabet Med
10
:
958
–961,
1993
435
Ajani UA, Hennekens CH, Spelsberg A, Manson JE: Alcohol consumption and risk of type 2 diabetes mellitus among US male physicians.
Arch Intern Med
160
:
1025
–1030,
2000
436
Tsumura K, Hayashi T, Suematsu C, Endo G, Fujii S, Okada K: Daily alcohol consumption and the risk of type 2 diabetes in Japanese men: the Osaka Health Study.
Diabetes Care
22
:
1432
–1437,
1999
437
Wei M, Gibbon LW, Mitchell TL, Kampert JB, Blair SN: Alcohol intake and incidence of type 2 diabetes in men.
Diabetes Care
23
:
18
–22,
2000
438
Sacco RL, Elkind M, Boden-Albala B, Lin IF, Kargman DE, Hauser WA, Shea D, Paik MC: The protective effect of moderate alcohol consumption on ischemic stroke.
JAMA
281
:
53
–60,
1999
439
Mayer EJ, Newman B, Quesenberry CP, Friedman GD, Selby JV: Alcohol consumption and insulin concentrations: role of insulin in associations of alcohol intake with high-density lipoprotein cholesterol and triglycerides.
Circulation
88
:
2190
–2197,
1993
440
Facchini F, Chen Y-D, Reaven GM: Light-to-moderate alcohol intake is associated with enhanced insulin sensitivity.
Diabetes Care
17
:
115
–119,
1994
441
Bell RA, Mayer-Davis EJ, Martin MA, D’Agostino RB, Haffner SM: Associations between alcohol consumption and insulin sensitivity and cardiovascular disease risk factors: the Insulin Resistance and Atherosclerosis Study.
Diabetes Care
23
:
1630
–1636,
2000
442
Valmadrid CT, Klein R, Moss SE, Klein BK, Cruickshanks KJ: Alcohol intake and the risk of coronary heart disease mortality in persons with older-onset diabetes mellitus.
JAMA
282
:
239
–246,
1999
443
Solomon CG, Hu FB, Stampfer MJ, Colditz GA, Speizer FE, Rimm EB, Willett WC, Manson JE: Moderate alcohol consumption and risk of coronary heart disease among women with type 2 diabetes mellitus.
Circulation
102
:
494
–499,
2000
444
Ajani UA, Gaziano M, Lotufo PA, Liu S, Hennekens CH, Buring JE, Manson JE: Alcohol consumption and risk of coronary heart disease by diabetes status.
Circulation
102
:
500
–505,
2000
445
Israelsson B: Role of alcohol, glucose intolerance and obesity in hypertriglyceridemia.
Atherosclerosis
62
:
123
–127,
1986
446
Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.
Arch Intern Med
157
:
2413
–2446,
1997
447
Tsuruta M, Adachi H, Hirai Y, Fujiura Y, Imaizumi T: Association between alcohol intake and development of hypertension in Japanese normotensive men: 12-year follow-up study.
Am J Hypertens
13
:
482
–487,
2000
448
Nanchahal K, Ashton WD, Wood DA: Alcohol consumption, metabolic cardiovascular risk factors and hypertension in women.
Int J Epidemiol
29
:
57
–64,
2000
449
Keil U, Liese A, Filipiak B, Swales JD, Grobbee DE: Alcohol, blood pressure and hypertension.
Novartis Found Symp
216
:
125
–151,
1998
450
MacMahon SW: Alcohol consumption and hypertension.
Hypertension
9
:
111
–121,
1987
451
Friedman GD, Selby JV, Quesenberry CP, Armstrong MA, Klatsky AL: Precursors of essential hypertension: body weight, alcohol and salt use, and parental history of hypertension.
Prev Med
17
:
387
–402,
1988
452
Working Group Report on Primary Prevention of Hypertension: National High Blood Pressure Education Program. U.S. Department of Health and Human Services, May 1993 (NIH publ. no. 93–2669)
453
The DCCT Research Group: Weight gain associated with intensive therapies in the Diabetes Control and Complications Trial.
Diabetes Care
11
:
567
–573,
1988
454
Wing RR, Klein R, Moss SE: Weight gain associated with improved glycemic control in population-based sample of type 1 diabetic subjects.
Diabetes Care
13
:
1106
–1109,
1990
455
Carlson MG, Campbell PJ: Intensive insulin therapy and weight gain in IDDM.
Diabetes
42
:
1700
–1707,
1993
456
Purnell JQ, Hokanson JE, Marcovina SM, Steffes MW, Cleary PA, Brunzell JD: Effect of excessive weight gain with intensive therapy of type 1 diabetes on lipid levels and blood pressure.
JAMA
280
:
140
–146,
1998
457
Williams KV, Erbey JR, Becker D, Orchard TJ: Improved glycemic control reduces the impact of weight gain on cardiovascular risk factors in type 1 diabetes.
Diabetes Care
22
:
1084
–1091,
1999
458
The DCCT Research Group: Epidemiology of severe hypoglycemia in the Diabetes Control and Complications Trial.
Am J Med
90
:
450
–459,
1990
459
Cryer PE, Fisher JN, Shamoon H: Hypoglycemia (Technical Review).
Diabetes Care
17
:
734
–755,
1994
460
Slama G, Traynard, P-Y, Desplanque N, Pudar H, Dhunputh I, Letanoux M, Bornet FRJ, Tchobroutsky G: The search for an optimized treatment of hypoglycemia: carbohydrates in tablets, solution, or gel for the correction of insulin reactions.
Arch Intern Med
150
:
589
–593,
1990
461
The American Diabetes Association: Diabetes mellitus and exercise (Position Statement).
Diabetes Care
25(Suppl. 1)
:
S64
–S68,
2002
462
Wasserman DH, Zinman B: Exercise in individuals with IDDM (Technical Review).
Diabetes Care
17
:
924
–937,
1994
463
Rabasa-Lhoret R, Bourque J, Ducros F, Chiasson J-L: Guidelines for premeal insulin dose reduction for postprandial exercise of different intensities and durations in type 1 diabetic subjects treated intensively with a basal-bolus insulin regimen (Ultralente-Lispro).
Diabetes Care
24
:
625
–630,
2001
464
Lamb DR, Brodowicz GR: Optimal use of fluids of varying formulation to minimize exercised-induced disturbances in homeostasis.
Sport Med
3
:
247
–274,
1986
465
Coyle EF, Hagberg JM, Hurley BS, Martin WH, Ehsani AA, Holloszy JO: Carbohydrate feeding during prolonged strenuous exercise can delay fatigue.
J Appl Physiol
55
:
230
–235,
1983
466
Wahren J, Felig P, Hagenfeldt PL: Physical exercise and fuel homeostasis in diabetes mellitus.
Diabetologia
14
:
213
–222,
1978
467
Ivy JL, Katz SL, Cutler CL, Sherman WM, Coyle EF: Muscle glycogen synthesis after exercise: effects of time of carbohydrate ingestion.
J Appl Physiol
64
:
1480
–1485,
1988
468
Wing RR, Blair EH, Bononi P, Marcus MD, Watanabe R, Bergman RN: Caloric restriction per se is a significant factor in improvements in glycemic control and insulin sensitivity during weight loss in obese NIDDM patients.
Diabetes Care
17
:
30
–36,
1994
469
Kelley DE, Wing R, Buonocore C, Sturis J, Polonsky K, Fitzsimmons M: Relative effects of calorie restriction and weight loss in noninsulin-dependent diabetes mellitus.
J Clin Endocrinol Metab
77
:
1287
–1293,
1993
470
Markovic TP, Jenkins AB, Campbell LV, Furler SM, Kraegen EW, Chisholm DJ: The determinants of glycemic responses to diet restriction and weight loss in obesity and NIDDM.
Diabetes Care
21
:
687
–694,
1998
471
Albright A, Franz M, Hornsby G, Kriska A, Marrero D, Ullrich I, Verity LS: American College of Sports Medicine position stand: exercise and type 2 diabetes.
Med Sci Sports Exerc
32
:
1345
–1350,
2000
472
Barnard RJ, Jung T, Inkeles S: Diet and exercise in treatment of NIDDM: the need for early emphasis.
Diabetes Care
17
:
1469
–1472,
1994
473
Wing RR, Koeske R, Epstein LH, Nowalk MP, Gooding W, Becker D: Long-term effects of modest weight loss in type II patients with diabetes.
Arch Intern Med
147
:
1749
–1753,
1987
474
Watts NB, Spanheimer RG, DiGirolamo M, Gebhart SS, Musey VC, Siddiq K, Phillips LS: Prediction of glucose response to weight loss in patients with non-insulin-dependent diabetes mellitus.
Arch Intern Med
150
:
803
–806,
1990
475
Markovic TP, Campbell LV, Balasubramanian S, Jenkins AB, Fleury AC, Simons LA, Chisholm DJ: Beneficial effect on average lipid levels from energy restriction and fat loss in obese individuals with or without type 2 diabetes.
Diabetes Care
21
:
695
–700,
1998
476
Pi-Sunyer FW: Weight loss and non-insulin dependent diabetes mellitus.
Am J Clin Nutr
63 (Suppl.):426S−429S, 1996
477
Williamson DF, Thompson TJ, Thun M, Flanders D, Pamuk E, Byers T: Intentional weight loss and mortality among overweight individuals with diabetes.
Diabetes Care
23
:
1499
–1504,
2000
478
Schneider SH, Khachadurian AK, Amorosa LF, Lemow L, Ruderman NB: Ten-year experience with exercise-based outpatient life-style modification program in the treatment of diabetes mellitus.
Diabetes Care
15
:
1800
–1810,
1992
479
Yamanouchi K, Shinozaki T, Chikada K, Nishikawa T, Ito K, Shimizu S, Ozawa N, Suzuki Y, Maeno H, Kato K, Oshida Y, Sato Y: Daily walking combined with diet therapy is a useful means for obese NIDDM patients not only to reduce body weight but also to improve insulin sensitivity.
Diabetes Care
18
:
775
–778,
1995
480
Mayer-Davis EJ, D’Agostino R Jr, Karter AJ, Haffner SM, Rewers MJ, Saad M, Bergmans RN: Intensity and amount of physical activity in relation to insulin sensitivity: the Insulin Resistance and Atherosclerosis Study (IRAS).
JAMA
279
:
669
–674,
1998
481
Hu FB, Stampfer MJ, Solomon C, Liu S, Colditz GA, Speizer FE, Willett WC, Manson JE: Physical activity and risk for cardiovascular events in diabetic women.
Ann Intern Med
134
:
96
–105,
2001
482
Wei M, Gibbons LW, Kampert JB, Nichaman MZ, Blair SN: Low cardiorespiratory fitness and physical inactivity as predictors of mortality in men with type 2 diabetes.
Ann Intern Med
132
:
605
–611,
2000
483
Arnold L, Mann J, Ball M: Metabolic effects of alterations in meal frequency in type 2 diabetes.
Diabetes Care
20
:
1651
–1654,
1997
484
Beebe CA, Van Cauter E, Shapiro T, Tillel H, Lyons R, Rubenstein A, Polonsky K: Effect of temporal distribution of calories on diurnal patterns of glucose levels and insulin secretion in NIDDM.
Diabetes Care
13
:
748
–755,
1990
485
Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D, Khoury PR, Zeitler P: Increased incidence of non-insulin-dependent diabetes mellitus among adolescents.
J Pediatr
128
:
608
–615,
1996
486
Kitagawa T, Owada M, Urakami T, Yamauchi K: Increased incidence of NIDDM among Japanese school children correlates with an increased intake of animal protein and fat.
Clin Pediatr (Phila)
37
:
111
–115,
1998
487
Dabelea D, Hanson RL, Bennett PH, Roumain J, Knowler WC, Pettitt DJ: Increasing prevalence of Type II diabetes in American Indian children.
Diabetologia
41
:
904
–910,
1998
488
Kim C, McHugh C, Kwok Y, Smith A: Type 2 diabetes mellitus in Navajo adolescents.
West J Med
170
:
210
–213,
1999
489
Wise E, Kolb E, Sauder S: Effect of glycemic control on growth velocity in children with IDDM.
Diabetes Care
15
:
826
–830,
1992
490
Danne T, Weber B, Hartman R, Enders I, Burger W, Hovener G: Long-term glycemic control has a nonlinear association to the frequency of background retinopathy in adolescents with diabetes.
Diabetes Care
17
:
1390
–1396,
1994
491
Donaghue KC, Fung A, Hing S, Fairchild J, King J, Chain A, Howard NJ, Silink M: The effect of prepubertal diabetes duration on diabetes.
Diabetes Care
20
:
77
–80,
1997
492
Weissberg-Benchell J, Glasgow AM, Tynan WD, Wirtz P, Turek J, Ward J: Adolescent diabetes management and mismanagement.
Diabetes Care
18
:
77
–82,
1995
493
Brink SJ, Moltz, K: The message of the DCCT for children and adolescents.
Diabetes Spectrum
10
:
259
–267,
1997
494
American Diabetes Association: Type 2 diabetes in children and adolescents (Consensus Statement).
Diabetes Care
23
:
381
–389,
2000
495
Food and Nutrition Board, National Research Council: Recommended Dietary Allowances, 10th ed, Washington, DC, National Academy Press, 1989, p. 285
496
Position of the American Dietetic Association: Dietary guidance for healthy children aged 2 to 11 years.
J Am Diet Assoc
99
:
93
–101,
1999
497
Expert Panel on Blood Cholesterol Levels in Children and Adolescents: Treatment recommendations of the National Cholesterol Education Program report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents.
Pediatrics
89 (Suppl.):525–584, 1992
498
U.S. Department of Agriculture:
The Food Guide Pyramid
. Hyattsville, MD, USDA Human Nutrition Information Service, 1992
499
Centers for Disease Control/National Center for Health Statistics: U.S. Growth Charts, 2000: Available from http://www.cdc.gov/growthcharts. Accessed November 2000
500
American Academy of Pediatrics Committee on Nutrition: Cholesterol in children.
Pediatrics
101
:
141
–147,
1998
501
Williams CL, Bollella M, Wynder EL: A new recommendation for dietary fiber in childhood.
Pediatrics
96
:
985
–988,
1995
502
Andersen RE, Crespo CJ, Bartlett SJ, Cheskin LJ, Pratt M: The relationship of physical activity and television watching with body weight and level of fatness among children.
JAMA
279
:
938
–942,
1998
503
Austin A, Warty V, Janosky J, Arslanian S: The relationship of physical fitness to lipid and lipoprotein(a) levels in adolescents with IDDM.
Diabetes Care
16
:
421
–425,
1993
504
Ferguson MA, Gutin B, Le N-A, Karp W, Litaker M, Humphries M, Okuyama T, Riggs S, Owens S: Effects of exercise training and its cessation on components of the insulin resistance syndrome in obese children.
Int J Obes Relat Metab Disord
23
:
889
–895,
1999
505
McClain MR, Srinivassan SR, Chen W, Steinmann WC, Berenson GS: Risk of type 2 diabetes mellitus in young adults from a biracial community: the Bogalusa Heart Study.
Prev Med
31
:
1
–7,
2000
506
Cogswell ME, Serdula MK, Hungerford DW, Yip R: Gestational weight gain among average-weight and overweight women. What is excessive?
Am J Obstet Gynecol
172
:
705
–712,
1995
507
Edwards LE, Hellerstedt WL, Alton IR, Story M, Himes JH: Pregnancy complications and birth outcomes in obese and normal-weight women: effects of gestational weight change.
Obstet Gynecol
87
:
389
–394,
1996
508
Food and Nutrition Board: Recommended Dietary Allowances. 10th ed. Washington, DC, National Academy of Sciences, 1989, p. 59–62
509
Durnin JVGA: Energy requirements of pregnancy.
Diabetes
40(Suppl. 2)
:
152
–156,
1991
510
Kaplan JS, Iqbal S, England BG, Zawacki CM, Herman WH: Is pregnancy in diabetic women associated with folate deficiency?
Diabetes Care
22
:
1017
–1021,
1999
511
ACOG Committee on Obstetrics: Folic acid and the prevention of recurrent neural tube defects.
Int J Gynaecol Obstet
42
:
75
–77,
1993
512
Department of Health and Human Services, Public Health Service: Recommendation for the use of folic acid to reduce the number of cases of spina bifida and other neural tube defects.
MMWR Morb Mortal Wkly Rep
41(RR-14):1–7, 1992
513
Czeizel AE: Prevention of congenital abnormalities by periconceptional multivitamin supplementation.
BMJ
306
:
1645
–1648,
1993
514
Shaw GM, Lammer EJ, Wasserman CR, O’Malley CD, Tolarova MM: Risks of orofacial clefts in children born to women using multivitamins containing folic acid periconceptually.
Lancet
346
:
393
–397,
1995
515
Scholl TO, Hediger ML, Schall JI, Fischer RL, Khoo CS: Low zinc intake during pregnancy: its association with preterm and very preterm delivery.
Am J Epidemiol
137
:
1115
–1124,
1993
516
Goldenberg RL, Tamura T, Neggers Y, Copper RL, Johnston KE, Du Bard MB, Hauth JC: The effect of zinc supplementation on pregnancy outcome.
JAMA
274
:
463
–468,
1995
517
American Dietetic Association: Position of the American Dietetic Association: Use of nutritive and nonnutritive sweeteners.
J Am Diet Assoc
98
:
580
–587,
1998
518
The American Dietetic Association:
Nutrition Practice Guidelines for Gestational Diabetes Mellitus
. Available from http://eatright.com. Accessed October 2001
519
Pitkin RM, Reynolds WA, Filer LJ, Kling TG: Placental transmission and fetal distribution of saccharin.
Am J Obstet Gynecol
111
:
280
–286,
1971
520
London RS, Rorick Jr, JT: Safety evaluation in pregnancy. In
The Clinical Evaluation of a Food Additive: Assessment of Aspartame
. Tschanz C, Butchko HH, Stargel WW, Kotsonis FN, Eds. New York, Marcel Dekker, 2001, p. 115–123
521
Pitkin RM: Aspartame ingestion during pregnancy. In Aspartame. Stegink LD, Filer LJ, Eds. New York, Marcel Dekker, 1984, p. 555–563
522
Sturtevant FM: Use of aspartame during pregnancy (Review).
Int J Fertil
30
:
85
–87,
1985
523
London R: Saccharin and aspartame. Are they safe to consume during pregnancy?
J Reprod Med
33
:
17
–21,
1988
524
Grice HC, Goldsmith LA: Sucralose: an overview of the toxicity data.
Food Chem
  Toxicol
38(Suppl. 2)
:
S1
–S6,
2000
525
The Diabetes Control and Complications Trial Research Group: Pregnancy outcomes in the Diabetes Control and Complications Trial.
Am J Obstet Gynecol
174
:
1343
–1353,
1996
526
Gestational diabetes. ACOG Practice Bulletin No. 30. American College of Obstetricians and Gynecologists.
Obstet Gynecol
98
:
525
–538,
2001
527
Rizzo T, Metzger BE, Burns WJ, Burns K: Correlations between antepartum maternal metabolism and intelligence of offspring.
N Engl J Med
325
:
911
–916,
1991
528
Rizzo TA, Dooley SL, Metzger BE, Cho NH, Ogata ES, Silverman BL: Prenatal and perinatal influences on long-term psychomotor development in offspring of diabetic mothers.
Am J Obstet Gynecol
173
:
1753
–1758,
1995
529
American Diabetes Association: Proceedings of the Fourth International Workshop: Conference on Gestational Diabetes Mellitus.
Diabetes Care
21(Suppl. 2)
:
B161
−B167, 1998
530
McFarland MB, Langer O, Conway DL, Berkus MD: Dietary therapy for gestational diabetes. How long is long enough?
Obstet Gynecol
93
:
978
–982,
1999
531
Mello G, Parretti E, Mecacci F, Carbone C, Lucchetti R, Lagazio C, Pratesi M, Scarselli G: Anthropometric features in infants of mothers with gestational diabetes: relationship with treatment modalities.
Biol Neonate
72
:
22
–27,
1997
532
Langer O, Conway DL, Backus MD, Xenakis EMJ, Gonzales O: The comparison of glyburide and insulin in women with gestational diabetes.
N Engl J Med
343
:
1134
–1138,
2000
533
Garcia-Patterson A, Corcoy R, Balsells M, Altirriba O, Adelantado JM, Cabero L, De Leiva A: In pregnancies with gestational diabetes mellitus and intensive therapy, perinatal outcome is worse in small-for-gestational-age newborns.
Am J Obstet Gynecol
179
:
481
–485,
1998
534
Peterson CH, Jovanovic-Peterson L: Percentage of carbohydrate and glycemic response to breakfast, lunch, and dinner in women with gestational diabetes.
Diabetes
40(Suppl. 2)
:
172
–174,
1991
535
Major CA, Henry MJ, DeVeciana M, Morgan MA: The effects of carbohydrate restriction in patients with diet-controlled gestational diabetes.
Obstet Gynecol
91
:
600
–604,
1998
536
Jovanovic-Peterson L, Peterson CM: Dietary manipulation as primary treatment strategy for pregnancies complicated by diabetes.
J Am Coll Nutr
9
:
320
–325,
1990
537
Clapp JF: Effect of dietary carbohydrate on the glucose and insulin response to mixed caloric intake and exercise in both nonpregnant and pregnant women.
Diabetes Care
21(Suppl. 2)
:
B107
−B112, 1998
538
Gunderson EP: Intensive nutrition therapy for gestational diabetes: rationale and current issues.
Diabetes Care
20
:
221
–226,
1997
539
Maggee MS, Knopp RH, Benedetti TJ: Metabolic effects of 1200 kcal diet in obese pregnant women with gestational diabetes.
Diabetes
39
:
234
–240,
1990
540
Knopp RH, Magee MS, Raisys V, Benedetti T, Bonet B: Hypocaloric diets and ketogenesis in the management of obese gestational diabetic women.
J Am Coll Nutr
10
:
649
–667,
1991
541
Snyder J, Gray-Donald K, Koski KG: Predictors of infant birth weight in gestational diabetes.
Am J Clin Nutr
59
:
1409
–1414,
1994
542
Jovanovic-Peterson L (Ed.):
Medical Management of Pregnancy Complicated by Diabetes
. 3rd ed. Alexandria, VA, American Diabetes Association, 2000
543
Avery MD, Leon AS, Kopher RA: Effects of a partially home-based exercise program for women with gestational diabetes.
Obstet Gynecol
89
:
10
–15,
1997
544
Combs CA, Gunderson E, Kitzmiller JL, Gavin LA, Main EK: Relationship of fetal macrosomia to maternal postprandial glucose control during pregnancy.
Diabetes Care
15
:
1251
–1257,
1992
545
De Veciana M, Major CA, Morgan MA, Asrat T, Toohey JS, Lien JM, Evans AT: Postprandial versus preprandial blood glucose monitoring in women with gestational diabetes mellitus requiring insulin therapy.
N Engl J Med
333
:
1237
–1241,
1995
546
Gunderson E, Adams B: Epidemiology of gestational weight gain and body weight change after pregnancy.
Epidemiol Rev
21
:
261
–275,
1999
547
Murtaugh MA, Ferris AM, Capacchione CM, Reese EA: Energy intake and glycemia in lactating women with type 1 diabetes.
J Am Diet Assoc
98
:
642
–648,
1998
548
American Diabetes Association: Gestational diabetes mellitus (Position Statement).
Diabetes Care
25(Suppl. 1)
:
S94
–S96,
2002
549
Institute of Medicine: Nutrition During Lactation. Washington, DC, National Academy Press, 1991
550
Mooradian AD: Biology of aging. In Rehabilitation of the Aging and Elderly Patient. Felsenthal G, Garrison SJ, Steinberg FU, Eds. Baltimore, MD, Williams & Wilkins, 1994, p. 3–10
551
Reed RL, Mooradian AD: Nutritional status and dietary management of elderly patients with diabetes.
Clin Geriatr Med
6
:
883
–901,
1990
552
Mooradian AD, McLaughlin S, Boyer CC, Winter J: Diabetes care for older adults.
Diabetes Spectrum
12
:
70
–77,
1999
553
Millward DJ, Fereday A, Gibson N, Pacy PJ: Aging, protein requirements and protein turnover.
Am J Clin Nutr
66
:
774
–786,
1997
554
Roberts SB, Fuss P, Heyman MB, Young VR: Influence of age on energy requirements.
Am J Clin Nutr
62 (Suppl.):1053S−1058S, 1995
555
Visser M, Deurenberg P, van Staveren WA, Hautrat JG: Resting metabolic rate and diet-induced thermogenesis in young and elderly subjects: relationship with body composition, fat distribution, and physical activity level.
Am J Clin Nutr
61
:
772
–778,
1995
556
Mooradian AD, Osterweil D, Petrasek D, Morley JE: Diabetes mellitus in elderly nursing home patients: a survey of clinical characteristics and management.
J Am Geriatr Soc
36
:
391
–396,
1988
557
Morley JE, Mooradian AD, Silver AJ, Heber D, Alfin-Slater RB: Nutrition in the elderly.
Ann Intern Med
109
:
890
–904,
1988
558
Morais JA, Gougeon R, Pencharz PB, Jones PJ, Ross R, Marlish EM: Whole body protein turnover in the healthy elderly.
Am J Clin Nutr
66
:
880
–889,
1997
559
Toth MJ, Arciero PJ, Gardner AW, Calles-Escandon J, Poehlman ET: Rates of free fatty acid appearance and fat oxidation in healthy younger and older men.
J Appl Physiol
80
:
506
–511,
1996
560
Roberts SB, Fuss P, Dallal GE, Atkinson A, Evans WJ, Joseph L, Fiatarone MA, Greenberg AS, Young VR: Effects of age on energy expenditure and substrate oxidation during experimental overfeeding in healthy men.
J Gerontol
51
:
B142
–B157,
1996
561
Roberts SB, Fuss P, Heyman MB, Dallal GE, Young VR: Effects of age on energy expenditure and substrate oxidation during experimental underfeeding in healthy men.
J Gerontol
51
:
B158
–B166,
1996
562
Coulston AM, Mandelbaum D, Reaven GM: Dietary management of nursing home residents with non-insulin dependent diabetes mellitus.
Am J Clin Nutr
51
:
62
–71,
1990
563
American Diabetes Association: Translation of the diabetes nutrition recommendations for health care institutions.
Diabetes Care
25(Suppl. 1)
:
S61
–S63,
2002
564
Schafer R, Bohannon B, Franz MJ, Freeman J, Holmes A, McLaughlin S, Haas L, Kruger D, Lorenz R, McMahon M: Translation of the diabetes nutrition recommendations for health care institutions (Technical Review).
Diabetes Care
20
:
96
–105,
1997
565
Pannemans DL, Van den Berg H, Westerterp KR: The influence of protein intake on Vitamin B6 metabolism differs in young and elderly humans.
J Nutr
124
:
1207
–1214,
1994
566
Lindenbaum J, Rosenberg IH, Wilson PWF, Stabler SP, Allen RH: Prevalence of cobalamin deficiency in the Framingham elderly population.
Am J Clin Nutr
60
:
2
–11,
1994
567
Koehler KM, Pareo-Tubbeh SL, Romero LJ, Baumgartner RN, Garry PJ: Folate nutrition and older adults: challenges and opportunities.
J Am Diet Assoc
97
:
167
–173,
1997
568
Lindeman RD, Romero LJ, Kohler KM, Liang HC, LaRue A, Baumgartner RN, Garry PJ: Serum Vitamin B12, C and folate concentrations in the New Mexico elder health survey: correlations with cognitive and affective functions.
J Am Coll Nutr
19
:
68
–76,
2000
569
Selhub J, Jacques PF, Wilson PWF, Rush D, Rosenberg IH: Vitamin status and intake as primary determinants of homocysteinemia in an elderly population.
JAMA
270
:
2693
–2698,
1993
570
Lindenbaum J, Healton EB, Savage DG, Brust JC, Garrett TJ, Podell ER, Marcell PD, Stabler SP, Allen RH: Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocystosis.
N Engl J Med
318
:
1720
–1728,
1988
571
Kinyamu HK, Gallagher JC, Balhorn KE, Petranick KM, Rafferty KA: Serum vitamin D metabolites and calcium absorption in normal young and elderly free living women and women living in nursing homes.
Am J Clin Nutr
65
:
790
–797,
1992
572
Volkert D, Kruse W, Oster P, Schlierf G: Malnutrition in geriatric patients: diagnostic and prognostic significance of nutritional parameters.
Ann Nutr Metab
36
:
97
–112,
1992
573
Hallfrisch J, Muller DC: Does diet provide adequate amounts of calcium, iron, magnesium and zinc in a well educated adult population?
Exp Gerontol
28
:
473
–483,
1993
574
Hallfrisch J, Muller DC, Singh VN: Vitamin A and E intakes and plasma concentrations of retinal, beta-carotene and alpha tocopherol in men and women of the Baltimore Longitudinal Study of Aging.
Am J Clin Nutr
60
:
176
–182,
1994
575
Selhub J, Jacques PF, Bostom AG, D’Agostino RB, Wilson PW, Belanger AJ, O’Leary DH, Wolf PA, Schaefer EJ, Rosenberg IH: Association between plasma homocysteine concentrations and extracranial carotid artery disease.
N Engl J Med
332
:
286
–291,
1995
576
Amato P, Morales AJ, Yen SSC: Effects of chromium picolinate supplementation on insulin sensitivity, serum lipids, and body composition in healthy, nonobese older men and women.
J Gerontol
55A
:
M250
–M263,
2000
577
Hagberg JM: Effect of training on the decline of Vo2max with aging.
Fed Proc
46
:
1830
–1833,
1987
578
LaCroix AZ, Leveille SG, Hecht JA, Grothaus LC, Wagner EH: Does walking decrease the risk of cardiovascular disease hospitalizations and death in older adults?
J Am Geriatr Soc
44
:
113
–120,
1996
579
Schwartz RS: Exercise training in treatment of diabetes mellitus in elderly patients.
Diabetes Care
13 (Suppl 2):77–85, 1990
580
Clark WL, Cox DJ, Gonder-Frederick L, Julian D, Kovatchev B, Young-Hyman D: Biopsychobehavioral model of risk of severe hypoglycemia.
Diabetes Care
22
:
580
–584,
1999
581
Brodows RG, Williams C, Amatruda JM: Treatment of insulin reactions in diabetics.
JAMA
252
:
3378
–3381,
1984
582
Wiethop BV, Cryer PE: Alanine and terbutaline in the treatment of hypoglycemia in IDDM.
Diabetes Care
16
:
1131
–1136,
1993
583
Schvarcz E, Palmer M, Aman J, Berne C: Hypoglycemia increases the gastric emptying rate in healthy subjects.
Diabetes Care
18
:
674
–676,
1995
584
Levy CJ, Kinsley BT, Bajaj M, Simonson DC: Effect of glycemic control on glucose counterregulation during hypoglycemia in NIDDM.
Diabetes Care
21
:
1330
–1338,
1998
585
Dinneen S, Gerich J, Rizza: Carbohydrate metabolism in non-insulin-dependent diabetes mellitus.
N Engl J Med
327
:
707
–713,
1992
586
Owen OE, Morgan AP, Kemp HG, Sullivan JM, Herrara MG, Cahill GF: Brain metabolism during fasting.
J Clin Invest
46
:
1589
–1595,
1967
587
Cahill GF, Owen OE, Felig P: Insulin and fuel homeostasis.
Physiologist
11
:
97
–102,
1968
588
Macdonald I: Metabolic requirements for dietary carbohydrate.
Am J Clin Nutr
45
:
1193
–1195,
1987
589
Whelton PK, Appel LJ, Espeland MA, Applegate WB, Ettinger WH Jr, Kostis JB, Kumanyika S, Lacy CR, Johnson KC, Folmar S, Cutler JA, the TONE Collaborative Research Group: Sodium restriction and weight loss in the treatment of hypertension in older person: a randomized controlled trial of nonpharmacologic intervention in the elderly.
JAMA
279
:
839
–846,
1998
590
Wylie-Rosett J, Wassertheil-Smoller S, Blaufox MD, Davis BR, Langford HG, Oberman A, Jennings S, Hataway H, Stern J, Zimbaldi N: Trial of Antihypertensive Intervention and Management: a greater efficacy with weight reduction than with a sodium-potassium intervention.
J Am Diet Assoc
93
:
408
–414,
1993
591
Wassertheil-Smoller S, Blaufox D, Oberman A, Langford HG: Adequate weight loss alone and combined with drug therapy in the treatment of mild hypertension.
Arch Intern Med
152
:
131
–136,
1993
592
Trial of Hypertension Prevention Collaborative Research Group: The effects on nonpharmacological intervention on blood pressure of persons with high normal blood levels: results of the Trial of Hypertension Prevention Phase I.
JAMA
267
:
1213
–1220,
1992
593
Kaplan NM: Evidence in favor of moderate sodium reduction.
Am J Hypertens
13
:
8
–13,
2000
594
Kotchen TA, Kotchen JM: Dietary sodium and blood pressure: interactions with other nutrients.
Am J Clin Nutr
65 (Suppl.):708S−711S, 1997
595
Hamet P, Mongeau E, Lambert J, Bellavance F, Daignault-Gelinas M, Ledour M: Interactions among calcium, sodium, and alcohol intake as determinants of blood pressure.
Hypertension
17(Suppl. 1)
:
I150
–I154,
1991
596
Whelton PK, He J, Cutler JA, Brancati FL, Appel LJ, Follmann D, Klag MJ: Effects of oral potassium on blood pressure: meta-analysis of randomized controlled clinical trials.
JAMA
277
:
1624
–1632,
1997
597
Hamet P: The evaluation of the scientific evidence for a relationship between calcium and hypertension.
J Nutr
125 (Suppl.):311S−411S, 1995
598
Resnick LM: Dietary calcium and hypertension.
J Nutr
117
:
1806
–1808,
1987
599
Gruchow HW, Sobocinski KA, Barboriak JJ: Calcium intake and the relationship of dietary sodium and potassium to blood pressure.
Am J Clin Nutr
48
:
1463
–1470,
1988
600
McCarron DA, Reusser ME: Nonpharmacologic therapy in hypertension: from single components to overall dietary management.
Prog Cardiovasc Dis
41
:
451
–460,
1999
601
Tuck M, Corry D, Trujillo A: Salt-sensitive blood pressure and exaggerated vascular reactivity in the hypertension of diabetes mellitus.
Am J Med
88
:
210
–216,
1991
602
Imanishi M, Yoshioka K, Okumura M, Konishi Y, Okada N, Morikawa T, Sato T, Tanaka S, Fujii S: Sodium sensitivity related to albuminuria appearing before hypertension in type 2 patients with diabetes.
Diabetes Care
24
:
111
–116,
2001
603
Cutler JA, Follmann D, Allender PS: Randomized trials of sodium reduction: an overview.
Am J Clin Nutr
65(Suppl. 1)
:
643S
−651S, 1997
604
Midgley JP, Matthew AG, Greenwood CMT, Logan AG: Effect of reduced dietary sodium on blood pressure: a meta-analysis of randomized controlled trials.
JAMA
275
:
1590
–1597,
1996
605
Alam S, Johnson AG: A meta-analysis of randomised controlled trials (RCT) among healthy normotensive and essential hypertensive elderly patients to determine the effect of high salt (NaCl) diet on blood pressure.
J Hum Hypertens
13
:
367
–374,
1999
606
Sacks FM, Obarzanek E, Windhauser MM, Svetkey LP, Vollmer WM, McCullough M, Karanja N, Lin PH, Steele P, Proschan MA: Rationale and design of the Dietary Approaches to Stop Hypertension trial (DASH): a multi-center controlled-feeding study of dietary patterns to lower blood pressure.
Ann Epidemiol
5
:
108
–118,
1995
607
Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetky LP, Sacks FM, Bray GA, Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N, the DASH Collaborative Research Group: A clinical trial of the effects of dietary pattern on blood pressure.
N Engl J Med
336
:
1117
–1124,
1997
608
Svetkey LP, Simons-Morton D, Vollmer WM, Appel LJ, Conlin PR, Ryan DH, Ard J, Kennedy BM for the DASH Collaborative Research Group: Effects of dietary patterns of blood pressure: subgroup analysis of the Dietary Approaches to Stop Hypertension (DASH) randomized clinical trial.
Arch Intern Med
159
:
285
–293,
1999
609
Sacks FM, Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Bray GA: Dietary approaches to prevent hypertension: a review of the Dietary Approaches to Stop Hypertension (DASH) Study.
Clin Cardiol
22 (Suppl.):III6−10, 1999
610
Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER, Simons-Morton DG, Karanja N, Lin P-H for the DASH-Sodium Collaborative Research Group: Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet.
N Engl J Med
344
:
3
–10,
2001
611
Staessen J, Fagard R, Lijnen P, Amery A: Body weight, sodium intake, and blood pressure.
J Hypertens
7 (Suppl.):S19−S23, 1989
612
Puddey IB, Beilin LJ, Vandongen R, Rouse IL, Rogers P: Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men: a randomized controlled trial.
Hypertension
7
:
707
–713,
1985
613
Puddey IB, Beilin LJ, Vandongen R: Regular alcohol use raises blood pressure in treated hypertensive subjects: a randomized controlled trial.
Lancet
i
:
647
–651,
1987
614
World Hypertension League: Alcohol and hypertension: implications for management. A consensus statement by the World Hypertension League.
J Hum Hypertens
5
:
227
–232,
1991
615
Allender PS, Cutler JA, Follmann D, Cappuccio PP, Pryer J, Elliott P: Dietary calcium and blood pressure: a meta-analysis of randomized clinical trials.
Ann Intern Med
124
:
825
–831,
1996
616
Feingold KR, Grunfield C, Pang M, Doerrler W, Krauss RM: LDL subclass phenotypes and triglyceride metabolism in non-insulin-dependent diabetes.
Arterioscler Thromb Vasc Biol
12
:
1496
–1502,
1992
617
Selby JV, Austin MA, Newman B, Zhang D, Quesenberry CP Jr, Mayer EF, Krauss RM: LDL subclass phenotypes and the insulin resistance syndrome in women.
Circulation
88
:
381
–387,
1993
618
Haffner SM, Mykkanen L, Stern MP, Paidi M, Howard BV: Greater effect of diabetes on LDL size in women than in men.
Diabetes Care
17
:
1164
–1171,
1994
619
Singh AT, Rainwater DL, Haffner SM, VandeBerg JL, Shelledy WR, Moore PH Jr, Dyer TD: Effect of diabetes on lipoprotein size.
Arterioscler Thromb Vasc Biol
15
:
1805
–1811,
1995
620
Siegel RD, Cupples A, Schaefer EJ, Wilson PW: Lipoproteins, apolipoproteins, and low-density lipoprotein size among diabetics in the Framingham offspring study.
Metabolism
45
:
1267
–1272,
1996
621
Temelkova-Kurktschiev T, Hanefeld M, Leonhardt W: Small dense low-density lipoprotein (LDL) in non-insulin-dependent diabetes mellitus (NIDDM): impact of hypertriglyceridemia.
Ann N Y Acad Sci
827
:
279
–286,
1997
622
Fujimoto WY, Abbate SL, Kahn SE, Hokanson JE, Brunzell JD: The visceral adiposity syndrome in Japanese-American men.
Obes Res
2
:
364
–371,
1994
623
Tchernof A, Lamarche B, Prud’Homme D, Nadeau A, Moorjani S, Labrie F, Lupian PJ: The dense LDL phenotype: association with plasma lipoprotein levels, visceral obesity, and hyperinsulinemia in men.
Diabetes Care
19
:
629
–637,
1996
624
Rönnemaa T, Mattila K, Lehtonen A, Kallio V: A controlled randomized study on the effect of long-term physical exercise on metabolic control in type 2 patients.
Acta Med Scand
220
:
219
–224,
1986
625
Weinsier RL, Seeman A, Herrera MG, Assal JP, Soeldner JS, Gleason RE: High- and low-carbohydrate diets in diabetes mellitus: study of effects on diabetic control, insulin secretion, and blood lipids.
Ann Intern Med
80
:
332
–341,
1974
626
Kiehm TG, Anderson TW, Ward K: Beneficial effects of a high carbohydrate, high fiber diet on hyperglycemic diabetic men.
Am J Clin Nutr
29
:
895
–899,
1976
627
Anderson JW, Ward K: High-carbohydrate, high fiber diets for insulin-treated men with diabetes mellitus.
Am J Clin Nutr
32
:
2312
–2321,
1979
628
Howard BV, Abbott WG, Swinburn BA: Evaluation of metabolic effects of substitution of complex carbohydrates for saturated fat in individuals with obesity and NIDDM.
Diabetes Care
14
:
786
–795,
1991
629
Coulston AM, Hollenbeck CB, Swislocki ALM, Chen Y-DI, Reaven G: Deleterious metabolic effects of high-carbohydrate, sucrose-containing diets in patients with non-insulin-dependent diabetes mellitus.
Am J Med
82
:
213
–220,
1987
630
Coulston AM, Hollenbeck CB, Swislocki ALM, Reaven GM: Persistence of hypertriglyceridemic effect of low-fat high-carbohydrate diets in NIDDM patients.
Diabetes Care
12
:
94
–101,
1989
631
Grundy SM, Baldy GJ, Criqui MH, Fletcher G, Greenland P, Hiratzka LF, Houston-Miller N, Kris-Etherton P, Krumholz HM, LaRosa J, Ockene IS, Pearson TA, Reed J, Smith SC, Washington R: When to start cholesterol-lowering therapy in patients with coronary heart disease: a statement for healthcare professionals from the American Heart Association task force on risk reduction.
Circulation
95
:
1683
–1685,
1997
632
Pyorala K, Pedersen TR, Kjekshus J, Faergeman O, Olsson AG, Thorgeirsson G: Cholesterol lowering with simvastatin improves prognosis of patients with diabetes with coronary heart disease.
Diabetes Care
20
:
614
–620,
1997
633
Goldberg RB, Mellies MJ, Sacks FM, Moye LA, Howard BV, Howard WJ, Davis BR, Cole TG, Pfeffer MA, Braunwald E: Cardiovascular events and their reduction with pravastatin in diabetic and glucose-intolerant myocardial infarction survivors with average cholesterol levels: subgroup analyses in the cholesterol and recurrent events (CARE) trial. The Care Investigators.
Circulation
98
:
2513
–2519,
1998
634
Elkeles RS, Diamond JR, Poulter C, Dhanji S, Nicolaides AN, Mahmood S, Richmond W, Mather H, Sharp P, Feher MD: Cardiovascular outcomes in type 2 diabetes: a double-blind placebo- controlled study of bezafibrate. The St. Mary’s, Ealing, Northwick Park Diabetes Cardiovascular Disease Prevention (SENDCAP) Study.
Diabetes Care
21
:
641
–648,
1998
635
Chait A, Brunzell JD: Chylomicronemia syndrome.
Adv Intern Med
37
:
249
–273,
1992
636
Santamarina-Fojo S: The familial chylomicronemia syndrome.
Endocrinol Metab Clin North Am
27
:
551
–567, viii, 1998
637
Elam MB, Hunninghake DB, Davis KB, Garg R, Johnson C, Egan D, Kostis JB, Sheps DS, Brinton EA: Effect of niacin on lipid and lipoprotein levels and glycemic control in patients with diabetes and peripheral arterial disease. The ADMIT study: a randomized trial. Arterial Disease Multiple Intervention Trial.
JAMA
284
:
1263
–1270,
2000
638
American Diabetes Association: Diabetic nephropathy (Position Statement).
Diabetes Care
25(Suppl. 1)
:
S85
–S89,
2002
639
Tapp DC, Wortham WG, Addison JF, Hammonds DN, Barnes JL, Venkatachalam MA: Food restriction retards body growth and prevents end-stage renal pathology in remnant kidneys of rats regardless of protein intake.
Lab Invest
60
:
184
–194,
1989
640
Kobayashi S, Venkatachalam MA: Differential effects of caloric restriction on glomeruli and tubules of the remnant kidney.
Kidney Int
42
:
710
–717,
1992
641
Allen TJ, Waldron MJ, Casley D, Jerums G, Cooper ME: Salt restriction reduces hyperfiltration, renal enlargement and albuminuria in experimental diabetes.
Diabetes
46
:
19
–24,
1997
642
Craven PA, DeRubertis FR, Kagan VE, Melhem M, Studer RK: Effects of supplementation with vitamin C or E on albuminuria, glomerular TGF-β1, and glomerular size in diabetes.
J Am Soc Nephrol
8
:
1405
–1411,
1997
643
Koya D, Lee IK, Ishii H, Kanoh H, King GL: Prevention of glomerular dysfunction in diabetic rats by treatment of d-α-tocopherol.
J Am Soc Nephrol
8
:
426
–435,
1997
644
Bouhanick B, Suraniti S, Berrut G, Bled F, Simard G, Lejeune JJ, Fressinaud P, Marre M: Relationship between fat intake and glomerular filtration rate in normotensive insulin-dependent patients with diabetes.
Diabetes Metab
21
:
168
–172,
1995
645
Pijls LTJ, deVries H, Donker AJM, vanEijk JTM: The effect of protein restriction on albuminuria in patients with type 2 diabetes mellitus: a randomized trial.
Nephrol Dial Transplant
14
:
1445
–1453,
1999
646
Pomerleau J, Verdy M, Garrel DR, Nadeau MH: Effect of protein intake on glycaemic control and renal function in type 2 (non-insulin-dependent) diabetes mellitus.
Diabetologia
36
:
829
–834,
1993
647
Hansen HP, Christensen PK, Tauber-Lassen E, Klausen A, Jenen BR, Parving HH: Low-protein diet and kidney function in insulin-dependent patients with diabetes with diabetic nephropathy.
Kidney Int
55
:
621
–628,
1999
648
Dullaart RPF, vanDoormaal JJ, Beusekamp BJ, Sluiter WJ, Meijer S: Long-term effects of protein-restricted diet on albuminuria and renal function in IDDM patients without clinical nephropathy and hypertension.
Diabetes Care
2
:
483
–492,
1993
649
Raal FJ, Kalk WJ, Lawson M, Esser JD, Buys R, Fourie L, Panz VR: Effect of moderate dietary protein restriction on the progression of overt diabetic nephropathy: a 6-month prospective study.
Am J Clin Nutr
60
:
579
–585,
1994
650
Ciavarella A, DiMizio G, Stefoni S, Borgnino LC, Vannini P: Reduced albuminuria after dietary protein restriction in insulin-dependent patients with diabetes with clinical nephropathy.
Diabetes Care
10
:
407
–413,
1987
651
Zeller K, Whittaker E, Sullivan L, Raskin P, Jacobson HR: Effect of restricting dietary protein on the progression of renal failure in patients with insulin-dependent diabetes mellitus.
N Engl J Med
324
:
78
–84,
1991
652
Walker JD, Bending JJ, Dodds RA, Mattock MB, Murrells TJ, Keen H, Viberti GC: Restriction of dietary protein and progression of renal failure in diabetic nephropathy.
Lancet
i 
i
:
1411
–1415,
1989
653
Pecis M, DeAzevedo MJ, Gross JL: Chicken and fish diet reduces glomerular hyperfiltration in IDDM patients.
Diabetes Care
17
:
665
–672,
1994
654
Jibani MM, Bloodworth LL, Foden E, Griffiths KD, Galpin OP: Predominantly vegetarian diet in patients with incipient and early clinical diabetic nephropathy: effects on albumin excretion rate and nutritional status.
Diabet Med
8
:
949
–953,
1991
655
Barsotti G, Ciardella F, Morelli E, Cupisti A, Mantovanelli A, Giovannetti S: Nutritional treatment of renal failure in type 1 diabetic nephropathy.
Clin Nephrol
29
:
280
–287,
1988
656
Kontessis PS, Trevisan R, Bossinakou I, Roussi D, Sarika L, Stipsanelli K, Iliopoulou E, Grigorakis S, Papantoniou A, Souvatzoglou A: Renal, metabolic, and hormonal responses to proteins of different origin in normotensive, nonproteinuric type 1 diabetic subjects.
Diabetes Care
18
:
1233
–1240,
1995
657
McMahon MM, Farnell MB, Murray MJ: Nutritional support of critically ill patients.
Mayo Clin Proc
68
:
911
–920,
1993
658
Wilmore DW: Catabolic illness: strategies of enhancing recovery.
N Engl J Med
325
:
695
–702,
1991
659
McMahon MM: Nutrition support and diabetes. In
American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes
. Franz MJ, Bantle JP, Eds. Alexandria, VA, American Diabetes Association, 2000, p. 335–348
660
Peters AL, Davidson MB: Effects of various enteral feeding products on postprandial blood glucose response in patients with type 1 diabetes.
JPEN J Parenter Enteral Nutr
16
:
69
–74,
1992
661
Harris MI, Hadden WC, Knowler WC, Bennett PH: Prevalence of diabetes and impaired glucose tolerance and plasma glucose levels in the US population aged 20–74 years.
Diabetes Care
36
:
523
–534,
1987
662
Harris MI, Flegal KM, Cowie CC, Eberhardt MS, Goldstein DE, Little RR, Wiedmeyer HM, Byrd-Holt DD: Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in US adults: the Third National Health and Nutrition Examination Survey, 1988–
1994
. Diabetes Care
21
:
518
–524,
1998
663
Mokdad AH, Bowman BA, Ford ES, Vinicor F, Marks JS, Koplan JP: The continuing epidemics of obesity and diabetes in the United States.
JAMA
12
:
1195
–1200,
2001
664
Edelstein SL, Knowler WC, Bain RP, Andres R, Barrett-Connor EL, Dowse GK, Haffner SM, Pettitt DJ, Sorkin JD, Muller DC, Collins VR, Hamman RF: Predictors of progression from impaired glucose tolerance to NIDDM: an analysis of six prospective studies.
Diabetes
46
:
701
–710,
1997
665
Kuczmarski RJ, Flegal KM, Campbell SM, Johnson CL: Increasing prevalence of overweight among US adults: the National Health and Nutrition Examination Surveys, 1960 to
1991
. JAMA
272
:
205
–211,
1994
666
Eriksson J, Lindstrom J, Valle T, Aunola S, Hamalainen H, Ilanne-Parikka P, Keinanen-Kiukaanniemi S, Laakso M, Lauhkonen M, Lehto P, Lehtonen A, Louheranta A, Mannelin M, Martikkala V, Rastas M, Sundvall J, Turpeinen A, Viljanen T, Uusitupa M, Tuomilehto J: Prevention of Type II diabetes in subjects with impaired glucose tolerance: the Diabetes Prevention Study (DPS) in Finland. Study design and 1-year interim report on the feasibility of the lifestyle intervention program.
Diabetologia
42
:
793
–801,
1999
667
Wing RR: Physical activity in the treatment of adulthood overweight and obesity: current evidence and research issues.
Med Sci Sports Exerc
31 (Suppl.):S547–S552, 1999
668
Apfelbaum M, Vague P, Ziegler O, Hanotin C, Thomas F, Leutenegger E: Long-term maintenance of weight loss after a very-low-calorie diet: a randomized blinded trial of the efficacy and tolerability of sibutramine.
Am J Med
106
:
179
–184,
1999
669
Hauptman J, Lucas C, Boldrin MN, Collins H, Segal KR: Orlistat in the long-term treatment of obesity in primary care settings.
Arch Fam Med
9
:
160
–167,
2000
670
Rossner S, Sjostrom L, Noack R, Meinders AE, Noseda G: Weight loss, weight maintenance, and improved cardiovascular risk factors after 2 years treatment with orlistat for obesity: European Orlistat Obesity Study Group.
Obes Res
8
:
49
–61,
2000
671
National Heart Lung and Blood Institute Expert Panel: Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: the evidence report.
Obes Res
6(Suppl. 2)
:
102S
−125S, 1998
672
Pan XR, Li GW, Hu YH, Wang JX, Yang WY, An ZX, Hu ZX, Lin J, Xiao JZ, Cao HB, Liu PA, Jiang XG, Jiang YY, Wang JP, Zheng H, Zhang H, Bennett PH, Howard BV: Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance.
Diabetes Care
20
:
537
–544,
1997
673
Eriksson KF, Lindgarde F: Prevention of type 2 (non-insulin dependent) diabetes mellitus by diet and physical exercise.
Diabetologia
34
:
891
–898,
1991
674
Viswanathan M, Snehalatha C, Viswanathan V, Vidyavathi P, Indu J, Ramachandran A: Reduction in body weight helps to delay the onset of diabetes even in non-obese with strong family history of the disease.
Diabetes Res Clin Pract
35
:
107
–112,
1997
675
Heymsfield SB, Segal KR, Hauptman J, Lucas CP, Boldrin MN, Rissanen A, Wilding JP, Sjostrom L: Effects of weight loss with Orlistat on glucose tolerance and progression to type 2 diabetes in obese adults.
Arch Intern Med
160
:
1321
–1326,
2000
676
Sjostrom CD, Lissner L, Weedel H, Sjostrom L: Reduction in incidence of diabetes, hypertension and lipid disturbances after intentional weight loss induced by bariatric surgery: the SOS Intervention Study.
Obes Res
5
:
477
–484,
1999
677
Moore LL, Visioni AJ, Wilson PW, D’Agostino RB, Finkle WD, Ellison RC: Can sustained weight loss in overweight individuals reduce the risk of diabetes mellitus?
Epidemiology
3
:
269
–273,
2000
678
Wannamethee SG, Shaper AG: Weight change and duration of overweight and obesity in the incidence of type 2 diabetes.
Diabetes Care
22
:
1266
–1272,
1999
679
Hu FB, Manson JE, Stampfer MJ, Colditz G, Liu S, Solomon CG, Willett WC: Diet, lifestyle and the risk of type 2 diabetes mellitus in women.
N Engl J Med
345
:
790
–797,
2001
680
Wing RR, Goldstein M, Acton K, Birch L, Jakicic JM, Sallis JF, Smith-West D, Jeffrey R, Surwit R: Lifestyle changes related to obesity, eating behavior, and physical activity.
Diabetes Care
24
:
117
–123,
2001
681
Helmrich SP, Ragland DR, Leung RW, Paffenbarger RS Jr: Physical activity and reduced occurrence of non-insulin-dependent diabetes mellitus.
N Engl J Med
325
:
147
–152,
1991
682
Frisch RE, Wyshak G, Albright E, Albright NL, Schiff I: Lower prevalence of diabetes in female former college athletes compared with nonathletes.
Diabetes
35
:
1101
–1105,
1986
683
Manson JE, Rimm EB, Stampfer MJ, Colditz GA, Willett WC, Krolewski AS, Rosner B, Hennekens CH, Speizer FE: Physical activity and incidence of non-insulin-dependent diabetes in women.
Lancet
338
:
774
–778,
1991
684
Manson JE, Nathan DM, Krolewski AS, MJ Stampfer MJ, Willett WC, Hennekens CH: A prospective study of exercise and incidence of diabetes among US male physicians.
JAMA
268
:
63
–67,
1992
685
Perry IJ, Wannamethee M, Walker MK, Thomson AG, Whincup PH, Shaper AG: Prospective study of risk factors for development of non-insulin-dependent diabetes in middle aged British men.
BMJ
310
:
560
–564,
1995
686
Kohl HW, Gordon NF, Villegas JA, Blair SN: Cardiorespiratory fitness, glycemic status, and mortality risk in men.
Diabetes Care
15
:
185
–192,
1992
687
Lee DC, Blair SN, Jackson AS: Cardiorespiratory fitness, body composition, and all-cause and cardiovascular disease mortality in men.
Am J Clin Nutr
69
:
373
–380,
1999
688
Tsunehara CH, Leonetti DL, Fujimoto WY: Diet of second-generation Japanese-American men with and without non-insulin-dependent diabetes.
Am J Clin Nutr
52
:
731
–738,
1990
689
Meyer KA, Kushi LH, Jacobs DR, Folsom AR: Dietary fat and incidence of type 2 diabetes in older Iowa women.
Diabetes Care
24
:
1528
–1535,
2001
690
Hughes VA, Fiatarone MA, Fielding RA, Ferrara CM, Elahi D, Evans WJ: Long-term effects of a high-carbohydrate diet and exercise on insulin action in older subjects with impaired glucose tolerance.
Am J Clin Nutr
62
:
426
–433,
1995
691
Louheranta AM, Turpeinen AK, Vidgren HM, Schwab US, Uusitupa MI: A high-trans fatty acid diet and insulin sensitivity in young healthy women.
Metabolism
48
:
870
–875,
1999
692
Sarkkinen E, Schwab U, Niskanen L, Hannuksela M, Savolainen M, Kervinen K, Kesniemi A, Uusitupa MI: The effects of monounsaturated-fat enriched diet and polyunsaturated-fat enriched diet on lipid and glucose metabolism in subjects with IGT.
Eur J Clin Nutr
50
:
592
–598,
1996
693
Ahren B, Gudbjartsson T, Al-Amin AM, Martensson H, Myrsen-Axcrona U, Karlsson S, Mulder H, Sundler F: Islet perturbations in rats fed a high-fat diet.
Pancreas
18
:
75
–83,
1999
694
Larsson H, Elmstahl S, Beglund G, Ahren B: Habitual dietary intake versus glucose tolerance, insulin sensitivity and insulin secretion in postmenopausal women.
J Intern Med
245
:
581
–591,
1999
695
Mayer-Davis EJ, Levin S, Bergman RN, D’Agostino RB Jr, Karter AJ, Saad MF: Insulin secretion, obesity, and potential behavioral influences: results from the Insulin Resistance Atherosclerosis Study (IRAS).
Diabetes Metab Res Rev
17
:
137
–145,
2001
696
Wolever TM, Hamad S, Gittelsohn J, Gao J, Hanley AJ, Harris SB, Zinman B: Low dietary fiber and high protein intakes associated with newly diagnosed diabetes in a remote aboriginal community.
Am J Clin Nutr
66
:
1470
–1474,
1997
697
Meyer KA, Kushi LH, Jacobs DR Jr, Slavin J, Sellers TA, Folsom AR: Carbohydrates, dietary fiber, and incident type 2 diabetes in older women.
Am J Clin Nutr
71
:
921
–930,
2000
698
Paolisso G, D’Amore A, Giugliano D, Ceriello A, Varricchio M, D’Onofrio F: Pharmacologic doses of vitamin E improve insulin action in healthy subjects and non-insulin-dependent patients with diabetes.
Am J Clin Nutr
57
:
650
–656,
1993
699
Reunanen A, Knekt P, Aaran R-K, Aromaa A: Serum antioxidants and risk of non-insulin dependent diabetes mellitus.
Eur J Clin Nutr
52
:
89
–93,
1998
700
Lukaksi HC: Magnesium, zinc, and chromium nutriture and physical activity.
Am J Clin Nutr
72 (Suppl.):585S−593S, 2000
701
Singh RB, Niaz MA, Rastogi SS, Bajaj S, Gaoli Z, Shoumin Z: Current zinc intake and risk of diabetes and coronary artery disease and factors associated with insulin resistance in rural and urban populations of North India.
J Am Coll Nutr
17
:
564
–570,
1998
702
Anderson RA: Effects of chromium on body composition and weight loss.
Nutr Rev
56
:
266
–270,
1998
703
Anderson RA: Chromium in the prevention of diabetes.
Diabetes Metab
26
:
22
–27,
2000
704
Hypponen E, Kenward MG, Virtanen SM, Piitulainen A, Virta-Autio P, Tuomilehto J, Knip M, Akerblom HK: Infant feeding, early weight gain, and risk of type 1 diabetes: Childhood Diabetes in Finland (DiMe) Study Group.
Diabetes Care
22
:
1961
–1965,
1999
705
Norris JM, Scott FW: A meta-analysis of infant diet and insulin-dependent diabetes mellitus. Do biases play a role?
Epidemiology
7
:
87
–92,
1996
706
Meloni T, Marinaro AM, Mannazzu MC, Ogana A, La Vecchia C, Negri E, Colombo C: IDDM and early infant feeding: Sardinian case-control study.
Diabetes Care
20
:
340
–342,
1997
707
Vaarala O, Knip M, Paronen J, Hamalainan AM, Muona P, Vaatainen M, Ilonan J, Simell O, Akerblom HK: Cow’s milk formula feeding induces primary immunization to insulin in infants at genetic risk for type 1 diabetes.
Diabetes
48
:
1389
–1394,
1999
708
Virtanen SM, Hypponen E, Laara E, Vahasalo P, Kulmala P, Savola K, Rasanen L, Aro A, Knip M, Akerblom HK: Cow’s milk consumption, disease-associated autoantibodies and type 1 diabetes mellitus: a follow-up study in siblings of diabetic children. Childhood Diabetes in Finland Study Group.
Diabet Med
15
:
730
–738,
1998
709
Bodington MJ, McNally PG, Burden AC: Cow’s milk and type 1 childhood diabetes: no increase in risk.
Diabet Med
11
:
663
–665,
1994
710
Norris JM, Beaty B, Klingensmith G, Yu Liping, Hoffman M, Chases HP, Erlich HA, Hamman RF, Eisenbarth GS, Rewers M: Lack of association between early exposure to cow’s milk protein and beta-cell autoimmunity: Diabetes Autoimmunity Study in the Young.
JAMA
276
:
609
–614,
1996

Address correspondence and reprint requests to Marion J. Franz, MS, RD, CDE, Nutrition Concepts by Franz, Inc., 6635 Limerick Dr., Minneapolis, MN 55439. E-mail: [email protected].

This paper was peer-reviewed, modified, and approved by the Professional Practice Committee, October 2001.

A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.