Evidence-Based Nutrition Principles and Recommendations ... · Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications

Evidence-Based Nutrition Principles andRecommendations for the Treatment andPrevention of Diabetes and RelatedComplicationsMARION J. FRANZ, RD, CDE, CO-CHAIR

1

JOHN P. BANTLE, MD, CO-CHAIR2

CHRISTINE A. BEEBE, RD, CDE3

JOHN D. BRUNZELL, MD4

JEAN-LOUIS CHIASSON, MD5

ABHIMANYU GARG, MD6

LEA ANN HOLZMEISTER, RD, CDE7

BYRON HOOGWERF, MD8

ELIZABETH MAYER-DAVIS, PHD, RD9

ARSHAG D. MOORADIAN, MD10

JONATHAN Q. PURNELL, MD11

MADELYN WHEELER, RD, CDE12

H istorically, nutrition principles andrecommendations for diabetes andrelated complications have been

based on scientific evidence and diabetesknowledge when available and, when ev-idence was not available, on clinical expe-rience and expert consensus. Often it hasbeen difficult to discern the level of evi-dence used to construct the nutritionprinciples and recommendations. Fur-thermore, in clinical practice, many nutri-tion recommendations that have noscientific supporting evidence have beenand are still being given to individualswith diabetes. To address these problemsand to incorporate the research done inthe past 8 years, this 2002 technical re-view provides principles and recommen-dations classified according to the level of

evidence available. It reviews the evi-dence from randomized, controlled trials;cohort and case-controlled studies; andobservational studies, which can also pro-vide valuable evidence (1,2), and takesinto account the number of studies thathave provided consistent outcomes ofsupport. In this review, nutrition princi-ples are graded into four categories basedon the available evidence: those withstrong supporting evidence, those withsome supporting evidence, those withlimited supporting evidence and thosebased on expert consensus.

Evidence-based nutrition recommen-dations attempt to translate research dataand clinically applicable evidence intonutrition care. However, the best avail-able evidence must still be moderated by

individual circumstances and prefer-ences. The goal of evidence-based recom-mendations is to improve the quality ofclinical judgments and facilitate cost-effective care by increasing the awarenessof clinicians and patients with diabetes ofthe evidence supporting nutrition ser-vices and the strength of that evidence,both in quality and quantity.

Before 1994, the American DiabetesAssociation’s (ADA’s) nutrition principlesand recommendations attempted to de-fine an “ideal” nutrition prescription thatwould apply to everyone with diabetes(3–5). Although individualization was amajor principle of all recommendations,it was usually done within defined limitsfor recommended energy intake and ma-cronutrient composition. The 1994 nutri-tion recommendations shifted this focusto one that emphasized effects of nutritiontherapy on metabolic control (6,7). Thenutrition prescription is determined con-sidering treatment goals and lifestylechanges the diabetic patient is willing andable to make, rather than predeterminedenergy levels and percentages of carbohy-drate, protein, and fat. The goal of nutri-tion intervention is to assist and facilitateindividual lifestyle and behavior changesthat will lead to improved metabolic con-trol. This focus continues with the 2002nutrition principles and recommenda-tions.

Medical nutrition therapy (MNT) isan integral component of diabetes man-agement (8,9) and diabetes sel f-management education (10). (Medicalnutrition therapy is the preferred termand should replace other terms, such asdiet, diet therapy, and dietary manage-ment.) MNT for diabetes includes theprocess and the system by which nutri-tion care is provided for diabetic individ-uals and the specific lifestyle recommen-dations for that care. However, recom-mendations should not only be based onscientific evidence but should also takeinto consideration lifestyle changes the

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From 1Nutrition Concepts by Franz, Inc., Minneapolis, Minnesota; 2Division of Endocrinology and Diabetes,Department of Medicine, University of Minnesota, Minneapolis, Minnesota; 3University of Illinois, Chicago,Illinois; 4Department of Medicine, University of Washington, Seattle, Washington; 5Research Center, CentreHospitalier de l’Universite de Montreal, Campus Hotel-Dieu and Department of Medicine, University ofMontreal, Montreal, Ontario, Canada; 6Department of Internal Medicine and Center for Human Nutrition,University of Texas Southwestern Medical Center, Dallas, Texas; 7Holzmeister Nutrition Consulting, Tempe,Arizona; 8Department of Endocrinology, Cleveland Clinic Foundation, Cleveland, Ohio; 9Department ofEpidemiology and Biostatistics, School of Public Health, University of South Carolina, Columbia, SouthCarolina; 10Division of Endocrinology, St. Louis University Medical Center, St. Louis, Missouri; 11Divisionof Endocrinology, Diabetes, and Clinical Nutrition, Oregon Health and Science University, Portland, Ore-gon; and 12Diabetes Research and Training Center, Indiana University School of Medicine, Indianapolis,Indiana.

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

This paper was peer-reviewed, modified, and approved by the Professional Practice Committee, October2001.

Abbreviations: ADA, American Diabetes Association; ADI, acceptable daily intake; DASH, Dietary Ap-proaches to Stop Hypertension; DCCT, Diabetes Control and Complications Trial; DPP, Diabetes PreventionProgram; DRI, Dietary Reference Intake; FDA, U.S. Food and Drug Administration; FPG, fasting plasmaglucose; GFR, glomerular filtration rate; GRAS, Generally Recognized as Safe; MNT, medical nutritiontherapy; NCEP, National Cholesterol Education Program; NHANES, National Health and Nutrition Exam-ination Survey; RD, registered dietitian; RDA, recommended dietary allowance; UKPDS, U.K. ProspectiveDiabetes Study; VLCD, very-low-calorie diet.

A table elsewhere in this issue shows conventional and Systeme International (SI) units and conversionfactors for many substances.

R e v i e w s / C o m m e n t a r i e s / P o s i t i o n S t a t e m e n t sT E C H N I C A L R E V I E W

148 DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002

individual can make and maintain. Cul-tural and ethnic preferences should betaken into account, and the person withdiabetes should be involved in the deci-sion-making process.

Results from the Diabetes Controland Complications Trial (DCCT) and theU.K. Prospective Diabetes Study (UK-PDS) convincingly demonstrated the im-portance of g lycemic contro l inpreventing the microvascular complica-tions of diabetes (11,12). In both trials,MNT was important in achieving treat-ment goals (13,14). MNT in diabetes ad-dresses not only glycemic control butother aspects of metabolic status as well,including dyslipidemia and hyperten-sion—major risk factors for cardiovascu-lar disease. This is important, asmacrovascular complications are the ma-jor contributors to the morbidity andmortality associated with diabetes (15).

The current nutrition principles andrecommendations for diabetes focus onlifestyle goals and strategies for the treat-ment of diabetes. Now, for the first time,the 2002 recommendations specificallyaddress lifestyle approaches to diabetesprevention; they distinguish MNT fortreating and managing diabetes fromMNT for preventing or delaying the onsetof diabetes, as the two may not necessarilybe the same.

Whether for management or preven-tion of diabetes and its complications, ba-sic to the nutrition recommendations isthe underlying concern for optimal nutri-tion through healthy food choices and anactive lifestyle. The ADA supports and in-corporates the nutrition recommenda-tions from major organizations, such asthe U.S. Department of Agriculture (Di-etary Guidelines for Americans) (16),American Heart Association (17), Na-tional Cholesterol Education Program(18), American Institute for Cancer Re-search (19), and Joint National Commit-tee on Prevention, Detection, Evaluation,and Treatment of High Blood Pressure(20).

Although many studies have focusedon the role of single nutrients, food, orfood groups in disease prevention or pro-motion, emerging research suggests thereare health benefits from food patterns thatinclude mixtures of food containing mul-tiple nutrients and nonnutrients (21–27).Although this approach makes it difficultto elucidate mechanisms through whichthe diet composition affects a particular

health outcome, it does represent a prac-tical approach to making realistic nutri-tion recommendations for improvinghealth.

The health professional with thegreatest expertise in providing MNT fordiabetes is the registered dietitian (RD)knowledgeable and skilled in diabetesmanagement (8–10,28). Outcome stud-ies (13,29–34) have demonstrated thatMNT provided by RDs results in a 1.0%decrease in HbA1c in patients with newlydiagnosed type 1 diabetes (29), a 2.0%decrease in HbA1c in patients with newlydiagnosed type 2 diabetes (14), and a1.0% decrease in HbA1c in patients withan average 4-year duration of type 2 dia-betes (30). The effectiveness of dietitian-de l i ve red MNT in improv ingdyslipidemia has also been demonstrated(35–41). However, it is essential that allteam members involved in diabetes treat-ment and management be knowledgeableabout MNT and supportive of the pa-tient’s need to make lifestyle changes (42–45).

GOALS OF MEDICALNUTRITION THERAPY FORDIABETES — Goals of MNT that ap-ply to all persons with diabetes are as fol-lows:

1. To attain and maintain optimal meta-bolic outcomes, including

a. blood glucose levels in the normalrange or as close to normal as issafely possible to prevent or reducethe risk for complications of diabe-tes

b. a lipid and lipoprotein profile thatreduces the risk for macrovasculardisease

c. blood pressure levels that reducethe risk for vascular disease

2. To prevent and treat the chronic com-plications of diabetes; modify nutrientintake and lifestyle as appropriate forprevention and treatment of obesity,dyslipidemia, cardiovascular disease,hypertension, and nephropathy

3. To improve health through healthyfood choices and physical activity

4. To address individual nutritionalneeds, taking into consideration per-sonal and cultural preferences and life-style while respecting the individual’swishes and willingness to change

The goals of MNT that apply to spe-cific situations include the following:

1. For youth with type 1 diabetes, to pro-vide adequate energy to ensure normalgrowth and development, and to inte-grate insulin regimens into usual eat-ing and physical activity habits

2. For youth with type 2 diabetes, to fa-cilitate changes in eating and physicalactivity habits that reduce insulin re-sistance and improve metabolic status

3. For pregnant or lactating women, toprovide adequate energy and nutrientsneeded for optimal outcomes

4. For older adults, to provide for the nu-tritional and psychosocial needs of anaging individual

5. For individuals being treated with in-sulin or insulin secretagogues, to pro-vide self-management education fortreatment (and prevention) of hypo-glycemia, acute illnesses, and exercise-related blood glucose problems

6. For individuals at risk for diabetes, todecrease the risk by encouraging phys-ical activity and promoting foodchoices that facilitate moderate weightloss or at least prevent weight gain

The next sections of this technical reviewpaper focus on MNT for the managementof diabetes. The first section includes nu-trition recommendations for type 1 andtype 2 diabetes—intake of carbohydrate,sweeteners, protein, fat, micronutrients,and alcohol; energy balance and obesity;and special considerations. The secondsection reviews MNT for special popula-tions—children and adolescents, preg-nant and lactating women, and olderadults. The third section reviews MNT foracute complications—hypoglycemia andacute illness—and comorbid condi-tions—hypertension, dyslipidemia, ne-phropathy, and catabolic illness. The lastsection reviews lifestyle recommenda-tions for the prevention or delay of diabe-tes.

MEDICAL NUTRITIONTHERAPY FOR TYPE 1 ANDTYPE 2 DIABETES

Carbohydrate and diabetesWhen referring to common food carbo-hydrates, the following terms are pre-ferred: sugars, starch, and fiber (Table 1).This classification is based on the recom-mendations of the Food and Agriculture

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DIABETES CARE, VOLUME 25, NUMBER 1, JANUARY 2002 149

Organization of the United Nations andthe World Health Organization in whichcarbohydrates are classified according totheir degree of polymerization and are ini-tially divided into three principalgroups—sugars, oligosaccharides, andpolysaccharides (46). Terms such as sim-ple sugars, complex carbohydrates, andfast-acting carbohydrates are not well de-fined; use of these terms should be aban-doned.

A number of factors influence glyce-mic response to food, including theamount of carbohydrate (47), type ofsugar (glucose, fructose, sucrose, lactose)(48), nature of the starch (amylose, amy-lopectin, resistant starch) (49), cookingand food processing (degree of starch ge-latinization, particle size, cellular form)(50), and food structure (51), as well asother food components (fat and naturalsubstances that slow digestion—lectins,phytates, tannins, and starch-protein andstarch-lipid combinations) (52). Fastingand preprandial glucose concentrations(53–56), the severity of glucose intoler-ance (57), and the second meal or lenteeffect (58) are other factors affecting theglycemic response to food.

Carbohydrate and type 1 diabetesIn trying to establish nutrition recom-mendations for the prescription of carbo-hydrate for patients with type 1 diabetes,there are several problems: the paucity ofstudies, the small number of subjectsstudied, and the lack of long-term studies.Although several studies in subjects withtype 1 diabetes have been done compar-ing differing amounts or percentages of

calories from carbohydrate (59 – 61),there is no body of evidence to suggestchanging the 1994 recommendation that60–70% of total energy be distributed be-tween carbohydrate and monounsatu-rated fat based on nutrition assessmentand treatment goals (6). A basis for choos-ing between carbohydrate and monoun-saturated fat, other than ethnic or culturalpreferences, is not readily available. Insome studies (59,60), a high-carbohy-drate diet compared to a high�mono-unsaturated fat diet resulted in a higherglycemic profile, with no differences inthe lipid profile; however, insulin may nothave been adjusted appropriately to coverthe amount of carbohydrate ingested. Inanother study (61) comparing a high-carbohydrate diet to a high�monoun-saturated fat diet, there were nodifferences in glycemia, but there was anincrease in postprandial triglycerides withthe high�monounsaturated fat diet.

More information is available regard-ing the effects of different types of carbo-hydrate on postprandial glycemia. In type1 patients with diabetes, the ingestion of avariety of starches or sucrose, bothacutely (62–68) and for up to 6 weeks(69–72), was shown to produce no sig-nificant differences in glycemic responseif the total amount of carbohydrate is sim-ilar. Studies in controlled settings (62–69) and in free-living subjects (70–72)have demonstrated similar results.

Studies show a strong relationshipbetween the premeal insulin dosage andthe postprandial response to the carbohy-drate content of the meal (73–76). In in-dividuals receiving intensive insulin

therapy, the total amount of carbohydratein the meal did not influence glycemicresponse if the premeal insulin was ad-justed for the carbohydrate content of themeal (73). The premeal insulin dosage re-quired was not affected by the glycemicindex, fiber, fat, or caloric content of themeal. Furthermore, wide variations inmeal carbohydrate content did not mod-ify the basal (long-acting) insulin require-ment. The concept of total mealcarbohydrate determining the premealinsulin dosage is further supported by theDCCT, in which it was shown that indi-viduals who adjusted their premeal insu-lin dosages based on the carbohydratecontent of meals had 0.5% (P � 0.03)lower HbA1c levels than those who didnot adjust premeal insulin (13).

For individuals receiving fixed dos-ages of short- and intermediate-acting in-sulin, day-to-day consistency in theamount and source of carbohydrate hasbeen associated with lower HbA1c levels(77). Day-to-day variations in energy andprotein or fat intakes were not signifi-cantly related to HbA1c.Glycemic index. The usefulness oflow�glycemic index diets in individualswith type 1 diabetes is controversial. Fivestudies (n � 48; range 12 days to 6 weeks)(78–82) have compared low�glycemicindex diets to high�glycemic index dietsfor longer than 1 day. The results fromthese studies did not provide convincingevidence of benefit. Four studies (78,80–82) measured HbA1c, and none reporteddifferences in HbA1c between low� andhigh�glycemic index diets. Four studies(78–81) measured glycated albumin or

Table 1 —Carbohydrate classification and terminology

Major dietary carbohydrate classes based ondegree of polymerization and subgroups Components

U.S. food labelingdesignation

Sugars* (1–2 molecules)Monosaccharides Glucose, galactose, fructose SugarsDisaccharides Sucrose, lactose SugarsPolyols (sugar alcohols) Sorbitol, mannitol, xylitol, isomalt, malitol, lactitol,

hydrogenated starch hydrolysatesSugar alcohol

Oligosaccharides (3–9 molecules)Malto-oligosaccharides Maltodextrins Other carbohydrateOther oligosaccharides Raffinose, stachyose, fructo-oligosaccharides Other carbohydrate

Polysaccharides (�9 molecules)Starch* Amylose, amylopectin, modified starches Other carbohydrateFiber* (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 AgricultureOrganization of the United Nations: Carbohydrates in Human Nutrition. Food and Agriculture Organization of the United Nations, Rome, 1998.

Technical Review


fructosamine; three of those (78–80) re-ported decreases in glycated albumin orserum fructosamine after the incorpora-tion of low�glycemic index food in thediet, and one reported no differences inserum fructosamine (81). Three studies(78–80) measured fasting plasma glu-cose (FPG) concentrations, and none re-ported differences in FPG between low�and high�glycemic index diets. Insulinrequirements were measured in fourstudies (79–82); one (79) reported lowerinsulin requirements from low� com-pared to high�glycemic index diets,whereas three (80–82) reported no dif-ferences in insulin dosages. Therefore, al-though the use of low�glycemic indexfood may reduce postprandial glucoselevels, there is not sufficient evidence oflong-term benefit to recommend generaluse of low�glycemic index diets in indi-viduals with type 1 diabetes.

In a cross-sectional study of 2,810people with type 1 diabetes from the EU-RODIAB IDDM Complications Study(83), the glycemic index calculated from3-day food records was examined for itsrelation to HbA1c and serum lipid con-centrations. HbA1c levels were lower inthe lowest glycemic index quartile com-pared with the highest quartile. Of theserum lipids, only HDL cholesterol wasindependently related to the glycemic in-dex. Interestingly, the consumption ofbread and pasta had the biggest effect onthe overall glycemic index.

The effects on lipids after low� com-pared to high�glycemic index diets ap-pear to be minimal. Two studies (79,80)measured cholesterol concentrations andthree studies (78 – 80) measured HDLcholesterol concentrations, but none re-ported differences in the low� comparedto the high�glycemic index diets. Onestudy (80) reported lower triglyceride lev-els, but one (78) did not.

Although it is clear that carbohy-drates do have differing glycemic re-sponses, the data reveal no clear trend inoutcome benefits. If there are long-termeffects on glycemia and lipids, these ef-fects appear to be modest. Moreover, thenumber of studies is limited, and the de-sign and implementation of several ofthese studies is subject to criticism.Fiber. Early short-term studies usinglarge amounts of fiber (�30 g/day) insmall numbers of suboptimally controlledtype 1 subjects (84–87) suggested a pos-itive effect of fiber on glycemia. However,

in a study of type 1 diabetes subjects onintensive insulin therapy, 56 g of fiber hadno beneficial effect on glycemic control(81). A recent study (88) randomizedsubjects being treated with two or moreinjections of insulin per day and HbA1c

levels of 7–10% to either a high-fiber (50g/day), low�glycemic index diet or a low-fiber (15 g/day), high�glycemic indexdiet for 24 weeks. The high-fiber diet sig-nificantly reduced mean daily blood glu-cose concentration (P � 0.05), thenumber of hypoglycemic events (P �0.01), and, in the subgroup of patientscompliant to diet, HbA1c (P � 0.05), buthad no beneficial effect on cholesterol,HDL cholesterol, or triglyceride concen-trations. Conversely, a cross-sectionalanalysis of dietary fiber in type 1 diabetespatients enrolled in the EURODIABIDDM Complications Study revealed thata higher intake of total fiber (grams perday) was independently associated withhigher levels of HDL cholesterol in bothmen and women, and lower LDL choles-terol levels in men but not women (89).No substantial differences were observedbetween soluble and insoluble fiber in-takes. Mean total fiber intake was 18.5g/day in men and 16.2 g/day in women.

The Dietary Guidelines for Americans(16) recommends that all Americanschoose a variety of fiber-containing food,such as whole grains, fruits, and vegeta-bles, because they provide vitamins, min-erals, fiber, and other substancesimportant for good health. This is an ap-propriate recommendation for peoplewith type 1 diabetes as well.

There is strong evidence for the fol-lowing statements:

● Studies in healthy subjects support theimportance of including food contain-ing carbohydrate from whole grains,fruits, vegetables, and low-fat milk inthe diet.

● With regard to the glycemic effects ofcarbohydrates, the total amount of car-bohydrate in meals and snacks is moreimportant than the source or type.

● Individuals receiving intensive insulintherapy should adjust their premeal in-sulin dosages based on the carbohy-drate content of meals.

There is some evidence for the follow-ing statements:

● Individuals receiving fixed daily insulindosages should try to be consistent inday-to-day carbohydrate intake.

● Although the use of low�glycemic in-dex food may reduce postprandial hy-perglycemia, there is not sufficientevidence of long-term benefit to recom-mend use of low�glycemic index dietsas a primary strategy in food/meal plan-ning for individuals with type 1 diabe-tes.

● As for the general public, consumptionof fiber is to be encouraged; however,there is no reason to recommend thatpeople with type 1 diabetes consume agreater amount of fiber than otherAmericans.

● Percentages of carbohydrate should bebased on individual nutrition assess-ment.

The following statement is based onexpert consensus:

● Carbohydrate and monounsaturatedfat together should provide 60–70% ofenergy intake.

Carbohydrate and type 2 diabetesAs is the case for type 1 diabetes, there isno body of evidence relating to peoplewith type 2 diabetes to suggest changingthe 1994 recommendation that 60–70%of total energy be divided between carbo-hydrate and monounsaturated fat. Inweight-maintaining diets for type 2 pa-tients with diabetes, replacing carbohy-drate with monounsaturated fat reducespostprandial glycemia and triglyceride-mia (90,91), but there is concern that in-creased fat intake in ad libitum diets maypromote weight gain and potentially con-tribute to insulin resistance (92–100).Thus the contributions of carbohydrateand monounsaturated fat to energy intakeshould be individualized based on nutri-tion assessment, metabolic profiles, andweight and treatment goals.

In individuals with type 2 diabetes,postprandial glucose levels and insulin re-sponses to a variety of starches and su-crose are similar if the amount ofcarbohydrate is constant (69,71,101–106). This has been demonstrated in bothcontrolled (69,101–104) and in free-living subjects (71,105,106). When stud-ied, the effects of starches and sucrose onplasma lipids were similar and no adverseeffects were observed (103–106).



Glycemic index. There have been ninestudies (80,82,107–113) involving type 2diabetes subjects (n � 129) that havecompared low�glycemic index andhigh�glycemic index diets for longerthan 1 day. One study (107) reportedlower HbA1c levels in low� compared tohigh�glycemic index diets, whereas fourstudies (80,82,108,109) reported no dif-ferences in HbA1c levels. Three studies(110–112) reported significantly lowerfructosamine levels in low� compared tohigh�glycemic index diets, whereasthree other studies (108,109,113) re-ported no significant differences in fruc-tosamine. No differences in fastingplasma glucose concentrations were re-ported in eight studies (80,107–113), andno differences in insulin levels were foundin two studies (107,109).

In studies that also assessed the effectsof low� and high�glycemic index dietson plasma lipids, there were no consistentresults. One study (112) reported positivedifferences on cholesterol levels, whereasfour (80,107,108,113) reported no differ-ences. One study reported positive differ-ences in HDL cholesterol levels (109),whereas five (80,108,110,112,113) re-ported no differences. Four studies (108–110,112) reported no differences in LDLcholesterol levels. One study (80) re-ported positive differences in triglyceridelevels; five studies (107,108,110 –112)reported no differences.

Although studies in type 2 diabetessubjects have not consistently reported arelation between glycemic index and in-sulin and lipid levels, studies in otherpopulations have reported an associationbetween either lower glycemic index dietsor lower glycemic loads with lipids, inparticular HDL cholesterol, and insulinlevels. In a cross-sectional study of mid-dle-aged adults, the glycemic index of thediet was the only dietary variable signifi-cantly related to serum HDL cholesterolconcentration (114), and a recent analysis(115) of the Third National Health andNutrition Examination Survey (NHANESIII) reported a change in HDL concentra-tion of –2.3 mg/dl per 15-unit increase inglycemic index. In a study of 32 patientswith advanced coronary heart disease, 4weeks of a low�glycemic index diet im-proved glucose tolerance and insulin sen-sitivity compared to a high�glycemicindex diet over the same period (116).The same group reported that a low�compared to a high�glycemic index diet

improved adipocyte insulin sensitivity inwomen at risk for coronary heart disease(117).

The glycemic load, defined as theproduct of the glycemic index value of afood and its carbohydrate content, hasbeen reported to be positively associatedwith the risk of developing type 2 diabetesin men and women (118,119) and coro-nary heart disease in women (120). In across-sectional study of healthy post-menopausal women, dietary glycemicload was inversely related to plasma HDLcholesterol and positively related to fast-ing triglycerides (121). In the analysis ofthe NHANES III results, a high glycemicload was associated with a lower concen-tration of plasma HDL cholesterol (115).Fiber. Early studies of the effects of fiberon glycemia showed promising results,but may have suffered from methodolog-ical errors (i.e., poor control of confound-ing variables such as weight loss,differences in energy consumed, differentfood sources with potential differences instarch digestibility, and differences in di-etary fat content) (122). In a study inwhich dietary variables were controlledfor, increasing the fiber content of the dietfrom 11 to 27 g/1,000 kcal did not lead toimprovements in glycemia, insulinemia,or lipemia (123).

In contrast, a diet supplemented withlarge amounts of water-soluble, gel-forming fiber, such as guar gum, reducedpostprandial glycemia (124). In supportof this finding, another study comparing adiet containing 24 g fiber per day (highusual intake) to a diet containing 50 gfiber per day found that the intake of foodhigh in dietary fiber improved glycemiccontrol, reduced hyperinsulinemia, anddecreased plasma lipids (125). It thus ap-pears that ingestion of large amounts offiber is necessary to confer metabolic ben-efit. It is not clear whether the palatabilityand gastrointestinal side effects of fiber inthis amount would be acceptable to mostpeople.

A meta-analysis of 67 controlled clin-ical trials indicated that diets high in sol-uble fiber decrease total and LDLcholesterol, but had a small HDL-lowering effect and did not affect triglyc-eride concentrations (126). Patients withhypercholesterolemia were not more re-sponsive to dietary fiber than healthy in-dividuals. However, the authors concludedthat the effect of soluble fiber within prac-tical ranges on cholesterol was modest

(daily intake of 3 g soluble fiber, e.g.,3 apples or 3 bowls [29-g servings] oat-meal can decrease total cholesterol by �5mg/dl, an �2% reduction), and on risk ofheart disease may be only small.

Newer fiber supplements such aspsyllium (127) and �-glucan (128,129)have mixed short-term effects on glyce-mia and lipemia and require furtherstudy.


● Studies in healthy subjects and those atrisk for type 2 diabetes support the im-portance of including food containingcarbohydrate from whole grains, fruits,vegetables, and low-fat milk in the diet.

● With regard to the glycemic effect ofcarbohydrates, the total amount of car-bohydrate in meals or snacks is moreimportant than the source or type.


● Although the use of low�glycemic in-dex food may reduce postprandial hy-perglycemia, there is not sufficientevidence of long-term benefit to recom-mend general use of low�glycemic in-dex diets in type 2 diabetes patients.

● As for the general population, con-sumption of fiber is to be encouraged.Although large amounts of dietary fiber(�50 g per day) may have beneficialeffects on glycemia, insulinemia, and li-pemia, it is not known if such high lev-els of fiber intake can be maintainedlong-term.


● Carbohydrate and monounsaturatedfat should together provide 60–70% ofenergy intake. However, the individu-al’s metabolic profile and need forweight loss should be considered whendetermining the monounsaturated fatcontent of the diet. Increasing fat intakemay result in increased energy intake.

Nutritive sweetenersSucrose. Sucrose is a common, naturallyoccurring disaccharide composed of aglucose and a fructose molecule. Averageper capita consumption of sucrose andother sugars in the U.S. is estimated to be94 g/day, accounting for 22% of energy

Technical Review


intake (130). Historically, the mostwidely held belief about nutrition and di-abetes was that added sugars should beavoided and naturally occurring sugarsrestricted. This belief was based on theassumption that sucrose and other sugarswere more rapidly digested and absorbedthen starch-containing food and therebyaggravated hyperglycemia. However, sci-entific evidence does not support this as-sumption.

The available evidence from clinicalstudies demonstrates that dietary sucrosedoes not increase glycemia more than iso-caloric amounts of starch (67,69,101,103,104,106,131,132). Thus the intake ofsucrose and sucrose-containing food indiabetic individuals need not be restrictedbecause of a concern about aggravatinghyperglycemia. If sucrose is part of thefood/meal plan, it should be substitutedfor other carbohydrate sources or, ifadded, should be adequately coveredwith insulin or other glucose-loweringmedication. In addition, the intake ofother nutrients (such as fat) often ingestedwith sucrose-containing food should betaken into account. In one study, whenindividuals with type 2 diabetes includedsucrose in their daily meal plan, no nega-tive impact on dietary habits or metaboliccontrol was observed (133).Fructose. Fructose is a common, natu-rally occurring monosaccharide that ac-counts for �9% of average energy intakein the U.S. (134). Fructose is somewhatsweeter than sucrose. It has been reportedthat �33% of dietary fructose comes fromfruits, vegetables, and other naturalsources in the diet and �67% comes fromfood and beverages to which fructose hasbeen added (135).

In several studies in diabetic subjects,fructose produced a reduction in post-prandial glycemia when it replaced su-crose or starch as a carbohydrate source(69,106,136,137). Thus fructose mightbe a good sweetening agent in the diabeticdiet. However, this potential benefit istempered by the concern that fructosemay have adverse effects on plasma lipids.Consumption of large amounts of fruc-tose (15–20% of daily energy intake [90th

percentile of usual intake]) has beenshown to increase fasting total and LDLcholesterol in subjects with diabetes(137) and fasting total and LDL choles-terol and triglycerides in nondiabetic sub-jects (138–141).

Sugar alcohols (polyols). Sugar alco-hols are classified as hydrogenatedmonosaccharides (e.g., sorbitol, manni-tol, xylitol), hydrogenated disaccharides(e.g., isomalt, maltitol, lactitol), and mix-tures of hydrogenated mono- (sorbitol),di- (maltitol), and oligosaccharides (e.g.,hydrogenated starch hydrolysates) (46).They are used in food as sweeteners andbulking agents. Sugar alcohols have beendesignated by the U.S. Food and DrugAdministration (FDA) as safe for use asfood additives or as Generally Recognizedas Safe (GRAS) by affirmation petitionsaccepted for filing by the FDA (Table 2).The FDA has not indicated a need to des-ignate an acceptable daily intake. Foodprepared with sugar alcohols may claimon the label that there is an associationbetween sugar alcohols and reduced riskof dental caries. Because sugar alcoholsare only partially absorbed from the smallintestine, the claim of reduced energy val-ues per gram is allowed. However, if cer-tain polyols are used in food, a warningconcerning excess consumption and lax-ative effects of polyols is required on thefood label (Table 2).

In some studies, ingestion of sugar al-cohols (�50 g) by healthy and diabeticindividuals has produced lower post-prandial glucose responses than after in-gestion of fructose, sucrose, or glucose(142–147). Because of the reduced avail-able energy of sugar alcohols, the possi-bility exists that they could be used toreduce energy intake (as with fat replacersand nonnutritive sweeteners). However,

no studies have been published showingthis to be the case, and the small energysavings do not appear to result in a signif-icant reduction in total daily energy in-take. Intake of food containing sugaralcohols such as sorbitol has been re-ported to cause diarrhea in children withdiabetes (148) and adults (149).


● Sucrose does not increase glycemia to agreater extent than isocaloric amountsof starch.

● Sucrose and sucrose-containing fooddo not need to be restricted by peoplewith diabetes based on a concern aboutaggravating hyperglycemia. However,if sucrose is included in the food/mealplan, it should be substituted for othercarbohydrate sources or, if added, beadequately covered with insulin orother glucose-lowering medication.


● Fructose reduces postprandial glyce-mia when it replaces sucrose or starchin the diabetic diet.

● Consumption of fructose in largeamounts may have adverse effects onplasma lipids.

● The use of sugar alcohols as sweeteningagents appears to be safe.

● Sugar alcohols may cause diarrhea, es-pecially in children.

Table 2 —Sugar alcohols: caloric content and regulatory status

Sugar alcoholCaloric content

(kcal/g) FDA designation

Erythritol 0.2 GRAS affirmation petition accepted for filingHydrogenated starch

hydrolysates3.0 GRAS affirmation petitions accepted for filing

Isomalt 2.0 GRAS affirmation petition accepted for filingLactitol 2.0 GRAS affirmation petition accepted for filingMaltitol 3.0 GRAS affirmation petition accepted for filingMannitol* 1.6 Food additive permitted in food or in contact with

food on an interim basis pending additional studySorbitol* 2.6 Affirmed as GRASXylitol 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 theenergy of certain polyols used as food ingredients,” June 1994, (unpublished), and Life Sciences ResearchOffice: “Evaluation of the net energy value of maltitol,” April 1999 (unpublished). *“Excess consumptionmay have a laxative effect” must be on label for foods whose reasonably foreseeable consumption may resultin the daily ingestion of 20 g mannitol or 50 g sorbitol.



There is limited evidence for the fol-lowing statement:

● The use of added fructose as a sweeten-ing agent is not recommended.

The following statements are basedon expert consensus:

● Sucrose and sucrose-containing foodshould be eaten in the context of ahealthy diet, and the intake of other nu-trients ingested with sucrose, such asfat, should be taken into account.

● There is no reason to recommend thatdiabetic individuals avoid naturally oc-curring fructose in fruits, vegetables,and other food.

● It is unlikely that sugar alcohols in theamounts likely to be ingested in indi-vidual food servings or meals will con-tribute to a significant reduction in totalenergy or carbohydrate intake, al-though no studies have been conductedto support this.

Resistant starch. Resistant starch (non-digestible oligosaccharides and the starchamylose) (Table 1) is not digested andtherefore not absorbed as glucose in thesmall intestine. It is, however, almostcompletely fermented in the colon andproduces about 2 kcal/g of energy (46). Itis estimated that resistant starch and un-absorbed starch represent �2–5% (usu-ally �10 g/day) of the total starchingested in the average Western diet(150). Legumes are the major food sourceof resistant starch in the diet, containing2–3 g resistant starch per 100 g cookedlegumes. Uncooked cornstarch containsabout 6 g resistant starch per 100 g dryweight (151). It has been suggested thatingestion of resistant starch produces alesser increase in postprandial glucosethan digestible starch and correspond-ingly lower insulin levels. As a result, ithas been proposed that food containingnaturally occurring resistant starch (corn-starch) or food modified to contain moreresistant starch (high amylose cornstarch)may modify postprandial glycemic re-sponse, prevent hypoglycemia, and re-duce hyperglycemia; these effects mayexplain differences in the glycemic in-dexes of some food.

There have been several one-meal(152–154) and second-meal studies(155–157) in nondiabetic subjects, com-paring subjects’ physical response to food

high in resistant starch and their responseto food with an equivalent amount of di-gestible starch. All studies found some re-duction in postprandial glucose andinsulin responses to the first meal, but ob-served mixed results after the secondmeal. Long-term studies have not consis-tently confirmed these results (155,158–161).

Published studies involving peoplewith diabetes have focused on uncookedcornstarch and its potential to preventnighttime hypoglycemia (162–165). Inuncontrolled studies, evening cornstarchin specific dosages or dosages based ong/kg body weight resulted in less hypogly-cemia around 0200 h in all groups (166,167). Longer term studies of eveningcornstarch snacks in adults with type 1diabetes reported less hypoglycemia at0300 h (168). In subjects with type 2 di-abetes, evening cornstarch snacks in-creased nocturnal glucose and insulin(165). It has not been established thatbedtime cornstarch snacks are more effec-tive in preventing nocturnal hypoglyce-mia than other types of carbohydrate.

The is limited evidence for the follow-ing statement:

● Resistant starches have no establishedbenefit for people with diabetes.

Nonnutritive sweeteners. There arepresently four nonnutritive sweeteners(also referred to as high-intensity sugaralternatives, low calorie, or alternativesweeteners) approved for use in the U.S.:saccharin, aspartame, acesulfame potas-sium (acesulfame K), and sucralose. Sac-charin, originally linked to human cancerbased on a study in rats more than two

decades ago, has now been dropped fromthe FDA list of cancer-causing chemicals(169).

The newest product approved by theFDA is sucralose (made from sucrosethrough a multistep process in whichthree hydrogen-oxygen groups are re-placed with three chlorine atoms). Sucra-lose has been shown to have no effect onglucose homeostasis in diabetic subjects(170,171). FDA approval is being soughtfor three other nonnutritive sweeteners:alitame (formed from the amino acids as-partic acid and alanine), cyclamates (re-moved from the market in 1970), andneotame (similar to aspartame but 30–60times sweeter and will not require speciallabeling for phenylketonuria) (172). A re-cent trend in the food industry is to blendhigh-intensity sweeteners. This decreasesthe total amount of individual sweetenersused and may improve taste.

Nonnutritive sweeteners approved bythe FDA must undergo rigorous scrutinyand are not allowed on the market unlessthey are demonstrated to be safe for thepublic, including people with diabetes, toconsume. For all food additives, includ-ing nonnutritive sweeteners, the FDA de-termines an acceptable daily intake (ADI),defined as the amount of a food additivethat can be safely consumed on a dailybasis over a person’s lifetime without risk.Actual intake is much less than the ADI.Although the daily ADI for aspartame is50 mg/kg body wt, the range of actualdaily aspartame intake at the 90th percen-tile is 2–3 mg/kg body wt (173). Table 3lists ADIs of nonnutritive sweeteners(174).

Studies to determine the effects ofnonnutritive sweeteners during preg-

Table 3—ADI of nonnutritive sweeteners

ADI(mg/kg

body wt)

Averageamount in

12-oz can ofsoda* (mg)

Cans of soda toreach ADI for

60-kg (132-lb)person (n)

Amount inpacket ofsweetener

(mg)

Packets toreach ADI for

60-kg (132-lb)person (n)

Acesulfame K 15 40† 25† 50 18Aspartame 50 200 15 35 86Saccharin 5‡ 140 2 40 7.5Sucralose 5 70 4.5 5 60

*Fountain drinks may have different amounts and may contain a sweetener blend. †based on most typicalblend with 90 mg aspartame. ADIs are independent. With this sweetener blend, it takes 35 cans to reach theADI 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 toMedical Nutrition Therapy for Diabetes. Franz MJ, Bantle JP, Eds. Alexandria, VA, American Diabetes Associ-ation, 1999.

Technical Review


nancy and lactation have been conductedin animals. No adverse effects have beenreported (175).

There is strong evidence for the fol-lowing statement:

● Nonnutritive sweeteners are safe forpeople with diabetes when consumedwithin the ADI levels established by theFDA.


● It is unknown if use of nonnutritivesweeteners improves long-term glyce-mic control or assists in weight loss.

Protein and diabetesIn the U.S., protein intake accounts for15–20% of average adult energy intake, astatistic that has varied little from 1909 tothe present. Protein intake is also fairlyconsistent across all ages, from infancy toolder age (176, 177), and appears to besimilar in individuals with diabetes. Pro-tein intake in subjects with type 2 diabe-tes in the U.K. Prospective Diabetes Studywas 21% of daily energy (32); protein in-take in children with type 1 diabetes hasbeen reported to be 17% of daily energy(178).Protein needs. It has been assumed thatin people with diabetes, abnormalities ofprotein metabolism are less affected byinsulin deficiency and insulin resistancethan abnormalities of glucose metabolism(179). However, moderate hyperglyce-mia may contribute to increased turnoverof protein in type 2 diabetic subjects. Dur-ing moderate hyperglycemia, obese sub-jects with type 2 diabetes, compared tonondiabetic obese subjects, had an in-crease in whole-body nitrogen flux and ahigher rate of protein synthesis andbreakdown (180,181).

A high-quality protein (95 g protein/day), very-low-energy diet capable ofmaintaining nitrogen balance in obesesubjects without diabetes did not preventnegative nitrogen balance in diabetic sub-jects, despite weight loss and improvedglycemic control (181). This increasedprotein turnover was restored to normalonly with oral glucose-lowering agents orexogenous insulin sufficient to achieveeuglycemia and with increased protein in-take (182,183). These study results sug-gest that people with type 2 diabetes havean increased need for protein during

moderate hyperglycemia and an alteredadaptive mechanism for protein sparingduring weight loss. Thus with energy re-striction, the protein requirements of peo-ple with diabetes may be greater than therecommended dietary allowance (RDA)of 0.8 g protein/kg body wt, although notgreater than usual intake, which is �1.0 gprotein/kg body wt or �100 g protein/day (32). However, individuals consum-ing very low energy intakes may have adeficiency in protein intake and requirean assessment of protein adequacy.

Protein degradation and conversionof endogenous and exogenous protein toglucose in type 1 diabetes depends on thestate of insulinization and correspondingglycemic control. Insulin deficiency in-creases whole-body protein synthesis,protein breakdown, oxidation of essentialamino acids (184), and gluconeogenesis(185). Conversion of excess dietary pro-tein or endogenous protein to glucosemay occur and, in turn, adversely influ-ence glycemia.

Short-term kinetic studies have dem-onstrated increased protein catabolism intype 1 diabetic subjects treated with con-ventional insulin therapy (186–188). Inone study, to protect against increasedprotein catabolism, type 1 subjects re-quired near-normal glycemia and an ade-quate protein intake (188). Because mostadults eat at least 50% more protein thanrequired, people with diabetes appear tobe protected against protein malnutritionwhen consuming a usual diet.Protein and development of nephropa-thy. An association between dietary pro-tein intake and the development of renaldisease has been suggested. In seven stud-ies, dietary protein intake was reported tobe similar in patients with diabetes withand without nephropathy (189–195). Inall studies, protein intake was in the rangeof usual intake and rarely exceeded 20%of the energy intake. In a cross-sectionalstudy of 2,500 type 1 diabetic subjects,those who reported protein consumption�20% of total energy had average albu-min excretion rates �20 mcg/min (196).Those in whom protein intake was �20%of daily energy (22% of patients) had av-erage albumin excretion rates �20 mcg/min (in the range of microalbuminuria).In individuals with macroalbuminuria,32% consumed �20% of total energyfrom protein versus 23% for those withmicroalbuminuria and 20% for thosewith normal albumin excretion. This sug-

gests that a high-protein intake may havea detrimental effect on renal function.

The long-term effects of consuming�20% of energy as protein on the devel-opment of nephropathy has not been de-termined. However, intake of protein inthe usual range does not appear to be as-sociated with the development of diabeticnephropathy.Glucose responses to protein. A num-ber of studies in healthy, normal-weightsubjects (197) and subjects with con-trolled type 2 diabetes (blood glucose�200 mg/dl) (198–200) have demon-strated that ingested protein does not in-crease plasma glucose concentration.Gannon et al. (200) reported that duringthe 8-h period after subjects with type 2diabetes ingested 50 g protein in the formof very lean beef, �20–23 g of proteinwere deaminated, which in theory couldyield �11–13 g glucose. However, theamount of glucose appearing in the circu-lation was only �2 g, confirming that in-gested protein does not result in asignificant increase in glucose concentra-tion. This raises the question that if glu-coneogenesis from protein is occurring,why does the glucose produced not ap-pear in the general circulation after theingestion of protein?

In type 2 diabetic subjects, the peakplasma glucose response to carbohydrateis similar to the response to carbohydrateplus protein (197–199), suggesting thatprotein does not slow the postprandialabsorption of carbohydrate.

In individuals capable of secreting in-sulin, protein ingestion is just as potent asglucose ingestion in stimulating insulinsecretion (197–200). The net effect onglucose output by the liver depends onthe ratio of insulin to glucagon. In type 1or type 2 diabetic subjects, the glucagonresponse to protein is considerablygreater than in nondiabetic subjects(201).

In one study of subjects with well-controlled type 1 diabetes, the addition ofprotein to a meal did not slow the absorp-tion of carbohydrate or change either thepostprandial peak glucose response to themeal or glucose levels at 5 h (202). Fur-thermore, in type 1 diabetic subjects, therate of restoration to euglycemia after hy-poglycemia did not differ when treatmentwas given with carbohydrate or carbohy-drate plus protein (203). Glucose levels,the time to peak plasma glucose levels,



and subsequent rate of glucose fall weresimilar after both treatments.Protein’s effect on satiety and/or en-ergy balance. It has been claimed thathigh-protein, low-carbohydrate dietsproduce weight loss and improvements inglycemia. It should be noted that most ofthese diets tend to be high in fat. In onestudy of high-protein diets, there was asignificant decrease in weight and plasmatriglycerides at 12 weeks (204). However,plasma LDL cholesterol levels were in-creased. There is no research available todocument that high-protein diets main-tain long-term weight reduction any bet-ter than traditional weight-loss diets andthat they are safe for long-term use.

The Continuing Survey of Food In-take by Individuals 1994 –1996 (177)was used to examine the relationshipamong prototype popular diets (205). In acomparison of low-carbohydrate diets(�30% of energy from carbohydrate[h igh pro te in d ie t s ] ) and high-carbohydrate diets (�55% of energy fromcarbohydrate), diet quality was lower andtotal and saturated fat intake was higheron the lower carbohydrate diet, whereasenergy intake and BMI were approxi-mately similar between the two.

The effects of dietary protein on theregulation of energy intake and satietyhave not been adequately studied(206,207). Short-term meal studies sug-gest that protein does exert a positive ef-fect on satiety (208 –211). However,results from one study demonstrated thatalthough hunger was suppressed to agreater extent after a high-protein than ahigh-fat or high-carbohydrate breakfast,the changes in hunger were not of suffi-cient magnitude to change ad libitumlunchtime energy intake 5 h later or en-ergy intake for the rest of the day, whichwere similar after all three breakfast types(210).

There is strong evidence for the fol-lowing statement:

● In individuals with controlled type 2diabetes, ingested protein does not in-crease plasma glucose concentrations,although ingested protein is just as po-tent a stimulant of insulin secretion ascarbohydrate.


● For diabetic individuals, there is no ev-idence to suggest that usual protein in-take (15–20% of total daily energy)should be modified if renal function isnormal.

● For diabetic individuals, especiallythose with less-than-optimal glycemiccontrol, the protein requirement maybe greater than the RDA, but not greaterthan usual intake.

● Contrary to advice often given to pa-tients with diabetes, the available evi-dence suggests the following: 1) dietaryprotein does not slow the absorption ofcarbohydrate and 2) dietary proteinand carbohydrate do not raise plasmaglucose later than carbohydrate aloneand thus do not prevent late-onset hy-poglycemia.


● It may be prudent to avoid protein in-take �20% of total daily energy.


● The long-term effects of diets high inprotein and low in carbohydrate are un-known. Although such diets may pro-duce short-term weight loss andimproved glycemia, it has not been es-tablished that weight loss is main-tained. The long-term effect of suchdiets on plasma LDL cholesterol is alsoa concern.

Dietary fat and diabetesSaturated fats and dietary cholesterol.The primary goal regarding dietary fat inpatients with diabetes is to decrease in-take of saturated fat and cholesterol (212–214). Saturated fat is the principal dietarydeterminant of LDL cholesterol (213).Compared to nondiabetic subjects, dia-betic subjects have an increased risk ofcoronary heart disease with higher in-takes of dietary cholesterol (215). TheADA (8,212) and the National Choles-terol Education Program’s Adult Treat-ment Panel III (18) have recommendedthat the serum LDL cholesterol goal be�100 mg/dl. To assist in achieving thisgoal, it is recommended that food with ahigh content of saturated fatty acids andcholesterol be limited (17,18).

In a meta-analysis (216) of 37 dietaryintervention studies in free-living sub-

jects, plasma total cholesterol decreasedfrom baseline by 24 mg/dl (10%), LDLcholesterol by 19 mg/dl (12%), and trig-lycerides by 15 mg/dl (8%) in Step I (10%saturated fat and 300 mg cholesterol) in-terventions (P � 0.01 for all). In Step IIinterventions (7% saturated fat and 200mg cholesterol), total cholesterol de-creased 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 cholesteroldecreased by 7% (P � 0.05) in responseto Step II but not Step I dietary interven-tions. Positive correlations betweenchanges in dietary total and saturatedfatty acids and changes in total, LDL, andHDL cholesterol were observed. Addingexercise resulted in greater decreases intotal and LDL cholesterol and triglycer-ides and prevented the decrease in HDLcholesterol associated with low-fat diets.However, studies in diabetic subjectsdemonstrating the effects of specific per-centages of saturated fatty acids (e.g., 10vs. 7% of energy) and specific amounts ofdietary cholesterol (e.g., 300 vs. 200 mg)are not available. Therefore, the goal forpatients with diabetes remains the sameas for the general population: to reducesaturated fat intake to �10% of energyintake. Some individuals (i.e., those withLDL cholesterol �100 mg/dl) may benefitby reducing saturated fat to �7% of en-ergy intake. The goal for dietary choles-terol intake is �300 mg/day and forindividuals with LDL cholesterol �100mg/dl, �200 mg/day.

For patients with diabetes, the debatehas focused not on the extent to whichsaturated fatty acids and cholesterol in-take should be limited, but rather on whatis the best alternative energy source.Plasma cholesterol reductions of 9–29%have been reported in four studies inwhich saturated fat was replaced with car-bohydrate in diabetic diets (217–220).Two of these studies also measuredplasma LDL and HDL cholesterol and re-ported that substituting a low-fat (�30%of total daily calories), high-carbohydratediet for a high�saturated fat diet resultedin reductions in LDL, but not HDL, cho-lesterol. (217,218) Glycemic control wasimproved or unchanged as a result of re-stricting dietary saturated fat and replac-ing it with carbohydrate (217,219,221–224). See Table 4 for classification of fattyacids (225).

Technical Review


Monounsaturated fats. Diets high incis-monounsaturated fatty acids (hereaf-ter referred to simply as monounsaturatedfat) (90,226–229) or low in fat and highin carbohydrate (216–223) result in im-provements in glucose tolerance and lip-ids compared with diets high in saturatedfat. Diets enriched with monounsaturatedfat may also reduce insulin resistance(227); however, some studies have re-ported total dietary fat to be associatedwith insulin resistance (96–100). Meta-bolic study diets in which energy intake ismaintained and that are high in either car-bohydrate or monounsaturated fat lowerplasma LDL cholesterol equivalently (90).Low�saturated fat (i.e., 10% of energy),high-carbohydrate diets increase post-prandial levels of plasma glucose and in-sulin, increase plasma triglycerides (90),and, in some studies, were shown to de-crease plasma HDL cholesterol whencompared in metabolic studies to isoca-

loric high�monounsaturated fat diets(91,230). However, high�monoun-saturated fat diets have not been shown toimprove fasting plasma glucose or HbA1cvalues. Therefore, if saturated fat caloriesneed to be replaced, they can be replacedwith carbohydrate or monounsaturatedfat, either of which can contribute to areduction in plasma LDL cholesterol.There is, however, concern that whenhigh�monounsaturated fat diets areeaten ad libitum outside of a controlledsetting, they may result in increased en-ergy intake and weight gain (216). Studiescomparing diets high in monounsatu-rated fat with diets high in carbohydratewith ad libitum energy intake are neededto evaluate the efficacy of these diets anddetermine which dietary intervention issuperior for reducing cardiovascular risk.Each individual’s metabolic profile andneed to lose weight will determine theMNT recommendations. For example, a

diet in which 60–70% of energy is to bederived from carbohydrate and monoun-saturated fat may emphasize carbohy-drate intake for the patient to achieveweight loss and monounsaturated fat forthe patient to improve plasma triglyceridelevels or postprandial glycemia. Further-more, an Asian patient may be more com-fortable with a high-carbohydrate diet,whereas a patient of Mediterranean de-scent may prefer a monounsaturatedfat�containing diet. Monounsaturatedfats can also be considered for food prep-aration and substituted for saturated fatsin fat spreads and snacks.Polyunsaturated fats. Only a few stud-ies have evaluated the effects of polyun-saturated fat on plasma lipid levels andglycemic control in subjects with diabe-tes. In one study of type 2 subjects withdiabetes, a diet high in total and polyun-saturated fat resulted in lower plasma to-tal and LDL cholesterol than a diet high in

Table 4 —Composition of some common dietary fatty acids and typical food sources

Fatty acid (common name) Chemical notation

Amount found in U.S.diet (g/day)

Food sourcesMen Women

Polyunsaturated fatty acidsLinoleic acids 18:2, n-6 14.7 10.4 Vegetable oil, nuts, seeds�-linolenic acid 18:3, n-3 1.6 1.1 Flaxseed oil (linseed oil), canola

oil, soybean oil, walnutsEicosapentaenoic 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 acidsOleic 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 foodcontaining partiallyhydrogenated oil

Saturated fatty acidsLauric 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 withcoconut oil

Palmitic acid 16:0 1.7 11.6 Dairy products, meat, processedgrain products

Stearic acid 18:0 8.1 5.4 Dairy products, meat, processedgrain products, chocolate

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



total and saturated fat, but produced nodifference in other plasma lipid levels(231). Another study in type 2 diabeticsubjects compared a diet high in polyun-saturated fat with one high in monounsat-urated fat and reported higher plasmatotal and LDL cholesterol, fasting glucose,and insulin levels with the polyunsatu-rated fat diet (232).N-3 polyunsaturated fat (omega-3 fattyacids). Food sources of n-3 polyunsatu-rated fatty acids include fish, especiallyfatty fish, as well as plant sources such asflaxseed and flaxseed oil, canola oil, soy-bean oil, and nuts. N-3 fatty acid supple-ments have been shown to reduce plasmatriglyceride levels, especially in hypertri-glyceridemic individuals (233), and tohave beneficial effects on platelet aggrega-tion and thrombogenicity (234). Increas-ing the intake of n-3 polyunsaturated fattyacids has been shown to be beneficial insubjects with diabetes (235–237). Al-though fish oil supplementation may bebeneficial in lowering plasma triglyceridelevels in type 2 diabetic subjects, the ac-companying rise in plasma LDL choles-terol is of concern (238,239). Therefore, ifn-3 fatty acid supplements are used, theeffects on plasma LDL cholesterol shouldbe monitored. Glucose metabolism is notlikely to be adversely affected with the useof n-3 supplements (236,237,240). N-3supplements may be most beneficial inthe treatment of severe hypertriglyceride-mia (236,241). Although studies of theeffects of n-3 fatty acids in patients withdiabetes have primarily used supple-ments, there is evidence from the generalpopulation that food containing n-3 fattyacids, specifically eicosapentaenoic acidand docosahexaenoic acid, has cardiopro-tective benefits (242–246).Transunsaturated fatty acids. Transfats— unsaturated fatty acids formedwhen vegetable oils are processed andmade more solid (hydrogenation)—arefound in some margarines and in foodprepared or fried in hydrogenated vegeta-ble oils. Trans fats also occur naturally insmall amounts in meats and dairy prod-ucts. The mean intake of trans fatty acidsin the U.S. has been estimated at 2.6% oftotal caloric intake and 7.4% of total fatintake (247). When studied indepen-dently of other fatty acids, the effect oftrans fatty acids is similar to that of satu-rated fats in raising plasma LDL choles-terol. Trans fatty acids also lower plasmaHDL cholesterol (248–250). Studies in

nondiabetic subjects support limiting theintake of trans fatty acids.Stanols/sterols. Plant stanols are foundin very small amounts in food from plantssuch as corn and soy and in other vegeta-ble or plant oils. Within plant tissue theyare derived from plant phytosterols. Theydiffer from plant sterols in that their ringstructure is saturated. Plant stanols are es-terified to other vegetable oil fatty acids toenhance their lipid solubility and makethem easier to use as an ingredient infood. Plant sterol and stanol esters blockthe intestinal absorption of dietary andbiliary cholesterol (251) by competingwith cholesterol for entry into the mixedmicelles that must form during digestionfor dietary fatty acids, cholesterol, and fat-soluble vitamins to be absorbed. Plantstanols/sterols in the amount of �2 g/dayhave been shown to lower serum totalcholesterol by up to 10% and LDL cho-lesterol by up to 14% (251–255).Low-fat diets. There are potential bene-fits from low-fat diets. Low-fat diets areusually associated with modest loss ofweight, which can be maintained as longas the diet is continued (230,256) and ifcombined wi th aerob ic exerc i se(216,257,258). In studies evaluating theeffect of ad libitum energy intake as afunction of dietary fat content, low-fat,high-carbohydrate intake is associatedwith a transient decrease in caloric intakeand modest weight loss, leading to a newequilibrium body weight (221,259–268).With this modest weight loss, a decreasein total cholesterol and plasma triglycer-ides and an increase in HDL cholesteroloccur. Consistent with this, low-fat, high-carbohydrate diets over long periods oftime have been shown to not increaseplasma triglycerides and, when reported,have led to modest weight loss (230,269,270). Although the significance of the ef-fects of reduced dietary fat intake arecontroversial (256,271–279), reduced-fat diets have been shown to maintainweight loss better than other types of re-duced energy diets (216,257,280–283).

In type 2 diabetic subjects, restrainedeating behaviors combined with dietaryfat restriction have been shown to havebeneficial effects on glycemia, plasma lip-ids, and/or weight (284–286). A higherintake of total dietary fat is associated withhigher levels of plasma LDL cholesterol,and the adverse effect of a higher carbo-hydrate intake on triglycerides has beenfound in individuals who have undiag-

nosed diabetes or have gained weight dur-ing the previous year (287).Fat replacers/substitutes. Dietary fatintake can be decreased by reducing theamount of high-fat food in the diet. An-other option is to provide lower fat or fat-free versions of food and beverages. Thiscan be accomplished by removing somefat or by using fat replacers (ingredientsthat mimic the properties of fat with sig-nificantly fewer calories than fat) in foodformulations. The FDA has approved themajority of the fat replacers as GRAS be-cause the substances’ ingredients have along history of safe use in food. A fewreplacers (notably olestra) have been ap-proved as food additives; approval ofthese requires both demonstration ofsafety and premarket approval (288 –290). Although olestra has no effect onwater-soluble nutrients, it can lead to aloss of fat-soluble vitamins.

Two recent studies involving diabeticsubjects and food made with fat replacershave been reported (291,292). One ofthese, a short-term study (292), providedcorrectly labeled regular or fat-free foodto free-living subjects with and withoutdiabetes. Use of fat substitutes/replacersin reasonable amounts (five low-fat or no-fat products per day) produced a smalldecrease in dietary fat, saturated fat, andcholesterol intake with little or no de-crease in total energy intake or weight.When fat replacers are used in largeramounts (293,294), there can be a signif-icant decrease in energy intake. Long-term studies are needed to assess theeffect of food containing fat replacers/substitutes on the macronutrient contentof the diets patients with diabetes andtheir utility in achieving treatment goals.

Studies in nondiabetic subjects pro-vide strong evidence for the followingstatements:

● In all, �10% of energy intake should bederived from saturated fats. Some indi-viduals (i.e., those with LDL cholesterol�100 mg/dl) may benefit from lower-ing saturated fat intake to �7% of en-ergy intake.

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

● Intake of transunsaturated fatty acidsshould be minimized.

● Current fat replacers/substitutes ap-

Technical Review


proved by the FDA are safe for use infood.

Studies in diabetic subjects providestrong evidence for the following state-ment:

● To lower plasma LDL cholesterol, en-ergy derived from saturated fat can bereduced if concurrent weight loss is de-sirable or replaced with carbohydrateor monounsaturated fat if weight loss isnot a goal.


● Polyunsaturated fat intake should be�10% of energy intake.

● In weight-maintaining diets, whenmonounsaturated fat replaces carbohy-drate, it may beneficially affect post-prandial glycemia and plasma tri-glycerides but not necessarily fastingplasma glucose or HbA1c.

● Incorporation of two to three servingsof plant stanols/sterols (�2 g) food perday, substituted for similar food, willlower total and LDL cholesterol.

● Reduced-fat diets when maintainedlong term contribute to modest loss ofweight and improvement in dyslipide-mia.


● Two or more servings of fish per weekprovide dietary n-3 polyunsaturated fatand can be recommended.


● Monounsaturated fat and carbohydratetogether should provide �60–70% ofenergy intake. However, increasing fatintake may result in increased energyintake.

● Fat intake should be individualized anddesigned to fit ethnic and cultural back-grounds.

● Use of low fat food and fat replacers/substitutes by patients with diabetesmay reduce total fat and energy intakeand thereby facilitate weight loss.

Energy balance and obesityMany individuals with type 2 diabetes areoverweight, with �36% having a BMI

�30 kg/m2, which would classify them asobese (295). The prevalence of obesity ishigher in women and members of minor-ity populations with type 2 diabetes(295). As body adiposity increases, sodoes insulin resistance (296–298). Obe-sity may also aggravate hyperlipidemiaand hypertension in type 2 patients withdiabetes (299).

Because of the effects of obesity oninsulin resistance, weight loss is an im-portant therapeutic objective for obese in-dividuals with type 2 diabetes. Short-termstudies lasting 6 months or less have dem-onstrated that weight loss in type 2 dia-betic subjects is associated with decreasedinsulin resistance, improved measures ofglycemia, reduced serum lipids, and re-duced blood pressure (300–302). Long-term data assessing the extent to whichthese improvements can be maintained inpeople with type 2 diabetes are not avail-able.

Data from the general public suggestthat long-term maintenance of weight lossis challenging. In two observational stud-ies on weight maintenance after weightloss in nondiabetic subjects, one study(303) reported that only 6% in the finalstudy group maintained a 5% weight lossover 9–15 years, while in a random tele-phone survey (304), 21% of 228 over-weight subjects reported that they hadintentionally lost weight and maintained aweight loss of 10% for at least �5 years.However, long-term data assessing the ex-tent to which weight loss is maintained inpatients with diabetes are not available. Instudies of weight loss in type 2 diabeticsubjects (305–307), the most successfullong-term weight loss from diet was re-ported in the Diabetes Treatment Study(307), with weight loss of 9 kg maintainedover the 6-year study period. To accom-plish this required long-term access totherapeutic contact.

The reason that long-term weight lossis difficult for most people to accomplishis probably because energy intake and en-ergy expenditure, and thereby bodyweight, are controlled and regulated bythe central nervous system (308–310).Although our understanding of centralnervous system regulation of energy bal-ance is incomplete, it is thought that thehypothalamus may be the center of con-trol. Neuropeptide Y, leptin, insulin, anda variety of other neural, endocrine, andgastrointestinal signals also appear to beinvolved. Individual characteristics of

central nervous system control of energybalance may be genetically determined.For example, in a study of Danish adopt-ees, there was a strong relation betweenBMI of the adoptees and their biologicalparents, and no relation whatsoever be-tween the BMI of the adoptees and theiradoptive parents (311). These study re-sults suggest that genetic factors have animportant role in determining bodyweight. Other data support this conclu-sion (312,313). Furthermore, environ-mental factors often make losing weightdifficult for those genetically predisposedto obesity.

The National Weight Control Regis-try has enrolled over 3,000 subjects suc-cessful at long-term maintenance ofweight loss (314). A group of �800 peo-ple who lost an average of 30 kg andmaintained a minimum weight loss of13.6 kg (30 lb) for 5 years were identifiedfrom the registry (315). Slightly morethan half lost weight through formal pro-grams, and the remainder lost weightwith a program of their own. Average en-ergy consumption was �1,400 kcal/day,with 24% of energy derived from fat. Av-erage energy expenditure through addedphysical activity was 2,800 kcal/week.Importantly, nearly 77% of this sample ofpeople who were successful in achievingand maintaining weight loss reported atriggering event that preceded the weightloss. The most common triggering eventswere acute medical conditions and emo-tional problems. Thus a new diagnosis oftype 2 diabetes could trigger lifestylechanges that result in reduced fat and en-ergy intake, increased physical activity,and associated weight loss.Structured programs to produce life-style change. The recently completedDiabetes Prevention Program (DPP) dem-onstrated long-term benefit in peoplewith glucose intolerance from structured,intensive lifestyle programs (316,317). Inthe DPP, participants randomly assignedto an intensive lifestyle intervention thatincluded a low-fat diet, increased physicalactivity, educational sessions, and fre-quent follow-up were able to lose 7% ofbody weight in the first year and sustain a5% weight loss over an average follow-upperiod of 3 years. DPP program partici-pants received training in diet, exercise,and behavior modification from casemanagers who met with them for at least16 sessions in the first 24 weeks andmonthly thereafter. With intensive life-



style intervention, the risk of developingdiabetes was reduced by 58% relative tostandard care. Wing et al. (318) demon-strated a 2.5-kg weight loss and Tuo-milehto et al. (319) documented a 3.5-kgweight loss at 2 years with such programs,and also demonstrated that lifestylechanges reduce the risk of developing di-abetes. A recently initiated clinical trialcalled Look AHEAD (Action for Health inDiabetes) will assess the long-term effectsof diet and exercise in type 2 patients withdiabetes.

For weight loss, dietary fat is probablythe most important nutrient to be re-stricted. Spontaneous food consumptionand total energy intake are increasedwhen the diet is high in fat and decreasedwhen the diet is low in fat (259,260).Moreover, epidemiological studies havedemonstrated that dietary fat intake ispositively associated with adiposity andBMI (320,321). In healthy individuals,simply reducing the fat content of the dietcan result in reduced energy intake andweight loss of 2–3 kg (260,322,323).Toubro and Astrup (283) compared theefficacy of an ad libitum, low-fat, high-carbohydrate diet with that of afixed�energy intake diet for long-termmaintenance of weight loss. Both treat-ment groups attended reinforcement ses-sions 2–3 times weekly. At 1-year followup, the ad libitum group had maintaineda greater weight loss than the fixed�energy intake group.

Exercise improves insulin sensitivity,can acutely lower blood glucose in pa-tients with diabetes, and may also im-prove cardiovascular status. Exercise byitself has only a modest effect on weight(324). Exercise is to be encouraged, butlike behavioral therapies, may be mostuseful as an adjunct to other weight-lossstrategies, such as dietary fat reduction.Exercise is, however, important in long-term maintenance of weight loss(325,326).

Behavioral approaches to weight lossinclude strategies such as self-monitoringof food intake and exercise, nutrition ed-ucation, stimulus control, preplanning offood intake, and self-reinforcement.Weight loss with behavioral therapy alonehas been modest (327,328); behavioralapproaches may be most useful as an ad-junct to other weight-loss strategies.Other nutrition interventions. Stan-dard weight-reduction diets, meal re-placements, and very-low-calorie diets

(VLCDs) are other nutrition options.Standard weight-reduction diets provide500–1,000 fewer calories than are esti-mated to be necessary for weight mainte-nance. An ADA technical review paper onthe prevention and treatment of obesity(326) concluded when such diets areused alone in patients with type 2 diabetesas well as in the general population, par-ticipants generally lose �10% of initialbody weight (329). However, an averageof 33% of the lost weight is usually re-gained in the year after treatment, and al-most all of the lost weight may beregained within 5 years (330). Neverthe-less, standard weight-reduction diets maystill be recommended for overweight pa-tients with type 2 diabetes as some peoplecan lose weight with them and maintainthe weight loss, particularly if they in-crease their physical activity.

Structured meal replacements pro-vide a defined amount of energy (usually200–300 calories), often as a prepack-aged meal, snack bar, or formula product.Most of the energy is derived from proteinand carbohydrate. Vitamins, minerals,and fiber may also be included. Use ofmeal replacements once or twice daily toreplace a usual meal can result in signifi-cant weight loss (331–335). Presumablythe meal replacement causes a reductionin energy intake by eliminating the choiceof type and amount of food. Weight losscan be as much as 11% of starting weightat 2 years, but meal replacement therapymust be continued if weight loss is to bemaintained; attrition may occur in about33% of patients (331).

VLCDs provide 800 or fewer caloriesdaily, primarily from protein and carbo-hydrate, with mineral and vitamin sup-plementation. These diets can producesubstantial weight loss and rapid im-provements in glycemia and lipemia inpatients with type 2 diabetes (301,336).

Of note, reductions in glycemia occur be-fore significant weight loss, suggestingthat caloric restriction plays an importantrole in correcting hyperglycemia. Unfor-tunately, when VLCDs are stopped andself-selected meals are reintroduced,weight gain is common (337,338). Mostpeople treated with VLCDs are not able tomaintain long-term weight loss. ThusVLCDs appear to have limited utility inthe treatment of type 2 diabetes andshould be considered only in conjunctionwith a structured weight-maintenanceprogram.Pharmacological therapy. If energy bal-ance is regulated by a hypothalamic con-trol center that produces and responds tobiochemical signals, it might be possibleto influence the control center pharmaco-logically. This possibility first received at-tention with the publication of alandmark study by Weintraub, who de-scribed the effects of fenfluramine andphentermine to induce weight loss (339).When the study was published in 1992, itinitiated widespread increased use of fen-fluramine and phentermine (fen-phen)for weight loss and maintenance (340).Before the withdrawal of fenfluramine be-cause of cardiac effects, the combinationof fenfluramine and phentermine wasdemonstrated to have beneficial weight-loss effects in type 2 diabetic subjects(341).

Since the withdrawal of fenfluramineand its dextroenantiomer dexfenflura-mine, only a limited number of weight-loss medications remain available in theU.S. Some are listed in Table 5. Phenter-mine continues to be available, but ap-pears to have limited efficacy when usedas a single agent. Sibutramine suppressesthe appetite by inhibiting reuptake of se-rotonin and norepinephrine in the centralnervous system. A 24-week, placebo-controlled study compared sibutramine

Table 5 —Selected weight-loss drugs available in the U.S.

Drug Mechanism of action FA Labeling

Phentermine Nonadrenergic; appetitesuppression and/orstimulation of metabolic rate

Short-term usage

Sibutramine Serotonin and norepinephrinereuptake inhibition; appetitesuppression

Safety and effectiveness beyond1 year not determined

Orlistat Inhibition of pancreatic lipase;partial malabsorption of fat

Safety and effectiveness beyond2 years not determined

Technical Review


and diet to placebo and diet in type 2 di-abetic subjects (342). Subjects treatedwith sibutramine lost 4.0 kg more weight,but did not have a significant improve-ment in HbA1c levels when compared tosubjects treated with placebo. Orlistat is amedication that inhibits pancreatic lipaseand causes malabsorption of a portion ofingested fat. In a 1-year, placebo-controlled study comparing orlistat anddiet to placebo and diet in type 2 diabeticsubjects, the orlistat group lost 6.2% ofinitial body weight as compared to 4.3%weight loss in the placebo group (343). Inthe orlistat group, HbA1c decreased by0.2%, whereas in the placebo group it in-creased by 0.3%. In a second 1-year, pla-cebo-controlled study of orlistat, adiabetic subgroup experienced a reduc-tion in HbA1c that was 0.5% more withorlistat than with placebo (344).

The available data suggest that weightloss medications may be useful in thetreatment of overweight patients withtype 2 diabetes. However, the effect ofthese medications is modest. The dataalso suggest that these drugs work best inconjunction with lifestyle strategies. Inaddition, like antihypertensive and anti-hyperlipidemic medications, these medi-cations must be continued to maintainany beneficial effect. As more is learnedabout the regulation of energy balance,new weight-loss drugs should becomeavailable.Gastric reduction surgery. Gastric re-duction surgery can be an effective weightloss treatment for severely obese patients(including those with type 2 diabetes)(345–347). A National Institute of HealthConsensus Development Panel has rec-ommended that such surgery be consid-ered in patients with type 2 diabetes andwith a BMI �35 kg/m2 (348). The twosurgical procedures most widely used arevertical banded gastroplasty and gastricbypass. Both procedures involve creationof a small (25–50 ml) gastric pouch toreceive food. This small pouch permitsconsumption of small meals without epi-gastric pain or vomiting. Larger meals orlarge fluid intakes cause pain and vomit-ing.

In a series of 70 obese patients treatedwith vertical banded gastroplasty, medianweight losses 1 and 3 years after surgerywere 37 and 32 kg, respectively (345). Ina large series of 515 obese patients treatedwith gastric bypass, mean weight losses at1 and 3 years were 50 and 45 kg, respec-

tively, and weight loss was well main-tained in 44 patients who achieved 10years of follow-up (346). Within the sub-group of 137 patients in this study whohad type 2 diabetes, 107 (78%) experi-enced clinical remission of diabetes. Froma group of 500 patients consecutivelytreated with laparoscopic adjustable gas-tric band surgery, 50 patients with type 2diabetes were studied preoperatively andagain 1 year after surgery (347). Theirpostoperative mean weight loss was 27kg, with significant improvement in allmeasures of glucose metabolism and re-mission of diabetes in 32 (64%) patients,major improvement in control of diabetesin 13 (26%), and no change in 5 (10%).

Potential adverse effects of gastric re-duction surgery include perioperativemortality in 1–2% of patients, wound de-hiscence, vitamin and mineral deficien-cies, cholelithiasis, inability to eat certaintypes of food (particularly meat, un-toasted bread, and raw fruit), and persis-tent vomiting (345–348). Prophylactictreatment with ursodiol may prevent gall-stone formation (349).

It is unfortunate that there are no datacomparing medical and surgical ap-proaches to weight loss in obese patientswith type 2 diabetes; thus the relativebenefits and risks of surgical approachesare uncertain. In the absence of data de-fining benefits and risks, gastric reductionsurgery probably should be consideredunproven in treating diabetes.


● In insulin-resistant individuals, re-duced energy intake and modestweight loss improve insulin resistanceand glycemia in the short term.

● Structured programs that emphasizelifestyle changes, including education,reduced fat (�30% of daily energy) andenergy intake, regular physical activity,and regular participant contact can pro-duce long-term weight loss of 5–7% ofstarting weight.

● Exercise and behavior modification aremost useful as adjuncts to other weight-loss strategies. Exercise is helpful inmaintaining weight loss.

● Nutrition interventions, such as stan-dard weight-reduction diets, whenused alone are unlikely to producelong-term weight loss. Structured, in-tensive lifestyle programs are neces-sary.

● Optimal strategies for preventing andtreating obesity long-term have yet tobe defined.

There is some evidence for the follow-ing statement:

● Currently available weight-loss drugshave modest beneficial effects in pa-tients with diabetes. These drugsshould be used only in people with BMI�27.0 kg/m2.


● Gastric reduction surgery can be con-sidered for patients with diabetes and aBMI �35.0 kg/m2. Long-term datacomparing the benefits and risks of gas-tric reduction surgery to those of med-ical therapy are not available.

Micronutrients and diabetesAdequate intake of micronutrients withinthe range of Dietary Reference Intake(DRI) prevents deficiency diseases and isimportant in maintaining the health andwell-being of patients with diabetes. Nu-trient recommendations for adults, ado-lescents, and children with type 1 or type2 diabetes and for women with diabetesduring pregnancy and lactation are simi-lar for people with or without diabetes(350–355). However, uncontrolled dia-betes is often associated with micronutri-ent deficiencies (356,357).

Individuals with diabetes should beeducated about the importance of acquir-ing daily vitamin and mineral require-ments from natural food sources, andabout the potential toxicity of megadosesof vitamin and mineral supplements. Inselect groups, such as elderly individuals,pregnant or lactating women, strict vege-tarians, or individuals on calorie-restricted diets, supplementation with amultivitamin preparation is advisable(16). However, vitamin and mineral sup-plementation in pharmacological dosagesshould be viewed as a therapeutic inter-vention and, as with medications, be sub-jected to placebo-controlled trials todemonstrate its safety and efficacy.

To determine how much of a specificmicronutrient an individual needs on adaily basis, four estimates of DRIs havebeen made by the Institute of Medicine’sFood and Nutrition Board: Estimated Av-erage Requirement (EAR), the Recom-



mended Dietary Allowance (RDA), theAdequate Intake (AI), and the TolerableUpper Intake Level (UL). The RDA is adaily intake level that is sufficient to meetthe nutrient requirement of nearly all(97–98%) healthy individuals within aspecific age, sex, life stage, and physiolog-ical state; the UL is the largest amount of anutrient that is likely to pose no risk ofadverse health effects for almost all thegeneral population (350–353). Table 6provides RDAs for certain vitamins andminerals and upper limits for thosedeemed harmful at high dosages.

Evaluation of the micronutrient sta-tus of patients with diabetes begins with acareful clinical history and should include

a food/nutrition history to document useof “health food”; over-the-counter vita-min, mineral, and herbal supplements;food supplements; and methods of pre-paring food. Laboratory evaluation of mi-cronutrient status is confounded bymethodological problems and, as a result,does not always define micronutrient de-ficiencies. For example, wide seasonalvariations for vitamin D occur in someparts of the country, and serum mea-surements of intracellular cat ions poorlyreflect body stores. However, measure-ments of serum folate, vitamin B12, vita-min D, calcium, potassium, magnesium,and iron concentrations may be clinicallyuseful.

Antioxidants and vitamins. An Insti-tute of Medicine report concluded thatconsuming megadoses of dietary antioxi-dants—vitamin C, vitamin E, selenium,beta carotene, and other carotenoids—has not been demonstrated to protectagainst cardiovascular disease, diabetes,or various forms of cancer, nor doesmegavitamin use necessarily prevent ba-sic nutritional deficiencies. In fact, the op-posite may be true. High dosages ofantioxidants may lead to health problems,including diarrhea, bleeding, and toxicreactions (350). Although results from alarge number of population-based studieshave suggested a link between antioxi-dants and a lower incidence of certain

Table 6 —Adult DRIs for select vitamins and minerals

RDA Tolerable upper intake levelAdverse effects upon whichupper intake level is based

Vitamin A 700 �g/day for women 900 �g/dayfor men

3,000 �g/day

Vitamin B6 1.3 mg/day 100 mg/day Sensory neuropathyVitamin B12 2.4 �g/day Insufficient data to set upper intake levelFolic acid 400 �g/day of dietary folate

equivalents1,000 �g/day from fortified food and

supplement intake (exclusive of foodintake)

Niacin 14 mg/day niacin equivalents forwomen, 16 mg/day niacinequivalents for men

35 mg/day niacin equivalents Flushing

Riboflavin 1.1 mg/day for women, 1.3 mg/dayfor men

Insufficient data to set upper intake level

Thiamin 1.1 mg/day for women, 1.3 mg/dayfor men

Insufficient data to set upper intake level

Vitamin C 75 mg/day for women, 90 mg/dayfor men

2,000 mg/day Diarrhea and othergastrointestinal disturbances

Vitamin E 15 mg/day �-tocopherol 1,000 mg/day HemorrhageCalcium 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; adequateintake is 25 �g/day for women and35 �g/day for men

Not established

Iron 8 mg/day for men and postmeno-pausal women, 18 mg/day forpremenopausal women

45 mg/day Gastrointestinal disturbances

Magnesium 320 mg/day for women, 420 mg/dayfor men

350 mg/day from supplements(exclusive of intake from food andwater)

Selenium 55 �g/day 400 �g/day SelenosisVanadium Insufficient data to set RDA or

adequate intake1.8 mg/day

Zinc 8 mg/day for women, 11 mg/dayfor men

40 mg/day Interference with theabsorption of copper

From the Institute of Medicine Food and Nutrition Board.

Technical Review


chronic diseases, the Institute of Medi-cine’s comprehensive review of the scien-tific evidence concluded it was not certainthat antioxidants were responsible for anybenefit.Antioxidants. Because diabetes may be astate of increased oxidative stress, therehas been interest in prescribing antioxi-dant vitamins to patients with diabetes.Large observational studies have shown acorrelation between dietary or supple-mental consumption of antioxidants anda variety of clinical outcomes, such as pre-vention of disease states (358 –377).However, large, placebo-controlled clini-cal trials have failed to show a benefitfrom antioxidants and, in some instances,have suggested adverse effects (378 –383). Of particular interest is the HeartOutcomes Prevention Evaluation Trial,which included 9,541 subjects, 38% ofwhom had diabetes (378). Supplementa-tion with vitamin E (400 IU/day) for 4.5years did not result in any significant ben-efit.

Several placebo-controlled studies ofsmall numbers of subjects have foundbeneficial effects of antioxidants on phys-iological and biochemical end points(384–388). However, most of these find-ings have not been confirmed. In addi-tion, concern remains about potentiallong-term toxicity of antioxidants. Twotrials with beta carotene found an unex-pected increase in the incidence of lungcancer in those randomized to beta caro-tene (380,382).Folate. The role of folate in preventingbirth defects is widely accepted and hasbeen the impetus for folate fortification ofwheat and grain products in the U.S.(351). Because of the association betweenelevated serum homocysteine levels andcardiovascular disease, there has been in-creasing interest in folate supplementa-tion to lower homocysteine (389).However, the role of folate supplementa-tion in reducing cardiovascular events isfar from settled. It is noteworthy thatthere are no health concerns with folatesupplementation, except for aggravatingvitamin B12 deficiency and occasionallycausing seizures in people with epilepsyand marginal folate status who are receiv-ing anticonvulsants. Folate supplementa-tion trials are currently ongoing and arelikely to yield important information.B vitamins. The role of vitamins B1, B6,and B12 in the treatment of diabetic neu-ropathy has not been established; there-

fore, supplementing diet with B vitaminscannot be recommended as a standard orroutine therapeutic option (356,357). Ithas been suggested from some studiesthat nicotinamide might preserve �-cellmass in newly diagnosed type 1 diabeticsubjects, but the number of subjects en-rolled in these studies has not been largeenough and the treatment effect was notclear enough to warrant application of thefindings (390,391).Minerals. Deficiencies of certain miner-als, such as potassium and magnesium,and possibly zinc and chromium, maypredispose a person to carbohydrate in-tolerance. Whereas the need for potas-sium or magnesium replacement isrelatively easy to detect based on low se-rum levels of these minerals, the need forzinc or chromium supplementation ismore difficult to detect (356,357).Chromium. There have been two ran-domized, placebo-controlled studies inChinese diabetic subjects where chro-mium supplementation has had benefi-cial effects on glycemia (392,393).However, the study populations mayhave had marginal baseline chromiumstatus. In the first study (392), the chro-mium status was not evaluated either atbaseline or after supplementation. Othersmaller studies have also suggested a rolefor chromium supplementation in themanagement of diabetes (394), glucoseintolerance (395), gestational diabetes(396), and corticosteroid-induced diabe-tes (397). Results from these studies indi-cate that the dosage and formulation ofchromium used significantly influencesthe outcome. In one study of patients withdiabetes (392), 1,000 �g/day of chro-mium picolinate was more effective than200 �g/day. Similarly, in gestational dia-betes, 8 �g � kg�1 � day�1 of chromiumwas more effective than 4 �g � kg�1 �day�1 (396). In contrast, two well-designed studies in the U.S. (398,399)and two in Finland (400,401) failed todemonstrate any significant benefit ofchromium supplementation in patientswith diabetes. The latter studies usedchromium chloride, which may not be asbioavailable as chromium picolinate. Atthe present time, benefit from chromiumsupplementation in diabetic individualshas not been conclusively demonstrated.

The Institute of Medicine Food andNutrition Board’s DRIs found insufficientevidence to set an estimated average re-quirement for chromium. An adequate

intake was determined based on esti-mated mean intakes. The adequate intakefor adult men �51 years is 30 �g/day andfor women �51 years is 20 �g/day. How-ever, few serious adverse effects have beenassociated with excess intake of chro-mium from food, and therefore a tolerableupper intake level has not been estab-lished (352).Zinc. Another area of current interest inmicronutrient supplementation is the roleof zinc in diabetic individuals. Small stud-ies in older subjects with diabetes havesuggested some benefit from zinc supple-mentation in healing skin ulcerations(356,357). A more recent placebo-controlled trial with a formulation of zincand rabbit prostatic extracts found a sig-nificant reduction in HbA1c in subjectsrandomized to the active treatment arm(402). However, in that study, those ran-domized to the active treatment hadhigher baseline HbA1c levels than thoserandomized to placebo.Calcium. The rationale for recommend-ing daily intakes of 1,000–1,500 mg ofcalcium, especially in older subjects withdiabetes (403), is based on the recom-mendations of the Institute of MedicineFood and Nutrition Board (353) and theNational Institutes of Health ConsensusDevelopment Panel on Osteoporosis Pre-vention, Diagnosis, and Therapy (404).This recommendation appears to be safeand likely to reduce the incidence of os-teoporosis in older individuals. Vitamin Dis also required for optimal calcium ab-sorption, and a recommended vitamin Dintake of 400–600 IU/day has been estab-lished for adults (353,404). The uncer-ta in ty o f the va lue of ca lc iumsupplementation in younger individualsand potential long-term benefits havebeen discussed in a critical review by Ka-nis (405).Vanadium. The role of vanadium salts indiabetes has been explored in severalsmall studies. There is no clear evidenceof efficacy and there is a potential for tox-icity (406–409).Herbal preparations. A full review ofherbal preparations and issues is outsidethe scope of this technical review paper. Avariety of herbal preparations have beenshown to have modest short-term benefi-cial effects on glycemia. Of these, the beststudied is American ginseng (410,411).Many herbal supplements used to treatobesity also have caffeine and ephedrine-containing herbs in them. Commercially



available products are not well standard-ized, varying greatly in content of activeingredients. In addition, some herbalpreparations have been found to surrep-titiously include pharmaceutical agentsthat produce hypoglycemia. Herbal prep-arations also have the potential to interactwith other medications. Therefore, it isimportant that health care providersknow when their patients with diabetesare using these products.


● There is no clear evidence of benefitfrom vitamin or mineral supplementa-tion in patients with diabetes who donot have underlying deficiencies. Ex-ceptions include folate for preventionof birth defects (strong evidence) andcalcium for prevention of bone disease(some evidence).

● Although difficult to ascertain, if defi-ciencies of vitamins and minerals areidentified, supplementation can bebeneficial.

● Routine supplementation of the dietwith antioxidants is not advised be-cause of uncertainties related to long-term efficacy and safety.


● Select populations, such as elderly in-dividuals, pregnant or lactatingwomen, strict vegetarians, and peopleon calorie-restricted diets, may benefitfrom supplementation with a multivita-min preparation.

● In individuals with diabetes, there is noevidence to suggest long-term benefitfrom herbal preparations.

Alcohol and diabetesAccording to data for the period 1989–1991, alcohol accounts for �2.5% of en-ergy intake in U.S. adults (412) comparedwith the previous �5% based onNHANES II data (1976–1980) (413). It isnot clear whether this change is attribut-able to decreased intake or to method-ological differences in the measurementof alcohol intake. Nearly 67% of the adultU.S. population are reported to drink al-coholic beverages, whereas 33% claim toabstain from them (414). People with di-abetes undoubtedly fall into both catego-ries.

The alcohol in distilled spirits (hardliquor), wine, and beer is ethanol (ethylalcohol, C2H5OH). It is the by-product ofthe oxidation of sugars by yeast enzymes(fermentation). One drink or alcoholicbeverage is commonly defined as 12-ozbeer, 5-oz glass of wine, or 1.5-oz glass ofdistilled spirits, each of which contains�15 g of alcohol. The cardioprotectiveeffects of alcohol are not determined bythe type of alcoholic beverage (415,416).A summary of ecological, case-control,and cohort studies concluded that all al-coholic drinks are linked with lower riskof coronary heart disease, so that much ofthe benefit is from the alcohol itself ratherthan other components of each type ofdrink (415).

The same precautions that apply tothe general population regarding the useof alcohol apply to individuals with dia-betes. Abstention from alcohol should beadvised for women during pregnancy andfor people with medical problems such aspancreatitis, advanced neuropathy, se-vere hypertriglyceridemia (417), or alco-hol abuse. The Dietary Guidelines forAmericans (16) recommends no morethan two drinks per day for adult men andno more than one drink per day for adultwomen. After consuming comparableamounts of alcohol, women have higherblood ethanol concentrations than men,even with allowances for size differences.Women, compared to men, have an in-creased bioavailability of alcohol resultingfrom decreased gastric first-pass metabo-lism and decreased gastric alcohol dehy-drogenase activity; this may contribute tothe enhanced susceptibility of women tothe effects of alcohol (418).Alcohol and blood glucose levels. Al-coholic beverages can have both hypo-and hyperglycemic effects in patients withdiabetes, depending on the amount of al-cohol acutely ingested, if alcohol is con-sumed with or without food, and ifalcohol use is chronic or excessive. Mod-erate (419) or severe hypoglycemia (420),no hypoglycemia (421,422), and hyper-glycemia (423,424) have all been re-ported in patients with diabetes afteralcohol ingestion. Ingestion of moderateamounts of alcohol has also been shownto blunt the awareness of hypoglycemia intype 1 diabetic subjects (425).

Moderate amounts of alcohol can en-hance the glucose-lowering action of ex-ogenous insulin and certain oral glucose-lowering agents. Although alcohol does

not affect the rate and degree of decline inplasma glucose, it appears to alter thephase of glucose recovery by interferingwith hepatic gluconeogenesis. The hypo-glycemia induced by alcohol is not ame-liorated by glucagon because it is causedby indirect impairment of gluconeogene-sis and is not associated with excessiveinsulin secretion (420).

In type 1 and type 2 diabetic subjects,it has been shown that ingesting moderateamounts of alcohol with food has no acuteeffect on blood glucose or insulin levels(419,421,422,426–434). The risk of al-cohol-induced hypoglycemia during fast-ing is modest for type 2 diabeticindividuals, and is probably present onlyif they are being treated with insulin orinsulin secretagogues.Relationship of alcohol to other healthrisks. Heavy or excessive alcohol con-sumption is a leading, avoidable cause ofdeath in the U.S. There may be additionalspecific adverse effects of chronic alcoholconsumption for patients with diabetes.In people with type 2 diabetes, chronicalcohol ingestion (customary intake of�45 g/day) causes deterioration in long-and short-term glucose metabolism(423). Therefore metabolic controlshould be carefully monitored if alcohol isan important component of a patient’sdiet. The effects induced by excess alco-hol are reversed after abstinence from al-cohol for 3 days (423,424).

Epidemiological evidence in nondia-betic individuals suggests that light-to-moderate alcohol ingestion in adults isassociated with decreased risk of type 2diabetes (435–437) and stroke (438) andincreased insulin sensitivity (439–441),although insulin sensitivity may be atten-uated by central adiposity (441). In adultswith diabetes, chronic intake of light-to-moderate amounts of alcohol (5–15g/day) is associated with a decreased riskfor coronary heart disease, perhaps be-cause of the concomitant increase in HDLcholesterol (442– 444). Prospective,long-term studies are needed to confirmthese observations.

Alcohol ingestion increases the ca-pacity for lipoprotein synthesis, especiallyof VLDL particles. This increase in syn-thesis is enhanced by a genetic predispo-sition, high-fat diet, and diabetes (445).Increased lipoprotein synthesis may bemore an effect of chronic or excessive al-cohol intake, as nondiabetic subjects withfasting hypertriglyceridemia who, in one

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study, consumed the equivalent of twoalcoholic beverages did not demonstratean acute increase in triglycerides (417).This suggests that even people with hy-pertriglyceridemia may occasionally usealcohol in moderation.

There appears to be a U- or J-shapedrelationship between alcohol intake andblood pressure. Light-to-moderateamounts of alcohol do not raise bloodpressure (446–451). However, a strongassociation exists between chronic, exces-sive intake of alcohol (�30–60 g/day)and blood pressure elevation in men andwomen. Each additional 10-g incrementof alcohol intake above 30 g/day increasessystolic blood pressure by an average of1–2 mmHg and diastolic blood pressureby 1 mmHg (452). In addition to being arisk factor for hypertension, alcohol mayinterfere with antihypertensive therapyand may be a risk factor for stroke(446,452).


● If individuals choose to drink alcohol,daily intake should be limited to onedrink for adult women and two drinksfor adult men. One drink is defined as a12-oz beer, 5-oz glass of wine, or 1.5-ozglass of distilled spirits.

● The type of alcoholic beverage con-sumed does not make a difference.

● When moderate amounts of alcohol areconsumed with food, blood glucoselevels are not affected.

● To reduce risk of hypoglycemia, alco-hol should be consumed with food.

● Ingestion of light-to-moderate amountsof alcohol does not raise blood pres-sure; excessive, chronic ingestion of al-cohol raises blood pressure and may bea risk factor for stroke.

● Pregnant women and people with med-ical problems such as pancreatitis, ad-vanced neuropathy, severe hypertri-glyceridemia, or alcohol abuse shouldbe advised to not ingest alcohol.


● There are potential benefits from the in-gestion of moderate amounts of alco-hol, such as decreased risk of type 2diabetes, coronary heart disease, andstroke.


● Alcoholic beverages should be consid-ered an addition to the regular food/meal plan for all patients with diabetes.No food should be omitted.

Special considerationsType 1 diabetes. Nutrition recommen-dations for a healthy lifestyle for the gen-eral public are also appropriate forindividuals with type 1 diabetes. Whatdiffers for individuals requiring insulin isthe integration of an insulin regimen intotheir lifestyle. With the many insulin op-tions available, if an individual’s preferredmeal routine and food choices are known,an appropriate insulin regimen can usu-ally be developed. The food/meal planshould be based on an assessment of theindividual’s appetite, preferred types offood, and usual eating and exercise sched-ule, and should reflect cultural and ethnicpreferences. The food/meal plan shouldbe shared with the entire health profes-sional team so that insulin therapy can beintegrated into the individual’s preferredfood and physical activity patterns (4–6).

As discussed in the CARBOHYDRATE AND

DIABETES section, above, for individuals re-quiring insulin, the total carbohydratecontent of meals and snacks is the firstpriority and determines the premeal insu-lin dosage and postprandial glucose re-sponse (62–76,81). Glycemic index andusual fiber content of meals and snacks donot affect the premeal insulin dosage(73,81). Subjects in the DCCT who re-ported following their meal plan at least90% of the time and adjusted their pre-meal insulin based on changes in usualcarbohydrate intake had HbA1c levels1.0% lower than those who reported fol-lowing their meal plan less often (13). Forindividuals who are on fixed insulin reg-imens and do not adjust premeal insulindosages, consistency of carbohydrate in-take is the first priority (77).

Improved glycemic control with in-tensive insulin therapy is often associatedwith an increase in body weight (453–455). In DCCT subjects, a BMI �30kg/m2 has been associated with increasesin lipids and blood pressure (456). In thePittsburgh Epidemiology of DiabetesComplications study, moderate weightgain did not adversely affect lipid profilesif glycemic control was improved (457).

Given the potential for weight gain to ad-versely affect glycemia, lipemia, bloodpressure, and general health, the preven-tion of weight gain is desirable. Becausestrategies effective in preventing weightgain have not been defined, treatment ofthe adverse metabolic effects of weightgain is indicated (456).

For individuals with type 1 diabetes,attention also must be paid to nutritiontherapy for improving lipids and bloodpressure control, and, if present, reducingmicroalbuminuria. (See MEDICAL NUTRITION

THERAPY FOR THE TREATMENT/PREVENTION OF

ACUTE COMPLICATIONS OF DIABETES AND CO-MORBID COMPLICATIONS, below, for the con-ditions comorbid with diabetes).

Hypoglycemia is more frequent in in-dividuals with type 1 diabetes as bloodglucose levels and HbA1c are reduced(458), and needs to be treated appropri-ately to prevent cognitive changes, re-bound hyperglycemia, and weight gain.With hypoglycemia, 10 g of oral glucosecan raise blood glucose levels by �40mg/dl (2.2 mmol/l) over 30 min, and 20 gof oral glucose can raise blood glucoselevels by �60 mg/dl (3.3 mmol/) over 45min (459). With both treatments, how-ever, glucose levels begin to fall 60 minafter glucose ingestion. Although glucosemay be the preferred treatment choice,any form of carbohydrate will raise bloodglucose (460). In one study, adding pro-tein to the treatment of hypoglycemia didnot affect the response to carbohydratetreatment or prevent later-onset hypogly-cemia (203). (See MEDICAL NUTRITION THER-APY FOR THE TREATMENT/PREVENTION OF

ACUTE COMPLICATIONS OF DIABETES AND CO-MORBID COMPLICATIONS, below, for more de-tails on the treatment/prevention of acutecomplications of diabetes.)

Additional carbohydrate may beneeded for unplanned exercise. Carbohy-drate supplementation is based on theblood glucose level before exercise, previ-ous experience with the particular form ofexercise, and the individual’s insulin reg-imen (461). Exercise of moderate inten-sity increases glucose uptake by 2–3 mg �kg�1 � min�1 above usual requirements(e.g., a 70-kg person would need 8.4–12.6g of carbohydrate per hour of exercise)(10–15 g). During high-intensity exercise,glucose uptake increases by 5–6 mg � kg�1

� min�1; however, exercise of this inten-sity usually cannot be sustained for longintervals (462). For planned exercise, re-duction in the insulin dosage may be the



preferred choice to prevent hypoglycemia(463). Regardless , carbohydrate-containing food should be readily avail-able during and after exercise (461,464).

Carbohydrate is needed during exer-cise lasting longer than 60 –90 min(465,466) as well as after such exercise toreplenish muscle glycogen stores (467).Fluid intake is also essential. It has beenfound that 6–8% carbohydrate solutionsare absorbed better and cause less gastricupset than regular soft drinks and fruitjuices, which are 13–14% carbohydratesolutions (464).Type 2 diabetes. Nutrition recommen-dations for a healthy lifestyle for the gen-eral public are also appropriate forindividuals with type 2 diabetes. Becausemost type 2 patients with diabetes areoverweight and resistant to insulin, MNTshould emphasize lifestyle strategies thatresult in reduced energy intake (468 –470), usually through reducing the fatcontent of the diet, and increased energyexpenditure through exercise (471). Mostpatients with diabetes also have dyslipi-demia and hypertension, making reduc-tions in dietary intake of saturated fat,cholesterol, and sodium desirable. There-fore, the emphasis of nutrition therapy fortype 2 diabetes is on lifestyle strategies toreduce glycemia, dyslipidemia, and bloodpressure. These strategies should be im-plemented as soon as the diagnosis of di-abetes is made (472).

Moderate amounts of short-termweight loss improve metabolic abnormal-ities in many individuals with type 2 dia-betes (473), but not in all (474). Moderateamounts of weight loss, especially of in-tra-abdominal fat, reduce insulin resis-tance and help correct dyslipidemia(475,476). Intentional weight loss is alsoassociated with reductions in mortality inoverweight individuals with diabetes(477). However, the best strategy for ac-complishing and maintaining weight lossis unclear and may vary from person toperson.

In the UKPDS, before being random-ized into study groups, subjects received3 months of intensive nutrition therapy,which resulted in an �2% reduction inHbA1c and a mean 5% weight loss (14).The initial glucose response was reportedto be more related to the decreased energyintake, with the decrease in body weightbeing a secondary response. Fastingplasma glucose levels of 100 mg/dl (5.6mmol/l) were maintained only in indi-

viduals who continued a restricted ener-gy intake; once caloric intake was in-creased, fasting plasma glucose levels in-creased, even when weight loss wasmaintained.

Increased physical activity is impor-tant for the maintenance of weight loss.Furthermore, increased physical activitycan improve glycemia (478), decrease in-sulin resistance (479,480), and reducecardiovascular risk factors in women withdiabetes (481) and may independently re-duce the risk of mortality in men withtype 2 diabetes (482). A minimum cumu-lative total of 1,000 kcal/week from phys-ical activities is recommended (471).

Food intake frequency—three mealsor smaller meals and snacks—is not asso-ciated with long-term differences in glu-cose, l ipid, or insul in responses(483,484). Therefore, division of food in-take should be based on individual pref-erences.

Food containing carbohydrate is animportant component of a healthy diet.Individuals with type 2 diabetes may ben-efit by knowing what types of food con-tain carbohydrate (starches, fruits,starchy vegetables, milk, sweets), portionsizes, and the number of servings formeals and, if desired, for snacks. The ef-fect of carbohydrate on blood glucose andplasma lipids may depend on the severityof glucose intolerance (57). With the useof pre- and postmeal blood glucose mon-itoring data, it can be determined if ad-justments in food/meal planning will behelpful or if medication(s) need to becombined with nutrition therapy.

When individuals with type 2 diabe-tes require insulin, consistency in the tim-ing of meals and carbohydrate contentbecomes important. As with type 1 diabe-tes, flexible insulin dosing regimens allowfor variations in food intake and a moreflexible lifestyle. Treatment with sulfonyl-ureas and other insulin secretagogues alsorequires consistency in timing and carbo-hydrate content of meals. Short-acting in-sulin secretagogues may allow for greaterflexibility in mealtimes. People with type2 diabetes are more resistant to hypogly-cemia than people with type 1 diabetes;nevertheless, when type 2 patients withdiabetes being treated with insulin or in-sulin secretagogues may need to reducemedication dosages if they are not able toeat.

MEDICAL NUTRITIONTHERAPY FOR SPECIALPOPULATIONS

Children and adolescents withdiabetesMost diabetes cases diagnosed in childrenare type 1 diabetes, although the preva-lence of type 2 diabetes in youth is in-creasing (485– 488). Nutrition recom-mendations for children and adolescentswith type 1 diabetes should focus on achiev-ing blood glucose goals without excessivehypoglycemia (489–492). This can be ac-complished through individualized foodand meal planning, flexible insulin regi-mens and algorithms, self-blood glucosemonitoring, and education promoting deci-sion making based on outcomes (493). Nu-trition recommendations for youth withtype 2 diabetes focus on a healthy lifestyleand treatment goals to normalize glycemia(494).

There is no research on the nutrientrequirements for children and adoles-cents with diabetes; therefore, nutrientrecommendations are based on require-ments for all healthy children and adoles-cents (350 –353,495). Children andadolescents should achieve healthful eat-ing habits to ensure adequate intake ofessential vitamins and minerals. In gen-eral, U.S. children are not eating the rec-ommended amounts of fruits andvegetables (496), although children withdiabetes may be doing somewhat betterthan the general population in some ar-eas. A 1996 report (178) on dietary intakeof children with type 1 diabetes, ages 4–9years, found that their energy, vitamin,and mineral intakes were adequate,whereas fiber intake was less than recom-mended. Of concern was a reported meansaturated fat intake that exceeded the Na-tional Cholesterol Education Program(NCEP) recommendations (497). Manychildren consumed levels of saturated fatwell above recommendations. The FoodGuide Pyramid, which is a broad tool en-compassing food preferences and differ-ences in food choices among varioussegments of the population, can be usedto increase selection of fruits, vegetables,whole grains, and nuts and reduce intakeof total and saturated fat (498).Energy. Many children with type 1 dia-betes present at diagnosis with weight lossthat must be restored through insulin ini-tiation, hydration, and adequate energyintake. The best method for estimating a

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child or adolescent’s energy needs is afood/nutrition history of a typical dailyintake as obtained from a 24-h recall or3-day food record, provided that growthand development are within normal lim-its. The typical daily energy intake can becompared to reference intakes for normalgrowth and development. An evaluationof weight gain and growth begins at diag-nosis by recording height and weight onthe Centers for Disease Control pediatricgrowth charts (499). Adequacy of energyintake can be evaluated by followingweight gain and growth patterns on a reg-ular basis.

Consideration of a child’s appetitemust be given when determining energyrequirements and the nutrition prescrip-tion. Because energy requirementschange with age, physical activity, andgrowth rate, an evaluation of height,weight, and energy intake is recom-mended every 3–6 months (29). Achiev-ing good metabolic control is essential tonormal growth and development (489).However, the practice of withholdingfood or having the child eat consistentlywithout an appetite for food in an effort tocontrol blood glucose is discouraged.Macronutrients. Macronutrient com-position of the nutrition prescription isindividualized according to blood glucoseand plasma lipid goals and requirementsfor growth and development. Childrenand adolescents with type 1 diabetes arenot at high risk for developing lipid ab-normalities, but should be screened andmonitored according to guidelines issuedby the NCEP in the report of its ExpertPanel on Blood Cholesterol Levels in Chil-dren and Adolescents (497) and by theAmerican Academy of Pediatrics (500).The stepwise approach to dietary man-agement of lipid abnormalities suggestedby the NCEP recommends a reduction intotal fat, saturated fat, and cholesterol forchildren over age 2 years.Fiber. Dietary fiber recommendationsfor children with diabetes are the same asfor nondiabetic children. It has been rec-ommended that children older than age 2years increase their intake of dietary fiberto an amount equal to or greater than theirage plus 5 g/day (501).Physical activity. Physical inactivity isassociated with adverse health effects(502). Intervention strategies for the en-tire family that promote lifelong physicalactivity may help children overcomethese adverse effects. Physical activity

may also provide a lipid-lowering effect inadolescents with diabetes (503).Type 2 diabetes in youth. Successfultreatment of type 2 diabetes in childrenand adolescents with nutrition therapyand exercise is comprised of the cessationof excessive weight gain with normal lin-ear growth and the achievement of bloodglucose and HbA1c goals (494). Nutritionrecommendations for children and ado-lescents with type 2 diabetes should alsoaddress comorbidities, such as hyperten-sion and dyslipidemia (494). Behaviormodification strategies to decrease intakeof high-calorie, high-fat food while en-couraging healthy eating habits and regu-lar physical activity for the entire familyshould be considered. Regular exercise inobese children, without dietary interven-tion, has been shown to lead to favorablechanges in plasma triglycerides, serum in-sulin concentrations, and percent bodyfat (504). However, the benefits of exer-cise were lost when the children becameless active. Intervention strategies shouldbe culturally appropriate, sensitive tofamily resources, provided to all caregiv-ers, and followed consistently by allhealth care providers.

Adolescents whose parents have type2 diabetes have more risk factors—higherBMI, plasma cholesterol, plasma triglyc-erides, serum insulin, plasma glucose,and insulin-resistance index and lowerplasma HDL cholesterol— comparedwith adolescents whose parents do nothave diabetes (505). These risk factorscan be detected early and provide incen-tive for interventions, such as control ofweight gain and increased exercise.


● Individualized food/meal plans, insulinregimens using basal and bolus insu-lins, and insulin algorithms can provideflexibility for children with type 1 dia-betes and their families to accommo-date i r regu lar mea l t imes andschedules, varying appetite, and vary-ing activity levels.

● Blood glucose monitoring data can beused to integrate an insulin regimeninto the meal/snack and exercise sched-ules.

● Nutrient requirements for children andadolescents with type 1 or type 2 dia-betes appear to be similar to those forsame-age nondiabetic children and ad-olescents.

● In obese children, increased physicalactivity improves plasma lipids and in-sulin sensitivity.


● Successful lifestyle treatment regimensfor youth with type 2 diabetes have notbeen defined.

Pregnant and lactating womenDuring pregnancy, the goals of nutritionare similar for women with and withoutdiabetes. MNT goals are to provide ade-quate maternal and fetal nutrition, energyintake for appropriate maternal weightgain (506), and any necessary vitamin andmineral supplements. For pregnancycomplicated by diabetes, nutrition ther-apy should also attempt to achieve andsustain optimal maternal blood glucosecontrol. A favorable pregnancy outcomeis defined as gestational duration of39–41 weeks and live birth of an infantweighing 6.6–8.8 lb. (3–4 kg) (355).Weight gain/energy requirements. In-fant birth weight is related to maternalsize and weight gain during pregnancy.Recommended weight gain goals arebased on pregravid BMI and should besteady and progressive (355). For obesewomen (BMI �30 kg/m2), a relativelysmall weight gain of �7 kg is recom-mended during pregnancy (507). For un-derweight women (BMI �19.8 kg/m2),greater weight gain (up to 18 kg) is rec-ommended. A normal-weight womanshould gain 1.4–2.3 kg/month during thefirst trimester and 0.5–0.9 kg/week dur-ing the rest of her pregnancy. Overweightwomen should gain weight at �50% ofthese rates (355).

Energy intake should be sufficient topromote appropriate weight gain. Unlessa woman begins pregnancy with depletedbody reserves, energy needs do not in-crease in the first trimester. An additional300 kcal/day are suggested during thesecond and third trimesters for increasesin maternal blood volume and breast,uterus, and adipose tissue; placentalgrowth; fetal growth; and amniotic fluids(508). Obese women with ample body fatstores may require fewer calories. Studieshave reported successful pregnancy out-comes for women with energy intake ofonly 100 kcal/day above prepregnancyintake during the second and third tri-mesters (509). Energy estimates must be



individualized based on a food/nutritionassessment, physical activity, and weightgain patterns during pregnancy.Protein requirements and vitamin andmineral supplementation. In additionto adequate energy intake, pregnantwomen need to eat a balanced diet withadequate protein. Protein requirementsfor women with diabetes during preg-nancy are the same as for nondiabeticwomen during pregnancy—0.75 g � kg�1

� day�1 plus an additional 10 g/day (508).A balanced diet resulting in appropri-

ate weight gain generally supplies all thevitamins and minerals needed for preg-nancy. However, assessment of the preg-nant woman’s eating patterns may yieldspecific individual needs. Although ab-normal folate metabolism does not appearto occur in pregnant women with diabetes(510), 400 �g/day of folic acid from for-tified food and/or as a supplement as wellas food folate from a varied diet is recom-mended for all women of childbearing agewho are capable of becoming pregnant forthe prevention of neural tube defects andother congenital abnormalities (351,511–514). Low-dosage iron supplementation(30 mg/day) during the second and thirdtrimesters is often recommended (508).The average zinc intake of pregnantwomen is 11 mg/day, whereas the RDA is15 mg/day (515). Zinc supplementationfor women with low pregravid weight andlow plasma zinc levels leads to infantswith a higher birth weight (516). Food isconsidered the optimal vehicle for nutri-ent intake. However, prenatal vitaminand mineral supplements are often pre-scribed because of uncertainty of nutri-tional status and intake.Nonnutritive sweeteners. The FDA hasapproved four nonnutritive sweetenersfor general use: saccharin, aspartame, ace-sulfame-K, and sucralose. These sweeten-ers appear to be safe for use duringpregnancy. However, moderation is oftenrecommended (517,518).

Although saccharin can cross the pla-centa and remain in fetal tissues becauseof slow fetal clearance (519), there is noevidence that saccharin causes ill effects.If a woman chooses to use saccharin dur-ing pregnancy, the evidence suggests it issafe.

In animal studies, aspartame use hasshown no risk to the fetus when ingestedin amounts three t imes the ADI(520,521). Phenylalanine, aspartate, andmethanol are dietary components of as-

partame. Maximum maternal plasmaphenylalanine concentrations occurringafter ingestion of aspartame would be lessthan those after ingestion of protein food,making it highly unlikely that customaryintakes of aspartame would raise fetal lev-els to a toxic range. Clinical trials withsingle and repeated doses of aspartamehave shown that aspartame has minimalimpact on serum concentrations of aspar-tate, phenylalanine, and methanol, andno clinical effects in healthy women andwomen heterozygous for phenylketonu-ria (520). Aspartate does not cross the pla-centa at any intake level less thanenormous amounts (100 times normal)(521,522). Plasma methanol does not in-crease significantly after an aspartameload. Thus, if placental transport of thesecompounds occurs, the amount is notclinically significant (523).

Multigenerational studies of rats thatreceived acesulfame-K and sucralose haveshown no adverse effects on fertility,number of offspring, birth weight, mor-tality, or fetal development (169,524).Acesulfame-K and sucralose are thus con-sidered safe during pregnancy.Pregnancy with prior onset of type 1 ortype 2 diabetes. For women with type 1(525) or type 2 diabetes, achieving opti-mal glycemic control before and afterconception has been shown to lower theincidence of birth defects and spontane-ous abortion (526). Prepregnancy nutri-tion therapy includes an individualprenatal food/meal plan to optimizeblood glucose control. During pregnancy,the distribution of calories and carbohy-drates in the meal plan should be basedon the woman’s food and eating habits,blood glucose records, and the expectedphysiological effects of pregnancy on herbody. Regular meals and snacks are im-portant to avoid hypoglycemia mademore likely by the continuous fetal drawof glucose from the mother. Moreover,the accelerated starvation of pregnancyleads to fat catabolism, ketonemia, andketonuria after only 12–14 h of fasting.This ketonemia has been associated withlower intelligence scores in offspring atages 2–5 years (527,528).

An evening snack is usually necessaryfor pregnant women with diabetes to de-crease the potential for overnight hypo-glycemia and fasting ketosis. Bloodglucose monitoring and daily foodrecords provide valuable information forinsulin and meal plan adjustments.

Gestational diabetes. Prevention of ad-verse perinatal outcomes is the primaryfocus of antepartum management of ges-tational diabetes (526). Women who failto achieve or maintain glycemic goals orwho show signs of excessive fetal growthwith nutrition therapy should be consid-ered for pharmacological therapy with in-sulin (529–531). Results from a singlestudy have suggested that glyburide maybe an alternative strategy that merits fu-ture consideration (532). Intensive treat-ment of hyperglycemia in women withgestational diabetes can reduce the risk ofinfants having excessive fetal size for ges-tational age. However, the perinatal out-comes of small-for-gestational-ageneonates in pregnancies with gestationaldiabetes may be worse with intensivetherapy than for appropriate size andlarge-for-gestational-age neonates (533).

The goal of nutrition therapy forwomen with gestational diabetes is to pro-mote nutrition necessary for maternal andfetal health, with adequate energy levelsfor appropriate gestational weight gain,achievement and maintenance of normo-glycemia, and absence of ketones. Carbo-hydrate is distributed throughout the dayamong three small-to-moderate-sizemeals and two to four snacks. An eveningsnack may be needed to prevent acceler-ated ketosis overnight. Specific nutrition/food recommendations are determinedand modified based on individual assess-ment and self�blood glucose monitoringdata (518).

Diets containing 40–45% of total en-ergy intake from carbohydrate have beenshown to reduce postprandial glucoselevels (534–536), with carbohydrate be-ing less well tolerated at breakfast than atother meals (534). Nutrition manage-ment should include evaluation of the in-dividual glycemic response to food atdifferent times of the day (537,538). Ifinsulin therapy is added to nutrition ther-apy, a primary goal must be to maintaincarbohydrate consistency at meals andsnacks to facilitate insulin adjustments.

Several research studies have focusedon use of energy-restricted diets duringpregnancy. Hypocaloric diets (�1,200calories per day) in obese women withgestational diabetes have been shown toresult in ketonemia and ketonuria (539).In one study, a modest energy reduction(33% calorie restriction of estimated en-ergy needs or �1,600–1,800 kcal/day)resulted in reduced mean blood glucose

Technical Review


levels without elevations in plasma freefatty acids or ketonuria, whereas a moresevere energy reduction (50% calorie re-striction) increased ketonuria by abouttwofold (540). Energy intake shouldmaintain desirable weight gain duringpregnancy. Daily food records, weeklyweight checks, and ketone testing can beused to determine individual energy rec-ommendations and if a woman is under-eating to avoid insulin therapy (541,542).

Regular aerobic exercise has beenshown to lower fasting and postprandialglucose concentrations and may be usedas an adjunct to nutritional therapy to im-prove maternal glycemia (529). Otherbenefits of exercise during pregnancy in-clude cardiovascular fitness (543) and re-duced discomfort in later pregnancy. Theoptimal frequency and intensity of exer-cise for lowering maternal glucose con-centrations have not been determined,but it appears that a minimum of threeepisodes of exercise per week, each �15min, is required to modify maternal glu-cose levels. In addition, 2–4 weeks of reg-ular exercise may be required before alowering of glycemia is seen (529). Insuf-ficient evidence exists to recommend anyspecific type of exercise as being superiorto another in the management of gesta-tional diabetes.

Blood glucose data allow evaluationof the effectiveness of nutrition therapyand the need for pharmacological ther-apy. Postprandial glucose levels may bemore closely related to fetal risks than arefasting levels (544,545). Pre-breakfast ke-tone measurements are recommended forpatients receiving hypocaloric or carbo-hydrate-restricted diets to allow the de-tection and treatment of ketones.However, the effectiveness of ketonemonitoring in improving fetal outcomeshas not been demonstrated (529).

Although most women with gesta-tional diabetes return to normal glucosetolerance postpartum, they are at in-creased risk of developing gestational di-abetes in subsequent pregnancies andtype 2 diabetes later in life. Evidence sug-gests that a single birth results in a 2–3 kghigher average body weight for themother, and thus increases the risk of be-coming overweight after delivery. Bodyweight changes during the postpartumperiod are likely to be a combination ofretention of gestational weight gain andweight changes caused by the lifestyle al-terations associated with child rearing

(546). Lifestyle behaviors aimed at reduc-ing weight and increasing physical activ-ity may be beneficial to reduce thesubsequent risk of developing diabetes.Lactation. Breastfeeding is recom-mended for women with preexisting dia-betes or gestational diabetes (547,548),although achieving desired metaboliccontrol during lactation may be difficultfor women with type 1 diabetes. Breast-feeding lowers blood glucose, often re-quiring insulin-treated women to eat asnack containing carbohydrate either be-fore or during breastfeeding. Evening orlate night snacks may also be necessary(547). Energy requirements during thefirst 6 months of lactation require an ad-ditional �200 calories above the preg-nancy meal plan. However, an energyintake of 1,800 kcal/day usually meets thenutritional requirements for lactation andmay allow a slow weight loss of 1–2 lb/month (549). Although not all womenlose weight while breastfeeding, it is nor-mal for weight loss to occur as maternalfat stores are mobilized. Overweightwomen may lose up to 2 kg/month with-out affecting milk volume.


● Nutrient requirements during preg-nancy and lactation are similar forwomen with and without diabetes. Forall women of childbearing age who arecapable of becoming pregnant, 400 �g/day of folic acid from fortified foodand/or a supplement as well as folatefrom a variety of types of food is recom-mended for the prevention of neuraltube defects and other congenital ab-normalities in any potential offspring.

● Because previous gestational diabetes isa risk factor for subsequent develop-ment of impaired glucose tolerance andtype 2 diabetes, lifestyle modificationsaimed at reducing weight or preventingweight gain and increasing physical ac-tivity after pregnancy is recommended.

● Use of nonnutritive sweeteners is safeduring pregnancy.

● As with nondiabetic women, diabeticwomen should avoid alcoholic bever-ages during pregnancy.


● In women with type 1 or type 2 diabe-tes, MNT is important in achieving and

maintaining optimal glycemic controlduring pregnancy.

● MNT for gestational diabetes focuseson food choices for appropriate weightgain, normoglycemia, and absence ofketones. For some women, modest en-ergy and carbohydrate restriction maybe appropriate.

● To prevent ketosis, adequate energy in-take and appropriate distribution ofmeals and snacks is important. Anevening snack may be needed to pre-vent accelerated ketosis overnight.

● Although regular exercise has beenshown to lower fasting and postpran-dial glucose concentrations, there is in-sufficient evidence to recommend anyspecific type of exercise in the manage-ment of gestational diabetes.

● Successful lactation requires planningand coordination of care following de-livery.


● There is inadequate evidence to sup-port the benefit of prenatal vitamin-mineral supplementation; however,these supplements are often prescribedbecause of uncertainty about nutri-tional status and intake.

Older adults with diabetesAging is associated with many biologicalchanges that may predispose the olderadult to nutritional deficiencies (550,551). These include alterations in taste,smell, mastication and salivary flow, gas-tric acidity, hepatic function, and renalfunction. In addition, difficulty in prepar-ing food, polypharmacy, and alcoholismare common problems in elderly individ-uals and may interfere with adequate nu-trition. Given these concerns, it is prudentthat any nutritional intervention startwith a thorough assessment that includesa clinical and nutritional history and apsychosocial and environmental evalua-tion (552).

There is limited research on thechanging nutritional needs with agingand virtually none in aging diabetic sub-jects. Therefore, nutritional recommen-dations for older adults with diabetesmust be extrapolated from what is knownfor the general population. The most reli-able indicator of poor nutritional status inan elderly individual is probably changein body weight. In general, involuntary



gain or loss of �10 pounds or 10% ofbody weight in less than 6 months shouldbe evaluated to determine if the reason isnutrition related (552).Energy intake/nutrient requirements.Because of the changes in body composi-tion (i.e., loss of lean body mass) and ex-ercise patterns, the energy requirementsof older adults are 20–30% lower thanthose of younger adults (553). However,it has been suggested that the currentRDA for energy may underestimate theenergy needs of healthy elderly individu-als (554). Nevertheless, in one cross-sectional study, the resting metabolic ratewas lower in elderly subjects, even afteradjustment for body composition (555).

The need for weight loss in over-weight older adults should be carefullyevaluated. Older patients with diabetes,especially those in nursing homes, tend tobe under- rather than overweight (556).Low body weight has been associatedwith greater morbidity and mortality inthis age group (557). Aging does not ap-pear to alter the synthesis or breakdownrate of proteins when results are adjustedfor fat-free mass (553,558). Similarly, theage-related changes in appearance of freefatty acids and fat oxidation can be attrib-uted to reduced lean body mass (559).Finally, older men do not demonstrate animpairment in energy conservation or dis-position during experimental conditionso f under f eed ing or ove r f eed ing(560,561).

In long-term care settings, malnutri-tion and dehydration may develop be-cause of lack of food choices, poor qualityof food, and unnecessary restrictions.Specialized diabetic diets do not appear tobe superior to standard (regular) diets insuch settings (562). Therefore, it is rec-ommended that residents be served theregular menu with consistent amounts ofcarbohydrate (/�15 g) for meals andsnacks (563,564). It may often be prefer-able to make medication changes to con-trol blood glucose than to implementfood restrictions.

The recommended macronutrientcomposition of the diet and the individu-alization of carbohydrate and fat compo-nents for older adults do not differ fromthe general recommendations for patientswith diabetes. However, any increase indietary fiber should be done cautiously inelderly individuals, especially in thosewho are not ambulatory or are likely tobecome dehydrated (552). Because of re-

duced alcohol tolerance with age, alcoholingestion by elderly patients should belooked at carefully.Micronutrients. Restricting sodium in-take to �2,400 mg/day (the current limitrecommended for the management of hy-pertension and congestive heart failure)may predispose older subjects who enjoysalty food to further limit their caloric in-take and increase their risk of nutritionaldeficiencies. Older subjects are morelikely to have deficiencies in micronutri-ents such as thiamine, vitamin B12, folate,vitamin C, and vitamin D (565–570). Cal-cium, zinc, and magnesium deficienciesare also common (571–573). All olderadults should be advised to have a cal-cium intake of at least 1,200 mg/day. TheBaltimore Longitudinal Study of Agingfound that daily intake and plasma levelsof certain antioxidants, such as vitamin Aand vitamin E, were suboptimal in the el-derly population (574). In the Framing-ham Study, poor intake of folate, vitaminB6, and vitamin B12 was related to higherplasma homocysteine concentrations andincreased prevalence of carotid artery ste-nosis (569,575). In a study in healthy el-derly subjects supplemented withchromium picolinate (1,000 �g/day),chromium did not alter insulin sensitiv-ity, serum lipid profile, or body composi-tion (576).

Vitamin D deficiency has been foundin 8% of nursing home residents; 17% ofthose had evidence of secondary hyper-parathyroidism (571). Minority popula-tions, such as elderly Hispanic adults,may have low serum vitamin B12, vitaminC, and folate levels compared to elderlywhite adults (568).

Use of nutritional supplements is ap-propriate when the patient cannotachieve nutritional needs through food.Daily supplementation with 1,000 –1,500 mg of elemental calcium is proba-bly safe and may reduce the risk ofosteoporosis (352).Physical activity. Exercise training cansignificantly reduce the decline in maxi-mal aerobic capacity (VO2) that occurswith age (577), improve risk factors foratherosclerosis (578), slow the decline inage-related lean body mass, decrease cen-tral adiposity (579), and improve insulinsensitivity, all of which are beneficial forthe older adult with diabetes. However,because of the potential risks of exercise(cardiac ischemia, musculoskeletal andfoot injuries, and hypoglycemia in pa-

tients treated with insulin or insulinsecretagogues), an evaluation and educa-tion session should be undertaken beforeinitiating an exercise training program.Physical activity should increase gradu-ally, and appropriate stretching, warm-up, and cool-down periods shouldaccompany all exercise (579).


● Energy requirements for older adultsare less than those for younger adults.

● All older adults should be advised tohave a calcium intake of at least 1,200mg/day.

● Physical activity should be encouragedin elderly individuals.

● Undernutrition is more likely thanovernutrition in older adults, andtherefore caution should be exercisedwhen prescribing weight-loss diets.


● A daily multivitamin supplement maybe appropriate for elderly individuals,especially for those with reduced en-ergy intake.

● The imposition of dietary restrictionson elderly, diabetic residents in long-term care health facilities is not war-ranted. Residents with diabetes shouldbe served regular (unrestricted) menus,with consistency in the amount andtiming of carbohydrate.


● There is no evidence to support the pre-scribing of diets such as “no concen-trated sweets” or “no sugar added,”which are often served to elderly indi-viduals in long-term care facilities.

MEDICAL NUTRITIONTHERAPY FOR THETREATMENT/PREVENTIONOF ACUTE COMPLICATIONSOF DIABETES ANDCOMORBID CONDITIONS

Acute complicationsHypoglycemia. Hypoglycemia is pri-marily an issue for individuals taking in-jected insulin, although those takinginsulin secretagogues can also be affected.Changes in food intake, physical activity,

Technical Review


and medication(s) can contribute to thedevelopment of hypoglycemia. Two treat-ment modalities are the ingestion of car-bohydrate and an adjustment inmedication(s). A logistic regression anal-ysis of 6,425 self-monitored blood glu-cose events in 93 adults with type 1diabetes showed that more insulin, lessfood, or more exercise predicted 61% ofall blood glucose values �70 mg/dl (�3.9mmol/l), but did not predict severe hypo-glycemia (580).

Although rigid definitions of hypo-glycemia are useful for epidemiologicalstudies, more flexible definitions areneeded in the management of diabetes. Ingeneral, a glucose level �50 mg/dl (�2.8mmol/l) should be treated promptly(459). However, even a level of 60–80mg/dl (3.3–4.4 mmol/l) may require amanagement decision (e.g., carbohydrateingestion, deferral of exercise, change ininsulin dosage) (459).

Treatment of hypoglycemia requiresingestion of glucose or carbohydrate-containing food. The glycemic responsecorrelates better with the glucose contentthan with the carbohydrate content of thefood (581). Although any carbohydratewill raise glucose levels, glucose is pre-ferred (460,581). Treatment of insulin-induced hypoglycemia with 20 g glucosehas been shown to produce a greater risein plasma glucose than treatment with20 g carbohydrate from orange juice ormilk (581), a difference presumably at-tributable to the fact that some of the car-bohydrate in juice is fructose and some ofthe carbohydrate in milk is galactose, andneither is as effective as glucose in raisingplasma glucose levels. In another study(460), type 1 diabetic subjects with in-duced hypoglycemia who were treatedwith 15 g carbohydrate from glucose so-lution or tablets, sucrose solution or tab-lets, or corn syrup had alleviation ofsymptoms in 10 min. Treatment with 15 gcarbohydrate from glucose gel or orangejuice was less effective in alleviating theirsymptoms. Although pure glucose may bethe preferred treatment, any form of car-bohydrate that contains glucose will raiseblood glucose levels.

In a study of insulin-induced hypo-glycemia (582), 10 g oral glucose raisedplasma glucose from 60 mg/dl (3.3mmol/l) to 97 mg/dl (5.4 mmol/l) over 30min, with the glucose level starting to de-cline after 60 min; 20 g oral glucose raisedplasma glucose from 58 mg/dl (3.2

mmol/l) to 122 mg/dl (6.8 mmol/l) over45 min, with the glucose level again start-ing to decline after 60 min. Although10–20 g glucose may be an effective treat-ment for adults (0.3 g/kg body wt in chil-dren), these amounts of glucose are onlytemporarily effective. If glucagon is re-quired, a standard dosage of 1.0 mg (15�g/kg in children) produces rapid andsubstantial hyperglycemia, with glucoselevels beginning to fall after �1.5 h (459).Treatment with glucagon is also a tempo-rary measure. Treatment of hypoglycemiarequires continued evaluation of glycemiato determine if additional carbohydrate isneeded to prevent recurrent hypoglyce-mia.

Adding protein to carbohydrate in thetreatment of hypoglycemia does not ac-celerate the treatment response to carbo-hydrate and does not prevent subsequenthypoglycemia (201). Adding fat, how-ever, may retard the acute glycemic re-sponse. Furthermore, during hypogly-cemia, gastric emptying rates are twice ashigh as during euglycemia (56,583), andare similar for liquids and solid food (56).

Treatment of sulfonylurea-inducedhypoglycemia in type 2 patients with di-abetes differs from insulin-induced hypo-g l ycemia . Su l fony lu rea - inducedhypoglycemia can be prolonged and re-cur and therefore requires more persis-tent treatment. However, type 2 diabeticsubjects, compared to type 1 diabetic sub-jects, release counterregulatory hormonesat higher plasma glucose levels and main-tain glucagon response to hypoglycemia,reducing their risk of severe hypoglyce-mia (584).


● Glucose is the preferred treatment forhypoglycemia, although any form ofcarbohydrate that contains glucose maybe used.

● Ingestion of 15–20 g of glucose is effec-tive treatment for hypoglycemia, butblood glucose may be only temporarilycorrected.


● The form of the carbohydrate—liquidor solid—used to treat hypoglycemiadoes not make a difference.

● Adding protein to the carbohydratedoes not assist in the treatment of hy-

poglycemia or prevent subsequent hy-poglycemia.

The following statement is based on ex-pert consensus:

● Initial response to treatment for hypo-glycemia should be seen in �10–20min; however, blood glucose should beevaluated again in �60 min, as addi-tional treatment may be necessary.

Acute illness. Acute illness in individu-als with type 1 diabetes can result indiabetic ketoacidosis. To prevent ketoac-idosis, individuals with type 1 diabetesneed to know how to handle illnesses ap-propriately. During acute illnesses, withthe accompanying increases in counter-regulatory hormones, the need for insulincontinues and additional insulin is oftenrequired. Testing blood glucose andblood or urine for ketones, drinking ade-quate amounts of fluids, and ingestingcarbohydrate, especially if blood glucoselevel is �100 mg/dl (�5.5 mmol/l) areimportant actions during an acute illness.

Fluid intake should be increased toprevent dehydration. To avoid depletionof intravascular volume, replacement flu-ids containing sodium, such as broth, to-mato juice and sports drinks, are helpful.

In adults, ingestion of 150–200 g car-bohydrate daily (45–50 g or three or fourcarbohydrate choices every 3–4 h) willreduce or prevent starvation ketosis(585–588). If regular food is not toler-ated, liquid or soft carbohydrate-containing food, such as sugar-sweetenedsoft drinks, juices, soups, and ice cream,should be eaten. However, if nausea,vomiting, or obtundation prevents fluidand carbohydrate intake, prompt consul-tation with a health care professional isadvisable. Most importantly, individualswith type 1 diabetes should not omit in-sulin. Supplemental insulin may also berequired.


● During acute illnesses, individuals withtype 1 diabetes should continue insu-lin.

● During acute illnesses, testing bloodglucose and blood or urine ketones,drinking adequate amount of fluids,and ingesting carbohydrate are impor-tant.




● During acute illness, oral ingestion of�150–200 g of carbohydrate per dayshould be sufficient, along with medi-cation adjustments, to keep glucose inthe goal range and to prevent starvationketosis.

HypertensionMNT for the management of hyperten-sion has focused on reducing weight(589 –591) and sodium intake (592–594). Other variables that have been con-sidered include alcohol intake (595),potassium (592,596) and calcium levels(597–599), and diet composition (totalfat, saturated fat, cholesterol) (600). Fewstudies have been done exclusively in di-abetic subjects. However, there is no com-pelling reason to believe that differencesexist between diabetic and nondiabeticindividuals with regard to the benefits ofweight reduction. The response to so-dium reduction may be greater in subjectswho are salt sensitive, a factor that mayapply to many individuals with diabetes(601,602). Currently there is no availableroutine clinical measure to identify indi-viduals who may be salt sensitive.Sodium. Several meta-analyses and re-views have examined the relationship be-tween sodium intake and blood pressure(603–605). A review of 32 trials covering2,635 subjects concluded that moderatereduction of dietary sodium lowers sys-tolic and diastolic blood pressure (603).The mean effect was modest, with a re-duction of 5 mmHg systolic and 2 mmHgdiastolic in hypertensive subjects and areduction of 3 mmHg systolic and 1mmHg diastolic in normotensive sub-jects. It should be noted that there was awide variation in the blood pressure re-sponses to alterations in sodium intakes.A similar conclusion was reached in ameta-analysis of 56 trials (26 studies inhypertensive and 28 in normotensivesubjects) (604). Mean reduction in dailyurinary sodium excretion was 95 mmol/day in 1,131 hypertensive subjects and125 mmol/day in 2,374 normotensivesubjects. In hypertensive subjects, themean decrease in blood pressure per each100 mmol decrease in sodium intake perday was 4 mmHg systolic and 1 mmHgdiastolic. In the normotensive subjects,the mean decrease was 1 mmHg systolicand only negligible for diastolic.

The Dietary Approaches to Stop Hy-pertension (DASH) study evaluated theeffect of three dietary patterns on bloodpressure: 1) a control diet that was similarto a traditional American diet, 2) a diethigh in fruit and vegetables, and 3) theDASH diet, which was higher in fruits,vegetables, and low-fat dairy products,and lower in total fat, saturated fat, andcholesterol (606–609). Sodium intake,physical activity, and body weight re-mained constant. Compared to the con-trol diet, both of the other diets wereassociated with lower systolic and dia-stolic blood pressure over the 8-weekstudy periods. The DASH diet loweredsystolic and diastolic blood pressure by 6and 3 mmHg more, respectively, than thecontrol diet. Although the DASH diet waseffective in all subgroups, systolic bloodpressure in blacks and hypertensive indi-viduals decreased more than in whitesand nonhypertensive individuals. In an-other study, the effects of three levels ofsodium intake were compared in 412subjects randomly assigned to the controlor DASH diet (610). Within the assigneddiet, subjects ate food with high (150mmol/day Na [3.6 g Na or 8.7 g NaCl]),intermediate (100 mmol/day Na [2.4 g Naor 6 g Na]), and low (50 mmol/day Na)levels of sodium for 30 days each. Weightremained stable in all subjects. Reducingthe sodium intake from the high to theintermediate level reduced systolic bloodpressure by 2.1 mmHg (P � 0.001) dur-ing the control diet and by 1.3 mmHg(P � 0.03) during the DASH diet. Reduc-ing the sodium intake from the interme-diate to the low level caused additionalreductions of 4.6 mmHg during the con-trol diet (P � 0.001) and 1.7 mmHg dur-ing the DASH diet (P � 0.01). Therefore,the lower the sodium intake, the greaterthe lowering of blood pressure. The ef-fects of sodium reduction were greater inhypertensive participants, blacks, andwomen.Weight. In patients with diabetes, thereis a general association between weightreduction and a reduction in blood pres-sure, but there is a great deal of variabilityin the response. Reductions in blood pres-sure occur before (and without) desirablebody weight is achieved. In a meta-analysis of 11 weight loss trials, the aver-age systolic and diastolic blood pressurereductions per kilogram of weight losswere 2 and 1 mmHg, respectively (611).

Alcohol. An association between highalcohol intake (more than three drinksper day) and elevated blood pressure hasbeen reported in a number of observa-tional studies (612,613). However, largestudies do not show much difference inblood pressure among people who con-sume less than three drinks per day com-pared to nondrinkers (614).Potassium, magnesium, and calcium.Clinical trials have reported a beneficialeffect of potassium supplementation onblood pressure (596,615). Evidence for abeneficial effect from calcium and magne-sium supplementation is not consistent(615). Because a high dietary intake ofpotassium, magnesium, and calcium canbe achieved from food sources, it is rec-ommended that appropriate types of foodrather than supplements be used to in-crease the intake of these minerals (20).


● In both normotensive and hypertensiveindividuals, a reduction in sodium in-take lowers blood pressure. The goalshould be to reduce sodium intake to2,400 mg sodium (100 mmol sodium)or 6,000 mg sodium chloride (salt) perday. In nondiabetic subjects, this re-duction in sodium intake lowered sys-tolic blood pressure by 4–5 mmHg.

● A modest amount of weight loss bene-ficially affects blood pressure.

● Drinking small-to-moderate amountsof alcohol will not adversely affectblood pressure levels.


● A low-fat diet that includes fruits andvegetables (five to nine servings perday) and low-fat dairy products (two tofour servings per day) will be rich inpotassium, magnesium, and calciumand will modestly reduce blood pres-sure and body weight.

DyslipidemiaDyslipidemia (abnormal lipid levels, li-poprotein composition, or both) is oftenfound in individuals with type 1 or type 2diabetes before the initiation of therapyfor hyperglycemia. For most individualswith type 1 diabetes, effective insulintherapy returns lipid serum levels to nor-mal and usually lowers plasma triglycer-

Technical Review


ides; LDL cholesterol may decreasemodestly as well (212).

For all individuals with diabetes, ele-vated LDL cholesterol is identified as theprimary target of cholesterol-loweringtherapy (8,212). Therapy begins with amultifaceted lifestyle approach. In adultindividuals with elevated LDL cholesterollevels, saturated and trans fatty acidsshould be limited to �10% and prefera-bly to �7% of energy intake (17,18), cho-lesterol intake should be limited to �200mg/day, and modest weight loss andphysical activity should be encouraged.The LDL cholesterol response should beevaluated after 6 weeks (18). If the LDLcholesterol goal is not achieved, LDLcholesterol�lowering therapy should beintensified by reinforcing the need for di-etary reduction in saturated fat and cho-lesterol. Adding plant stanols/sterols (2g/day) has been reported to lower totalcholesterol by 10–32 mg/dl and LDL cho-lesterol by 8–29 mg/dl (251,253,255).Increasing soluble fiber intake (10 –25g/day) can also be suggested (18). A re-cent meta-analysis concluded that for ev-ery gram of increase in soluble fiber, LDLcholesterol would be expected to decreaseby an average of 2.2 mg/dl—an effect thatis small within the practical range of sol-uble fiber intake (126). The LDL choles-terol response should be monitored againafter 6 weeks, and if the LDL goal is notachieved, weight management and phys-ical activity should be intensified anddrug therapy considered. It is recom-mended that adherence to therapeuticlifestyle changes be monitored every 4–6months (18).

Obese individuals with type 1 diabe-tes (456) and many individuals with type2 diabetes (616–621) manifest a dyslipi-demia consisting of increased plasma trig-l yce r ides , r educed se rum HDLcholesterol levels, and small, dense serumLDL cholesterol particles that persist de-spite improved glycemic control. Thisdyslipidemia is strongly associated withincreased body adiposity that is abdomi-nal (visceral) in distribution (622,623).Dietary fat restriction and weight loss willlead to decreased plasma triglycerides anda modest lowering of LDL cholesterol(300,326,475). Regular physical activityalso reduces plasma triglycerides(461,471,481) and improves insulin sen-sitivity (624). However, with one excep-tion (624), most studies have not shownimprovements in HDL cholesterol from

exercise in individuals with type 2 diabe-tes. This may be because of the relativelymodest exercise intensities used (461).

In type 2 diabetic subjects with mild-to-moderate elevations of plasma triglyc-erides and low HDL cholesterol, replacingsaturated fat with carbohydrate has beenshown by most (217,219,625–628), butnot all (629,630), studies to result in im-provements in LDL cholesterol, with ben-eficial or neutral effects on plasmatriglycerides and HDL cholesterol. Mono-unsaturated fat can also be substituted forsaturated fat (90,227–229). However, in-creased dietary fat may cause weight gainand, although controversial, also causeinsulin resistance (96–100).

If goals for serum lipid levels are notachieved with lifestyle improvement, in-cluding MNT and exercise, lipid-loweringmedications should be added (18,212).Maximal changes in nutrition typically re-duce LDL cholesterol 15–25 mg/dl(0.40–0.65 mmol/l) (631). Therefore, ifLDL cholesterol exceeds the goal by �25mg/dl (0.65 mmol/l), pharmacologicaltherapy is likely to be necessary (632–634).

For patients with persistently ele-vated plasma triglycerides despite the ad-dition of medication, supplementationwith fish oils that include n-3 fatty acidsmay be recommended. However, fish oilsmay increase LDL cholesterol, the levelsof which should then be monitored(236,237). Patients with plasma triglycer-ides �1,000 mg/dl are at increased riskfor chylomicronemia syndrome and pan-creatitis and should restrict all types ofdietary fat (635,636) and institute lipid-lowering medication, such as a fibric acidderivative or perhaps niacin (637).


● For individuals with diabetes and ele-vated LDL cholesterol, saturated fattyacids and transunsaturated fatty acidsshould be limited to �10% and per-haps to �7% of energy, and if replaced,can be substituted by carbohydrates ormonounsaturated fats.

● For individuals with diabetes and ele-vated plasma triglycerides, reducedHDL cholesterol, and small dense LDLcholesterol (the metabolic syndrome),improved glycemic control, modestweight loss, restricted intake of satu-rated fats, increased physical activity,

and incorporation of monounsaturatedfats may be beneficial.

● LDL cholesterol lowering can be en-hanced 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 typesof dietary fat (except for n-3 fatty acids)and be treated with medication to re-duce plasma triglycerides.


● Supplementation with fish oils contain-ing n-3 fatty acids may benefit thosewith resistant hypertriglyceridemia.

NephropathyIn individuals with type 1 or type 2 dia-betes, microalbuminuria predicts thelater development of macroalbuminuriaand overt nephropathy. Once clinical ne-phropathy has developed, end-stage renaldisease is almost always the consequence.Recommended treatments focus on re-versing or at least retarding the progres-sion of proteinuria and preventingnephropathy. Improved glycemic con-trol, reduction of blood pressure—particularly by the use of ACE inhibitorsand MNT—all are important in this re-gard (638).

Several dietary factors have beenidentified as having a role in the preven-tion of nephropathy. Animal studies havesuggested a beneficial effect from energy(639,640) and sodium (641) restrictionand supplementation with vitamin C(642) and vitamin E (642,643). Humanstudies have identified associations be-tween urinary microalbumin and dietarysaturated fat (193) and between glomer-ular filtration rate (GFR) and total fat(644). However, the majority of humanstudies have focused on dietary protein.

Several studies have attempted to re-duce protein intake in people with type 1or type 2 diabetes and microalbuminuria.The achieved protein reductions (mea-sured 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 pro-tein intake, the GFR improved signifi-cantly in all four studies and the albuminexcretion rate was reduced significantly inthree. In a dosage-response analysis(645), a 0.1 g � kg�1 body wt � day�1



change in intake of animal protein wasrelated to an 11.1% change in albumin-uria.

Many studies have been conducted intype 1 diabetic subjects with macroalbu-minuria (overt nephropathy). Theachieved 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 thelatter two studies, reduced protein intakeslowed the rate of decline in the GFR sig-nificantly over 33–35 months (P � 0.05and P � 0.001, respectively). However, inone of the studies (652), antihypertensivetreatment might have been responsiblefor part of the beneficial effect on the GFR.

A few studies have explored the po-tential beneficial effects of plant proteinrather than animal protein. When pre-dominantly plant protein replaced animalprotein in three studies of type 1 diabeticsubjects, the amount of protein con-sumed was also reduced significantly(653– 655). Any beneficial effects mayhave been from reduction in the amountor change in the protein source. In theonly published study (656) comparingapproximately equivalent amounts of an-imal and plant protein, type 1 diabeticsubjects were normoalbuminuric, nor-motensive, and not hyperfiltering, so thatrenal benefits may not have been ex-pected. Long-term clinical trials areneeded to determine whether reductionsin certain types of protein (plant versusanimal) or changes in various plant pro-teins such as soy or various animal pro-teins will have a beneficial effect ondiabetic nephropathy.

Because of the small number of clini-cal studies and their methodologicalproblems (e.g., food intake not closelycontrolled, lack of success in reducingprotein to prescribed levels), there is in-sufficient evidence to make definite rec-ommendations for patients with diabetesand microalbuminuria or clinical ne-phropathy. There is, however, suggestiveevidence that even small reductions in di-etary protein intake from usual amounts(e.g., achieved reduction of 0.8–1.0 g �kg�1 body wt � day�1 in people with mi-croalbuminuria, 0.8 g � kg�1 body wt �day�1 or lower for people with clinicalnephropathy) will retard the progressionof renal disease. However, reduction ofprotein intake should be done in the con-text of overall good nutrition. A dietitianfamiliar with MNT for both diabetes and

renal diseases should be involved in de-veloping the reduced-protein diet.


● In patients with diabetic nephropathy,reduction of dietary protein to 0.8–1.0g � kg�1 body wt � day�1 for people withmicroalbuminuria and 0.8 g � kg�1

body wt � day�1 for people with overtnephropathy may slow the progressionof nephropathy.


● There is insufficient evidence to makerecommendations regarding the sourceof dietary protein (animal versus plant).

Catabolic illnessThe catabolic state induced by injury, in-flammation, or severe illness is associatedwith special nutrition considerations.Most studies of nutrient needs are in non-diabetic subjects, but the results are likelyapplicable to patients with diabetes. Manyof the changes in nutrient requirementsappear to be cytokine mediated. Cyto-kines reduce albumin production, de-crease plasma levels of some traceproteins through tissue redistribution, in-duce negative nitrogen balance, and alterintermediary metabolism in such a way asto increase glucose levels through the ac-tions of the counterregulatory hormones(657). These changes, as well as alteredfluid balance, make nutritional assess-ment difficult during times of critical ill-ness. Overall, catabolic disease statesresult in a change in body compartmentsthat may be characterized by an increasedextracellular fluid compartment (fre-quently with an actual increase in bodyweight) and an associated shrinkage ofbody fat and body cell mass (body cellmass is defined as the actively functioningprotein-rich tissue and associated intra-cellular fluid) (658).

The magnitude of recent weight loss,taking into account the presence of excessfluid that is often present in critically illpatients, along with the presence or ab-sence of clinical markers of stress and theamount of time the patient will be unableto eat should determine the need for nu-tritional intervention (657). A recentweight loss of �10% of usual weight ne-cessitates a thorough nutritional assess-ment; an unintentional loss of 10–20%

suggests moderate protein-calorie malnu-trition, and a loss of �20% usually indi-cates severe malnutr i t ion (659) .Numerous studies have shown that theneeds of most hospitalized patients can bemet by providing 25–35 kcal/kg body wt(657). Care should be taken not to over-feed the patient, as this can exacerbate hy-perglycemia, cause abnormal liverfunction, and increase oxygen consump-tion and carbon dioxide production(657).

Protein needs are �1.0 g/kg body wtfor mildly stressed patients and 1.5 g/kgbody wt for moderately to severelystressed patients with normal hepatic andrenal function. This intake of protein willnot decrease protein catabolism, but willresult in an increase in protein synthesis.At least 30% of total energy should begiven as lipids (659).

For the hospitalized patient with dia-betes who requires parenteral or enteralnutrition, the goal is to provide adequatenutrition while avoiding extremes of hy-per- and hypoglycemia. For stressed hos-pitalized patients, a reasonable aim is tomaintain glucose levels at 100–200 mg/dl(5.6–11.1 mmol/l) (659). As with solidfood, the total grams of carbohydrate inthe feeding will have the greatest impacton the blood glucose response (660). Theenteral route is preferred if the gastroin-testinal tract is functional. A standard en-teral formula (50% carbohydrate) or alower carbohydrate (33–40% carbohy-drate) formula may be used in individualswith diabetes (660). Careful monitoringof vital signs, hemodynamic data, weight,fluid balance, plasma glucose and electro-lytes, and acid-based status is essential(659). Medications, usually insulin, mayneed to be adjusted to maintain glycemiccontrol.

There is limited evidence for the fol-lowing statements:

● Careful monitoring of nutritional statusindicators (e.g., change in body weight)and glycemia are necessary to ensurethat nutrient needs are being met andhyperglycemia is prevented. The en-ergy needs of most hospitalized pa-tients can be met by providing 25–35kcal/kg body wt.

● Protein needs are 1.0–1.5 g/kg bodywt, with the higher end of the rangebeing for more stressed patients.

Technical Review


DIABETES PREVENTION — Theimportance of preventing diabetes inhigh-risk individuals is highlighted by thesubstantial increase in the prevalence ofdiabetes in the U.S. over an 11-year pe-riod (661,662). From the most recentdata available, the increase in the preva-lence of diabetes continued unabated wellthrough the late 1990s (663) and, mostlikely, continues to the present day.

Genetic susceptibility appears to playa powerful role in the occurrence of type 2diabetes in certain populations; however,given that population gene pools shiftquite slowly, the current epidemic likelyreflects marked changes in lifestyle. Life-style changes that are characterized by de-creased physical activity and increasedenergy consumption have together pro-moted obesity, which is a remarkablystrong risk factor for diabetes that itself isinfluenced by both genes and behavior.

Weight lossExcess body fat is perhaps the most nota-ble modifiable risk factor for the develop-ment of type 2 diabetes (664). It isestimated that the risk of type 2 diabetesattributable to obesity is as much as 75%(92). A striking increase in the prevalenceof obesity, as well as diabetes, was re-ported between NHANES II and III. As ofthe early 1990s, over 50% of the U.S.adult population was overweight (665). Ifthe prevalence of obesity continues to in-crease, it is expected that the prevalenceof diabetes in the population will also in-crease.

Numerous interventions focusing onweight loss through hypocaloric, low-fatdiets, increased physical activity, and avariety of behavior change strategies haveemerged (316,318,327,338,666,667). Itis unfortunate that preventing obesity andeffectively reducing body weight haveproven difficult to accomplish and partic-ularly challenging to maintain over thelong term. Accordingly, pharmacologicalagents to enhance weight reduction andmaintenance of weight loss have recentlybeen recommended for individuals athigh risk for obesity-related conditionswhen other weight-loss methods havefailed (668–671).

Despite these difficulties, several re-cent studies have demonstrated the po-tential for moderate, sustained weight lossto substantially reduce risk for type 2 di-abetes (672– 677). Wannamethee andShaper (678) reported increased risk for

diabetes in men who gained weight over a12-year period of follow-up. Overweightmen who lost weight had a reduced risk ofdiabetes. In the Framingham Study co-hort, sustained weight loss over two con-secutive 8-year periods led to a 37% lowerrisk of diabetes; however, those who re-gained the lost weight failed to experienceany reduction in diabetes incidence(677).

Clinical trial data also support the po-tential for weight loss to reduce risk fordiabetes. In the Malmo Feasibility Study(673), both weight reduction and in-creased fitness were associated with re-duced incidence of diabetes in a lifestyleintervention group when compared to acontrol group. In the Da Qing Study, diet,exercise, and diet plus exercise all re-duced the incidence of diabetes com-pared to the control condition (672). Inthe Swedish Obese Subjects Study, obeseindividuals with sustained weight loss 2years after bariatric surgery demonstratedsubstantially lower risk of type 2 diabetesand hyperinsulinemia compared to con-trol subjects (676). Results from a 2-yearclinical trial showed reduced risk for pro-gression from impaired glucose toleranceto diabetes among individuals random-ized to orlistat compared to those ran-domized to behavioral therapy (675).

The Finnish Diabetes PreventionStudy (319) included 522 overweight in-dividuals with impaired glucose tolerancerandomized to control or intensive life-style intervention, which included weightreduction (5% or more), reduction of to-tal (�30% of energy intake) and saturatedfat (�10% of energy intake), increasedfiber (�15 g/1,000 kcal), and increasedphysical activity (�4 h/week). The sub-jects in the intervention group were morelikely to report changes in dietary and ex-ercise habits than subjects in the controlgroup. Success in achieving goals in theintervention group varied from 25% (fi-ber intake) to 86% (exercise). The cumu-lative incidence of diabetes after 4 yearswas 11% in the intervention group and23% in the control group. The risk of di-abetes was reduced by 58% in the inter-vention group, an outcome directlyassociated with changes in lifestyle.

In the U.S., the DPP study tested thesafety and efficacy of pharmacologicaltherapy and lifestyle modification ofweight management and physical activity(316). The study was recently completed,approximately 1 year earlier than

planned, because of the remarkable suc-cess of both interventions (317). The DPPstudy included 3,234 individuals of di-verse ethnic backgrounds (45% minorityinclusion), all of whom had impaired glu-cose tolerance at study entry. Participantsrandomly assigned to intensive lifestylereduced their risk of developing type 2diabetes by 58% over nearly 3 years offollow-up. Significant risk reduction wasobserved across subgroups of ethnicity,age, gender, BMI, and fasting glucose.Among individuals over age 60 years, therisk reduction was 71%. On average, in-dividuals in the lifestyle interventiongroup reduced their percent calories fromfat from �34 to �27.5%; maintainedtheir physical activity at �30 min/day,usually with walking or other moderateintensity physical activity; and lost 5–7%of their baseline body weight. Of interestwas the finding that the pharmacologicalagent tested, metformin, reduced diabe-tes risk by 31%, which was less than therisk reduction observed for the lifestyleintervention. However, unlike lifestyle,metformin was not uniformly successful.Although effective in men and womenand in all ethnic groups, metformin wasrelatively ineffective in the older volun-teers and in those who were less over-weight.

The consistency of beneficial effectsof lifestyle interventions used in the Finn-ish Diabetes Study and the DPP is furthersupported by an analysis of data from theNurses’ Health Study (679) in which in-dividuals categorized as low risk based ona BMI �25 and a set of related lifestylevariables experienced reduced risk for di-abetes incidence over 16 years of follow-up. Thus there is clearly strong evidencethat comprehensive lifestyle interventionsreduce the incidence of type 2 diabetes.Additional work in the area of increasingadherence and long-term success of inter-vention strategies for sustained lifestylechange is needed (680).

ExerciseAlthough obesity is generally regarded asthe salient modifiable risk factor for type 2diabetes, decreased physical activity alsohas been identified as a diabetes risk fac-tor, independent of its impact on energybalance. A relationship between physicalactivity and type 2 diabetes was suggestedby studies in societies that had abandonedtraditional lifestyles typically involvinglarge amounts of habitual physical activity



and subsequently experienced major in-creases in rates of type 2 diabetes. Morerecently, the fact that an active lifestylemay prevent or delay the development oftype 2 diabetes has been demonstrated ina number of prospective studies (681–685). Protection from diabetes appears tooccur from moderate intensity activities,such as brisk walking, as well as from par-ticipation in vigorous physical activity.Moreover, physical activity may providesome protection against mortality at alllevels of glucose tolerance, as has beendemonstrated in middle-aged men (686).Of interest in this regard is a large pro-spective observational study demonstrat-ing that cardiorespiratory fitness levels inmen influence the effects of obesity onhealth (687). No elevated mortality risk inobese men was observed if they werephysically fit, and lean men had increasedlongevity only if they were physically fit.Thus moderate-to-high cardiorespiratoryfitness may reduce mortality risk acrossall categories of body composition.

Dietary fatDietary fat intake appears to be an impor-tant determinant of diabetes risk, inde-pendent of total caloric intake. Using acase-control design, increased intake ofdietary fat was associated with occurrenceof diabetes among second-generation Jap-anese-American men (688). After adjust-ment for total caloric intake and obesity,Marshall et al. (93) reported increased in-cidence of diabetes with increased intakeof dietary fat. However, three large pro-spective studies that relied on patient-report of physician-diagnosed diabetesdid not detect an effect of dietary fat ondiabetes incidence, or else suggested dif-ferential effects of various subtypes of di-etary fat (118,119,689). Results from tworecent studies (690,691) suggest that in-creased intake of polyunsaturated fat maybe associated with reduced risk of type 2diabetes, independent of BMI, total en-ergy intake, physical activity, and otherpotential confounders. Potential mecha-nisms underlying these findings are un-clear.

Several studies have identified dietaryfat as a contributor to insulin resistanceindependent of obesity (92–100), butother studies do not support this (690–692). Nevertheless, it appears that alltypes of dietary fat, except n-3 fatty acids,may have an adverse effect on insulin sen-sitivity. Results are most consistent for an

adverse effect of saturated fats. These ef-fects may be enhanced among individualswith obesity (99) or low levels of physicalactivity (98,99).

Although early animal studies sug-gested a potential deleterious effect of di-etary fat on insulin secretion (693), recentstudies in human populations have failedto demonstrate either clinically or statis-tically significant effects (694,695).

In total, the impact of dietary fat ondiabetes risk appears to lie primarily inthe impact of high-fat diets on long-termenergy balance. Other specific metaboliceffects of dietary fat may occur, but seemlikely to play only a minor role in overalldiabetes risk.

Whole grains/fiberRecent studies have provided preliminaryevidence for reduced risk of diabetes withincreased intake of whole grains and di-etary fiber (27,696,697). In both theNurses’ Health Study (27) and the IowaWomen’s Health Study (697), increasedintake of whole grain food was associatedwith significant reductions in incidence oftype 2 diabetes. A higher glycemic load,calculated and applied to food frequencydata, was related to increased incidence ofdiabetes in men (118) and women (119).The glycemic load is defined as the prod-uct of the glycemic index value of a foodand its carbohydrate content in an aver-age serving. It incorporates both the qual-i ty and quantity of carbohydrateconsumed. However, glycemic load orglycemic index was not related to diabetesincidence in the Iowa Women’s HealthStudy (697).

MicronutrientsSelected micronutrients may affect glu-cose and insulin metabolism, but the dataare scarce or inconsistent. Within therange that can be obtained from food in-take, men with higher plasma concentra-tions of �-tocopherol experiencedreduced risk for diabetes compared tomen with lower concentrations of �-to-copherol (374). Results of studies thatevaluated effects of vitamin E on insulinsens i t i v i t y have been equ ivoca l(363,698,699). Insufficient intake ofmagnesium, zinc, and chromium havebeen implicated as possible risk factorsfor the development of diabetes(118,697,700 –703); however, neitherthe efficacy nor the safety of supple-mented intake has been established.

AlcoholWhen compared to abstinence and heavydrinking, moderate alcohol intake hasbeen related to improved insulin sensitiv-ity (439–441) and reduced risk for dia-betes (437) However, insufficient dataexist to support a specific recommenda-tion for moderate alcohol intake for pre-vention of type 2 diabetes, and potentialadverse effects of heavy drinking must becarefully considered.

Cow’s milkType 1 diabetes accounts for �10% of alldiabetes and, like type 2 diabetes, hasboth genetic and environmental determi-nants. Early introduction of cow’s milk ininfants may be an environmental factorcontributing to the development of child-hood diabetes, but the research evidencehas been equivocal (704–710). Currentlythere are no clear dietary determinants oftype 1 diabetes.

Youth onset type 2 diabetesAlthough most of the diabetes diagnosedin children is type 1 diabetes, recentlynon�type 1 phenotypes, particularlyamong minority youth, have been re-ported. As such, youth-onset type 2 dia-betes is a relatively new area of research.Obesity and physical inactivity seemlikely to play an important role in devel-opment of this condition; however, nosufficient data have been collected fromyouth to justify any clear recommenda-tions for the prevention of diabetes inyouth at this time.


● Sustained, modest weight loss of�5–7% of body weight through re-duced energy intake, reduced intake ofdietary fat, and increased physical ac-tivity will reduce the risk for developingtype 2 diabetes.

● Structured programs that emphasizelifestyle changes are necessary to ac-complish these objectives.

● All individuals, especially family mem-ber of individuals with type 2 diabetes,should be encouraged to engage in reg-ular physical activity to decrease therisk of developing type 2 diabetes. Bothmoderate and vigorous exercise de-crease the risk of impaired glucose tol-erance and type 2 diabetes.

Technical Review


Table 7 —Major nutrition recommendations

Nutrition Recommendations Grading

Carbohydrate• Foods containing carbohydrate from whole grains, fruits, vegetables, and low-fat milk are important components and should be

included in a healthy diet.A

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

A

• Because sucrose does not increase glycemia to a greater extent than isocaloric amounts of starch, sucrose and sucrose-containingfoods 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.

A

• Nonnutritive sweeteners are safe when consumed within the ADI levels established by the FDA. A• Individuals receiving intensive insulin therapy should adjust their premeal insulin dosages based on the carbohydrate content of meals. B• 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.B

• As far the general public, consumption of dietary fiber is to be encouraged; however, there is no reason to recommend that peoplewith diabetes consume a greater amount of fiber than other Americans.

B

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

• Sucrose and sucrose-containing foods should be eaten in the context of a healthy diet. E

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.B

• For persons with diabetes, especially those not with less-than-optimal glucose control, the protein requirements may be greaterthan the RDA, but not greater than usual intake.

B

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

E

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

E

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.A

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

A

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

B

• Intake of transunsaturated fatty acids should be minimized. B• Reduced-fat diets when maintained long term contribute to modest loss of weight and improvement in dyslipidemia. B• Polyunsaturated fat intake should be �10% of energy intake. C

Energy balance and obesity• In insulin-resistant individuals, reduced energy intake and modest weight loss improve insulin resistance and glycemia in the

short-term.A

• 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.

A

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

A

• Standard weight-reduction diets, when used alone, are unlikely to produce long-term weight loss. Structured, intensive lifestyleprograms are necessary.

A

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.B

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

Continued on following page



Table 7 —Continued

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.B

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

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.E

• Nutrient requirements for children and adolescents with type 1 or type 2 diabetes appear to be similar to requirements for sameage nondiabetic children and adolescents.

E

Pregnancy and lactation• Nutrition requirements during pregnancy and lactation are similar for women with and without diabetes. E• Medical nutrition therapy for gestational diabetes focuses on food choices for appropriate weight gain, normoglycemia, and

absence of ketones.E

• For some women with gestational diabetes, modest energy and carbohydrate restriction may be appropriate. E

Older adults• Energy requirements for older adults are less than for younger adults. A• Physical activity should be encouraged A• In the elderly, undernutrition is more likely than overnutrition and therefore caution should be exercised when prescribing

weight-loss diets.E

Acute complications• Glucose is the preferred treatment for hypoglycemia, although any form of carbohydrate that contains glucose may be used. A• Ingestion of 15–20 g of glucose is an effective treatment for hypoglycemia, but blood glucose may be only temporarily corrected. B• During acute illnesses, testing blood glucose and blood or urine for ketones, drinking adequate amounts of fluids, and ingesting

carbohydrate are important.B

• 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.

E

Hypertension• In both normotensive and hypertensive individuals, a reduction in sodium intake lowers blood pressure. A• A modest amount of weight loss beneficially affects blood pressure. A• The goal should be to reduce sodium intake 2,400 mg (100 mmol) or sodium chloride to 6,000 mg per day. E

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.B

• Energy derived from saturated fat can be reduced if weight loss is desirable or replaced with either carbohydrates ormonounsaturated fats if weight loss is not a goal.

E

• For individuals with elevated plasma triglycerides, reduced HDL cholesterol, and small dense LDL cholesterol (the metabolicsyndrome), improved glycemic control, modest weight loss, dietary saturated fat restriction, increased physical activity, andincorporation of monounsaturated fats may be beneficial.

B

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.C

Catabolic illness• The energy needs of most hospitalized patients can be met by providing 25–35 kcal/kg body wt. E• 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. E

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.A

• All individuals, especially family members of individuals with type 2 diabetes, should be encouraged to engage in regular physicalactivity to decrease risk of developing type 2 diabetes.

B

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

Technical Review



● Increased intake of whole grains anddietary fiber may reduce diabetes risk.

● Reduced intake of total fat, particularlysaturated fat, may improve insulin sen-sitivity and reduce risk for diabetes, in-dependent of weight loss.


● Increased intake of polyunsaturated fat,in the context of appropriate total en-ergy intake for weight management,may reduce the risk for type 2 diabetes.


● No nutritional recommendations canbe made for the prevention of type 1diabetes. Breastfeeding may be benefi-cial.

● Although increasing obesity in youthmay be related to an increase in theprevalence of type 2 diabetes, particu-larly in minority adolescents, there isinsufficient data at present to warrantany specific recommendation for theprevention of type 2 diabetes in youth.Increased physical activity, reduced en-ergy and fat intake, and resultantweight management may prove to bebeneficial.

SUMMARY — Major nutrition rec-ommendations are listed in Table 7. Themajor nutrition recommendations listedin Table 7 are classified according to thelevel of evidence using the American Di-abetes Association evidence grading sys-tem. The principles reviewed in the abovetechnical review paper are the basis forthe recommendations. MNT for peoplewith diabetes should be individualized,with consideration given to each individ-ual’s usual food and eating habits, meta-bolic profile, treatment goals, and desiredoutcomes. Monitoring of metabolic pa-rameters, including glucose, HbA1c, lip-ids, blood pressure, body weight, andrenal function, when appropriate, as wellas quality of life is essential to assess theneed for changes in therapy and to ensuresuccessful outcomes. Ongoing nutritionself-management education and careneed to be available for individuals with

diabetes. Finally, many areas of nutritionand diabetes require additional research.

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Evidence-Based Nutrition Principles and Recommendations ... · Evidence-Based Nutrition Principles and Recommendations for the Treatment and Prevention of Diabetes and Related Complications