Medical Nutrition Therapy for Diabetes Mellitus … / Medical Nutrition Therapy for Diabetes...

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C H A P T E R 33Medical Nutrition Therapyfor Diabetes Mellitusand Hypoglycemia of Nondiabetic OriginM A R I O N J . F R A N Z , M S , R D , L D , C D E

C H A P T E R O U T L I N E

• Pathophysiology

• Diagnostic and Screening Criteria

• Management of Diabetes Mellitus

• Diabetes and Age-Related Issues

• Implementing Nutrition Self-Management

• Acute Complications

• Long-Term Complications

• Preventing Diabetes

• Hypoglycemia of Nondiabetic Origin

KEY TERMS

autonomic symptoms–symptoms of hypoglycemiathat are adrenergically based and that arise from the ac-tion of the autonomic nervous system

combination therapy–a form of therapy for diabetesusing combinations of oral medications or a combinationof oral medication(s) and insulin injection(s)

counterregulatory (stress) hormones–hormones,including glucagon, epinephrine (adrenaline), norepi-nephrine, cortisol, and growth hormone, released dur-ing stressful situations, which have the opposite effectof insulin and cause the liver to release glucose fromstored glycogen (glycogenolysis) and the adiposecells to release fatty acids for extra energy (lipolysis);these hormones counterbalance declining glucoselevels

dawn phenomenon–a natural increase in morningblood glucose levels and insulin requirements that oc-curs in people with and without diabetes but tends to bemore marked in people with diabetes; possibly caused

by a diurnal variation in growth hormone, cortisol, or cat-echolamines

Diabetes Control and Complications Trial (DCCT)–a 10-year study in people with type 1 diabetes who weretreated with either conventional therapy or intensivetherapy; follow-up evaluations proved that tight bloodglucose control reduces the risk of diabetic microvascu-lar complications

diabetic ketoacidosis (DKA)–severe, uncontrolled di-abetes, resulting from insufficient insulin, in which ke-tone bodies (acids) build up in the blood; if left untreated(with immediate administration of insulin and fluids),DKA can lead to coma and even death

fasting (food-deprived) hypoglycemia–low blood glu-cose concentrations in response to no food intake for 8hours or longer

gestational diabetes mellitus (GDM)–glucose intol-erance, the onset or first recognition of which occursduring pregnancy

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33 / Medical Nutrition Therapy for Diabetes Mellitus and Hypoglycemia of Nondiabetic Origin 793

glucagon–a hormone produced by the �-cells of the pan-creas that causes an increase in blood glucose levels bystimulating the release of glucose from liver glycogen stores

glucotoxicity–pancreatic beta cells chronically exposedto hyperglycemia become progressively less efficient in re-sponding to a glucose challenge

glycosylated hemoglobin–a blood test that reflects theblood glucose concentration over the life span of red bloodcells (�120 days), expressed as a percentage of total hemo-globin with glucose attached; may also be called glycatedhemoglobin or glycohemoglobin. Hemoglobin A1 (HbA1) isan evaluation of a combination of all fractions of the hemo-globin molecule. Hemoglobin A1c (HbA1c) is a measure-ment of the glycosylation of the “c” fraction and is the recom-mended assay method (simplified to A1c). An A1c of 6.0%reflects an average plasma glucose level of �120 mg/dl. Ingeneral, each 1% increase in A1c is a reflection of an in-crease in average glucose levels of �30 mg/dl

honeymoon phase–the period after the initial diagnosisof type 1 diabetes when there may be some recovery of �-cell function and a temporary decrease in exogenous in-sulin requirement

hyperglycemia–an excessive amount of glucose in theblood (generally �180 mg/dl or above) caused by too littleinsulin, insulin resistance, or increased food intake; symp-toms include frequent urination, increased thirst, weightloss, and often tiredness or fatigue

hyperglycemic hyperosmolar state (HHS)–extremelyhigh blood glucose levels with an absence of or only slightketosis and profound dehydration

hypoglycemia (or insulin reaction)–low blood glucoselevel (usually �70 mg/dl), which can be caused by the ad-ministration of excessive insulin or insulin secretagogues,too little food, delayed or missed meals or snacks, in-creased amounts of exercise or other physical activity, or al-cohol intake without food

hypoglycemia of nondiabetic origin–low levels of bloodglucose that lead to neuroglycopenia symptoms that areameliorated by the ingestion of carbohydrate

immune-mediated diabetes mellitus–a form of type 1 di-abetes resulting from autoimmune destruction of the �-cellsof the pancreas

impaired glucose homeostasis–metabolic stages of im-paired glucose use (between normal glucose concentra-tions and diabetes), which are risk factors for future dia-betes and cardiovascular disease

insulin–a hormone released from the �-cells of the pan-creas that enables cells to metabolize and store glucoseand other fuels

insulin resistance–an impaired biologic response (sensi-tivity) to either exogenous or endogenous insulin; insulin re-sistance and insulin deficiencies are involved in the etiologyof type 2 diabetes

insulin secretagogues–oral medications that stimulateinsulin release from the �-cell of the pancreas, such as sul-fonylureas and nonsulfonylurea secretagogues (i.e., repag-linide and nateglinide)

insulin sensitizers–oral medications that enhance in-sulin action and include biguanides (metformin) and thiazo-lidinediones

macrovascular diseases–diseases of the large bloodvessels, including coronary artery disease, cardiovasculardisease, and peripheral vascular disease

metabolic syndrome–characterized by central obesityand insulin resistance with increased risk for cardiovasculardisease and type 2 diabetes; associated risk factors includedyslipidemia (elevated triglycerides, low high-density lipo-protein [HDL] cholesterol, and high low-density lipoprotein[LDL] cholesterol), hypertension, prothrombotic factors,and impaired glucose tolerance

microvascular diseases–diseases of the small bloodvessels, including retinopathy and nephropathy

neuroglycopenic symptoms–neurologic symptoms ofhypoglycemia that are related to an insufficient supply ofglucose to the brain

oral glucose-lowering medications–drugs, administeredorally, that are used to control or lower blood glucose levels,including first- and second-generation sulfonylureas, non-sulfonylureas, secretagogues, biguanides, �-glucosidaseinhibitors, and thiazolidinediones

polydipsia–excessive thirstpolyuria–excessive urinationpostprandial (after a meal) blood glucose–blood glu-

cose level 1 to 2 hours after eatingpostprandial (reactive) hypoglycemia–low blood glu-

cose within 2 to 5 hours after eatingpre-diabetes–blood glucose concentrations that are

higher than normal but not yet high enough to be diagnosedas diabetes; sometimes referred to as impaired glucose tol-erance (IGT) or impaired fasting glucose (IFG), dependingon which test was used to detect it

preprandial (fasting) blood glucose–blood glucose levelbefore eating

self-monitoring of blood glucose (SMBG)–a methodwhereby individuals can test their own blood glucose levelsusing a chemically treated strip and visually comparing thestrip to a color chart or by inserting the strip into a meterthat measures the glucose level; most blood glucose me-ters automatically convert capillary whole blood glucosevalues to plasma glucose values

Somogyi (rebound) effect–an episode of hypoglycemiausually caused by excessive exogenous insulin, whichstimulates the overproduction of counterregulatory hor-mones, resulting in an excessive release of glucose fromthe liver and hyperglycemia; often caused by inappropriateevening insulin doses; evening insulin doses should not beincreased in an attempt to improve glucose levels

target blood glucose goals–levels for capillary blood glu-cose tests that are as near normal as possible and that canbe achieved without risk of serious hypoglycemia

type 1 diabetes–a type of diabetes that usually occurs inpersons younger than 30 years of age but can occur at anyage; previously known as insulin-dependent diabetes melli-tus (IDDM) or juvenile-onset diabetes

type 2 diabetes–a type of diabetes usually occurring inpersons older than 30 years of age, previously knownas non–insulin-dependent diabetes mellitus (NIDDM) ormaturity-onset diabetes; now also frequently diagnosed inyouth and young adults; formerly called maturity onset di-abetes of youth (MODY)

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794 5 / MEDICAL NUTRITION THERAPY

D iabetes mellitus is a group of diseases char-acterized by high blood glucose concentra-tions resulting from defects in insulin secre-

tion, insulin action, or both. Abnormalities in themetabolism of carbohydrate, protein, and fat are alsopresent. Persons with diabetes have bodies that donot produce or respond to insulin, a hormone pro-duced by the �-cells of the pancreas that is necessaryfor the use or storage of body fuels. Without effectiveinsulin, hyperglycemia (elevated blood glucose) oc-curs, which can lead to both the short-term and long-term complications of diabetes mellitus.

In 2000, about 15 million U.S. adults 18 years ofage or older had diagnosed diabetes (6.3 million menand 8.7 million women), representing an increasefrom 4.9% of the adult population in 1990 to 7.3% in2000. If undiagnosed diabetes is considered as well,it is likely that almost 10% of U.S. adults have dia-betes (Mokdad et al, 2001). Much of the increase is be-cause type 2 diabetes is no longer a disease that af-fects mainly older adults. Between 1990 and 1998, theprevalence of diabetes increased by 76% among peo-ple in their thirties (Mokdad et al, 2001). Among chil-dren with newly diagnosed diabetes, the prevalenceof type 2 diabetes also increased dramatically in thepast decade, growing from less than 4% in the yearspreceding 1990 to as high as 45% in certainracial/ethnic groups in recent years (American Dia-betes Association [ADA], 2000).

Diabetes prevalence increases with increasingage, affecting 18.4% of those 65 years of age or older(ADA, 2001). Diabetes is particularly prevalent inminorities; indeed, the prevalence of type 2 dia-betes is highest in ethnic minorities in the UnitedStates, such as African Americans, Hispanic popu-lations (Latinos and Mexican Americans), NativeAmericans and Alaska Natives, Asian Americans,and Pacific Islanders (see Focus on: Diabetes DoesDiscriminate!).

Of great concern are the more than 20 millionadults reported to have impaired glucose tolerance(IGT) (2-hour postchallenge glucose of 140-199 mg/dl), the 13 to 14 million with impaired fasting glucose(IFG) (fasting plasma glucose 110-125 mg/dl), andthe 40 to 50 million with metabolic syndrome (ADA,2001). Persons with IGT or IFG are now classified ashaving pre-diabetes, and they are at high risk for con-version to type 2 diabetes if lifestyle preventionstrategies are not used and are at higher risk of car-

diovascular disease compared with persons withnormal blood glucose concentrations.

Diabetes mellitus contributes to a considerable in-crease in morbidity and mortality rates, which can bereduced by early diagnosis and treatment. In 2002 di-abetes costs in the United States were $132 billion. Di-rect medical expenditures, such as inpatient care,outpatient services, and nursing home care, totaled$91.8 billion. Indirect costs, totaling $39.8 billion,were associated with lost productivity, including pre-mature death and disability. Total medical expendi-tures incurred by people with diabetes totaled $91.8billion, or an average annual total direct cost of med-ical care of $13,243 per person compared with $2560per person without diabetes (ADA, 2003a).

In 1997 new recommendations for the classificationand diagnosis of diabetes mellitus were accepted andsupported by the ADA, the National Institute of Dia-betes and Digestive and Kidney Diseases (NIDDKD),and the Centers for Disease Control and Prevention,Division of Diabetes Translation. Recommendationswere also made to eliminate the terms insulin-dependent diabetes mellitus (IDDM) and non–insulin-dependent diabetes mellitus (NIDDM) and to keep theterms type 1 and type 2 diabetes but to use Arabicrather than Roman numerals (Expert Committee onthe Diagnosis and Classification of Diabetes Mellitus,1997) (Table 33-1).

Type 1 DiabetesAt diagnosis, people with type 1 diabetes are usuallylean and are experiencing excessive thirst, frequenturination, and significant weight loss. The primarydefect is pancreatic �-cell destruction, usually lead-ing to absolute insulin deficiency and resulting in hy-perglycemia, polyuria (excessive urination), polydip-sia (excessive thirst), weight loss, dehydration,electrolyte disturbance, and ketoacidosis. The rate of�-cell destruction is quite variable, proceeding rap-idly in some persons (mainly infants and children)and slowly in others (mainly adults). The capacity ofa healthy pancreas to secrete insulin is far in excess ofwhat is needed normally; therefore, the clinical onset

PATHOPHYSIOLOGY

United Kingdom Prospective Diabetes Study (UKPDS)–a 20-year multicenter trial in the United Kingdom of sub-jects with type 2 diabetes who were randomized into inten-sive therapy or conventional therapy; lowering of A1c andaggressive treatment of hypertension significantly reduced

the development of microvascular complications and low-ered the risk for macrovascular complications

Whipple’s triad–a triad of clinical features that includes(1) low blood glucose levels, (2) accompanied by symp-toms, which are (3) relieved by administration of glucose

KEY TERMS—Continued

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of diabetes may be preceded by an extensive asymp-tomatic period of months to years, during which �-cells are undergoing gradual destruction (Figure33-1).

Type 1 diabetes accounts for 5% to 10% of all diag-nosed cases of diabetes. Persons with type 1 diabetesare dependent on exogenous insulin to prevent ke-toacidosis and death. Although it may occur at anyage, even in the eighth and ninth decades of life, most

cases are diagnosed in people younger than 30 yearsof age, with a peak incidence at around ages 10 to 12years in girls and ages 12 to 14 years in boys.

Type 1 diabetes has two forms: immune-mediateddiabetes mellitus and idiopathic diabetes mellitus.Immune-mediated diabetes mellitus results from anautoimmune destruction of the �-cells of the pan-creas. Idiopathic type 1 diabetes mellitus refers to formsof the disease that have no known etiology. Although

Diabetes strikes particularly hard at minorities. Certainenvironmental or lifestyle factors may increase the

risk of developing type 2 diabetes in susceptible popula-tions. For example, an increase in the prevalence is ob-served in populations who have migrated to more urban-ized locations compared with people of the same groupwho remained in their traditional home. Urbanization isusually related to major changes in diet, physical activity,and socioeconomic status as well as increased obesity.

One theory that might explain the increased preva-lence of diabetes and insulin resistance among Nativepeople is the “thrifty” gene. Years of subsistence livinghave created a thrifty genotype that allows Native peo-ple to extract a lot of energy and fat from small amountsof food. In an era of store-bought processed food, thatgene backfires to induce obesity and diabetes. Adoptionof a “Western” lifestyle (which may include a diet high infat and a sedentary way of life) has been associated witha dramatically increased rate of type 2 diabetes in thePima Indians of Arizona (ADA, 2001). Among the PimaIndians of Arizona, about 55% of adults older than 35years of age have type 2 diabetes. This disease is in-creasingly being diagnosed in Native Americansyounger than 30 years of age and has been diagnosedin some as young as 7 years of age.

Ravussin and colleagues (1994) surveyed a closelyrelated population of Pima Indians living in Maycoba, asmall village in a remote, mountainous region of north-western Mexico. They found that individuals in this com-

munity ate a diet lower in fat than is typically consumedin Arizona, and both men and women were very physi-cally active. The men and women of Maycoba weighed,on average, 50 lb less than a comparable group of Pi-mas from the Phoenix area. More important, diabeteswas diagnosed in about 10% of the Maycoba Pimascompared with almost 50% of the Arizona Pimas.

The main staples of the Maycoba Pimas’ diet arebeans, corn (as tortillas), and potatoes. Several essen-tial nutrients are lacking because of the relative absenceof fruits and vegetables. Diet analysis reveals a dietcomposed of 13% protein, 23% fat, 63% carbohydrate,and less than 1% alcohol and containing more than 50 gof fiber.This is in sharp contrast to the present diet of theArizona Pimas. Even more striking than the low-fat dietof the Maycoba population, however, was the high levelof physical activity in this population; more than 40 hoursa week were spent engaged in hard physical work(Ravussin et al, 1994).

Interventions involving increased physical activityand a reduced fat and energy diet slowed the pro-gression to type 2 diabetes in high-risk populations (Diabetes Prevention Program Research Group, 2002).Health promotion activities through community-basedexercise programs and a return to more traditional dietsalso may help to reduce the diabetes epidemic that af-fects many developing countries as well as the under-privileged in industrialized nations.

Diabetes Does Discriminate!FOCUS ON

Types of Diabetes and Prediabetes

CLASSIFICATIONS DISTINGUISHING CHARACTERISTICS

Type 1 diabetes Affected persons are usually lean, have abrupt onset of symptoms before the age of 30 yr (although it may occur at any age), and are dependent on exogenous insulin to prevent ketoacidosis and death.

Type 2 diabetes Affected persons are often older than 30 yr at diagnosis, although it is now occurring frequently in young adults and children. Individuals are not dependent on exogenous insulin for survival; they may require it for adequate glycemic control.

Gestational diabetes A condition of glucose intolerance affecting pregnant women, the onset or discovery of which occurs mellitus (GDM) during pregnancy.

Other specific types Diabetes that results from specific genetic syndromes, surgery, drugs, malnutrition, infections, or other illnesses.

Pre-diabetes or impaired Metabolic stage of impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) that is between glucose homeostasis current definitions of normal glucose values and diabetes.

Modified from Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, Diabetes Care 20:1183, 1997.

TABLE 33-1

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CAUSE

MEDICAL MANAGEMENT NUTRITIONAL MANAGEMENT

PATHOPHYSIOLOGY

TYPE 1 DIABETES MELLITUS

TYPE 1DIABETESMELLITUS

(absolute insulindeficiency)

Idiopathic

Immune-mediated

(Autoimmunity)(viral infection, toxic

chemicals,etc.)

Circulatingauto-antibodies

MEDICATION Insulin injections

GlargineLisproAspartNPHLente

UltralenteRegular

Insulin pumps

Daily blood glucosemonitoring

Synchronization of insulinaction with preferred food intake;consistency in timing and amount

of carbohydrate eaten ifon fixed insulin doses

SYMPTOMSHyperglycemia

Excessive thirst

Frequent urination

Significant weight loss

Electrolyte disturbances

Ketoacidosis

Macrovascular diseasesCoronary artery disease

Peripheral vascular diseaseCerebrovascular disease

Microvascular diseasesRetinopathy

NeuropathyNephropathy

A1c testing

Adjust premeal insulindoses based on

carbohydrate contentof meal

Adequate energy andnutrient intake to promotegrowth and development

in children

• Pathophysiology algorithm: type 1 diabetes mellitus. (Algorithm content developed by John Anderson, PhD, and SanfordC. Garner, PhD, 2000. Updated by Marion J. Franz, MS, RD, LD, CDE, 2002.)FIGURE 33-1

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only a minority of persons with type 1 diabetes fallinto this category, of those who do, most are ofAfrican or Asian origin (Expert Committee on the Di-agnosis and Classification of Diabetes Mellitus, 1997).

The etiology of immune-mediated diabetes involvesa genetic predisposition and an autoimmune destruc-tion of the islet �-cells that produce insulin. Genetic fac-tors involve the association between type 1 diabetesand certain histocompatibility locus antigens (HLA),with linkage to the DQA and DQB genes and influ-enced by the DRB genes. These HLA-DR/DQ allelescan be either predisposing or protective (Expert Com-mittee on the Diagnosis and Classification of DiabetesMellitus, 1997).

At diagnosis, 85% to 90% of patients with type 1diabetes have one or more circulating autoantibodiesto islet cells, endogenous insulin, or other antigensthat are constituents of islet cells. Antibodies identi-fied as contributing to the destruction of �-cells are(1) islet cell autoantibodies (ICAs); (2) insulin autoan-tibodies (IAAs), which may occur in persons whohave never received insulin therapy; and (3) autoan-tibodies to glutamic acid decarboxylase (GAD), aprotein on the surface of �-cells. GAD autoantibodiesappear to provoke an attack by the T cells (killer Tlymphocytes), which may be what destroys the�-cells in diabetes.

Frequently, after diagnosis and the correction ofhyperglycemia, metabolic acidosis, and ketoacidosis,endogenous insulin secretion recovers. During thishoneymoon phase, exogenous insulin requirementsdecrease dramatically for up to 1 year; however, theneed for increasing exogenous insulin replacement isinevitable, and within 8 to 10 years after clinical on-set, �-cell loss is complete and insulin deficiency isabsolute.

Type 2 DiabetesType 2 diabetes may account for 90% to 95% of all di-agnosed cases of diabetes and is a progressive dis-ease that, in many cases, is present long before it is di-agnosed. Hyperglycemia develops gradually and isoften not severe enough in the early states for the pa-tient to notice any of the classic symptoms of dia-betes. Although undiagnosed, these individuals areat increased risk of developing macrovascular andmicrovascular complications.

Risk factors for type 2 diabetes include genetic andenvironmental factors, including a family history ofdiabetes, older age, obesity, particularly intraabdom-inal obesity, physical inactivity, a prior history of ges-tational diabetes, impaired glucose homeostasis, andrace or ethnicity. Total adiposity and a longer dura-tion of obesity are established risks factors for type 2diabetes. Nevertheless, type 2 diabetes is found inpersons who are not obese, and many obese personsnever develop type 2 diabetes. Obesity combinedwith a genetic predisposition may be necessary fortype 2 diabetes to occur. Another possibility is that a

similar genetic predisposition leads independently toboth obesity and insulin resistance, which increasesthe risk for type 2 diabetes (ADA, 2001) (Figure 33-2).

In most cases, type 2 diabetes results from a combi-nation of insulin resistance and �-cell failure, but theextent to which each of these factors contributes to thedevelopment of the disease is unclear (Ferrannini,1998). Endogenous insulin levels may be normal, de-pressed, or elevated, but they are inadequate to over-come concomitant insulin resistance (decreased tissuesensitivity or responsiveness to insulin); as a result,hyperglycemia ensues. Insulin resistance is first dem-onstrated in target tissues, mainly muscle and theliver. Initially, there is a compensatory increase ininsulin secretion, which maintains normal glucoseconcentrations, but as the disease progresses, insulinproduction gradually decreases. Hyperglycemia isfirst exhibited as an elevation of postprandial (after ameal) blood glucose caused by insulin resistance atthe cellular level and is followed by an elevation infasting glucose concentrations. As insulin secretiondecreases, hepatic glucose production increases, caus-ing the increase in preprandial (fasting) blood glucoselevels. Compounding the problem is the deleteriouseffect of hyperglycemia itself—glucotoxicity—onboth insulin sensitivity and insulin secretion (Yki-Jarvinen, 1997), hence the importance of achievingnear-euglycemia in persons with type 2 diabetes.

Insulin resistance is also demonstrated at the adi-pocyte level, leading to lipolysis and an elevationin circulating free fatty acids. Increased fatty acidscause a further decrease in insulin sensitivity atthe cellular level, impair pancreatic insulin secretion,and augment hepatic glucose production (lipotoxicity)(Bergman and Adler, 2000). The above defects con-tribute to the development and progression of type 2diabetes and are also primary targets for pharmaco-logic therapy.

Persons with type 2 diabetes may or may not ex-perience the classic symptoms of uncontrolled dia-betes, and they are not prone to develop ketoacidosis.Although persons with type 2 diabetes do not requireexogenous insulin for survival, about 40% or morewill eventually require exogenous insulin for ade-quate blood glucose control. Insulin may also be re-quired for control during periods of stress-inducedhyperglycemia, such as during illness or surgery.

Gestational Diabetes MellitusGestational diabetes mellitus (GDM) is defined asany degree of glucose intolerance with onset or firstrecognition during pregnancy. It occurs in about 7%of all pregnancies, resulting in more than 200,000cases annually (ADA, 2001). Women with known di-abetes mellitus before pregnancy are not classified ashaving GDM. GDM is usually diagnosed during thesecond or third trimester of pregnancy. At this point,insulin-antagonist hormone levels increase, and in-sulin resistance normally occurs.

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CAUSE

MEDICAL MANAGEMENT NUTRITIONAL MANAGEMENT

PATHOPHYSIOLOGY

TYPE 2 DIABETES MELLITUS

TYPE 2DIABETESMELLITUS

(insulin resistance; insulin

deficiency)

Riskfactors

(physical inactivity,older age,obesity)

Environmentalfactors

DIAGNOSISFBG �126 mg/dl

Nonfasting glucose �200 mg/dl(with symptoms)

Oral GTT �200 mg/dl

EXERCISE

MONITORINGBlood glucose

A1c testing

MEDICATIONSulfonylureas

Non-sulfonylurea secretagoguesBiguanides

�-Glucosidase inhibitorsThiazolidinediones

Lifestyle strategies (food/eating and physical

activity) that improve glycemia, dyslipidemia,

and blood pressure

Nutrition education(carbohydrate counting

and fat modification)

Energy restriction topromote 5%–10%

weight loss

SYMPTOMS(variable)

Hyperglycemia

Excessive thirst

Frequent urination

Polyphagia

Weight loss

Intake of excessivecalories

Geneticfactors

1. Abnormal pattern of insulin secretion and action

2. Decreased cellular uptakeof glucose and increased postprandial glucose

3. Increased release ofglucose by liver (gluconeogenesis) in early morning hours

Blood glucose monitoring to determine

adjustments in food or medications

• Pathophysiology algorithm: type 2 diabetes mellitus. (Algorithm content developed by John Anderson, PhD, and SanfordC. Garner, PhD, 2000. Updated by Marion J. Franz, MS, RD, LD, CDE, 2002.)FIGURE 33-2

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Other Types of DiabetesThis category includes diabetes associated with spe-cific genetic syndromes, surgery, drugs, malnutrition,infections, and other illnesses. Such types of diabetesmay account for 1% to 2% of all diagnosed cases ofdiabetes.

Impaired Glucose HomeostasisA stage of impaired glucose homeostasis includes IFGand IGT and is called pre-diabetes. This condition canbe detected by either a fasting plasma glucose (FPG)test or an oral glucose tolerance (OGT) test. Individu-als with pre-diabetes are at high risk for future dia-betes and cardiovascular disease.

Diagnostic criteria for diabetes are summarized inTable 33-2. Three diagnostic methods may be usedto diagnose diabetes; however, because of the ease,acceptability to the patient, and the cost, the FPGtest is recommended (ADA, 2002a). At this time, he-moglobin A1c (A1C), is not recommended for diag-nosis. In pregnant women, different criteria are ap-plied in establishing the diagnosis of gestationaldiabetes. One of the following three tests can beused to diagnose diabetes but must be confirmed ona subsequent day:

� An FPG value equal to or greater than 126 mg/dl� Symptoms of diabetes and a nonfasting plasma

glucose (casual) value of greater than or equal to200 mg/dl. Casual refers to any time of the day,without regard to the elapsed time since one’s lastmeal. Symptoms of diabetes include the classicones of polyuria, polydipsia, and unexplainedweight loss.

� A 2-hour postprandial glucose equal to or greaterthan 200 mg/dl during an OGT test involving ad-ministration of 75 g of glucose

Testing or screening for diabetes should be consid-ered in all patients 45 years of age and older; if nor-mal, the test should be repeated at 3-year intervals.Testing should be considered at a younger age or becarried out more frequently in patients who:

� Have a family history of diabetes (i.e., parents orsiblings with diabetes)

� Are overweight with a body mass index (BMI)�25 kg/m2

� Are members of a high-risk ethnic population(e.g., African Americans, Hispanic Americans,Native Americans, Asian Americans, and PacificIslanders)

DIAGNOSTIC AND SCREENINGCRITERIA

� Are women who have a history of GDM or a historyof having infants weighing more than 9 lb at birth

� Are hypertensive (blood pressure �140/90 mm Hg)� Have a high-density lipoprotein (HDL) cholesterol

level �35 mg/dl or a triglyceride level �250 mg/dl� Had IGT or IFG on previous testing� Have polycystic ovary syndrome

The incidence of type 2 diabetes in children andadolescents is increasing dramatically and is consis-tent with screening recommendations for adults: chil-dren and youth at increased risk for type 2 diabetesshould be tested. Youth who are overweight (bodymass index [BMI] �85th percentile for age and sex)and who have two of the following risk factors shouldbe screened: family history of type 2 diabetes, mem-bers of high-risk ethnic populations, signs of insulinresistance (such as acanthosis nigricans—gray-brownskin pigmentations). The age of initiation of screeningis age 10 years or onset of puberty, and the frequencyis every 2 years (ADA, 2002a).

Screening and diagnosis for GDM is discussed un-der Gestational Diabetes Mellitus in the Pregnancysection.

Optimal control of diabetes requires the restoration ofnormal carbohydrate, protein, and fat metabolism. In-sulin is both anticatabolic and anabolic and facilitates

MANAGEMENT OF DIABETESMELLITUS

Diagnosis of DiabetesMellitus and ImpairedGlucose Homeostasis

DIAGNOSIS CRITERIA

Diabetes FPG �126 mg/dl (�7.0 mmol/L)

CPG �200 mg/dl (�11.1 mmol/L)plus symptoms

2hPG �200 mg/dl (�11.1 mmol/L)

Impaired glucose homeostasisImpaired fasting glucose FPG �110 and �126 mg/dl

(�6.1 and �7.0 mmol/L)Impaired glucose tolerance 2hPG �140 and �200 mg/dl

(�7.8 and �11.1 mmol/L)Normal FPG �110 mg/dl

(�6.1 mmol/L)2hPG �140 mg/dl

(�7.8 mmol/L)

Modified from Expert Committee on the Diagnosis and Classification of Di-abetes Mellitus: Report of the Expert Committee on the Diagnosis and Clas-sification of Diabetes Mellitus, Diabetes Care 20:1183, 1997.FPG, Fasting plasma glucose (preferred testing method); CPG, casual plasmaglucose; 2hPG, 2-hour plasma glucose level (measured 2 hours after an oralglucose tolerance test with administration of 75 g of glucose).

TABLE 33-2

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cellular transport (Table 33-3). In general, the coun-terregulatory (stress) hormones (glucagon, growthhormone, cortisol, epinephrine, and norepinephrine)have the opposite effect of insulin.

Diabetes is a chronic disease that requires changesfor a lifetime. The management of diabetes includesmedical nutrition therapy (MNT), physical activ-ity, blood glucose monitoring, medications, and self-management education. An important goal of treat-ment is to provide the patient with the necessarytools to achieve the best possible control of glycemia,lipidemia, and blood pressure to prevent, delay, orarrest the microvascular and macrovascular compli-cations of diabetes while minimizing hypoglycemiaand excess weight gain (ADA, 2002a).

Glycemic treatment goals for persons with diabetesare listed in Table 33-4. Achieving goals requires opencommunication and appropriate self-managementeducation. Patients can assess day-to-day glycemiccontrol by self-monitoring of blood glucose (SMBG)and measurement of urine and blood ketones.

Longer-term glycemic control is assessed fromthe results of glycosylated hemoglobin (simplifiedas A1C) tests. When hemoglobin and other proteinsare exposed to glucose, the glucose becomes at-

tached to the protein in a slow, nonenzymatic, andconcentration-dependent fashion. Measurements ofA1C reflect a weighted average of plasma glucoseconcentration over the preceding weeks, therebycomplementing day-to-day testing. In nondiabeticpersons, A1C values are 4.0% to 6.0%; these valuescorrespond to mean blood glucose levels of about 90mg/dl (or about 5 mmol/L). Lipid levels and bloodpressure must also be monitored (Table 33-5). Lipidsshould be measured annually, and blood pressure atevery diabetes management visit (ADA, 2002a).

Control and OutcomesEvidence relating hyperglycemia and other metabolicconsequences of insulin deficiency to the developmentof complications comes from a series of studies in Eu-rope and North America; however, the Diabetes Con-trol and Complications Trial (DCCT) demonstrated be-yond a doubt the clear link between glycemic controland development of complications in persons withtype 1 diabetes. The DCCT, sponsored by the NationalInstitutes of Health, was a long-term, prospective,randomized, controlled, multicenter trial that studiedapproximately 1400 young adults (ages 13 to 39 years)

Action of Insulin on Carbohydrate, Protein, and Fat Metabolism

EFFECT CARBOHYDRATE PROTEIN FAT

Anticatabolic Decreases breakdown and release of Inhibits protein degradation, Inhibits lipolysis, prevents ex-(prevents breakdown) glucose from glycogen in the liver diminishes gluconeogenesis cessive production of

ketones and ketoacidosisAnabolic Facilitates conversion of glucose to Stimulates protein synthesis Facilitates conversion of pyru-

(promotes storage) glycogen for storage in liver and vate to free fatty acids, stim-muscle ulating lipogenesis

Transport Activates the transport system Lowers blood amino acids in Activates lipoprotein lipase, fa-of glucose into muscle and parallel with blood glucose cilitating transport of triglyc-adipose cells levels erides into adipose tissue

TABLE 33-3

Recommendationsfor Glycemic Control*

BIOCHEMICAL INDEX NORMAL GOAL

Plasma ValuesAverage preprandial glucose �110 90-130

(mg/dl)Peak postprandial average �140 �180

plasma glucose (mg/dl) (measured within 1-2 hr after eating)

A1c (%) �6 �7

Modified from American Diabetes Association: Standards of medical carefor patients with diabetes mellitus, Diabetes Care 26(suppl 1):S37, 2003.*Values are for nonpregnant individuals. A1c, glycosylated hemoglobin, isreferenced to a nondiabetic range of 4.0%-6.0%.

TABLE 33-4 Lipid and Blood PressureGoals*

LIPIDS (mg/dl) BLOOD PRESSURE (mm Hg)

Cholesterol �200 Systolic �130LDL Cholesterol �100 Diastolic �80HDL Cholesterol

Men �45Women �55

Triglycerides �150

Modified from American Diabetes Association: Standards of medical carefor patients with diabetes mellitus [Postition Statement], Diabetes Care25(suppl 1):S33, 2002.*Values are for nonpregnant adults.LDL, Low-density lipoprotein; HDL, high-density lipoprotein.

TABLE 33-5

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with type 1 diabetes who were treated with either in-tensive therapeutic regimens (multiple injections of in-sulin or use of insulin infusion pumps guided by bloodglucose monitoring results) or conventional regimens(one or two insulin injections per day) (Diabetes Con-trol and Complications Trial Research Group, 1995).Patients who achieved control similar to that of the in-tensively treated patients in the study could expect a50% to 75% reduction in the risk of progression toretinopathy, nephropathy, and neuropathy after 8 to 9years (DCCT Research Group, 1993).

Previously, small studies had demonstrated the re-lationship of blood glucose control to complications intype 2 diabetes (Kuusito et al, 1994; Ohkubbo et al,1995). However, the reports of the United KingdomProspective Diabetes Study (UKPDS) in 1998 demon-strated conclusively that elevated blood glucose levelscause long-term complications in type 2 diabetes justas in type 1 diabetes (UKPDS, 1998a). The UKPDS re-cruited and followed up on 5102 newly diagnosedtype 2 diabetic patients for an average of 10 to 11 years.Subjects were randomized into a group treated con-ventionally, primarily with nutrition therapy, and hadan average HbA1c of 7.9% compared with subjectsrandomized into an intensively treated group, initiallytreated with sulfonylureas, and who had an averageHbA1c of 7.0%. In the intensive therapy group, the mi-crovascular complications rate decreased significantlyby 25% and the risk of macrovascular disease de-creased by 16%. Combination therapy (combining in-sulin or metformin with sulfonylureas) was needed inboth groups to meet glycemic goals as loss of glycemiccontrol was noted over the 10-year trial. Aggressivetreatment of even mild-to-moderate hypertension wasalso beneficial in both groups (UKPDS, 1998b).

Before randomization into intensive or conven-tional treatment, subjects received individualized in-tensive nutrition therapy for 3 months. During thisrun-in period, the mean A1C decreased by 1.9%(�9% to �7%) and patients lost an average of 3.5 kg(8 lb). UKPDS researchers concluded that a reductionof energy intake was at least as important, if not moreimportant, than the actual weight lost in determiningthe FPG (UKPDS, 1990).

This study clearly illustrates the progressive na-ture of type 2 diabetes. An important lesson learnedfrom the UKPDS is that therapy needs to be intensi-fied over time and that as the disease progresses,MNT alone is not enough to keep most patients’ A1Clevel at 7%. Medication(s), and for many patients,eventually insulin, needs to be added to the treat-ment regimen. It is not the “diet” failing; it is the pan-creas failing to secrete enough insulin to maintain ad-equate glucose control.

Nutrition TherapyMedical nutrition therapy is integral to total dia-betes care and management. To integrate MNT ef-

fectively into the overall management of diabetesrequires a coordinated team effort, including a dieti-tian who is knowledgeable and skilled in imple-menting current principles and recommendationsfor diabetes. MNT requires an individualized ap-proach and effective nutrition self-management ed-ucation. Monitoring glucose, A1C and lipid levels,blood pressure, weight, and quality-of-life issues isessential in evaluating the success of nutrition-related recommendations. If desired outcomes fromMNT are not met, changes in overall diabetes careand management should be recommended (ADA,2001).

The ADA’s nutrition guidelines underscore theimportance of individualizing nutrition care. Be-fore 1994 nutrition recommendations attempted todefine optimal percentages for macronutrient in-take. Then, by determining a person’s energy needsbased on theoretic calorie requirements and usingthe ideal percentages for carbohydrate, protein,and fat, a nutrition prescription was developed—for example, 1800 calories, 225 g of carbohydrate(50%), 90 g of protein (20%), and 60 g of fat (30%).The problem with this approach is that the pre-scribed “diet” can not really be individualized, andit often lacks relevance to the patient’s personallifestyle, culture, or socioeconomic status. Further-more, this approach is not supported by scientificevidence and usually does not produce successfuloutcomes. Beginning in 1994, the ADA recom-mended that an individualized nutrition prescrip-tion be based on metabolic profiles, treatmentgoals, and changes that the person with diabetes iswilling and able to make, not on rigid, predeter-mined calorie levels and macronutrient percentages(Franz et al, 1994). This approach continues withthe 2002 ADA nutrition principles and recommen-dations for persons with diabetes (ADA, 2002b;Franz, 2002).

Goals and Outcomes of Medical Nutrition Therapy for Diabetes

The goals for MNT for diabetes emphasize the role oflifestyle in improving not only glucose control butalso lipid and lipoprotein profiles and blood pres-sure. Improving health through food choices andphysical activity is the basis of all nutrition recom-mendations for the treatment and prevention of dia-betes (Box 33-1).

Besides being skilled and knowledgeable in re-gard to assessing and implementing MNT, dieti-tians must also be aware of expected outcomesfrom nutrition therapy, when to assess outcomes,and what feedback, including recommendations,should be given to referral sources. Research sup-ports MNT as an effective therapy in reaching dia-betes treatment goals. Outcomes studies demon-strate that MNT provided by a registered dietitian

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(RD) is associated with a decrease of about 1.0% ofA1C in patients with newly diagnosed type 1 dia-betes (Kulkarni et al, 1998), a decrease of about 2.0%of A1C in patients with newly diagnosed type 2 di-abetes (Franz et al, 1995; UKPDS Group, 1990), anda decrease of about 1.0% of A1C in patients with anaverage 4-year duration of type 2 diabetes (Franz etal, 1995). These outcomes are similar to those fromoral glucose-lowering medications. Furthermore,the effect of MNT on A1C will be known by 6 weeksto 3 months, at which time the RD must assesswhether the goals of therapy have been met bychanges in lifestyle and whether changes or addi-tions of medications are needed (ADA, 2001).

Prioritizing Nutrition Therapy for Type 1 DiabetesThe priority for anyone who requires insulin therapyis first to determine a food and meal plan and then tointegrate an insulin regimen into his or her usual eat-ing habits and physical activity schedule. With themany insulin options now available (new rapid-acting and long-acting insulins), an insulin regimenusually can be developed that will conform to an in-dividual’s preferred meal routines and food choices

(ADA, 2002b; Franz et al, 2002). It is no longer neces-sary to create unnatural or artificial divisions ofmeals and snacks.

Flexible insulin regimens involve multiple injec-tions (three or more insulin injections per day) oruse of an insulin infusion pump. Half of the re-quired insulin dose is given as a basal or back-ground insulin, and the other half is divided andgiven before meals (bolus or premeal insulin). Thesetypes of insulin regimens allow increased flexibilityin choosing when and what to eat. The total carbo-hydrate content of meals is the major determinant ofthe mealtime rapid-acting insulin dose and post-prandial glucose response (Rabasa-Lhoret et al,1999). Thus, individuals can be taught how to adjustmealtime insulin doses based on the carbohydratecontent of the meal and how to delay mealtime in-sulin for late meals. Even with flexible insulin regi-mens, however, consistency in food intake facilitatesimproved glycemic control (Delahanty and Halford,1993). For persons who receive fixed insulin regi-mens, such as with the use of premixed insulins, orthose who do not adjust their mealtime insulindoses, day-to-day consistency in the timing andamount of carbohydrate eaten is recommended(Wolever et al, 1999).

Box 33-1. Goals of Medical Nutrition Therapy for Diabetes MellitusGoals of Medical Nutrition Therapy That Apply to All Persons With Diabetes

1. Attain and maintain optimal metabolic outcomes including:• Blood glucose levels in the normal range or as close to normal as is safely possible to prevent or reduce risk

or complications of diabetes.• A lipid and lipoprotein profile that reduces the risk for cardiovascular disease.• Blood pressure levels that reduce the risk for vascular disease.

2. Prevent and treat the chronic complications: Modify nutrient intake as appropriate for the prevention andtreatment of obesity, cardiovascular disease, hypertension, and nephropathy.

3. Improve health through healthy food choices and physical activity.4. Address individual nutritional needs, taking into consideration personal and cultural preferences and

lifestyle while respecting the individual’s needs and willingness to change.Goals of Nutrition Therapy That Apply to Specific Situations

1. For youth with type 1 diabetes, provide adequate energy to ensure normal growth and development; inte-grate insulin regimen into usual eating and exercise habits.

2. For youth with type 2 diabetes, facilitate changes in eating and exercise habits that reduce insulin resistanceand improve metabolic status.

3. For pregnant and lactating women, provide adequate energy and nutrients needed for successful outcomes.4. For older adults, provide for the nutritional needs of an aging individual.5. For individuals treated with insulin or insulin secretagogues, provide information on prevention and treat-

ment of hypoglycemia and exercise-related blood glucose problems and how to manage acute illness.6. For individuals at risk for diabetes, decrease risk by increasing physical activity and promoting food choices

that facilitate moderate weight loss or at least prevent weight gain.

From American Diabetes Association: Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes andrelated complications [Position Statement], Diabetes Care 25:202, 2002.

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Prioritizing Nutrition Therapy forType 2 Diabetes

The priority for individuals with type 2 diabetes isto adopt lifestyle strategies that improve the associ-ated metabolic abnormalities of glycemia, dyslipi-demia, and hypertension (ADA, 2002b; Franz et al,2002). Lifestyle strategies independent of weightloss that can improve glycemia include reducing en-ergy intake, monitoring carbohydrate servings, lim-iting consumption of saturated fats, and increasingphysical activity. These strategies should be imple-mented as soon as the diagnosis of diabetes (or pre-diabetes) is made.

In the short-term, small amounts of weight lossmay improve insulin resistance and glycemia, but,because of the difficulty in maintaining weight losslong term, it is unknown whether this benefit contin-ues. Short-term studies lasting 6 months or lessdemonstrate that modest amounts of weight loss im-prove metabolic abnormalities in many persons withtype 2 diabetes (Markovic et al, 1998a; Wing et al,1987) but not in all (Watts et al, 1990). Weight loss, es-pecially of intraabdominal fat, reduces insulin resist-ance and helps to correct dyslipidemia (Markovic etal, 1998b); however, long-term data assessing the ex-tent to which these improvements can be maintainedin persons with diabetes are not available, probablybecause long-term weight loss is difficult to achieve.Long-term weight loss of 5% to 7% from baselineweight requires frequent, regular, and long-termfollow-up of patients (Diabetes Prevention ProgramResearch Group, 2002; Tuomilehto et al, 2001).

An energy-restricted diet, however, can have animportant regulatory effect on glucose control in per-sons with type 2 diabetes, independent of any effectsfrom weight loss (Kelley et al, 1993; Wing et al, 1994).When energy intake is restricted, hyperglycemia im-proves more rapidly than with weight loss. Further-more, when calories are increased after weight reduc-tion, glucose levels increase despite no regain ofweight. This suggests that energy intake is more im-portant than weight loss.

Physical activity improves insulin sensitivity, canacutely lower blood glucose in diabetic persons, andmay also improve cardiovascular status; but by itself ithas only a modest effect on weight. Physical activity isuseful as an adjunct to other weight loss strategies andis essential for long-term maintenance of weight loss(Albright et al, 2000). It should be noted, however, thatcardiorespiratory fitness appears to be more importantthan thinness in relation to all-cause and cardiovascu-lar mortality (Lee et al, 1999). During an 8-year studyof about 25,000 men, fit men had greater longevitythan unfit men regardless of their body composition orrisk factor status. No elevated mortality risk was ob-served in obese men if they were physically fit, andobese fit men had a lower risk of all-cause and cardio-vascular mortality than lean unfit men.

Teaching which foods are carbohydrates (fruits,grains, starchy vegetables, milk, sweets), average por-tion sizes, how many servings to select at meals (andsnacks, if desired), and how to limit fat and especiallysaturated fat intake; encouraging physical activity;and using blood glucose monitoring to adjust foodand eating patterns and medications are importantcomponents of successful MNT for type 2 diabetes(Rickheim et al, 2002). Frequent follow-up with adietitian as outlined in nutrition practice guidelinesfor type 2 diabetes can provide the problem-solvingtechniques, encouragement, and support that lifestylechanges require (Monk et al, 1995).

Carbohydrate

Sugars, starch, and fiber are the preferred terms forcarbohydrates (Report of a Joint FAO/WHO ExpertConsultation, 1998). Foods that contain carbohy-drate from whole grains, fruits, vegetables, and low-fat milk are important components of a healthy dietfor all Americans, including those with diabetes.They are excellent sources of vitamins, minerals, di-etary fiber, and energy. Historically it was a long-held belief that sucrose must be restricted based onthe assumption that sugars, such as sucrose, aremore rapidly digested and absorbed than starchesand thus aggravate hyperglycemia; however, scien-tific evidence does not justify restricting sugars orsucrose based on this belief. In approximately 20studies in which sucrose was substituted for othercarbohydrates, sucrose did not increase glycemia toa greater extent than isocaloric amounts of starch(Bantle et al, 1993; Peterson et al, 1986; Rickard et al,1998). The glycemic effect of carbohydrate foods can-not be predicted based on their structure (i.e., starchversus sugar) owing to the efficiency of the humandigestive tract in reducing starch polymers to glu-cose. Starches are rapidly metabolized into 100%glucose during digestion, in contrast to sucrose,which is metabolized into glucose and fructose.Fructose has a lower glycemic index, which has beenattributed to its slow rate of absorption and its stor-age in the liver as glycogen (Nuttall et al, 1992) (seeChapters 3, 12, and 26).

Numerous factors influence glycemic responses offoods, including the amount of carbohydrate, type ofsugar (glucose, fructose, sucrose, lactose), nature ofthe starch (amylose, amylopectin, resistant starch),cooking and food processing, particle size, and foodform as well as the fasting and preprandial glucoseconcentrations, severity of the glucose intolerance,and the second meal or lente effect of carbohydrates.There is, however, strong evidence to state that the to-tal amount of carbohydrate is more important thanthe source (sugar or starch) or the type (glycemicindex) of carbohydrate. Numerous studies have re-ported that when subjects are allowed to choose froma variety of starches and sugars, the glycemic re-

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sponse is identical if the total amount of carbohydrateis similar (ADA, 2002b). Therefore, the first priorityfor food and meal planning is the total amount of car-bohydrate that the person with diabetes chooses tohave for meals or snacks. This is the basis of carbohy-drate counting, whereby food portions contributing15 g of carbohydrate (regardless of the source) areconsidered to be one carbohydrate serving.

Glycemic Index and Glycemic Load

Although different carbohydrates do have differentglycemic responses (glycemic index), there is limitedevidence to show long-term benefit when low gly-cemic index diets are compared with high glycemicindex diets in studies lasting 2 weeks or longer.In subjects with type 1 diabetes (five studies intotal, n � 48), no studies in which low versus highglycemic index diets are compared show a beneficialeffect of the low glycemic index diet on A1c; threestudies report the low glycemic index diet improvedfructosamine (a short-term measure of overall con-trol), whereas one study reported no improvement infructosamine. In subjects with type 2 diabetes (ninestudies in total, n � 129), one study reported benefi-cial effects of the low glycemic index diet on A1c,whereas four studies reported no beneficial effects onA1c. Three studies reported improvement in fruc-tosamine from the low glycemic index diet, whereasthree studies reported no improvement. FPG is re-ported in all studies; however, no studies in personswith type 1 or type 2 diabetes report improvementsin FPG from the low glycemic index diets (Franz,2001). Therefore, there is insufficient evidence to rec-ommend low glycemic index diets as the primarystrategy in food and meal planning for individualswith diabetes (ADA, 2002b). The concept of theglycemic index is perhaps best used for fine-tuningpostprandial responses after focusing on total carbo-hydrate.

The glycemic load is a newer concept and incorpo-rates both the number of grams of carbohydrate in ausual food serving or meal and the glycemic index(see Appendix 54). At this time, however, no inter-vention studies have been done that show benefitfrom using this technique in persons with diabetes.

Fiber

Early short-term studies using large amounts of fiber(�30 g daily) in small numbers of subjects suggesteda positive effect on glycemia; however, results fromlater studies have shown mixed effects. In subjectswith type 1 diabetes, a high-fiber diet (56 g daily) hadno beneficial effects on glycemic control (Lafrance etal, 1998). Another study of subjects with type 1 dia-betes showed positive effects from 50 g of fiber onglucose concentrations but no beneficial effects onlipids (Giacco et al, 2000). In persons with type 2 dia-

betes, increasing fiber from 11 to 27 g/1000 kcal didnot improve glycemia, insulinemia, or lipemia (Hol-lenbeck et al, 1986), whereas another study compar-ing 24 g of fiber per day with 50 g of fiber reported im-proved glycemic control, reduced hyperinsulinemia,and decreased plasma lipids (Chandalia et al, 2000).Therefore, it appears that ingestion of large amountsof fiber (�50 g/day) is necessary to have beneficial ef-fects on glycemia, insulinemia, and lipemia. It is un-known whether free-living individuals can maintainsuch high levels of fiber and whether this amountwould be acceptable to most people (ADA, 2002b).Although the consumption of fiber is to be encour-aged, just as it is for the general public, there is no rea-son to recommend that persons with diabetes eat agreater amount of fiber than other Americans.

Sweeteners

Even though sucrose restriction cannot be justified onthe basis of its glycemic effect, it is still good advice tosuggest that persons with diabetes be careful in theirconsumption of foods containing large amounts ofsucrose. Besides often being high in total carbohy-drate content, these foods may also contain signifi-cant amounts of fat. If sucrose is included in the foodand meal plan, it should be substituted for other car-bohydrate sources or, if added, be adequately cov-ered with insulin or other glucose-lowering medica-tions. Sucrose and sucrose-containing foods alsoshould be eaten in the context of a healthy diet (ADA,2002b).

There appears to be no significant advantage of al-ternative nutritive sweeteners over sucrose. Fructoseprovides 4 kcal/g, as do other carbohydrates, andeven though it does have a lower glycemic responsethan sucrose and other starches, large amounts (15%-20% of daily energy intake) of fructose have an ad-verse effect on plasma lipids (Bantle et al, 1992, 2000).There is no reason, however, to recommend that per-sons with diabetes avoid fructose, which occurs natu-rally in fruits and vegetables as well as in foodssweetened with fructose (ADA, 2002b).

Sorbitol, mannitol, xylitol, isomalt, lactitol, andhydrogenated starch hydrolysates are commonsugar alcohols that also have a lower glycemic re-sponse and lower caloric content than sucrose andother carbohydrates. Because they are not soluble inwater, they are often combined with fat; therefore,foods sweetened with sugar alcohols may have acaloric content that is similar to that of the foodsthey are replacing. It is unlikely, however, that sugaralcohols in the amounts likely to be ingested in indi-vidual food servings or meals will contribute to sig-nificant reduction in total energy or carbohydrateintake (ADA, 2002b). Some patients report gastricdiscomfort after eating foods sweetened with theseproducts, and consuming large quantities maycause diarrhea.

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Saccharin (Sweet’N Low), aspartame (Equal andNutraSweet), acesulfame K, and sucralose arenoncaloric sweeteners currently approved for use inthe United States. Approval of the U.S. Food andDrug Administration (FDA) is being sought for ali-tame and cyclamates. All such products must un-dergo rigorous testing by the manufacturer andscrutiny from the FDA before they are approved andmarketed to the public. For all food additives, in-cluding nonnutritive sweeteners, the FDA deter-mines an acceptable daily intake (ADI), defined asthe amount of a food additive that can be safely con-sumed on a daily basis over a person’s lifetime with-out risk (see Chapter 14). The ADI includes a100-fold safety factor and greatly exceeds averageconsumption levels. For example, aspartame actualdaily intake in persons with diabetes is 2 to 4 mg perkilogram of body weight daily, well below the ADIof 50 mg/kg daily (Butchko and Stargel, 2001). AllFDA-approved nonnutritive sweeteners can be usedby persons with diabetes, including pregnantwomen (ADA, 2002b).

Protein

The rate of protein degradation and conversion ofprotein to glucose in type 1 diabetes depends onthe state of insulinization and the degree of gly-cemic control. With less than optimal insulinization,conversion of protein to glucose can occur rapidly,adversely influencing glycemic control. In poorlycontrolled type 2 diabetes, gluconeogenesis is alsoaccelerated and may account for most of the in-creased glucose production in the postabsorptivestate (Henry, 1994). In those with controlled type 2 di-abetes Gannon et al, 2001a; Nuttall et al, 1984) andwell-controlled type 1 diabetes (Peters and Davidson,1993), ingested protein did not increase plasma glu-cose concentrations. Although nonessential aminoacids undergo gluconeogenesis, it is unclear why theglucose produced does not appear in the general cir-culation after ingestion of protein (Franz, 2000). Fur-thermore, protein does not slow the absorption ofcarbohydrate (Nordt et al, 1991; Nuttall et al, 1984),and adding protein to the treatment of hypoglycemiadoes not prevent subsequent hypoglycemia (Gray etal, 1996). In type 2 diabetic patients who are still ableto produce insulin, ingested protein is just as potent astimulant of insulin secretion as carbohydrate.

There is evidence that moderate hyperglycemia inpersons with type 2 diabetes (Gougeon et al, 1994)and uncontrolled diabetes in persons with type 1 dia-betes (Lariviere et al, 1994) cause increased proteincatabolism. Protection against increased protein ca-tabolism requires near-normal glycemia and an ade-quate protein intake (Brodsky and Devlin, 1996;Gougeon et al, 2000). Therefore, for persons with dia-betes, the protein requirement may be greater thanthe recommended dietary allowance (RDA) but not

greater than typical intake in the United States. Noevidence has been found to suggest that typical pro-tein intake (15%-20% of total daily energy) must bemodified if renal function is normal (ADA, 2002b). Instudies in which protein intake was in the range ofusual intake and rarely exceeded 20% of energy in-take, dietary protein intake was not associated withthe development of diabetic nephropathy. In a cross-sectional study (Toeller et al, 1997), patients in whomprotein intakes were 20% or greater of daily energyhad a higher incidence of albuminuria. This findingsuggests that it may be prudent to avoid protein in-take that is more than 20% of total daily energy.

The long-term effects of weight-loss diets high inprotein and low in carbohydrate are unknown. Al-though initially blood glucose levels may improveand weight may be lost, it is unknown whetherweight loss is maintained better with these dietsthan with other low-calorie diets. Furthermore, pro-tein is just as potent a stimulant of insulin as is car-bohydrate. Because these diets are usually high insaturated fat, the long-term effect on LDL choles-terol is also a concern (ADA, 2002b) (see Chapters24 and 35).

Dietary Fat

In all persons with diabetes, less than 10% of energyintake should be derived from saturated fats, and di-etary cholesterol intake should be less than 300 mgdaily. Some persons (i.e., those with LDL cholesterol�100 mg/dl) may benefit from lowering saturatedfat intake to less than 7% of energy intake and dietarycholesterol to less than 200 mg daily. To lower plasmaLDL cholesterol, saturated fat can be reduced if con-current weight loss is desirable or replaced with car-bohydrate or monounsaturated fat if weight loss isnot a goal. Intake of trans-fatty acids should also beminimized (see Chapter 35).

If saturated fat contributes less than 10% of totaldaily energy, if about 10% of energy is from polyun-saturated fat, and if protein contributes 15% to 20% ofenergy, then 60% to 70% of total energy intake re-mains to be distributed between carbohydrate andmonounsaturated fat. Diets high in monounsatu-rated fat or low in fat and high in carbohydrate resultin improvement in glucose tolerance and lipids com-pared with diets high in saturated fat. Diets enrichedwith monounsaturated fats may also reduce insulinresistance (Parillo et al, 1992); however, other studieshave reported high total dietary fat (regardless of thetype of fat) to be associated with insulin resistance(Lovejoy and DiGirolamo, 1992). In metabolic studiesin which energy intake is maintained so that subjectsdo not lose weight, diets high in either carbohydrateor monounsaturated fat lower LDL cholesterol equiv-alently, but the concern has been the potential of ahigh-carbohydrate diet (greater than 55% of energyintake) to increase triglycerides and postprandial

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glucose compared with a high–monounsaturated fatdiet (Garg et al, 1994). If energy intake is reduced and a low-fat, high-carbohydrate diet is comparedwith a high–monounsaturated fat diet, no detri-mental effects on triglycerides result from the high-carbohydrate diet (Heilbronn et al, 1999). Energy in-take, therefore, appears to a factor in determining theeffects of a high-carbohydrate versus high–monoun-saturated fat diet.

Low-fat, high-carbohydrate diets over long periodshave not been shown to increase triglycerides and havebeen shown to lead to modest weight loss (Kendall etal, 1991) and weight-loss maintenance (Carmichael etal, 1998). Thus, a person’s metabolic profile and need tolose weight will determine nutrition recommenda-tions. For persons who need to lose weight, a lowerenergy intake and a low-fat, moderate-carbohydrateapproach can be used. For persons who do not needto lose weight, a high–monounsaturated fat approachmay be recommended to improve triglycerides or post-prandial glycemia (ADA, 2002b).

There is evidence from the general population thatfoods containing omega-3 fatty acids are beneficial,and two to three servings of fish per week are recom-mended. Although most studies in persons with dia-betes have used omega-3 supplements and show ben-eficial lowering of triglycerides, an accompanying risein LDL cholesterol also has been noted (Montori et al,2000). If supplements are used, the effects on LDLcholesterol should be monitored. The omega-3 sup-plements may be most beneficial in the treatment ofsevere hypertriglyceridemia (Patti et al, 1999).

Fiber and Phytosterols

Evidence for the effects of fiber on lipids is providedby a metaanalysis of 67 controlled trials (Brown et al,1999). Within the practical range of intake, the au-thors concluded that the effect of soluble fiber on to-tal and LDL cholesterol is small. For example, dailyintake of 3 g of soluble fiber from oats (three servingsof oatmeal, 28 g each) or three apples can decrease to-tal cholesterol by about 5 mg/dl, an approximate 2%reduction.

Intake of 2 to 3 g of plant stanols or sterols per dayare reported to decrease total and LDL cholesterollevels by 9% to 20% (Hallikainen et al, 1999). Useof low-fat food and fat replacers or substitutes ap-proved by the FDA are safe for use and may reducetotal fat and energy intake.

Energy Balance and Obesity

Improved glycemic control with intensive insulintherapy is often associated with increases in bodyweight. Because of the potential for weight gain to af-fect lipids and blood pressure adversely, prevention ofweight gain is desirable; however, the benefits of im-proved blood glucose control outweigh concernsabout weight gain, at least initially (Chaturvedi et al,

1995). To prevent weight gain, insulin therapy shouldbe integrated into usual eating and exercise habits andinsulin doses adjusted accordingly. Overtreatment ofhypoglycemia should be avoided; total protein, fat,and calories ingested must be accounted for; and ad-justments in insulin should be made for exercise.

Many individuals with type 2 diabetes are over-weight, with about 36% having a BMI of 30 kg/m2 orgreater (Cowie and Harris, 1995). The risk of obesityand excess mortality is controversial. Obesity in per-sons with type 2 diabetes was not related to mortality(Chaturvedi and Fuller, 1995) or to the long-term in-cidence of microvascular and macrovascular com-plications (Klein et al, 1997). Short-term studies thatlasted 6 months or less, however, demonstrated thatweight loss in subjects with type 2 diabetes is associ-ated with improvement in insulin resistance, gly-cemia, serum lipids, and blood pressure. Long-termdata assessing the extent to which these improve-ments can be maintained in people with type 2 dia-betes are scarce, as already mentioned.

A genetic predisposition to obesity and possibleimpaired metabolic and appetite regulation as well asenvironmental factors make it difficult to lose and,more important, to maintain weight loss. Because ofthe psychological and physiologic impact of dieting,encouragement to attain and maintain a reasonablebody weight is crucial. Emphasis should be on bloodglucose control, improved food choices, increasedphysical activity, and moderate energy restrictionrather than weight loss alone.

Standard weight-reduction diets, when used alone,are unlikely to produce long-term weight loss. Struc-tured, intensive lifestyle programs are necessary toproduce long-term weight loss of 5% to 7% of start-ing weight (Diabetes Prevention Program ResearchGroup, 2002; Tuomilehto et al, 2001). Currently avail-able weight-loss drugs have a modest beneficial effectin persons with diabetes and should be used only inpeople with a BMI greater than 27. Gastric reductionsurgery can be an effective weight-loss treatment forseverely obese patients with type 2 diabetes; however,it should be considered only in patients with a BMIgreater than 35 because long-term data comparing thebenefits and risks of gastric reduction surgery withmedical therapy are not available (ADA, 2002b) (seeChapter 24).

Alcohol

The same precautions that apply to alcohol consump-tion for the general population apply to persons withdiabetes. The effect of alcohol on blood glucose levelsdepends not only on the amount of alcohol ingestedbut also on its relationship to food intake. In the fast-ing state, alcohol may cause hypoglycemia in personsusing exogenous insulin or insulin secretagogues.Alcohol is used as a source of energy, but it is not con-verted to glucose. It is metabolized in a manner simi-lar to fat. It also blocks gluconeogenesis and aug-

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ments or increases the effects of insulin by interferingwith the counterregulation response to insulin-induced hypoglycemia. All these factors contributeto the development of hypoglycemia when alcohol isconsumed without food (Franz, 1999).

If individuals choose to drink alcohol, daily intakeshould be limited to one drink for adult women andtwo drinks for adult men (1 drink � 12 oz beer, 5 ozof wine, or 11⁄2 oz of distilled spirits [15 g alcohol]).For most persons, blood glucose levels are not af-fected by moderate use of alcohol when diabetes iswell controlled (Koivisto et al, 1993). Alcoholic bever-ages should be considered an addition to the regularfood and meal plan for all persons with diabetes.No food should be omitted given the possibility ofalcohol-induced hypoglycemia and the fact that alco-hol does not require insulin to be metabolized. Preg-nant women and patients with medical problemssuch as pancreatitis, advanced neuropathy, severehypertriglyceridemia, or alcohol abuse should avoidalcohol (ADA, 2002b).

Epidemiologic evidence in nondiabetic individualssuggests that light to moderate alcohol ingestion inadults is associated with decreased risk of type 2 dia-betes and stroke and improved insulin resistance. Inadults with type 2 diabetes, light to moderate alcoholingestion is associated with decreased risk of coro-nary heart disease, perhaps because of the concomi-tant increase in HDL cholesterol. Long-term, prospec-tive studies are needed to confirm these observations(ADA, 2002b) (see Chapter 35). Ingestion of light tomoderate amounts of alcohol does not raise bloodpressure, whereas excessive, chronic ingestions of al-cohol does raise blood pressure and may be a risk fac-tor for stroke (Joint National Committee on Preven-tion, Detection, Evaluation and Treatment of HighBlood Pressure, 1997).

Micronutrients

No clear evidence has been established of benefitsfrom routine vitamin or mineral supplements in per-sons with diabetes who do not have underlying defi-ciencies. Exceptions include folate for the preventionof birth defects and calcium for prevention of bonedisease. Routine supplementation of the diet with an-tioxidants is not advised because of uncertainties re-lated to long-term efficacy and safety (ADA, 2002b).Observational studies and several placebo-controlledclinical trials with small subject numbers have foundbeneficial effects of antioxidants, especially vitamin E,on physiologic and biochemical end points. Largeplacebo-controlled clinical trials have failed to showbenefit from antioxidants and, in some instances, havesuggested adverse effects (Omenn et al, 1996). Of in-terest is the Heart Outcomes Prevention EvaluationTrial, which included 9541 subjects, 38% of whom haddiabetes (Yusuf et al, 2000). Supplementation with 400IU daily of vitamin E for 4.5 years did not result in anysignificant benefit on cardiovascular outcomes.

Because the response to supplements is determinedlargely by a person’s nutritional status, persons withmicronutrient deficiencies are most likely to respondfavorably. Although difficult to ascertain, if deficien-cies of vitamins or minerals are identified, supplemen-tation can be beneficial. Those at greatest risk of defi-ciency who may benefit from prescription of vitaminand mineral supplements include patients who con-sume extreme calorie-restricted diets, strict vegetari-ans, older adults, pregnant or lactating women, thosetaking medication known to alter micronutrient me-tabolism (see Chapter 19), patients in poor metaboliccontrol (glycosuria), and patients in critical care envi-ronments.

Chromium deficiency in animal models is associ-ated with elevated blood glucose, cholesterol, andtriglyceride levels. It is unlikely, however, that mostpersons with diabetes are chromium deficient. Inthree double-blind crossover studies of chromiumsupplementation in individuals with diabetes, noimprovement in blood glucose control was noted(Mooradian et al, 1994). In a randomized, placebo-controlled study in Chinese subjects with diabetes,chromium supplementation did have beneficial ef-fects on glycemia (Anderson et al, 1997; Cheng et al,1999); however, the study population may have hadmarginal baseline chromium status because thechromium status was not evaluated either at base-line or after supplementation. Therefore, beforechromium supplementation can be recommended,placebo-controlled clinical trials need to be under-taken in which people with diabetes with known di-etary intakes of chromium use chromium supple-ments that may be better absorbed than oldersupplements.

ExerciseExercise should be an integral part of the treatmentplan for persons with diabetes. Exercise helps allpersons with diabetes improve insulin sensitivity,reduce cardiovascular risk factors, control weight,and bring about a healthier mental outlook. Givenappropriate guidelines, people with diabetes can ex-ercise safely. The exercise plan will vary dependingon interest, age, general health, and level of physicalfitness.

Despite the increase in glucose uptake by musclesduring exercise, glucose levels change little in indi-viduals without diabetes. Muscular work causesinsulin levels to decline while counterregulatory hor-mones (primarily glucagon) rise. In this way, in-creased glucose utilization by the exercising muscleis matched precisely with increased glucose produc-tion by the liver. This balance between insulin andcounterregulatory hormones is the major determi-nant of hepatic glucose production, underscoring theneed for insulin adjustments in addition to adequatecarbohydrate intake during exercise for people withdiabetes.

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In persons with type 1 diabetes, the glycemic re-sponse to exercise varies depending on overall dia-betes control, plasma glucose, and insulin levels at thestart of exercise; timing, intensity and duration of theexercise; previous food intake; and previous condi-tioning. An important variable is the level of plasmainsulin during and after exercise. Hypoglycemia canoccur because of insulin-enhanced muscle glucose up-take by the exercising muscle. In contrast, insulin defi-ciency in a poorly controlled (underinsulinized) exer-ciser results in increases in glucose concentrations andfree fatty acids release continues with minimal uptake.This can result in large increases in plasma glucoseand ketone levels (Wasserman and Zinman, 1994).

In persons with type 2 diabetes, blood glucose con-trol can improve with exercise, largely because of de-creased insulin resistance and increased insulin sensi-tivity, which results in increased peripheral use ofglucose not only during but also after the activity. Thisexercise-induced enhanced insulin sensitivity occurswithout changes in body weight. Exercise also de-creases the effects of counterregulatory hormones;this, in turn, reduces the hepatic glucose output, con-tributing to improved glucose control. Exercise regi-mens at an intensity of 50% to 80% VO2max three to fourtimes a week for 30 to 60 minutes a session can resultin a 10% to 20% baseline improvement in A1c and aremost beneficial in persons with mild type 2 diabetesand in those who are likely to be the most insulin re-sistant. Regular exercise also has consistently beenshown to be effective in reducing triglyceride levels inpersons with type 2 diabetes; however, the effect of ex-ercise on HDL cholesterol levels is unclear. Reductionsin blood pressure and improvements in impaired fibri-nolysis have also been noted (ADA, 2002c).

Potential Problems With Exercise

Hypoglycemia is a potential problem associated withexercise in persons taking insulin or insulin secreta-gogues. Hypoglycemia can occur during, immedi-ately after, or many hours after exercise. Hypo-glycemia has been reported to be more common afterexercise, especially after exercise of long duration, af-ter strenuous activity or play, or after sporadic exer-cise, than during exercise (MacDonald et al, 1987).This is because of increased insulin sensitivity afterexercise and the need to replete liver and muscleglycogen, which can take up to 24 to 30 hours (seeChapter 26). Hypoglycemia can also occur during orimmediately after exercise. Blood glucose levels be-fore exercise reflect only the value at that time, and itis unknown if this is a stable blood glucose level or ablood glucose level that is dropping. If blood glucoselevels are dropping before exercise, adding exercisecan contribute to hypoglycemia during exercise. Fur-thermore, hypoglycemia on the day before exercise isreported to increase the risk of hypoglycemia on theday of exercise as well (Davis et al, 2000).

Hyperglycemia can also result from exercise. Whena person exercises at what for him or her is a high

level of exercise intensity, there is a greater than nor-mal increase in counterregulatory hormones. As a re-sult, hepatic glucose release exceeds the rise in glu-cose utilization. The elevated glucose levels may alsoextend into the postexercise state (Mitchell et al, 1988;Purdon et al, 1993). Although not as likely, hyper-glycemia and worsening ketosis can also result frominsulin deficiency if exercise is done when fastingblood glucose levels are higher than 250 to 300 mg/dl.With elevated fasting blood glucose and ketones, ex-ercise should be postponed until control improves(ADA, 2002b). The latter cause of hyperglycemia isnot as likely to occur as the first.

Exercise Guidelines

The variability of glucose responses to exercise con-tributes to the difficulty in giving precise nutrition (andinsulin) guidelines. Frequent blood glucose monitoringbefore, during, and after exercise helps individualsidentify their response to physical activities. To meettheir individual needs, patients must modify generalguidelines to ingest carbohydrate after (or before) andto reduce insulin doses before (or after) exercise.

Carbohydrate for Insulin Users

During moderate-intensity exercise, glucose uptakeis increased by 8 to 13 g per hour, and this is the basisfor the recommendation to add 15 g carbohydrate forevery 30 to 60 minutes of activity (depending on theintensity) over and above normal routines. Moderateexercise for less than 30 minutes rarely requires anyadditional carbohydrate or insulin adjustment; how-ever, a small snack may be needed if the blood glu-cose level is less than 100 mg/dl (Franz, 2002).

In all persons, blood glucose levels decline gradu-ally during exercise, and ingesting a carbohydratefeeding during prolonged exercise can improve per-formance by maintaining the availability and oxida-tion of blood glucose. For the exerciser with diabeteswhose blood glucose levels may drop sooner andlower than the exerciser without diabetes, ingestingcarbohydrate after 40 to 60 minutes of exercise is im-portant and may also assist in preventing hypo-glycemia. Drinks containing 6% or less of carbohy-drate empty from the stomach as quickly as waterand have the advantage of providing both neededfluids and carbohydrate (see Chapter 26). Consum-ing carbohydrate immediately after exercise opti-mizes repletion of muscle and liver glycogen stores.For the exerciser with diabetes, this takes on addedimportance because of increased risk for late-onsethypoglycemia (Franz, 2002).

Insulin Guidelines

It is often necessary to adjust the insulin dosage toprevent hypoglycemia. This occurs most often withmoderate to strenuous activity lasting more than 45to 60 minutes. For most persons, a modest decrease

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(of about 1 to 2 U) in the rapid- or short-acting insulinduring the period of exercise is a good starting point.For prolonged vigorous exercise, a larger decrease inthe total daily insulin dosage may be necessary. Afterexercise, insulin may also need to be decreased. Inaddition to these acute reductions in insulin dosages,individuals who participate in a regular, long-termfitness program often find their usual total dosage ofinsulin decreasing by as much as 15% to 20% (Was-serman and Zinman, 1994).

Insulin doses should be reduced in anticipation ofexercise after a meal, depending on the duration andintensity of the exercise. In persons with type 1 dia-betes, Rabasa-Lhoret and colleagues validated thatexercise at 25% VO2max for 60 minutes required a 50%reduction in mealtime rapid-acting insulin, and exer-cise at 50% VO2max for 30 and 60 minutes required a50% and 75% reduction in mealtime rapid-acting in-sulin, respectively. Such reductions in mealtimerapid-acting insulin for postprandial exercise re-sulted in a 75% decrease in exercise-induced hypo-glycemia (Rabaca Lhoret et al, 2001).

Precautions for Persons With Type 2 Diabetes

Persons with type 2 diabetes may have a lower VO2maxand therefore need a more gradual training program.Rest periods may be needed; this does not impair thetraining effect from physical activity. Autonomic neu-ropathy or medications, such as for blood pressure,may not allow for increased heart rate, and individu-als must learn to use perceived exertion as a means ofdetermining exercise intensity. Blood pressure mayalso increase more in persons with diabetes than inthose who do not have diabetes, and exercise shouldnot be undertaken if systolic blood pressure is greaterthan 180 to 200 mm Hg.

Exercise Prescription

The type of exercise one chooses to perform shouldbe tailored to his or her physical capacity and inter-ests. A complete exercise program includes warm-upand cool-down periods. This not only prepares mus-cles for an aerobic workout, but it also improvesrange of motion. Cardiovascular conditioning is alsohelpful. Most people can at least undertake a walkingprogram safely. Those with type 2 diabetes shouldstrive to achieve a minimum cumulative total of 1000kcal per week from physical activities, which equatesto walking about 10 miles per week; 1 mile � �100kcal expenditure (Albright et al, 2000). Ideally, theaerobic portion of an exercise session should last aminimum of 20 minutes, with a goal of 30 to 40 min-utes; however, even three sessions of 10 minutes ofactivity during the day can improve physical fitness(Pate et al, 1995). Muscle-strengthening exercises,such as lifting light weights, are also an importantcomponent of an exercise session. Because musclesdispose of glucose, this type of exercise can also im-prove glucose control.

MedicationsOral Glucose-Lowering MedicationsThe use of the newer oral glucose-lowering medica-tions, alone or in combination, provides numerousoptions for achieving euglycemia in persons withtype 2 diabetes. Some persons with hyperglycemiathat is not adequately controlled by MNT alone can be treated with MNT, and oral medications—frequently combination therapy using two, and occa-sionally even three, oral medications may be needed.If glycemic control cannot be attained with MNT andoral medications, insulin, either alone or in combina-tion with oral medications, is required. The transitionto insulin often begins with an intermediate or long-acting insulin given at bedtime to control fasting glu-cose levels and oral medications given in the morningare to control daytime glucose levels. Eventually,however, many patients with type 2 diabetes will re-quire two or more insulin injections daily to achievecontrol. If large doses of insulin are required, oralmedications, such as insulin sensitizers, are oftencombined with the insulin regimen.

Currently, four classes of oral medications exist:(1) insulin secretagogues, which include the sulfony-lureas (first and second generation) and the megli-tinides (repaglinide and nateglinide); (2) biguanides(metformin); (3) thiazolidinediones (TZD; e.g., piogli-tazone, rosiglitazone); and (4) �-glucosidase inhibi-tors (acarbose, miglitol). Each class has a differentmechanism of action—in the pancreas, insulin secre-tion is stimulated; at the cellular level (muscle andadipose tissue), insulin resistance is decreased andglucose uptake enhanced; in the liver, hepatic glu-cose output is decreased, especially overnight, im-proving fasting glucose levels; or in the intestine, glu-cose absorption is slowed, improving postprandialglucose concentrations (Table 33-6). Because of thedifferent sites of action, the medications can be usedalone or in combination.

Insulin secretagogues (sulfonylureas and megliti-nides) promote insulin secretion by the �-cells of thepancreas. First- and second-generation sulfonylureadrugs differ from one another in their potency, phar-macokinetics, and metabolism. Disadvantages oftheir use include weight gain and the potential tocause hypoglycemia. The meglitinides differ fromthe sulfonylureas in that they have short metabolichalf-lives, which result in brief episodic stimulationof insulin secretion. As a result, a frequent dosingschedule is required with meals, postprandial glu-cose excursions are less, and because less insulin issecreted several hours after a meal, there is a de-creased risk of hypoglycemia between meals andovernight. Nateglinide only works in the presence ofglucose and is a somewhat less potent secretagogue(Inzucchi, 2002).

Insulin sensitizers enhance insulin action and in-clude biguanides (metformin) and TZD. Both classesrequire the presence of insulin, exogenous or endoge-nous, to be effective. Metformin (Glucophage) sup-

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presses hepatic glucose production and lowers in-sulin resistance, but it does not stimulate insulin se-cretion. It is not associated with hypoglycemia, maycause small weight losses when therapy begins, andimproves lipid levels. Adverse effects include gas-trointestinal distress, such as abdominal pain, nau-sea, and diarrhea, in up to 50% of patients. The fre-quency of these adverse effects can be minimizedwith food consumption and slow titration of dose. Arare side effect is severe lactic acidosis, which can befatal. Acidosis usually occurs in patients who use al-cohol excessively, have renal dysfunction, or haveliver impairments (Inzucchi, 2002). Biguanides can beused alone or in combination with other diabetesmedications. Other available agents include met-formin extended release (Glucophage XR) and gly-buride/metformin (Glucovance).

The TZDs decrease insulin resistance in peripheraltissues and thus enhance the ability of muscle and fatcells to take up glucose. TZDs also have certain lipidbenefits. HDL cholesterol increases and triglyceridesfrequently decrease with TZD therapy. AlthoughLDL cholesterol may increase because of a shift fromsmall and dense to large and buoyant LDL particles,these types of particles are less atherogenic, and thusthe increase in LDL cholesterol may not be a concern(Inzucchi, 2002). Adverse effects include weight gainand edema, and these effects are more common in pa-

tients who receive TZDs along with insulin. Patientswith advanced forms of congestive heart disease orhepatic impairment should not receive TZDs. Trogli-tazone (Rezulin), the first approved TZD, was re-moved from the market because of hepatocellularinjury. Rosiglitazone (Avandia) and pioglitazone (Ac-tos) are the two TZD drugs currently available andhave not been associated with liver injury.a-Glucosidase inhibitors work in the small intestine

to inhibit enzymes that digest carbohydrates, therebydelaying carbohydrate absorption and lowering post-prandial glycemia. Acarbose (Precose) and miglitol(Glyset) are competitive inhibitors of intestinal brush-border �-glucosidases required for the breakdown ofstarches, dextrins, maltose, and sucrose to absorbablemonosaccharides. They do not cause hypoglycemiaor weight gain when used alone, but they can fre-quently cause flatulence, diarrhea, cramping, or ab-dominal pain. Symptoms may be alleviated by initiat-ing therapy at a low dose and gradually increasingthe dose to therapeutic levels (Coniff, 1995).

Insulin

Persons with type 1 diabetes depend on insulin tosurvive. In persons with type 2 diabetes, insulin maybe needed to restore glycemia to near normal. Cir-cumstances that require the use of insulin in type 2

Oral Glucose-Lowering Medications for Type 2 Diabetes

PRINCIPAL MEAN DECREASECLASS AND GENERIC NAMES RECOMMENDED DOSE ACTION IN A1c

Sulfonylureas (Second Generation) Stimulate insulin secretion 1%-2%Glipizide (Glucotrol) 2.5-20 mg single or divided from the �-cellsGlipizide (Glucotrol XL) dose; single dose for XLGlyburide (Glynase Prestabs) 12 mg once dailyGlimepiride (Amaryl) 4 mg once daily

Meglitinides Stimulate insulin secretion 1%-2%Repaglinide (Prandin) 0.4-4.0 mg before meals from �-cellsNateglinide (Starlix) 120 mg before meals

Biguanides Decrease hepatic glucose 1.5%-2%Metformin (Glucophage) 500-850 mg tid or 1000 mg bid productionMetformin Extended Release 500-2000 mg once daily

(Glucophage XR)Metformin Glyburide 2.5/500 mg to 5.0/500 mg Also increases insulin

(Glucovance) [1.25/250 mg] once daily secretionMetformin/glipizide 2.5/250 mg to 5.0/500 mg Also increases insulin �2%

(Metaglip) [2.5 to 5./250 secretionto 500 mg]

Metformin/rosiglitazone 2.5/250 mg to 2.5/500 mg Improves insulin sensi- Unknown;(Avandamet) [1 to 4/500 tivity and reduces no clinicalmg] hepatic glucose pro- trials yet

duction

Thiazolidinediones Improve peripheral 1%-2%Pioglitazone (Actos) 15-45 mg daily insulin sensitivityRosiglitazone (Avandia) 4-8 mg daily

Alpha Glucosidase Inhibitors Delay carbohydrate 0.5%-1%Acarbose (Precose) 25-100 mg tid absorptionMiglitol (Glyset) 25-100 mg tid

From Franz MJ, Reader D, Monk A: Implementing group and individual medical nutrition therapy for diabetes, Alexandria, Va, 2002, American Diabetes Association.bid, Twice daily; tid, three times daily.

TABLE 33-6

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diabetes include the failure to achieve adequate con-trol with administration of oral medications; periodsof acute injury, infection, or surgery; pregnancy; andallergy or serious reactions to sulfonylurea agents.

Insulin has four properties: action, concentration,purity, and source. These properties determine its on-set, peak, and duration (Table 33-7). Most insulinnow is made biosynthetically, purified, and thentreated enzymatically to yield human insulin (Burgeand Schade, 1997). A major advantage of human in-sulin is that it produces fewer antibodies and, as a re-sult, can also be used for intermittent periods of in-sulin treatment, such as during surgery andpregnancy. U-100 is the concentration of insulinavailable in the United States. This refers to insulinactivity per milliliter of insulin; therefore, U-100means 100 U/ml of insulin. Pen injectors are now be-ing used more frequently as an alternative to the tra-ditional syringe-needle units.

Rapid-acting insulins include insulin lispro (Huma-log) and insulin aspart (Novolog) and are used as bo-lus (mealtime) insulins. They are insulin analogs thatdiffer from human insulin in amino acid sequence butbind to insulin receptors and thus function in a man-ner similar to human insulin. Both lispro and asparthave an onset of action within 15 minutes, a peak inactivity at 60 to 90 min, and a duration of action of 3 to5 hours. Both result in fewer hypoglycemic episodescompared with regular insulin. In the future, insulinadministered via the pulmonary route (inhaled in-sulin) also may be used as bolus insulin.

Regular is a short-acting insulin with an onset of ac-tion 15 to 60 minutes after injection and a duration ofaction ranging from 5 to 8 hours. For best results, theslow onset of regular insulin requires it to be taken 30to 60 minutes before meals.

Intermediate-acting insulins include NPH and lente.Their appearance is cloudy, and their onset, peak,

and duration are similar. Their onset of action isabout 2 hours after injection, and their peak effect isfrom 6 to 10 hours

Long-acting insulins are ultralente and glargine(Lantus). Ultralente has its peak activity 8 to 10 hoursafter injection and a duration of about 18 to 20 hours.Insulin glargine is the newest insulin on the marketand is also an insulin analog. Slow dissolution ofglargine at the site of the injection results in a relativelyconstant and peakless delivery over 24 hours.Glargine is clear in solution, similar to lispro, aspart,and regular, whereas NPH, lente, and ultralente arecloudy. Patients need to be sure they have their vialmarked clearly. Glargine cannot be mixed with otherinsulins and is usually given at bedtime. However,glargine can also be given before any meal, butwhichever time is chosen, glargine must be given con-sistently at that time. Clinical trials have demonstratedlower fasting glucose levels and less hypoglycemiawith glargine than with NPH (Vajo et al, 2001). De-temir is a long-acting insulin still under development.

Premixed insulins are also available: 70/30, whichis 70% NPH and 30% regular, and 50/50, which is50% NPH and 50% regular. The addition of neutralprotamine to lispro creates an intermediate-acting in-sulin that has been used in 75/25 combinations withlispro. Similarly, the addition of neutral protamine toaspart creates an immediate-acting insulin that hasbeen used in 10/30 combination with aspart.

All persons with type 1 diabetes and those withtype 2 diabetes who no longer produce adequate en-dogenous insulin need replacement of insulin thatmimics normal insulin action. After individuals with-out diabetes eat, their plasma glucose and insulinconcentrations increase rapidly, peak in 30 to 60 min-utes, and return to basal concentrations within 2 to 3hours. To mimic this, rapid-acting (or short-acting)insulin is given before meals, and this is referred to

Action Times of Human Insulin Preparations

ONSET OF USUAL EFFECTIVE MONITOR EFFECTTYPE OF INSULIN ACTION PEAK ACTION DURATION IN:

Rapid-acting �15 min 0.5-1.5 hr 2-4 hr 2 hrLisproAspart

Short-acting 0.5-1 hr 2-3 hr 3-6 hr 4 hrRegular

Intermediate-actingNPH 2-4 hr 6-10 hr 10-16 hr 8-12 hrLente 3-4 hr 6-12 hr 12-18 hr 8-12 hr

Long-actingUltralente 6-10 hr 10-16 hr 18-20 hr 10-12 hrGlargine (Lantus) 1.1 hr — 24 hr 10-12 hr

Mixtures 0.5-1 hr Dual 10-16 hr70/30 (70% NPH, 30% regular)50/50 (50% NPH, 50% regular)75/25 (75% neutral protamine

lispro [NPL], 25% lispro)70/30 (75% neutral protamine

aspart [NPA], 30% aspart)

From Franz MJ, Reader D, Monk D: Implementing group and individual medical nutrition therapy for diabetes, Alexandria, Va, 2002, American Diabetes Association.NPH, Neutral protamine Hagedorn.

TABLE 33-7

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as bolus or mealtime insulin. Mealtime insulin dosesare adjusted based on the amount of carbohydrate inthe meal. An insulin-to-carbohydrate ratio can be es-tablished for an individual that will guide decisionson the amount of mealtime insulin to inject.

Basal or background insulin dose is that amount ofinsulin required in the postabsorptive state to re-strain endogenous glucose output primarily from theliver. Basal insulin also limits lipolysis and excessflux of free fatty acids to the liver.

The type and timing of insulin regimens should beindividualized, based on eating and exercise habitsand blood glucose concentrations. For normal-weightpersons with type 1 diabetes, the required insulindosage is about 0.5 to 1.0 U per kilogram of bodyweight per day. About 50% of the total daily insulindose is used to provide for basal or background in-sulin needs (such as NPH or glargine). The remainder(rapid-acting insulins, such lispro or aspart) is dividedamong the meals either proportionate to the carbohy-drate content or by giving about 1.0 to 1.5 U insulinper 10 g carbohydrate consumed. The larger amount isusually needed to cover breakfast carbohydrate as aresult of the presence in the morning of higher levelsof counterregulatory hormones (Rabasa-Lhoret et al,1999). Persons with type 2 diabetes may require in-sulin doses in the range of 0.5 to 1.2 U per kilogram ofbody weight daily. Large doses, even �1.5 U kg of

body weight daily, may be required at least initially toovercome prevailing insulin resistance.

A single dose of insulin is seldom effective for op-timal blood glucose control in either type of diabetes,although occasionally insulin is added at bedtime tosuppress nocturnal hepatic glucose production andto normalize fasting glucose concentrations and oralmedications are continued during the day (Yki-Jarvinen et al, 1992).

The administration of basal insulin twice a daymay suffice for persons with type 2 diabetes who stillhave significant endogenous insulin production. Acommonly used insulin regimen combines a short-acting (such as regular) or a rapid-acting (such aslispro or aspart) insulin and a basal insulin (such asNPH) given twice a day. The prebreakfast dose con-sists of about one third regular and two thirds NPH.The presupper dose is usually divided into equalamounts of NPH and regular insulin (Figure 33-3).Another option is to combine regular (or lispro or as-part) and NPH before breakfast, regular (or lispro oraspart) before supper, and NPH or ultralente at bed-time. The NPH (or ultralente) is administered at bed-time to control the early morning surge in blood glu-cose levels (dawn phenomenon).

For persons with type 1 diabetes and many patientswith type 2 diabetes a flexible insulin regimen is pre-ferred. Basal insulin, such as NPH, may be adminis-

Morning Afternoon Evening Night

Regular Regular

NPH/Lente NPH/Lente


NPH/Lente NPH/Lente

Lispro/Aspart Lispro/Aspart

↑ B L ↑ S HS B

L ↑ S HS B

Insu

lin e

ffec

tIn

sulin

eff

ect

Meals (A)

Meals (B)

B, Breakfast; L, lunch; S, supper; HS, bedtime snack; arrow, time of insulin injectionSchematic representation only

↑ B

• Time actions of two-injection insulin regimens. (Modified from Skyler US: Medical management of type 1 diabetes, ed 3,Alexandria, Va, 1998, American Diabetes Association.)FIGURE 33-3

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tered twice a day, before breakfast and at bedtime.Meal insulin is provided by rapid-acting (lispro or as-part) insulin administered with each meal (Figure33-4). Because of the peaking action of NPH, this regi-men often results in erratic glucose levels. The intro-duction of glargine has provided a solution to many ofthese problems. With glargine as basal insulin at bed-time and rapid-acting insulin as bolus for meals, in-

sulin doses can be identified more accurately, and ini-tial dosing is simplified (Figure 33-5). These types ofinsulin regimens allow increased flexibility in the typeand timing of meals.

Insulin pump therapy provides basal rapid-acting or short-acting insulin pumped continuously by amechanical device in micro amounts through a sub-cutaneous catheter that is monitored 24 hours a day.


Regular Regular

NPH/Lente NPH/Lente

↑ B L ↑ S ↑ HS B

Insu

lin e

ffec

t

Meals (A)



NPH/Lente NPH/Lente

↑ B L ↑ S ↑ HS B

Insu

lin e

ffec

t

Meals (B)


• Time actions of multiple-action insulinregimens. (Modified from Skyler US: Medical management oftype 1 diabetes, ed 3, Alexandria, Va, 1998, American DiabetesAssociation.)

FIGURE 33-4



↑ B ↑ L ↑ S HS B

Insu

lin e

ffec

t

Meals (B)

Lispro/Aspart

Glargine


• Time actions of flexible insulin regimens.(Modified from Skyler US: Medical management of type 1 diabetes,ed 3, Alexandria, Va, 1998, Americam Diabetes Association.

FIGURE 33-5

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Both lispro and aspart work well in insulin pumps,resulting in improved glycemia and less hypogly-cemia than with regular insulin (Bode and Strange,2001). Boluses of the insulin are given before meals.Pump therapy requires a committed and motivatedperson who is willing to do a minimum of four bloodglucose tests per day, to keep blood glucose andfood records, and to learn the technical features ofpump use.

Blood Glucose MonitoringSelf-monitoring of blood glucose (SMBG) is used on aday-to-day basis to manage diabetes effectively andsafely; however, laboratory measurement of glycatedhemoglobin provides the best available index ofoverall diabetes control.

The health care team, including the individualwith diabetes, should work together to implementblood glucose monitoring and establish individualtarget blood glucose goals (see Table 33-4 for a listingof these goals). The frequency of monitoring dependson the type of diabetes and overall therapy.

Patients can perform SMBG up to eight times perday—before breakfast, lunch, and dinner; at bedtime;1 to 2 hours after meals; and during the night orwhenever needed to determine causes of hypogly-cemia or hyperglycemia. For most patients with type1 diabetes, SMBG is recommended four or moretimes a day, before each meal and at bedtime. SMBGin patients with type 2 diabetes should be sufficientto facilitate reaching glucose goals and is often per-formed one to four times a day, often before breakfastand before and 2 hours after the largest meal but only3 or 4 days per week. When adding to or modifyingtherapy, type 1 and type 2 patients with diabetesshould test more often than usual (ADA, 2002d).

Because the accuracy of SMBG is instrument anduser dependent, it is important for health care pro-viders to evaluate each patient’s monitoring tech-niques, both initially and at regular intervals there-after. Comparisons between results from patientself-testing in the clinic and simultaneous laboratorytesting are useful to assess the accuracy of patient re-sults. Most meters now automatically convert thecapillary whole-blood test to plasma glucose valuesso comparisons can readily be made with laboratoryvalues.

It is important that the results of SMBG be writtenin a record book and that patients be taught how to ad-just their management program based on these results.The first step in using such records is to learn how toidentify patterns in blood glucose levels and how toadjust basic insulin doses. For example, if blood glu-cose levels are consistently (generally 3 days in a row)elevated at a specific testing time, adjustments aremade in the insulin or medication acting at that time.After pattern management is mastered, algorithms forinsulin dose changes to compensate for an elevated orlow glucose value can be added.

In using blood glucose monitoring records, it shouldbe remembered that factors other than food affectblood glucose concentrations. An increase in blood glu-cose can be the result of insufficient insulin or insulinsecretagogue, too much food, or increases in glucagonand other counterregulatory hormones as a result ofstress, illness, or infection. Factors that contribute to hy-poglycemia include too much insulin or insulin secret-agogue, not enough food, unusual amounts of exercise,and skipped or delayed meals. Urine glucose testing,frequently used in the past, has so many limitationsthat it should not used.

It is now possible to do continuous ambulatoryblood glucose monitoring to determine 24-hourblood glucose patterns and to detect unrecognizedhypoglycemia. One such system consists of a subcu-taneous sensor that monitors interstitial glucose lev-els for up to 72 hours. Data can be downloaded in thephysician’s office after completion of the prescribedcycle. Another device is worn on the wrist and canprovide up to three glucose readings each hour for amaximum of 12 hours. It works through a processcalled reverse iontophoresis, in which a low-level elec-tric current passes through intact skin and extractsglucose molecules.

Urine or blood testing can be used to detect ke-tones. Testing for ketonuria or ketonemia should beperformed regularly during periods of illness andwhen blood glucose levels consistently exceed 240mg/dl. The presence of persistent, moderate, or largeamounts of ketones, along with elevated blood glu-cose levels, requires insulin adjustments. Personswith type 2 diabetes rarely have ketosis; however, ke-tone testing should be done when the person is seri-ously ill.

Self-Management EducationDiabetes management is a team effort. Persons withdiabetes must be at the center of the team because they have the responsibility for day-to-day manage-ment. Dietitians, nurses, physicians, and other healthcare providers contribute their expertise to developingtherapeutic regimens that help the person with dia-betes achieve the best metabolic control possible. Thegoal is to provide patients with the knowledge, skills,and motivation to incorporate self-management intotheir daily lifestyles.

For newly diagnosed patients, a staged approachto education should be used. Education initially fo-cuses on the needed basic skills (Box 33-2). Optimalself-management of diabetes requires changes in ex-isting behaviors in addition to the adoption of newones. Successful behavioral change requires compre-hensive education, skill development, and moti-vation (see Chapter 22). The knowledge and skillsneeded to implement nutritional recommendationscannot be acquired in one session; therefore, contin-ued nutrition education is essential and must be anongoing component of diabetes care (Box 33-3).

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Children and AdolescentsInvolvement of a multidisciplinary team, including aphysician, dietitian, nurse, and behavioral specialist,all trained in pediatric diabetes, is the best means ofachieving optimal diabetes management in youth.The most important team members, however, are thechild or adolescent and his or her family.

A complete nutrition assessment, which is thebasis for the food and meal plan for youth with dia-betes, includes anthropometric measurements, nutri-tion assessment and food history, biochemical in-dices, assessment of feelings and family concernsrelated to nutrition and diabetes, and typical activitypatterns (see Chapters 17 and 18).

A major nutrition goal for children and adolescentswith type 1 diabetes is maintenance of normal growthand development. Possible causes of poor weightgain and linear growth include poor glycemic control,inadequate insulin, and overrestriction of calories.The last may be a consequence of the common erro-neous belief that restricting food, rather than adjust-ing insulin, is the way to control blood glucose. Otherreasons unrelated to diabetes management includethyroid abnormalities and malabsorption syndromes.Excessive weight gain can be due to excessive caloricintake, overtreatment of hypoglycemia, or overin-sulinization. Other causes include low physical activ-ity levels and hypothyroidism (accompanied by poorlinear growth) (Drash, 1993).

DIABETES AND AGE-RELATEDISSUES

The nutrition prescription is based on the nutri-tion assessment. Newly diagnosed children oftenpresent with weight loss and hunger; as a result, theinitial meal plan must be based on adequate caloriesto restore and maintain appropriate body weight. Inabout 4 to 6 weeks, the initial caloric level may needto be modified to meet more usual caloric require-ments. Children have a natural ability to know howmuch to eat for normal growth and development.Table 33-8 lists a formula that can be used to confirmthat a child or adolescent is receiving the minimumnumber of calories necessary for growth and devel-opment. Height and weight should be recorded ongrowth charts every 3 to 6 months to make surechildren are growing normally. If not, the overalldiabetes management plan needs to be assessed.For growth charts see Appendixes 6 to 11, 18, and 19.Caloric needs in children change continuously, andso food intake should be evaluated every 3 to 6months.

Box 33-3. Essential Self-Management NutritionEducation Skills*

• Sources of carbohydrate, protein, fat• Understanding nutrition labels• Modification of fat intake• Alcohol consumption guidelines• Use of blood glucose monitoring data for

problem solving related to food choices andphysical activity options

• Use of blood glucose monitoring data to iden-tify blood glucose patterns and need for med-ication changes

• Adjustments in carbohydrate or insulin for ex-ercise

• Grocery shopping guidelines• Guidelines for eating out: restaurant, cafete-

ria, school lunch• Snack choices• Mealtime adjustments• Use of sugar-containing foods and nonnutri-

tive sweeteners• Recipes, menu ideas, cookbooks• Behavior modification techniques• Problem-solving tips for birthdays, special oc-

casions, holidays• Travel, schedule changes• Vitamin, mineral, and botanical supplements• Work shift rotation, if needed

Modified from American Dietetic Association: Medical nutrition therapyevidence-based guides for practice: nutrition practice guidelines for type 1 andtype 2 diabetes, CD-Rom, Chicago, Ill, 2001, American Dietetic Associa-tion.*Topics emphasized based on patient’s lifestyle, level of nutritionknowledge, and experiences in planning, purchasing, and preparingfood and meals.

Box 33-2. Medical NutritionTherapy Basic Self-Management Education Skillsfor PersonsWith Diabetes

• Basic food and meal planning guidelines• Physical activity guidelines• Self-monitoring of blood glucose levels• For insulin or insulin secretagogue users, signs,

symptoms, treatment, and prevention of hypo-glycemia

• For insulin or insulin secretagogue users,guidelines for managing short-term illness

• Plans for follow-up and ongoing education

Modified from American Dietetic Association: Medical nutrition ther-apy evidence-based guides for practice: nutrition practice guidelines for type1 and type 2 diabetes, CD-Rom, Chicago, Ill, 2001, American DieteticAssociation.

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Individualized food and meal plans, insulin regi-mens using basal (background) and bolus (mealtime)insulins, and insulin algorithms can provide flexibil-ity for children with type 1 diabetes and their families.This approach accommodates irregular meal timesand schedules and varying appetites and activity lev-els (ADA, 2002b).

Daily eating patterns in young children generallyinclude three meals and two or three snacks, depend-ing on the length of time between meals and thechild’s physical activity level. Children often prefersmaller meals and snacks. Snacks can prevent hypo-glycemia between meals and provide adequate calo-ries. Older children and teens may prefer only threemeals. Blood glucose monitoring data are then usedto integrate an insulin regimen into the meal, snack,and exercise schedules.

Realistic blood glucose goals should be determinedand discussed with the youth and family. Youth withdiabetes are also more likely than their age- and sex-matched nondiabetic peers to be at risk for cardiovas-cular disease. It is therefore essential to reduce the riskfactors in youth with type 1 diabetes. Lipid levelsshould be monitored regularly, and National Choles-terol Education Program treatment guidelines forchildren and adolescents should be followed (ADA,2003b) (see Chapter 35).

After the appropriate nutrition prescription hasbeen determined, the meal planning approach can beselected. Most pediatric educators agree that it is bet-ter to start with a more precise meal plan and thenteach flexibility than to start with flexibility and try toteach precise planning later. A number of meal plan-ning approaches can be used. Carbohydrate countingfor food planning provides youth and their familieswith guidelines that facilitate glycemic control while

still allowing the choice of many common foods thatchildren and adolescents enjoy. Whatever approachto food planning is used, however, the youth andfamily must find it understandable and applicable totheir lifestyle. Blood glucose records are essential toassist the dietitian and other team members in mak-ing appropriate changes in insulin regimens.

Type 2 Diabetes in Youth

Childhood obesity has been accompanied by an in-crease in the prevalence of type 2 diabetes among chil-dren and adolescents. Impaired glucose tolerance hasbeen shown to be highly prevalent in obese youth, ir-respective of ethnic group, and is associated with in-sulin resistance. Once type 2 diabetes develops, �-cellfailure is also a factor (Sinha et al, 2002). Thus, type 2diabetes in youth appears to follow a progressive pat-tern similar to type 2 diabetes in adults.

Successful lifestyle treatment of type 2 diabetes inchildren and adolescents involves cessation of exces-sive weight gain, promotion of normal growth anddevelopment, and the achievement of blood glucoseand A1C goals (ADA, 2000). Nutrition guidelinesshould also address comorbidities, such as hyperten-sion and dyslipidemia. Behavior modification strate-gies to decrease intake of high-caloric, high-fat foodwhile encouraging healthy eating habits and regularphysical activity for the entire family should be con-sidered. Unfortunately, successful lifestyle treatmentregimens for youth with type 2 diabetes have notbeen defined (ADA, 2002b). Metformin is often usedwhen lifestyle strategies alone have not achieved tar-get glucose goals and has been shown to be safe andeffective for the treatment of pediatric type 2 diabetes(Jones et al, 2002). Some youth may also require in-sulin therapy to achieve adequate glycemic control.

PregnancyNormalization of blood glucose levels during preg-nancy is very important for women who have preex-isting diabetes or who develop GDM. MNT goals areto assist in achieving and maintaining optimal bloodglucose control, to provide adequate maternal and fe-tal nutrition, to supply energy intake for appropriatematernal weight gain, and to provide necessary vita-min and mineral supplements (ADA, 2002b).

Preexisting Diabetes and Pregnancy

Preconception counseling and the ability to achievenear-normal blood glucose levels before pregnancyhave been shown to be effective in reducing the inci-dence of anomalies in infants born to women withpreexisting diabetes to nearly that of the general pop-ulation (Kitzmiller et al, 1996). Normal blood glucoselevels are lower during pregnancy. Table 33-9 outlinesblood glucose goals during pregnancy for preexistingdiabetes and for GDM (ADA, 2002e; Jovanovic, 2000).

Estimating Minimum EnergyRequirements for Youth

Base energy requirements on food and nutrition assessmentValidate energy needsAGE ENERGY REQUIREMENTS

1 yr 1000 kcal for the first year

Toddler2-11 yr Add 100 kcal/yr to 1000 kcal; up to 2000 kcal at

age 10

Girls12-15 yr 2000 kcal plus 50-100 kcal/yr per year after age 10�15 yr Calculate as for an adult

Boys12-15 yr 2000 kcal plus 200 kcal/yr per year after age 10�15 yr Sedentary: 16 kcal/lb (30-35 kcal/kg)

Moderate physical activity: 18 kcal/lb (40 kcal/kg)Very physically active: 23 kcal/lb (50 kcal/kg)

Modified from Franz MJ, Reader D, Monk D: Implementing group and individ-ual medical nutrition therapy for diabetes, Alexandria, Va, 2002, American Dia-betes Association.

TABLE 33-8

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As a result of hormonal changes during the firsttrimester, blood glucose levels are often erratic. Al-though caloric needs do not differ from those pre-ceding pregnancy, the meal plan may need to beadjusted to accommodate the metabolic changes.Women should be educated about the increased riskof hypoglycemia during pregnancy and cautionedagainst overtreatment.

The need for insulin increases during the secondand third trimesters of pregnancy. This is the reasonwhy screening for GDM is done between weeks 24 and28 of pregnancy. At 38 to 40 weeks’ postconception, in-sulin needs and levels peak at two to three timesprepregnancy levels. Pregnancy-associated hormonesthat are antagonistic to the action of insulin lead to anelevation of blood glucose levels. For women with pre-existing diabetes, this increased insulin need must bemet with increased exogenous insulin.

Meal plan adjustments are necessary to providethe additional calories required to support fetalgrowth. Weight gain should be monitored, and guide-lines for appropriate weight gain that apply towomen without diabetes also apply to women withdiabetes. Regular follow-up visits are needed to alsomonitor caloric and nutrient intake, blood glucosecontrol, and whether there is starvation ketosis.Urine or blood ketones during pregnancy may signalstarvation ketosis that can be caused by inadequateenergy or carbohydrate intake, omission of meals orsnacks, or prolonged intervals between meals (e.g.,more than 10 hours between the bedtime snack andbreakfast). Ketonemia during pregnancy has been as-sociated with reduced IQ scores in children (Rizzo etal, 1991). Women should be instructed to test for ke-tones periodically before breakfast.

Nutrition therapy is individualized according tothe food and nutrition history, prepregnancy weight,and physical activity levels. Generally, an additional100 to 300 kcal daily is added to the meal plan at the beginning of the second trimester. The increasedcalorie requirement can be met easily by the addition

of one or two cups of reduced-fat or skim milk and 1to 2 oz of meat or meat substitute. This also providesadequately for the increased protein need. Smallermeals and more frequent snacks are often needed toprevent hypoglycemia. A late-evening snack is espe-cially important to decrease the likelihood of over-night starvation ketosis. Records of food intake andblood glucose values are essential for determiningwhether glycemic goals are being met and for pre-venting and correcting ketosis.

Gestational Diabetes Mellitus

About 7% of all pregnancies are complicated by GDM,resulting in more than 200,000 cases annually (ADA,2002e). After delivery, about 90% of all women withGDM become normoglycemic but are at increased riskof developing GDM earlier in subsequent pregnanciesand are at increased risk for developing type 2 dia-betes. Although estimates vary, within 4 years afterpregnancy, about 30% to 40% of women with GDMwho are obese will develop type 2 diabetes (ADA,2001). Avoidance of obesity in women before and after pregnancy reduces the risk of subsequent type 2 diabetes.

Because fetal morbidity may be increased, a riskassessment for GDM should be done at the first pre-natal visit and for women at high risk (those withmarked obesity, previous history of GDM, glyco-suria, or a strong family history of diabetes) as soonas possible. An FPG of 126 mg/dl or higher or a ca-sual PG of 200 mg/dl meets the threshold for the di-agnosis of diabetes and, if confirmed on a second day,requires no further testing (ADA, 2002a). High-riskwomen not found to have GDM at the initial screen-ing and average risk women (a few women can beclassified as low-risk) should be tested between 24to 28 weeks’ gestation. An oral glucose challenge(which does not have to be preceded by fasting) witha 50-g glucose load is performed, and an elevatedplasma glucose level (�140 mg/dl) 1 hour later isconsidered an indication of the need for diagnostictesting. The criteria for the diagnosis of GDM basedon a 100-g oral glucose tolerance test (OGTT) arelisted in Table 33-10. Low-risk women who do notneed to be screened must meet all the following crite-ria: younger than 25 years of age; normal bodyweight; no family history of diabetes; no history ofabnormal glucose tolerance; and not a member of anethnic or racial group with a high prevalence of dia-betes (ADA, 2002a).

Limited research has been done to determine theideal diet for GDM. In general, the overall nutritionrecommendations for preexisting diabetes also applyto GDM, although the diagnosis is generally notmade before the second or third trimester. The goal ofnutrition therapy is to provide adequate energy lev-els for appropriate gestational weight gain, achieve-ment and maintenance of normoglycemia, and ab-sence of ketones. Individualization of the meal plan

Plasma Glucose Goals DuringPregnancy

PREEXISTING GESTATIONALDIABETES DIABETES

TEST (mg/dl) (mg/dl)

Fasting plasma glucose 65-100 80-110Premeal 65-1101 hr postprandial �145 �1552 hr postprandial �135 �1302 to 6 hr postprandial 65-135Normal values during

pregnancyFasting plasma glucose: 70-1051-2 hr postprandial: �140

Modified from Jovanovic L, editor: Medical management of pregnancy compli-cated by diabetes, ed 3, Alexandria, Va, 2000, American Diabetes Association,and American Diabetes Association: Gestational diabetes mellitus [PositionStatement], Diabetes Care 25(suppl 1):S94, 2002.

TABLE 33-9

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is recommended, as the ideal percentage and type ofcarbohydrate is controversial. Monitoring blood glu-cose, urine and blood ketones, appetite, and weightgain can aid in developing an appropriate, individ-ualized meal plan and in adjusting the meal planthroughout pregnancy (ADA, 2002b).

Nutrition practice guidelines for gestational dia-betes have been developed and field-tested (Readerand Sipe, 2001). With input from patients, the dieti-tian designs a food and meal plan; however, withoutblood glucose monitoring data, it is impossible to as-sess its effectiveness. Food and blood glucose recordsguide nutrition therapy, and alterations to food plansare used to assess outcomes of therapy and, alongwith weight changes, determine whether insulintherapy is needed. Insulin therapy is added if glucosegoals exceed target range (see Table 33-9) on two ormore occasions in a 1- to 2-week period without someobvious explanation from food records or if glucoselevels are consistently elevated because of patients’dietary indiscretions after MNT intervention. Weightgain or lack of weight gain and ketone testing can beuseful in determining whether patients are undereat-ing to keep glucose levels within target range toavoid insulin therapy.

Medical nutrition therapy involves developing acarbohydrate-controlled, consistent food and mealplan. Generally, 40% to 45% of total energy intake willbe from carbohydrate, which is distributed through-out the day in three small to moderate-sized mealsand two to four snacks. An evening snack is usuallyneeded to prevent accelerated ketosis overnight. Car-bohydrate is not as well tolerated at breakfast as it isat other meals because of increased levels of cortisoland growth hormones. To compensate for this, theinitial food plan may have 30 to 45 g of carbohy-drate at breakfast. To satisfy hunger, protein foods,because they do not affect blood glucose levels, can beadded.

Although caloric restriction must be viewed withcaution, in obese women with GDM, a 30% caloric re-striction (an intake of about 1700 to 1800 kcal daily)can reduce hyperglycemia with no increase in ke-tonuria (Knopp et al, 1991). Intake below these levelsis not advised. The pattern of weight gain during preg-nancy for women with GDM should be similar to thatof women without diabetes.

Exercise can also assist in overcoming peripheralresistance to insulin and in controlling postprandialhyperglycemia. It may be used as an adjunct to nutri-tion therapy to improve maternal glycemia. The idealform of exercise is unknown, but a brisk walk aftermeals is often recommended.

Older AdultsThe prevalence of diabetes and IGT increases dra-matically as people age. Many factors predisposeolder adults to diabetes: age-related decreases in in-sulin production and increases in insulin resistance,adiposity, decreased physical activity, multiple pre-scription medications, genetics, and coexisting ill-nesses. A major factor appears to be insulin resist-ance. Controversy persists as to whether the insulinresistance is itself a primary change or whether it isattributable to reduced physical activity, decreasedlean body mass, and increased adipose tissue, whichare all frequently seen in older adults. Abdominalobesity also correlates with insulin resistance in olderadults (Kohrt et al, 1993). Furthermore, medicationsused to treat coexisting diseases may complicate dia-betes therapy in older persons.

Despite the increase in glucose intolerance withage, aging per se should not be a reason for subopti-mal control of blood glucose. Even if it is incorrectlyassumed that preventing long-term diabetic compli-cations is not relevant to the care of older adults, per-sistent hyperglycemia has deleterious effects on thebody’s defense mechanisms against infection. It alsoincreases the pain threshold by exacerbating neuro-pathic pain, and it has a detrimental effect on the out-come of cerebrovascular accidents.

Exercise training can significantly reduce the de-cline in aerobic capacity that occurs with age, im-prove risk factors for atherosclerosis, slow the declinein age-related lean body mass, decrease central adi-posity, and improve insulin sensitivity.

A daily multivitamin supplement may be appro-priate for older adults, especially those with reducedenergy intake. All older adults should have a calciumintake of at least 1200 mg daily and a vitamin D in-take of 15 g or 600 IU per day.

Malnutrition, not obesity, is often the more preva-lent nutrition-related problem of older adults. It oftenremains subclinical or unrecognized because the re-sult of malnutrition—excessive loss of lean bodymass—resembles the signs and symptoms of the ag-ing process. Until a primary disease develops orchronic problems are exacerbated by illness or some

Diagnosis of GestationalDiabetes Mellitus (GDM)

TYPE OF TEST RESULTS

Screening during pregnancy— A plasma glucose level �140 a 50-g oral glucose chal- mg/dl (�7.8 mmol/L) 1 lenge (does not have to be hr later indicates the need fasting) at 24 to 28 wk ges- for further diagnostic tation testing.

Oral glucose tolerance test After a 100-g oral glucose with an abnormal screen load, GDM may be diag-

nosed if two plasma glu-cose values equal or exceed:Fasting: �95 mg/dl1 hr: �180 mg/dl2 hr: �155 mg/dl3 hr: �140 mg/dl

Modified from American Diabetes Association: Standards of medical carefor patients with diabetes mellitus [Position Statement], Diabetes Care25(suppl 1):S33, 2002.

TABLE 33-10

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other stress, malnutrition may remain unrecognized.Both malnutrition and diabetes adversely affectwound healing and defense against infection, andmalnutrition is associated with depression and cog-nitive deficits. The most reliable indicator of poor nu-tritional status in older adults is probably a change inbody weight. In general, involuntary weight gain orloss of more than 10 pounds or 10% of body weight in less than 6 months indicates a need to evaluatewhether the reason is nutrition related (ADA, 2002b).

Because of concern over malnutrition, it is essen-tial that older adults, especially those in long-termcare settings, be provided a diet that meets their nu-tritional needs, enables them to attain or maintain areasonable body weight, helps control blood glucose,and is palatable. The imposition of dietary restrictionon older residents in long-term health facilities is notwarranted. Residents should be served the regular(unrestricted) menu with consistency in the amountand timing of carbohydrate (ADA, 2002f).

In older adults, acute hyperglycemia and dehydra-tion can lead to a serious complication of diabetes: thehyperglycemic hyperosmolar state (HHS). Patientswith HHS have a very high blood glucose level (rang-ing from 400 to 2800 mg/dl, with an average of 1000mg/dl) without ketones. Patients are markedly dehy-drated, and mental status often ranges from mild con-fusion to hallucinations or coma. Treatment includesprovision of adequate fluids as well as blood glucosecontrol.

Medical nutrition therapy begins with developingrapport with the patient, and whether provided indi-vidually or in groups, MNT involves a commonprocess—assessment (evaluation at follow-up visits),intervention including self-management education,goal setting, and communication (documentation)(see Chapter 21). If MNT is to be implemented indi-vidually, the intervention is then individualizedbased on the needs of the patient and whether the in-tervention is for initial, continuing, or intensive care.

Providing MNT in groups is becoming increasinglymore important, since reimbursement criteria for dia-betes self-management education and for MNT rec-ommend that when possible group sessions are prefer-able. It is helpful if the group participants are similarin their stage of diabetes management and if they allspeak and understand the same language. Group edu-cation shifts more responsibility to the patient to pro-vide the needed initial assessment information, toevaluate outcomes, and to decide about therapychanges (Franz, Reader, and Monk, 2002). Group inter-ventions for diabetes self-management education,when compared with individual interventions, haveproduced similar positive outcomes (Rickheim et al,

IMPLEMENTING NUTRITION SELF-MANAGEMENT

2002). Implementation of group MNT is covered in Im-plementing Group and Individual Medical Nutrition Ther-apy for Diabetes (Franz, Reader, and Monk, 2002).

AssessmentTo develop an individualized nutrition care plan, thefollowing parameters are assessed: anthropometricmeasures (height, weight, BMI), laboratory data,food and nutrition history, learning style, culturalheritage, and socioeconomic status. Box 33-4 pro-vides a summary of such assessment data. Food andeating histories can be done several ways, with theobjective being to determine a schedule and patternof eating that will be the least disruptive to thelifestyle of the individual with diabetes and, at thesame time, will facilitate improved metabolic control.With this objective in mind, asking the individual ei-ther to record or report what, how much, and whenhe or she typically eats during a 24-hour period maybe the most useful.

Another approach is to ask the patient to keep andbring with him or her a 3-day or 1-week food intakerecord. This request can be made when an appoint-ment with the dietitian is scheduled. Assessment of themost typical daily pattern can then be made. The his-tory can also reveal other useful information, including(1) usual caloric intake; (2) quality of the usual diet; (3)times, sizes, and contents of meals and snacks; (4) foodidiosyncrasies; (5) frequency with which meals areeaten in restaurants; (6) who usually prepares food;

Box 33-4. Food/NutritionAssessment

• Minimum referral data: age, diagnosis of dia-betes and other pertinent medical history,diabetes and other pertinent medications, lab-oratory data (A1C, cholesterol fractionation,albumin-to-creatinine ratio, and blood pres-sure), and clearance for exercise

• Diabetes history: previous diabetes education,use of blood glucose monitoring, diabetesproblems/concerns (hypoglycemia, hyper-glycemia, fear of insulin)

• Food/nutrition history: current eating habitswith beginning modifications

• Social history: occupation, hours worked/away from home, living situation, financialissues

• Medications/supplements: medications taken,vitamin/mineral/supplement use, herbalsupplements

Modified from Franz MJ, Reader D, Monk A: Implementing group andindividual medical nutrition therapy for diabetes, Alexandria, Va, 2002,American Diabetes Association.

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(7) eating problems (e.g., as related to dental, gastroin-testinal or other problems); (8) alcoholic beverage in-take; and (9) supplements used (see Chapter 17).

It is also essential to learn about the patient’s dailyroutine and schedule. The following information isneeded: (1) time of waking; (2) usual meal and eatingtimes; (3) work schedule or school hours; (4) type,amount, and timing of exercise; and (5) usual sleephabits.

Using the assessment data and food and nutritionhistory information, a preliminary food and meal plancan then be designed and, if the patient desires, sam-ple menus provided. Developing a food and meal plandoes not begin with a set calorie or macronutrient pre-scription; instead, it is determined by modifying theusual food intake as necessary. The worksheet in Fig-ure 33-6 can be used to record the usual foods eatenand to modify the usual diet as necessary. The macro-nutrient and caloric values for the exchange lists arelisted on the form and in Table 33-11. See Appendix 33for portion sizes of the foods on the exchange lists.These tools are useful in evaluating nutrition assess-ments. Using the form in Figure 33-6, the dietitian be-gins by totaling the number of exchanges from eachlist and multiplying this number by the grams of car-bohydrate, protein, and fat contributed by each. Next

the grams of carbohydrate, protein, and fat are totaledfrom each column; the grams of carbohydrate and pro-tein are then multiplied by 4 (4 kcal/g of carbohydrateand protein), and the grams of fat are multiplied by 9(9 kcal/g of fat). Total calories and percentage of calo-ries from each macronutrient can then be determined.Numbers derived from these calculations are thenrounded off. Figure 33-7 provides an example of a pre-liminary food and meal plan. In this example, the nu-trition prescription would be the following:

1900-2000 calories230 g of carbohydrate (50%)90 g of protein (20%)65 g of fat (30%)

The number of carbohydrate choices for each mealand snack is the total of the starch, fruit, and milkservings. Vegetables, unless starchy or eaten in verylarge amounts (three or more servings per meal), aregenerally considered “free foods.” The carbohydratechoices are circled under each meal and snack col-umn. Table 33-12 is an example of a sample meal planand menu based on Figure 33-7.

The next step is to evaluate the preliminary mealplan. First and foremost, does the patient with dia-betes think it is feasible to implement the meal plan

Food Group

Starches

Fruit

Milk

Vegetables

Meats/Substitutes

Fats

Breakfast Snack Lunch

Meal/Snack/Time

Totalservings/

day

Snack Dinner Snack CHO(g)

Protein(g)

Fat(g)

Calories

15 3 1 80

15 60

12 8 1 90

X4=Calories/gram

Calculations are based on medium-fat meats and skim/very low-fat milk. If diet consists predominantly of low-fat meats, use the factor 3 g instead of 5 g fat; if predominantly high-fat meats, use 8 g fat. If low-fat (2%) milk is used, use 5 g fat; if whole milk is used, use 8 g fat.

Totalgrams

Percentcalories

X4= X9= Totalcalories

5 2 25

7 5(3) 75(55)

5 45

CHOChoices

• Worksheet for assessment and design of a meal or food plan. CHO, Carbohydrate.FIGURE 33-6

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into his or her lifestyle? Second, is it appropriate fordiabetes management? Third, are the calories appro-priate? Fourth, does it encourage healthful eating?

To answer the first question concerning the feasi-bility of the food plan, the food and meal plan is re-

viewed with the patient in terms of general food in-take. Timing of meals and snacks and approximateportion sizes and types of foods are discussed. Later,a meal-planning approach can be selected that willassist the patient in making his or her own food

Food Group

Starches

Fruit

Milk

Vegetables

Meats/Substitutes

Fats

Breakfast Snack Lunch

Meal/Snack/Time

Totalservings/

day

Snack Dinner Snack CHO(g)

Protein(g)

Fat(g)

Calories

15 3 1 80

15 60

12 8 1 90

X4=Calories/gram

Calculations are based on medium-fat meats and skim/very low-fat milk. If diet consists predominantly of low-fat meats, use the factor 3 g, instead of 5 g fat; if predominantly high-fat meats, use 8 g fat. If low-fat (2%) milk is used, use 5 g fat; if whole milk is used, use 8 g fat.

Totalgrams

Percentcalories

X4= X9= Totalcalories

5 2 25

7 5(3) 75(55)

5 45

7:30 AM 10:00 12:00 3:00 6:30 10:00

2 1 2–3 1 2–3 1–2

1 1 1 0–1

1 1

� �

2–3 3–4

1 0–1 1–2 0–1 1–2

150

45

24

30

16

10 4

42

10

229 92 67

916 368 603

50 19 301900–2000

1900–2000 calories230 g CHO-50%90 g protein-20%65 g fat-30%

2

30

25

10

3

2

6

50–1

3–4CHO

1CHO

3–4CHO

1CHO

4–5CHO

1–2CHO

CHOChoices

• An example of a completed worksheet from the assessment, the nutrition prescription, and a sample 1900- to2000-calorie meal plan. CHO, Carbohydrate.FIGURE 33-7

Macronutrient and Caloric Values for Exchange Lists*

GROUPS/LISTS CARBOHYDRATE (g) PROTEIN (g) FAT (g) CALORIES

Carbohydrate GroupStarch 15 3 0-1 80Fruit 15 — — 60Milk

Skim 12 8 0-3 90Reduced-fat 12 8 5 120Whole 12 8 8 150

Other carbohydrates 15 Varies Varies VariesVegetables 5 2 — 25

Meat and Meat Substitute GroupVery lean — 7 0-1 35Lean — 7 3 55Medium-fat — 7 5 75High-fat — 7 8 100

Fat Group — — 5 45

From American Diabetes Association and American Dietetic Association: Exchange lists for meal planning, Alexandria, Va, 1995, American Diabetes Association.*See Appendix 53.

TABLE 33-11

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choices. At this point, it needs to be determinedwhether this meal plan is reasonable for the patientwith diabetes. To determine the appropriateness ofthe meal plan for diabetes management involves as-sessing both distribution of the meals (and snacks, ifdesired) and the macronutrient percentages. Appro-priateness is based on the types of medications pre-scribed as well as treatment goals.

For patients receiving MNT alone, often the foodand meal plan begins with three or four carbohydrateservings per meal for women and four or five formen, and, if desired, one or two for a snack. Bloodglucose monitoring before the meal and 2 hours afterthe meal is recommended, with the plasma glucosegoal being premeal values below 130 mg/dl and2-hour postprandial values below 160 to 180 mg/dl.

Patients on oral glucose-lowering medications of-ten do better with smaller meals and snacks, espe-cially if they are taking an insulin secretagogue. Per-sons with type 2 diabetes, however, generally have

fewer problems with hypoglycemia and do not needsnacks unless this is their choice. If they choose tohave snacks, this cannot be in addition to the usualmeals. A portion of the meal should be saved to beeaten as a snack between meals.

For patients who require insulin, the timing of eat-ing is extremely important. Food consumption mustbe synchronized with the time actions of insulin (seeprevious section on medications). If the eating pat-tern is determined first, an insulin regimen can be se-lected that will fit with it. To prevent overnight hypo-glycemia, many patients require a bedtime snack.Often individuals who use morning intermediate-acting insulins (NPH or lente) also require an after-noon snack. Individuals using rapid-acting insulin(lispro or aspart) do not need a snack.

The next step is to determine whether the numberof calories is appropriate or realistic for the individ-ual patient. Energy requirements depend on severalfactors, such as age, gender, height, weight, and ac-tivity level. Box 33-5 outlines a simple method for de-termining approximate caloric requirements basedon actual weight. Many dietitians use handheld cal-culators to determine caloric requirements, and theHarris Benedict equation, with modifications, is gen-erally used in their calculations. The determination ofa caloric level for a child or adolescent is also basedon the nutrition assessment. Table 33-18 can be usedto confirm that the child is receiving the minimumnecessary calories.

Methods for determining caloric requirements areonly approximate. On a practical basis, they do pro-vide a starting point for evaluating the caloric ade-quacy of the meal plan. Adjustments in calories can be made during follow-up visits. Parameters that should be taken into consideration are weight

Sample Menu for 1900-2000Kilocalorie Meal Plan

MEAL/TIMING FOOD SELECTIONS

Breakfast—7:30 AM

3-4 Carbohydrate choices Raisin bran cereal, 1⁄2 c(i.e., 2 starch, 1 fruit, Bagel, 1⁄4 (1 oz)1 milk) Cantaloupe (5-inch), 1⁄3

Skim milk, 1 c1 Fat Reduced-fat cream cheese, 1 tbsp

Snack—10:00 AM

1 Carbohydrate choice Bagel, 1⁄4 (1 oz)(i.e., 1 starch or fruit)

0-1 Fat Reduced-fat cream cheese, 1 tbsp

Lunch—Noon3-4 Carbohydrate choices Whole-wheat bread, 2 slices

(i.e., 2-3 starches, 1 fruit) Vegetable-beef soup, 1 cApple, 1 small

Vegetable Lettuce and tomato slices2-3 Meats Turkey, 2 oz1-2 Fats Reduced-fat mayonnaise, 1 tbsp

Snack—3:00 PM

1 Carbohydrate choice Pretzels, 3⁄4 oz(i.e., 1 starch or fruit)

0-1 Fat

Dinner—6:30 PM

4-5 Carbohydrate choices Baked potato, 1 medium(i.e., 2-3 starch, 1 fruit, Dinner roll, 11 milk) Mandarin oranges, 3⁄4 c

Skim milk, 1 cVegetables Broccoli spears, 1⁄2 c

Dinner salad, 1 small3-4 Meats Chicken breast, baked, 3 oz1-2 Fats Sour cream, regular, 2 tbsp

Reduced-fat salad dressing, 2 tbsp

Snack—10:00 PM

1-2 Carbohydrate choices Ice cream, light, 1⁄2 c(i.e., 1-2 starches, Strawberries, 11⁄4 c0-1 fruit)

0-1 Fat

TABLE 33-12

Box 33-5. EstimatingApproximate EnergyRequirementsfor Adults

• Obese or very inactive 10-12 kcal/lb persons and chronic (20 kcal/kg)dieters

• Persons �55 yr, active 13 kcal/lb women, sedentary men (25 kcal/kg)

• Active men, very active 15 kcal/lb women (30 kcal/kg)

• Thin or very active men 20 kcal/lb (40 kcal/kg)

Data from Franz MJ, Reader D, Monk A: Implementing group and indi-vidual medical nutrition therapy for diabetes, Alexandria, Va, 2002, Ameri-can Diabetes Association.

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changes, feelings of satiety and hunger, and concernsabout palatability.

The best way to ensure that the meal plan encour-ages healthful eating is to encourage patients to eat avariety of foods from all the food groups. The FoodGuide Pyramid, with its suggested number of serv-ings from each food group, can be used to comparethe patient’s meal plan with the nutrition recommen-dations for all Americans (see Chapter 15).

Intervention and Self-ManagementEducationThis step involves selecting an appropriate meal-planning approach and identifying strategies forbehavioral change that enhance motivation and ad-herence to necessary lifestyle changes. A number of meal-planning approaches are available, rangingfrom simple guidelines or menus to more complexcounting methods (Table 33-13). No single meal-planning approach has been shown to be more effec-tive than any other, and the meal-planning approachselected should allow individuals with diabetes to se-lect appropriate foods for meals and snacks.

A popular approach to meal planning is carbohy-drate counting. It can be used as a basic meal-planning approach or for more intensive manage-ment. Carbohydrate-counting educational tools arebased on the concept that after eating, it is the carbo-hydrate in foods that is the major predictor of post-prandial blood glucose levels. One carbohydrateserving contributes 15 g of carbohydrate.

Facilitating Behavioral Changes

The transtheoretic model was proposed by Prochaskaas a general model of intentional behavior change(Prochaska et al, 1994). It includes a sequence ofstages along a continuum of behavioral change. Dif-ferent intervention strategies may be needed for indi-viduals at different stages of the change process. Mo-tivational interventions may work best with patientsin the earlier contemplative stages, whereas specificskill-training interventions may be most appropriatefor persons who have decided to change. Relapseand recycling through the stages occur quite fre-quently as patients attempt to modify behaviors (seeChapter 22).

Goal SettingShort-term goals (days or weeks) are often behavioralgoals and relate to lifestyle changes. Common self-management behavioral goals are consistent and include appropriate carbohydrate servings, regu-lar physical activity, correct medication dosage (ifneeded), and blood glucose monitoring as deter-mined to be needed. Goals should be specific, writtenin behavioral language, and realistic for the patient.

Before the patient leaves the initial session, plansand an appointment for a follow-up session shouldbe identified. In making plans for follow-up, the pa-tient is asked to keep a 3-day or weekly food recordwith blood glucose–monitoring data.

Evaluation and DocumentationOutcomes must be identified, and the effectiveness of nutrition interventions must be documented.Monitoring of medical and clinical outcomes shouldbe done after the second or third visit to determinewhether the patient is making progress toward estab-lished goals. If no progress is evident, the individualand dietitian need to reassess and perhaps revise thenutritional care plan. If altering food intake alone isnot achieving metabolic target ranges, the dietitianshould recommend that medications be added or ad-justed.

Finally, documentation is essential for communica-tion and reimbursement. Box 33-6 lists the areas of thenutrition intervention that require documentation.

Follow-Up and Continuing MedicalNutrition TherapySuccessful nutrition therapy involves a process ofassessment, problem solving, adjustment, and read-justment. Food records can be compared with themeal plan, which will help to determine whetherthe initial meal plan needs changing and can beintegrated with the blood glucose–monitoringrecords to determine changes that can lead to im-proved glycemic control. For patients receiving oralmedications or insulin, it can then be determinedwhether blood glucose values that are outside targetranges can be corrected with adjustments in themeal plan or whether adjustments in medicationsare needed.

After the basic food and nutrition strategies havebeen mastered, other aspects of nutrition educationshould be presented to increase flexibility in foodchoices and lifestyle while still maintaining glucosecontrol. Of particular importance is informationabout eating out and the use of information fromfood labels. Persons using insulin also need informa-tion about how to make adjustments in food intake orinsulin when schedules are disrupted.

Nutritional follow-up visits should provide en-couragement and ensure realistic expectations for thepatient. A change in eating habits is not easy for mostpeople, and they become discouraged without ap-propriate recognition of their efforts. Patients shouldbe encouraged to speak freely about problems theyare having with food and eating patterns. Further-more, there may be major life changes that requirechanges in the meal plan. Job and schedule changes,travel, illness, and other factors all have an impact onthe meal plan.

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Food-Planning Approaches for Diabetes

APPROACH PUBLICATION DESCRIPTION

Diabetes The First Step in Diabetes Meal Planning (American A pamphlet that provides general guidelines for meal plan-nutrition Diabetes Association and American Dietetic ning based on the Food Guide Pyramid. Designed to be guidelines Association) given to patients to use until an individualized meal plan

can be implemented; however, for some individuals theremay be no need to advance to more complex meal-planning approaches.

Healthy Food Choices (American Diabetes Associ- A pamphlet that promotes healthy eating. It is divided intoation and American Dietetic Association) two sections: (1) guidelines for making healthy food

choices and (2) simplified exchanges lists.Healthy Eating for People With Diabetes (Interna- Based on the plate method, which visualizes kinds and

tional Diabetes Center, Minneapolis, Minn.) amounts of food and is used to illustrate portions of com-mon foods in relation to plate size. General guidelines forchoosing healthy foods, lowering fat intake, and timing ofmeals and snacks are included.

Eating Healthy With Diabetes Easy Reading Guide A booklet designed specifically for persons with minimal(American Diabetes Association and reading skills. The amount of text is limited, symbols andAmerican Dietetic Association) color codes are used, and concepts and foods are pre-

sented visually.Menu Month of Meals: Classic Cooking, Old-Time Favorites, Separate books with each book containing 28 days of com-

approaches Meals in Minutes, Vegetarian Pleasures, and Ethnic plete menus for breakfast, lunch, dinner, and snacks.Delights (American Diabetes Association) Designed to help patients who need help in planning basic

menus for their diabetes.Carbohydrate Basic Carbohydrate Counting (American A pamphlet that outlines what foods are carbohydrates, and

counting Diabetes Association and American Dietetic average portions sizes. It can be used as a basic meal-Association) planning approach for anyone with diabetes and is based

on the concept that after eating, carbohydrate in foods hasthe major impact on blood glucose levels. One carbohy-drate serving � 15 g of carbohydrate.

Advanced Carbohydrate Counting (American A booklet for individuals who have chosen flexible insulinDiabetes Association and American regimens or an insulin pump. The relationship betweenDietetic Association) carbohydrate eaten and insulin injected can be shown as

an insulin-to-carbohydrate ratio. This ratio gives the indi-vidual a good guide to how much bolus rapid-acting in-sulin is needed when eating more or less carbohydratethan usual; however, before insulin ratios can be estab-lished, blood glucose levels must be under good control and the usual dose of both the basal and rapid-acting (bolus) insulin determined. The grams of carbohydrate consumed at a meal are divided by the number of units ofinsulin needed to maintain target glucose goals. This is called an insulin-to-carbohydrate ratio. For example, 75 g ofcarbohydrate may require 8 units of rapid-acting insulin and the insulin-to-carbohydrate ratio would be 1�10.Therefore, for each anticipated addition of 10 g of carbohy-drate an additional 1 unit of rapid-acting insulin is needed(or for 10 g less of carbohydrate, 1 less unit of rapid-actinginsulin is needed).

My Food Plan (International Diabetes Center, A pamphlet that combines both carbohydrate counting and Minneapolis, Minn.) calorie control in a simplified approach. It groups carbohy-

drate, meat, and fat choices by approximate portion sizes. A form for filling in an individualized meal plan is in-cluded.

Exchange list Exchange Lists for Meal Planning (American A booklet that contains lists that group foods in measuresapproaches Diabetes Association and American Dietetic that contribute approximately the same number of calo-

Association) (See Appendix 53.) ries, carbohydrate, protein, and fat. Foods are divided into three basic lists: carbohydrates, meat and meat substitutes, and fat. An individualized food plan that outlines the number of servings from each list for each meal and for snacks is included.

Modified from Franz MJ, Reader D, Monk A: Implementing group and individual medical nutrition therapy for diabetes, Alexandria, Va, 2002, American Diabetes As-sociation.

TABLE 33-13

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Hypoglycemia, diabetic ketoacidosis, and hypergly-cemic hyperosmolar state (HHS) are acute complica-tions related to diabetes.

HypoglycemiaHypoglycemia (or insulin reaction) is a common sideeffect of insulin therapy, although patients taking in-sulin secretagogues can also be affected. Autonomicsymptoms are often the first signs of mild hypo-glycemia and include shakiness, sweating, palpita-tions, and hunger. Neuroglycopenic symptoms canalso occur at similar glucose levels as autonomicsymptoms but with different manifestations. The ear-liest signs of neuroglycopenia include a slowingdown in performance and difficulty concentratingand reading. As blood glucose levels drop further, thefollowing symptoms occur: frank mental confusion

ACUTE COMPLICATIONS

and disorientation, slurred or rambling speech, irra-tional or unusual behaviors, extreme fatigue andlethargy, seizures, and unconsciousness.

Several common causes of hypoglycemia are listedin Box 33-7. In general, a glucose of 70 mg/dl orlower should be treated immediately (Cryer et al,1994). Even a level of 60 to 80 mg/dl may require amanagement decision (e.g., carbohydrate ingestion,deferral of exercise, change in insulin dosage). Treat-ment of hypoglycemia requires ingestion of glucoseor carbohydrate-containing food. Although any car-bohydrate will raise glucose levels, glucose is the pre-ferred treatment. Commercially available glucosetablets have the advantage of being premeasured tohelp prevent overtreatment. Ingestion of 15 to 20 g ofglucose is an effective but temporary treatment. Ini-tial response to treatment should be seen in about 10to 20 minutes; however, blood glucose should beevaluated again in about 60 minutes because addi-tional treatment may be necessary (Box 33-8). Theform of carbohydrate—liquid or solid—used to treatdoes not make a difference. Furthermore, addingprotein to the carbohydrate does not assist in treat-ment or prevent subsequent hypoglycemia (Gray etal, 1996). If patients are unable to swallow, adminis-tration of subcutaneous or intramuscular glucagonmay be needed. Parents, roommates, and spousesshould be taught how to mix, draw up, and adminis-ter glucagon so that they are properly prepared foremergency situations. Kits that include a syringe pre-filled with diluting fluid are available.

Self-monitoring of blood glucose is essential forprevention and treatment of hypoglycemia. Changesin insulin injections, eating, exercise schedules, andtravel routines warrant increased frequency of moni-toring (Cryer et al, 2003). Some patients experiencehypoglycemia unawareness, which means that they

Box 33-6. Nutrition CareDocumentation

Documentation of each MNT visit must include:Patient name and identification informationDate of MNT visit and amount of time spent

with patientReason for visitPatient’s current diagnosis (and relevant past

diagnoses)Pertinent test results and current medications

(name, dose)Names of others present during MNTPhysician’s referral for MNT (if billing Med-

icare)Summaries of:

Histories: nutrition, medical, social and familyNutrition risk factor assessmentNutrition problem listMNT intervention provided

Food and meal planShort- and long-term goalsEducational topics covered

Short- and long-term goalsRD’s impressions, patient progress

Patient acceptance and understandingAnticipated complianceSuccessful behavior changes

Plan of careAdditional needed skills or informationAdditional recommendationsPlans for ongoing care

From Franz MJ, Reader D, Monk A: Implementing group and individualmedical nutrition therapy for diabetes, Alexandria, Va, 2002, American Di-abetes Association.MNT, Medical nutrition therapy; RD, registered dietitian.

Box 33-7. Common Causesof Hypoglycemia

Medication errorsExcessive insulin or oral medicationsInadvertent or deliberate errors in insulin dosesImproper timing of insulin in relation to food

intakeIntensive insulin therapyInadequate food intakeOmitted or inadequate meals or snacksDelayed meals or snacksIncreased exercise or activityUnplanned activitiesProlonged duration or increased intensity of

exerciseAlcohol intake without food

Modified from Skyler JS, editor: Medical management of type 1 diabetes,ed 3, Alexandria, Va, 1998, American Diabetes Association.

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do not experience the usual symptoms. Patients needto be reminded of the need to treat hypoglycemia,even in the absence of symptoms. Patients with re-current hypoglycemia may not be good candidatesfor intensive insulin therapy.

Hyperglycemia and DiabeticKetoacidosisHyperglycemia can lead to diabetic ketoacidosis(DKA), a life-threatening but reversible complicationcharacterized by severe disturbances in carbohy-drate, protein, and fat metabolism. DKA is always theresult of inadequate insulin for glucose utilization.As a result, the body depends on fat for energy, andketones are formed. Acidosis results from increasedproduction and decreased utilization of acetoaceticacid and 3-�-hydroxybutyric acid from fatty acids.These ketones spill into the urine, hence the relianceon testing for ketones.

Diabetic ketoacidosis is characterized by elevatedblood glucose levels (�250 mg/dl but generally�600 mg/dl) and the presence of ketones in theblood and urine. Symptoms include polyuria, poly-dipsia, hyperventilation, dehydration, the fruity odorof ketones, and fatigue. SMBG, testing for ketones,and medical intervention can all help prevent DKA.If left untreated, DKA can lead to coma and death.Treatment includes supplemental insulin, fluid andelectrolyte replacement, and medical monitoring.Acute illnesses, such as flu, colds, vomiting, and diar-rhea, if not managed appropriately, can lead to thedevelopment of DKA. Patients need to know thesteps to take during acute illness to prevent DKA

(Box 33-9). During acute illness, oral ingestion ofabout 150 to 200 g of carbohydrate per day should besufficient, along with medication adjustments, tokeep glucose in the goal range and to prevent starva-tion ketosis (ADA, 2002b).

Fasting HyperglycemiaThe possible reasons for fasting hyperglycemia in-clude waning of insulin action, the dawn phenome-non, and the Somogyi (rebound) effect (phenomenon).The first situation is due to an inadequate insulin doseovernight and requires an adjustment in insulin doses.

The amount of insulin required to normalize bloodglucose levels during the night is less in the predawnperiod (from 1:00 to 3:00 AM) than at dawn (4:00 to8:00 AM). This rise in fasting blood glucose levels isreferred to as the dawn phenomenon and may resultif insulin levels decline between predawn and dawnor if overnight hepatic glucose output becomes ex-cessive as is common in type 2 diabetes. Blood glu-cose level is monitored at bedtime and at 2:00 to 3:00AM to identify the dawn phenomenon. With the dawn

Box 33-8.Treatmentof Hypoglycemia

• Immediate treatment with carbohydrate is es-sential.• If the blood glucose level falls below 70

mg/dl (3.9 mmol/L), treat with 15 g of car-bohydrate, which is equivalent to:

3 glucose tabletsFruit juice or regular soft drinks, 1⁄2 cSaltine crackers, 6Sugar or honey, 1 tbsp

• Wait 15 minutes and retest. If the blood glu-cose level remains �70 mg/dl (�3.9 mmol/L), treat with another 15 g of carbohydrate.

• Repeat testing and treatment until the bloodglucose level returns to within normal range.

• Evaluate the time to the next meal or snack todetermine the need for additional food. If it ismore than an hour to the next meal, add anadditional 15 g of carbohydrate.

Modified from Skyler JS, editor: Medical management of type 1 diabetes,ed 3, Alexandria, Va, 1998, American Diabetes Association.

Box 33-9. Sick-Day Guidelinesfor PersonsWith Diabetes

1. During acute illnesses, take usual doses of in-sulin. The need for insulin continues, or mayeven increase, during periods of illness. Fever,dehydration, infection, or the stress of illnesscan trigger the release of counterregulatory or“stress” hormones, causing blood glucose lev-els to become elevated.

2. Monitoring of blood glucose levels and urineor blood testing for ketones should be done atleast four times daily (before each meal and atbedtime). Blood glucose readings exceeding240 mg/dl and ketones are danger signals in-dicating that additional insulin is needed.

3. If regular foods are not tolerated, liquid or softcarbohydrate-containing foods (such as reg-ular soft drinks, soup, juices, and ice cream)should be eaten. At least 50 g of carbohydrate(3 to 4 carbohydrate choices) should be con-sumed every 3 to 4 hr in small, frequent feed-ings.

4. Ample amounts of liquid should be con-sumed every hour. If nausea or vomiting oc-curs, small sips—1 or 2 tbsp every 15 to30 min—should be consumed. If vomitingcontinues, the health care team should benotified.

5. The health care team should be called if ill-ness continues for more than 1 day.

Modified from Franz MJ, Joynes JO: Diabetes and brief illness, Minneapo-lis, 1993, International Diabetes Center.

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phenomenon, predawn blood glucose levels will bein the low range of normal but not in the hypo-glycemic range. For patients with type 2 diabetes,metformin is often used because of its effect onhepatic glucose output. For persons with type 1diabetes, administering insulin that does not peakat 1:00 to 3:00 AM should be considered. Takingintermediate-acting insulin at bedtime or substitut-ing a peakless, long-acting insulin, such as glargine,is often effective.

Hypoglycemia followed by “rebound” hyper-glycemia is called the Somogyi effect. This phenome-non originates during hypoglycemia with the secretionof counterregulatory hormones (glucagon, epineph-rine, growth hormone, and cortisol) and is usuallycaused by excessive exogenous insulin doses. Hepaticglucose production is stimulated, thus raising bloodglucose levels. If rebound hyperglycemia goes unrec-ognized and insulin doses are increased, a cycle ofoverinsulinization may result. Decreasing evening in-sulin doses or, as for the dawn phenomenon, takingintermediate-acting insulin at bedtime or substitutinga long-acting insulin should be considered.

Hyperosmolar Hyperglycemic StateHyperosmolar hyperglycemic state is defined as an ex-tremely high blood glucose level, the absence of orthe presence of only small amounts of ketones, and profound dehydration. Glucose levels generallyrange from greater than 600 to 2000 mg/dl. Patientswho have HHS have sufficient insulin to preventlipolysis and ketosis. This condition occurs rarely,usually in older patients with type 2 diabetes. Treat-ment consists of hydration and small doses of insulinto correct the hyperglycemia.

Long-term complications of diabetes include macro-vascular diseases, microvascular diseases, and neu-ropathy. Macrovascular diseases involve diseases of large blood vessels; microvascular diseases associ-ated with diabetes involve the small blood vesselsand include nephropathy and retinopathy. In con-trast, diabetic neuropathy is a condition character-ized by damage to the nerves.

Medical nutrition therapy is important in manag-ing several long-term complications of diabetes. Nu-trition therapy is also a major component in reducingrisk factors for chronic complications, especiallythose related to macrovascular disease. The DCCTand the UKPDS provided convincing evidence forthe relationship between improved control of bloodglucose and decreased risk of microvascular compli-cations (DCCT Research Group, 1993; UKPDSG,1998a). Although improved glycemic control has notbeen absolutely proven to reduce macrovascularcomplications, accumulating evidence is quite sug-

LONG-TERM COMPLICATIONS

gestive of such a benefit. Blood pressure control isdefinitely of benefit.

Macrovascular DiseasesInsulin resistance, which may precede the develop-ment of type 2 diabetes and macrovascular disease bymany years, induces numerous metabolic changes,known as the metabolic syndrome or the insulin resist-ance syndrome. It is characterized by intraabdominalobesity or the android distribution of adipose tissue(waist circumference greater than 102 cm [>40 in] inmen and greater than 88 cm [>35 inches] in women)and is associated with dyslipidemia, hypertension,glucose intolerance, and increased prevalence ofmacrovascular complications. Other risk factors in-clude genetics, smoking, sedentary lifestyle, high-fatdiet, renal failure, and microalbuminuria.

Macrovascular diseases—including coronary heartdisease (CHD), peripheral vascular disease (PVD), andcerebrovascular disease (CVD)—are more common,tend to occur at an earlier age, and are more extensiveand severe in people with diabetes. Furthermore, inwomen with diabetes, the increased risk of mortalityfrom heart disease is greater than in men, in contrast tothe nondiabetic population, in which heart diseasemortality is greater in men than in women (ADA, 2001).

Dyslipidemia

Lipid abnormalities occur in 11% to 44% of adults inthe United States with diabetes. In type 2 diabetes, theprevalence of an elevated cholesterol level is about28% to 34%, and about 5% to 14% have high triglyc-eride levels; also, lower HDL cholesterol levels arecommon. Furthermore, patients with type 2 diabetestypically have smaller, denser LDL particles, whichincreases atherogenicity even if the total LDL choles-terol level is not significantly elevated. Primary ther-apy is directed first at lowering LDL cholesterol levelswith the goal being to reduce LDL cholesterol concen-trations to 100 mg/dl or lower. Lifestyle interventionsshould be intensified at LDL cholesterol concentra-tions greater than 100 mg/dl, and pharmacologictherapy with a statin (HMG-CoA reductase in-hibitors) should be initiated at LDL cholesterol con-centrations of 130 mg/dl or greater. In addition, if theHDL cholesterol is less than 40 mg/dl, a fibric acidsuch as fenofibrate can be used (ADA, 2002g). Aspirintherapy should be used in all adult patients with dia-betes and macrovascular disease and for primary pre-vention in patients 40 years of age or older with dia-betes and one or more cardiovascular risk factors(ADA, 2002a).

Medical Nutrition Therapy for Dyslipidemia

For individuals with elevated LDL cholesterol, satu-rated fatty acids and trans fatty acids should be lim-ited to less than 10% of energy and perhaps to lessthan 7% of energy and, if replaced, can be substituted

CH33_Mahan_0792-0837 9/26/03 12:48 PM Page 827


with carbohydrates or monounsaturated fats (ADA,2002b).

For patients with the metabolic syndrome, im-proved glycemic control, modest weight loss, restrictedintake of saturated fats, increased physical activity, andif weight is not an issue incorporation of monounsatu-rated fats may be beneficial (ADA, 2002b). In addition,triglyceride lowering can be achieved with very-high-dose statins (for subjects with both high LDL choles-terol and triglyceride levels) or fibric acid derivatives(gemfibrozil or fenofibrate).

Individuals with triglyceride measurements of1000 mg/dl should restrict all types of dietary fat (ex-cept omega-3 fatty acids) and be treated with medica-tion to reduce triglycerides. Supplementation withfish oils may benefit those with resistant hypertri-glyceridemia (ADA, 2002b).

Hypertension

Hypertension is a common comorbidity of diabetes, af-fecting 20% to 60% of persons with diabetes, dependingon the person’s age, obesity, and ethnicity. Treatment ofhypertension in persons with diabetes should also bevigorous to reduce the risk of macrovascular and mi-crovascular disease. Blood pressure should be meas-ured at every routine visit with a goal for blood pres-sure control of less than 130/80 mm Hg. Patients with asystolic blood pressure of 130 to 139 mm Hg or a dia-stolic pressure of 80 to 89 mm Hg should be treatedwith MNT alone for a maximum of 3 months. Patientswith a systolic blood pressure of 140 mm Hg or greateror a diastolic pressure of 90 mm Hg or greater shouldreceive drug therapy in addition to MNT. Initial drugtherapy may be with angiotensin-converting enzyme(ACE) inhibition, angiotensin receptor blockers (ARBs),�-blockers, or diuretics. Additional drugs may be cho-sen from these classes or another drug class if necessaryto achieve target goals (ADA, 2002a).

Medical Nutrition Therapy for Hypertension

Although blood pressure response varies widely, thelower the sodium intake, the greater the lowering ofblood pressure (Sacks et al, 2001). Responses tosodium may be greater in subjects who are “sodiumsensitive,” a characteristic of many individuals withdiabetes. Therefore, in normotensive and hyperten-sive persons, the goal should be to reduce sodium in-take to 2400 mg of sodium or 6000 mg of sodiumchloride (salt) per day. A modest amount of weightloss and a low-fat diet that includes fruits and veg-etables (five to nine servings per day) and low-fatdairy products (two to four servings per day) will berich in potassium, magnesium, and calcium and willbeneficially affect blood pressure. Drinking small tomoderate amounts of alcohol will not adversely af-fect blood pressure; however, large alcohol intakes(more than three drinks per day) are related to an ele-vation in blood pressure (ADA, 2002b).

Microvascular DiseasesNephropathyIn the United States, diabetic nephropathy accountsfor about 40% of new cases of end-stage renal disease(ESRD). About 20% to 30% of patients with type 1 ortype 2 diabetes develop evidence of nephropathy, butin type 2 diabetes, a considerably smaller numberwill progress to ESRD; however, because of thegreater prevalence of type 2 diabetes, such patientsconstitute more than half of the patients with dia-betes currently starting on dialysis (ADA, 2002h).

The earliest clinical evidence of nephropathy is theappearance of low but abnormal urine albumin lev-els (�30 mg daily or 20 �g per minute), referred to as microalbuminuria or incipient nephropathy. Withoutspecific interventions, progression to overt nephrop-athy or clinical albuminuria (�300 mg daily or 200�g per minute) with hypertension and a gradual de-cline in glomerular filtration rate (GFR) can occur,leading to the development of ESRD in both patientswith type 1 diabetes and type 2 diabetes. An annualtest for microalbuminuria should be performed inpatients who have had type 1 diabetes for more than5 years and in all patients with type 2 diabetes start-ing at diagnosis (ADA, 2002h).

Although diabetic nephropathy cannot be cured,persuasive data indicate that the clinical course of thedisease can be modified. To reduce the risk or slow theprogression of nephropathy, glucose and blood pres-sure control should be optimized. In hypertensive andnonhypertensive patients with type 1 diabetes, ACEinhibitors are the initial agents of choice. In hyperten-sive patients with type 2 diabetes, angiotensin recep-tor blockers (ARBs) are the initial agents of choice. Ifone class is not tolerated, the other should be substi-tuted and their combination will decrease albuminuriamore than use of either agent alone (ADA, 2002h).

Medical Nutrition Therapy for Nephropathy

With the onset of nephropathy, restricted-protein di-ets may modify the underlying glomerular injuryand, along with control of hypertension and hyper-glycemia, delay the progression of renal failure(Pedrini et al, 1996; Zeller et al, 1991). Several studiesthat attempted to reduce protein intake in personswith type 1 or type 2 diabetes and microalbuminuriaachieved a protein reduction to about 1.0 g per kilo-gram of body weight. In a dose-response analysis (Pi-jls et al, 1999), a 0.1 g per kilogram of body weight perday decrease in the intake of protein was related toan improvement of 11.1% in albuminuria. In studiesconducted in subjects with type 1 diabetes andmacroalbuminuria (overt nephropathy), the achievedprotein restriction was for about 0.8 g per kilogram ofbody weight daily, which slowed the rate of declinein the GFR significantly over 32 to 35 months (Walkeret al, 1989; Zeller et al, 1991). In patients with mi-croalbuminuria, a limit of protein to 0.8 to 1.0 g per

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kilogram of body weight daily and for patients withovert nephropathy, limiting protein to 0.8 g per kilo-gram of body weight daily is recommended (ADA,2002b).

A few studies have explored the potential benefitof plant protein rather than animal protein (Kontesiset al, 1995). In general, the subjects have been nor-moalbuminuric, normotensive, and not hyperfilteringso that benefits may not have been expected. Further-more, when plant protein is substituted for animalprotein, the amount of protein consumed was also re-duced and the beneficial effect may have been from areduction in protein content or from the change inprotein source. Long-term clinical trials are needed todetermine whether reductions in animal protein orchanges in plant or animal protein will have a benefi-cial effect on diabetic nephropathy (ADA, 2002b).

Retinopathy

Diabetic retinopathy is estimated to be the most fre-quent cause of new cases of blindness among adults20 to 74 years of age. After 20 years of diabetes, nearlyall patients with type 1 diabetes and more than 60% ofpatients with type 2 diabetes have some degree ofretinopathy. Laser photocoagulation surgery can re-duce the risk of further vision loss but generally is notbeneficial in reversing already diminished acuity—thus the importance for a screening program to detectdiabetic retinopathy. An initial dilated and compre-hensive eye examination should be done in patients10 years of age and older with type 1 diabetes and inpatients with type 2 diabetes shortly after the diagno-sis of diabetes. Subsequent examinations for bothgroups should be done annually (ADA, 2002i).

There are three stages of diabetic retinopathy. Theearly stages of nonproliferative diabetic retinopathy(NPDR) are characterized by microaneurysms; apouchlike dilation of a terminal capillary; lesions thatinclude cotton-wool spots (also referred to as soft exu-dates); and the formation of new blood vessels as a re-sult of the retina’s great metabolic need for oxygenand other nutrients supplied by the bloodstream. Asthe disease progresses to the middle stages of moder-ate, severe, and very severe NPDR, gradual loss ofthe retinal microvasculature occurs, resulting in reti-nal ischemia. Extensive intraretinal hemorrhages andmicroaneurysms are common reflections of increas-ing retinal nonperfusion.

The most advanced stage—termed proliferative dia-betic retinopathy (PDR)—is the final and most vision-threatening stage of diabetic retinopathy. It is charac-terized by the onset of ischemia-induced new vesselproliferation at the optic disk or elsewhere in theretina. The new vessels are fragile and prone to bleed-ing, resulting in vitreous hemorrhage. With time, theneovascularization tends to undergo fibrosis and con-traction, resulting in retinal traction, retinal tears, vit-reous hemorrhage, and retinal detachment. Diabeticmacular edema, which involves thickening of the cen-

tral (macular) portion of the retina, and glaucoma, inwhich fibrous scar tissue increases intraocular pres-sure, are other clinical findings in retinopathy (Aielloet al, 1998).

Neuropathy

Chronic high levels of blood glucose are also associ-ated with nerve damage and affects 60% to 70% ofpatients with both type 1 and type 2 diabetes (ADA,2001). Peripheral neuropathy usually affects thenerves that control sensation in the feet and hands.Autonomic neuropathy affects nerve function con-trolling various organ systems. Cardiovascular ef-fects include postural hypotension and decreased re-sponsiveness to cardiac nerve impulses, leading topainless or silent ischemic heart disease. Sexual func-tion may be affected, with impotence the most com-mon manifestation. Damage to nerves innervatingthe gastrointestinal tract can cause a variety of prob-lems. Neuropathy can be manifested in the esopha-gus as nausea and esophagitis, in the stomach as un-predictable emptying, in the small bowel as loss ofnutrients, and in the large bowel as diarrhea or con-stipation. Intensive treatment of hyperglycemia re-duces the risk of developing diabetic neuropathy.

GastroparesisGastroparesis (impaired gastric motility) affectsabout 25% of this population and is perhaps the mostfrustrating condition that patients and dietitians ex-perience. It results in delayed or irregular contrac-tions of the stomach, leading to various gastrointesti-nal symptoms, such as feelings of fullness, bloating,nausea, vomiting, diarrhea, or constipation. It cancause detrimental effects on blood glucose control.

Medical Nutrition Therapy for Gastroparesis

Treatment involves minimizing abdominal stress.Small, frequent meals may be better tolerated thanthree full meals a day, and these meals should be lowin fiber and fat. If solid foods are not well tolerated,liquid meals may need to be recommended. As muchas possible, the timing of insulin administrationshould be adjusted to match the usually delayed nu-trient absorption. This may even require insulin in-jections after eating. Frequent blood glucose monitor-ing is important to determine appropriate insulintherapy.

The development of type 2 diabetes is strongly relatedto lifestyle factors, thus suggesting to researchers thatit might be a preventable disease. Supporting evi-dence comes from both observational and interven-

PREVENTING DIABETES

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tion studies. Observational studies addressing physi-cal activity, weight loss, and dietary intake, includingwhole grains and fiber and dietary fat, provided evi-dence for factors that might delay or prevent type 2diabetes (Wing, 1999). Early intervention trials alsoprovided support for the benefits of lifestyle inter-ventions, but all had methodologic limitations. Basedon these observational and intervention studies, theFinnish Diabetes Prevention Study (Tuomilehto et al,2001) and the Diabetes Prevention Program (DiabetesPrevention Program Research Group, 2002) were de-signed to investigate the effects of lifestyle interven-tions on prevention of diabetes in those at high risk(IGT).

In the Finnish study, 522 middle-aged, overweightsubjects with IGT were randomized to receive eitherbrief diet and exercise counseling (control group) orintensive individualized instruction on how to re-duce weight (goal of 5% weight reduction), total in-take of fat (goal of �30% of energy intake), and satu-rated fat (goal of �10% of energy intake) and how toincrease fiber intake (goal of �15 g/1000 kcal) andphysical activity (goal of �150 minutes weekly). Af-ter an average follow-up of 3.2 years, there was a 58%reduction in the incidence of type 2 diabetes in the in-tervention group compared with the control group.The reduction in the incidence of diabetes was di-rectly associated with the ability of the subjects toachieve one or more of the lifestyle strategies.

The Diabetes Prevention Program (DPP) random-ized 3234 persons (45% from minority groups) withIGT to placebo, metformin, or a lifestyle intervention.Subjects in the placebo and medication arms receivedstandard lifestyle recommendations that includedwritten information and an annual 20- to 30-minuteindividual session. Subjects in the lifestyle arm wereexpected to achieve and maintain a weight loss of atleast 7% and to perform 150 minutes of physical ac-tivity per week. Subjects were seen weekly for thefirst 24 weeks, followed by monthly sessions. Afteran average follow-up of 2.8 years, a 58% decrease inthe progression to diabetes was observed in thelifestyle group and a 31% relative reduction was ob-served in the metformin group. On average, 59% ofthe lifestyle group achieved the goal of 7% or greaterweight reduction and 74% maintained at least 150minutes per week of moderately intense activity.

The greater benefit of weight loss and physical ac-tivity over medication strongly suggests that lifestylemodification should be the first choices to prevent ordelay diabetes. Modest weight loss (5%-10% of bodyweight) and modest physical activity (30 minutesdaily) are the recommended goals (ADA, 2002j). Struc-tured programs that emphasize lifestyle changes arenecessary to accomplish these objectives.

No nutritional recommendations can be made forthe prevention of type 1 diabetes. Breast-feeding maybe of benefit. Although increased obesity in youthmay be related to an increased prevalence of type 2

diabetes, research supporting lifestyle interventionsis not available. Increased physical activity, reducedenergy and fat intake, and resultant weight manage-ment may be beneficial.

Hypoglycemia of nondiabetic origin has been de-fined as a clinical syndrome with diverse causes inwhich low levels of plasma glucose eventually leadto neuroglycopenia (Service, 1995). Hypoglycemialiterally means low (hypo) blood glucose (glycemia).Normally, the body is remarkably adept at maintain-ing fairly steady blood glucose levels—usually be-tween 60 and 100 mg/dl (3.3 to 5.6 mmol/L), despitethe intermittent ingestion of food. Maintaining nor-mal levels of glucose is important because body cells,especially the brain and central nervous system, musthave a steady and consistent supply of glucose tofunction properly. Under physiologic conditions, thebrain depends almost exclusively on glucose for itsenergy needs. Even with hunger, either because it ismany hours since food was eaten or because the lastmeal was small, blood glucose levels remain fairlyconsistent.

PathophysiologyIn a small number of people, however, blood glucoselevels become too low. If the brain and nervous sys-tem are deprived of the glucose they need to func-tion, symptoms, such as sweating, shaking, weak-ness, hunger, headaches, and irritability, can develop.Hypoglycemia can be difficult to diagnose becausethese typical symptoms can be caused by many dif-ferent health problems besides hypoglycemia. For ex-ample, adrenaline (epinephrine), released as a resultof anxiety and stress, can trigger the symptoms of hy-poglycemia. The only way to determine whether hy-poglycemia is causing these symptoms is to measureblood glucose levels while an individual is experienc-ing the symptoms (Brun, Fedou, and Mercier, 2000).Hypoglycemia, therefore, can best be defined by thepresence of three features known as Whipple’s triad:(1) a low plasma or blood glucose level; (2) symp-toms of hypoglycemia at the same time as the lowblood glucose values; and (3) amelioration of thesymptoms by correction of the hypoglycemia (Prince,1997). A fairly steady blood glucose level is main-tained by the interaction of several mechanisms. Af-ter eating, food is broken down into glucose and en-ters the bloodstream. As blood glucose levels rise, thepancreas responds by releasing the hormone insulin,which allows glucose to leave the bloodstream andenter various body cells where it fuels the body’s ac-tivities. Glucose is also taken up by the liver and

HYPOGLYCEMIA OF NONDIABETICORIGIN

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stored as glycogen for later use. When glucose con-centrations from the last meal decline, the body goesfrom a “fed” to a “fasting” state. Insulin levels de-crease, which keeps the blood glucose levels fromfalling too low. In addition, stored glucose is releasedfrom the liver back into the bloodstream with thehelp of glucagon, a hormone that is also released fromthe pancreas. Normally, the body’s ability to balanceglucose, insulin, and glucagon (and other counter-regulatory hormones) keeps glucose levels within thenormal range. Glucagon provides the primary de-fense against hypoglycemia; without it full recoverydoes not occur. Epinephrine is not necessary forcounterregulation when glucagon is present. In theabsence of glucagon, however, epinephrine has animportant role (Cryer, 1993).

Symptoms of hypoglycemia have been recognizedat plasma glucose levels of about 60 mg/dl, and im-paired brain function has occurred at levels of about50 mg/dl (Mitrakou et al, 1991). Symptoms are classi-fied into two major groups: those that arise from theaction of the autonomic nervous system (adrenergicsymptoms) and those related to an insufficient sup-ply of glucose to the brain (neuroglycopenic symp-toms). Adrenergic symptoms include sweating, trem-bling, feelings of warmth, anxiety, and nausea.Symptoms of neuroglycopenia include dizziness,confusion, tiredness, difficulty speaking, headaches,and inability to concentrate. Hunger, blurred vision,drowsiness, and weakness are other symptoms somepeople experience. Symptoms differ for differentpeople but are consistent from episode to episode forany one person. Furthermore, there is not a consis-tent chronologic order to the evolution of symptoms;autonomic symptoms do not always precede neuro-glycopenic ones. In many persons, neuroglycopenicsymptoms are the only ones observed. Hypo-glycemia is the cause for any of these symptoms onlyif blood glucose levels are determined to be belownormal at the time the symptoms occur.

Types of HypoglycemiaIf blood glucose levels fall below normal limitswithin 2 to 5 hours after eating, this is often referredto as reactive hypoglycemia (named because thebody is reacting to food) or postprandial (reactive)hypoglycemia. Postprandial hypoglycemia can becaused by an exaggerated insulin response caused byeither insulin resistance or elevated glucagon-like-peptide-1 (GLP-1), alimentary hyperinsulinism, renalglycosuria, defects in glucagon response, high insulinsensitivity, or rare syndromes, such as hereditaryfructose intolerance, galactosemia, leucine sensitivity,or a rare �-cell pancreatic tumor (insulinoma) (Brun,Fedou, and Mercier, 2000).

Alimentary hyperinsulinism is the most commontype of documented postprandial hypoglycemia andis seen in patients who have undergone gastric sur-

gery or some other type of gastric surgery (Gebhardet al, 2001) (see Chapter 29). These procedures are as-sociated with rapid delivery of food to the small in-testine, rapid absorption of glucose, and exaggeratedinsulin response. These patients respond best to mul-tiple, frequent feedings (Prince, 1997). �-Glucosidaseinhibitors such as acarbose may also be helpful be-cause they decrease the absorption of carbohydrates(Hasler, 2002).

The ingestion of alcohol after a prolonged fast, orthe ingestion of large amounts of alcohol and carbo-hydrate on an empty stomach (“gin-and-tonic” syn-drome) may also cause hypoglycemia within 3 to 4hours in some healthy persons.

Idiopathic reactive hypoglycemia is characterized bynormal insulin secretion but increased insulin sensitiv-ity and, to some extent, reduced response of glucagonto acute hypoglycemia symptoms (Brun, Fedou, andMercier, 2000). The increase in insulin sensitivity asso-ciated with a deficiency of glucagon secretion leads tohypoglycemia late postprandially (Leonetti et al,1996). Idiopathic reactive hypoglycemia has been in-appropriately overdiagnosed by both physicians andpatients, to the point that some physicians doubt itsexistence. Although rare, it does exist but can be docu-mented only in persons with hypoglycemia that oc-curs spontaneously and who meet the criteria ofWhipple’s triad.

Fasting (food-deprived) hypoglycemia may occurin response to having gone without food for 8 hoursor longer; however, generally, fasting hypoglycemiais the result of a serious underlying medical condi-tion. Causes of fasting hypoglycemia include hormonedeficiency states (e.g., hypopituitarism, adrenal in-sufficiency, catecholamine or glucagon deficiency),acquired liver disease, renal disease, certain drugs(e.g., alcohol, propranolol, salicylate), insulinoma (ofwhich most are benign, but 6% to 10% can be malig-nant), and other nonpancreatic tumors. Factitioushypoglycemia, or self-administration of insulin orsulfonylurea in persons who do not have diabetes, isa common cause as well (Prince, 1997). Symptomsrelated to fasting hypoglycemia tend to be particu-larly severe and can include a loss of mental acuity,seizures, and unconsciousness. If the underlyingproblem can be resolved, hypoglycemia is no longera problem.

Diagnostic CriteriaOne of the criteria used to confirm the presence of hy-poglycemia is a blood glucose level of less than 50mg/dl (�2.8 mmol/L). Previously, the oral glucosetolerance test was the standard test for this condition;however, this test is not helpful because it involves anonphysiologic stimulus and because results showlittle correlation with persons who later are docu-mented to have hypoglycemia. Recording fingerstickblood glucose measurements during spontaneously

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occurring symptomatic episodes at home is a methodthat is often used to establish the diagnosis. An alter-native method is to perform a glucose test in a med-ical office setting, in which case the patient is given atypical meal that has been documented in the past tolead to symptomatic episodes; Whipple’s triad can beconfirmed if symptoms occur (Prince, 1997). If bloodglucose levels are low during the symptomatic pe-riod, and if the symptoms disappear upon eating, hy-poglycemia is probably responsible. It is essential tomake a correct diagnosis in patients with fasting hy-poglycemia because the implications for therapy areserious.

Management of HypoglycemiaThe management of hypoglycemic disorders involvestwo distinct components: (1) relief of neuroglycopenicsymptoms by the restoration of blood glucose concen-trations to the normal range and (2) correction of theunderlying cause. The immediate treatment is to eatfoods or beverages containing carbohydrate. As theglucose from the breakdown of carbohydrate is ab-sorbed into the bloodstream, it will increase the levelof glucose in the blood and relieve the symptoms. Ifan underlying problem is causing hypoglycemia, ap-propriate treatment of this disease or disorder isessential.

Almost no research has been done to determinewhat type of food-related treatment is best for theprevention of hypoglycemia. Traditional advice hasbeen to avoid foods containing sugars and to eatprotein- and fat-containing foods. Recent research onthe glycemic index and sugars has raised questionsabout the appropriateness of restricting only sugarsbecause these foods have been reported to have alower glycemic index than many of the starches thatwere encouraged in the past. Restriction of sugarsmay contribute to a decreased intake in total carbo-hydrate, which may be more important than thesource of the carbohydrate.

Using the following information, guidelines forthe prevention of hypoglycemia have been published(International Diabetes Center, 1998). It is helpful toreview metabolism of carbohydrates, protein, andfat; their effects on blood glucose levels and their re-lationship to insulin secretion. It should be remem-bered that this research has been conducted usingnormal subjects, not subjects who have been diag-nosed with hypoglycemia.

After digestion, the major macronutrients ab-sorbed are glucose, fructose, galactose, amino acids,and fatty acids that are reconstituted into triglyceridesin chylomicrons. Glucose, fructose, and galactoseare the major absorbed products of carbohydrate-containing foods, with about 75% being glucose, 22%being fructose and 3% as galactose. The effect of theseabsorbed sugars on plasma glucose levels and insulinresponse is different for each (Nuttall and Gannon,1991a). Fructose ingestion in normal subjects results

in little increase in glucose concentrations and littleor no change in insulin concentrations. Ingestion ofgalactose (initially lactose) results in only a modestincrease in peripheral glucose concentrations and amodest rise in insulin, which is attributable to therise in glucose. Fructose and galactose appear to beused primarily for glycogen synthesis in the liver(Gannon et al, 2001). Blood glucose levels generallyreturn to premeal levels after about 4 hours; withsmaller amounts of carbohydrate, this time span isshortened.

The amount of insulin secreted after glucose in-gestion depends more on the amount of glucose in-gested than on the magnitude of the glucose in-crease (Castro et al, 1970). Quantitatively, theincrease in insulin concentration greatly exceeds theincrease in glucose concentration. For example, themaximal glucose concentration typically does notexceed 50% of the premeal value, whereas the in-crease in insulin concentration is commonly 800% to900%.

Overall, the system is designed to maintain the cir-culating glucose concentration in the nonfed statewithin narrowly defined limits. It is also designed toallow only a modest rise in glucose after carbohydrate-containing meals and to return glucose concentrationsrapidly to the nonfed state. Most of the insulin se-creted during a 24-hour period is secreted duringtimes of the day when ingested food is not being as-similated, that is, as basal insulin secretion (Nuttalland Gannon, 1991a).

Ingested protein does not raise the plasma glucoseconcentrations in normal subjects, even when in-gested in large amounts, although 50% to 70% of theingested protein can be accounted for by deaminatedamino acids and urea synthesis in the liver. Presum-ably, most deaminated amino acids are converted toglucose (Nuttall and Gannon, 1991b).

Although fat does not independently stimulateinsulin secretion, it also does not affect the circulat-ing glucose concentration. However, when fat is in-gested with carbohydrate, the plasma glucose andinsulin responses are modified. This is an area thatrequires additional research. Preliminary evidencealso suggests that a high fat intake may contribute toinsulin resistance.

The goal of treatment is to adopt eating habits thatwill keep blood glucose levels as static as possible.Recommended guidelines are listed in Box 33-10. Pa-tients with hypoglycemia may also benefit fromlearning carbohydrate counting and limiting carbo-hydrate servings (15 g of carbohydrate per serving)to two to four at a meal and one to two for snacks (seeAppendix 53). Foods containing protein that are alsolow in fat can be eaten at meals or with snacks. Thesefoods would be expected to have minimal effect onblood glucose levels and can add extra food for sati-ety and calories. Because protein as well as carbohy-drate stimulates insulin release, however, a moderateintake may be advisable.

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In summary, nutrition is a challenging aspect of themanagement of diabetes and hypoglycemia of nondi-abetic origin. Attention to nutrition and meal-planning principles is essential for glycemic control

SUMMARY

and overall good health. A registered dietitian who isknowledgeable and skilled in implementing currentnutrition principles and making recommendationsfor diabetes or hypoglycemia of nondiabetic origin isthe medical team member who should plan, imple-ment, and evaluate MNT. Outcomes must be identi-fied, and the effectiveness of nutrition interventionscontinually documented.

Box 33-10. Guidelinesfor AvoidingHypoglycemicSymptoms

1. Eat small meals, with snacks interspersed be-tween meals and at bedtime. This means eat-ing five to six small meals rather than two tothree large meals to steady the release of glu-cose into the bloodstream.

2. Spread the intake of carbohydrate foodsthroughout the day. Eating large amounts ofcarbohydrate at one time produces increasedamounts of glucose and stimulates the releaseof increased amounts of insulin, which cancause blood glucose levels to drop. Most indi-viduals can eat two to four servings of carbo-hydrate foods at each meal and one to twoservings at each snack. Furthermore, if carbo-hydrate is removed from the diet, the bodyloses its ability to handle carbohydrate prop-erly. Carbohydrate foods include starches,fruits and fruit juices, milk and yogurt, andfoods containing sugar.

3. Avoid foods that contain large amounts ofcarbohydrate. Examples of these foods areregular soft drinks, syrups, candy, regularfruited yogurts, pies, and cakes.

4. Avoid beverages and foods containing caf-feine. Caffeine can cause the same symptomsas hypoglycemia and make the individualfeel worse (Kerr et al, 1993).

5. Limit or avoid alcoholic beverages. Drinkingalcohol on an empty stomach and withoutfood can lower blood glucose levels by inter-fering with the liver’s ability to release storedglucose (gluconeogenesis) (Franz, 1999). If anindividual chooses to drink alcohol, it shouldbe done in moderation (one or two drinks no more than twice a week), and food shouldalways be eaten along with the alcoholicbeverage.

6. Decrease fat intake. A high-fat diet, especiallysaturated fat, has been shown to affect thebody’s ability to use insulin (insulin resist-ance). Decreasing fat intake can also help withweight loss, if weight is a problem. Excessweight also interferes with the body’s abilityto use insulin.

Modified from International Diabetes Center: Reactive and fasting hypo-glycemia, Minneapolis, 1998, International Diabetes Center.

Ellen is a 15-year-old girl with newly diagnosed type 1 dia-betes. She is 5 ft 2 in. tall, weighs 115 lb, and is active incheerleading and basketball in high school. Her physician willbe regulating the dosage and timing of her insulin regimen.

Her grandmother has diabetes and is supportive of Ellen’sneed for education. Ellen’s parents are divorced, and she nowlives with her grandmother.What steps should you, as her nu-trition counselor, take?

1. What food and meal-planning information needs to beshared with the health care team as insulin therapy is in-tegrated into Ellen’s normal eating and exercise habits?

2. What guidance should you offer regarding Ellen’s sportsactivities?

3. Ellen is worried about keeping up with her peers. Howwill you help her adapt to the possible need for snacksduring exercise and during a busy school day or duringactivities with her friends?

4. When Ellen travels on field trips or vacations, what typesof food can she pack to take along?

5. What signs and symptoms of lack of diabetes controlmust Ellen understand to manage her disease? Whichproblem is she more likely to experience—hyper-glycemia or hypoglycemia?

Clinical Scenario 1: Type 1 Diabetes

Debra is a 45-year-old woman with a known diagnosis oftype 2 diabetes for 3 years. She has not had a medicalcheck-up for 2 years. She returns at this time with a primarycomplaint of chronic fatigue. Her laboratory test resultsshow the following: HbA1c 8.3%; serum cholesterol 214mg/dl; triglycerides 275 mg/dl. Her current weight is 175 lb.,and her height is 64 in. (BMI � 30). She states she hasn’treturned for any follow-up visits because the only adviceshe gets is to lose weight and not to eat sugar, neither ofwhich she is able to do.

1. What advice will you offer to improve Debra’s metabolicparameters and, in particular, to improve her blood glu-cose control?

2. What guidelines for carbohydrate intake can help Debraimprove her glycemia?

3. What suggestions will you have about fat intake?4. What information will you share about exercise?5. What meal-planning method do you suggest for her?6. What will you recommend regarding her sugar intake?


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� R e l e v a n t We b S i t e sAmerican Association of Diabetes Educatorswww.aadenet.orgAmerican Diabetes Associationwww.diabetes.orgAmerican Dietetic Association, Diabetes Care andEducation Practice Groupwww.dce.orgChildren With Diabeteswww.childrenwithdiabetes.comCoverage for Medical Nutrition Therapywww.eatright.org/gov/reimbursement.htmlHealthy Weight Networkwww.healthyweight.netInternational Diabetes Center, Minneapolis,Minnesotawww.idcdiabetes.orgLifestyle Manuals Used in the Diabetes PreventionProgramwww.bsc.gwu.edu/dppNational Institute of Diabetes and DigestiveKidney Diseaseswww.niddk.nih.gov

� C i t e d R e f e r e n c e sAiello LP et al: Diabetic retinopathy [Technical Review], Diabetes

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stand: exercise and type 2 diabetes, Med Sci Sports Exerc 32:1345,2000.

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American Diabetes Association: Diabetes 2001 vital statistics,Alexandria, Va, 2001, American Diabetes Association.

American Diabetes Association: Standards of medical care for pa-tients with diabetes mellitus [Position Statement], Diabetes Care25(suppl 1):S33, 2002a.

American Diabetes Association: Evidence-based nutrition princi-ples and recommendations for the treatment and prevention ofdiabetes and related complications [Position Statement], Dia-betes Care 25:202, 2002b.

American Diabetes Association: Diabetes mellitus and exercise[Position Statement], Diabetes Care 25(suppl 1):S64, 2002c.

American Diabetes Association: Tests of glycemia in diabetes [Po-sition Statement], Diabetes Care 25(suppl 1):S97, 2002d.

American Diabetes Association: Gestational diabetes mellitus [Po-sition Statement], Diabetes Care 25(suppl 1):S94, 2002e.

American Diabetes Association: Translation of the diabetes nutri-tion recommendations for health care institutions, Diabetes Care25(suppl 1):S61, 2002f.

American Diabetes Association: Management of dyslipidemia inadults [Position Statement], Diabetes Care 25(suppl 1):S74, 2002g.

American Diabetes Association: Diabetic nephropathy [PositionStatement], Diabetes Care 25(suppl 1):S90, 2002h.

American Diabetes Association: Diabetic retinopathy [PositionStatement], Diabetes Care 25(suppl 1):S90, 2002i.

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American Dietetic Association: Medical nutrition therapy evidence-based guides for practice: nutrition practice guidelines for type 1 andtype 2 diabetes, CD-Rom, Chicago, 2001, American Dietetic As-sociation.

American Diabetes Association and American Dietetic Associa-tion: Exchange lists for meal planning, Alexandria, Va, 2003,American Diabetes Association.

American Diabetes Association: Economic costs of diabetes in theU.S. in 2002, Diabetes Care 26:917, 2003a.

American Diabetes Association: Management of dyslipidemia inchildren and adolescents with diabetes [Consensus Statement],Diabetes Care, 26:2194, 2003b.

Anderson RA et al: Beneficial effects of chromium for people withdiabetes, Diabetes 46:1786, 1997.

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Bantle JP et al: Metabolic effects of dietary sucrose in type II dia-betic subjects, Diabetes Care 16:1301, 1993.

Bantle JP et al: Effects of dietary fructose on plasma lipids inhealthy subjects, Am J Clin Nutr 72:1128, 2000.

Bergman RN, Adler M: Free fatty acids and pathogenesis of type 2diabetes mellitus, Trends Endocr Metab 11:351, 2000.

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Brodsky IG, Devlin JT: Effects of dietary protein restriction on re-gional amino acid metabolism in insulin-dependent diabetesmellitus, Am J Physiol 270:E148, 1996.

Brown L et al: Cholesterol-lowering effects of dietary fiber: a meta-analysis, Am J Clin Nutr 69:30, 1999.

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Carmichael HE et al: Lower fat intake as a predictor of initial andsustained weight loss in obese subjects consuming an other-wise ad libitum diet, J Am Diet Assoc 98:35, 1998.

Castro A et al: Plasma insulin and glucose responses of healthysubjects to varying glucose loads during three-hour oral glu-cose tolerance tests, Diabetes 19:842, 1970.

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John is a moderately obese (BMI � 29) 49-year-old manwho complains of increased thirst, polyuria, and fatigue. Hisfamily history includes his mother and an older brother withtype 2 diabetes. A random (casual) plasma glucose testshows a level of 480 mg/dl. His serum electrolyte level andanion gap are normal.

He reports finding it difficult to control his eating duringthe evening and because of his long working hours finds itdifficult to work in an hour for exercise most days. Whenasked what he is interested in learning about, he repliesthat he would like to learn how to control his eating becausehe is always hungry.

1. What type of diabetes does John likely have? Is it likelyto be controlled by nutrition therapy alone?

2. Given the symptoms of hyperglycemia, is it more likely thatan oral agent or insulin therapy will be recommended?

3. If John is started on medication, are lifestyle strategiesstill important?

4. What advice can you give to John to help him with hiseating problems?

5. What other lifestyle strategies will be helpful?


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