Nutritional Care of Diabetes - ContinuingEducation.com Online.pdf · Nutritional Care of Diabetes 1...

Nutritional Care of Diabetes Updated for 2014

By Joyce Green Pastors, RD, MS, CDE

Nutritional Care of Diabetes

By Joyce Green Pastors, RD, MS, CDE About the Author Joyce Green Pastors, RD, MS, CDE, is a diabetes nutrition specialist at the University of Virginia Diabetes Center. She has worked in the field for more than 35 years, has held numerous executive positions in the Diabetes Care and Education practice group of the Academy of Nutrition and Dietetics, and is active in the American Diabetes Association and the American Association of Diabetes Educators. EXPIRATION DATE: Students of all professions must submit this course for credit no later than February 28, 2019. Credit will not be awarded for this course after that date.

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Contents Introduction ....................................................................................................................................... 1 Chapter One: Classification, Diagnosis and Pathogenesis ............................................................... 3 Chapter Two: Treatment Options .................................................................................................... 11 Chapter Three: Nutrition Recommendations ................................................................................... 33 Chapter Four: Key Differences in Nutritional Management of Diabetes ......................................... 43 Chapter Five: Specific Nutrient Guidelines ....................................................................................... 49 Chapter Six: Process of Diabetes Medical Nutrition Therapy .......................................................... 65 Chapter Seven: Nutrition Intervention: Basic and In-Depth ............................................................. 73 Chapter Eight: Special Topics for Meal Planning ............................................................................. 89 Chapter Nine: Special Management Concerns ................................................................................ 99 Chapter Ten: Complications of Diabetes ......................................................................................... 107 Case Study ........................................................................................................................................ 117 Appendices ....................................................................................................................................... 129

Appendix 1: Diabetes Self-care Daily Record Appendix 2: Composition of Alcoholic Beverages Appendix 3: Fat and Fatty Acid Composition Appendix 4: Following the DASH Eating Plan Appendix 5: Resources for In-Depth Meal Planning Approaches Appendix 6: Mealtime or Bolus Insulin Supplement: Advanced Carbohydrate Counting Appendix 7: Mealtime or Bolus Insulin Supplement: Advanced Carbohydrate Counting: Answers

Test ................................................................................................................................................. 139

Goal and Objectives The goal of this course is to teach nutritionists, dietitians and other healthcare practitioners the nutritional management of diabetes to improve quality of life and decrease complications in patients with diabetes. After studying the information presented here, the learner will be able to: • Explain the classifications, diagnostic criteria and pathophysiology of diabetes

• List treatment options currently used for patients with diabetes, and explain the components, goals of therapy, recommendations and risks and benefits of each

• Explain the differences among the various types of insulin and show how they can be used with meal planning to achieve target blood glucose levels

• Define oral diabetes agents and give indications for their use

• Explain the nutrient recommendations for the various classifications of diabetes, listing carbohydrate, fiber, protein and fat amounts

• Explain the differences between meal planning, energy and nutrient requirements for type 1 and type 2 diabetes

• Define the glycemic response, and explain how this concept is applied to nutritional control of diabetes

• List three sugar substitutes presently used, and discuss their positive and negative features

• Describe the steps of the education process

• List several meal-planning approaches; explain the main characteristics, benefits and drawbacks of each; and cite the type of patient who would benefit from each

• Discuss the problems and guidelines for use of alcohol, eating out, snacking, hypoglycemic episodes and sick-day management

• Discuss the high-protein diet controversy

• Discuss the major problems associated with pre-existing diabetes in pregnancy

• Explain the difference between gestational and prepregnancy diabetes, and give nutritional recommendations for both

• Describe the characteristics, diagnosis and dangers of diabetic ketoacidosis, hyperosmolar hyperglycemic state (also known as hyperglycemic hyperosmolar nonketotic coma) and hypoglycemia, and explain the treatment options for each


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Introduction

f you have diabetes, you are not alone. Nearly 26 million Americans have diabetes — 18.8 million are diagnosed and 7 million are undiagnosed; another 79 million Americans have prediabetes and are at risk for developing type 2 diabetes. In those age 20 years and older, 11.3% (25.6 million)

have diabetes, and in those age 60 years and older, 26.9% (10.9 million) have diabetes. Since 1990, the prevalence has increased steadily. A 2012 Centers for Disease Control and Prevention study projected that as many as one in three U.S. adults could have diabetes by 2050 if current trends continue.1

Type 2 diabetes is the most prevalent type of diabetes, accounting for 90% to 95% of U.S. cases. The rise in the incidence of type 2 diabetes is associated with increases in obesity, decreases in leisure-time physical activity and an aging U.S. population. Type 1 diabetes accounts for 5% of all diagnosed cases of diabetes; about one in 400 to 600 children and adolescents has type 2 diabetes.

The significant increase in obesity and diabetes in recent years is of major importance. The most recent national data show that 35% of U.S. adults and almost 17% of youth were obese in 2011-2012.2 Differences in prevalence between men and women diminished between 1999 and 2000, and 2009 and 2010, with the prevalence of obesity among men reaching the same level as that among women.

By state, obesity prevalence ranged from 20.5% in Colorado to 34.7% in Louisiana in 2012. No state had a prevalence of obesity less than 20%. Nine states and the District of Columbia had prevalence between 20% and 25%. Thirteen states (Alabama, Arkansas, Indiana, Iowa, Kentucky, Louisiana, Michigan, Mississippi, Ohio, Oklahoma, South Carolina, Tennessee, and West Virginia) had a prevalence equal to or greater than 30%.

Diabetes strikes all ethnic groups and social classes, but American Indians/Alaska Natives (14.2% of the population), non-Hispanic blacks (12.6%) and Hispanics (11.8%), compared to non-Hispanic whites (7.1%), are affected disproportionately.

The fact that 7 million people have undiagnosed diabetes signifies a more serious problem. Until a serious complication arises, such as heart disease, stroke, high blood pressure, blindness, kidney disease, eye disease and nerve complications, these people are unaware they have diabetes.

Heart disease is the leading cause of death for people with diabetes, being noted on 68% of diabetes-related death certificates in 2004. People with diabetes are up to four times more likely to have heart disease. Stroke is two to four times more common in people with diabetes. Between 2005 and 2008, 67% of adults had blood pressure of 140/90 mmHg or higher. About 60% to 70% of people with diabetes have mild-to-severe nervous system damage. Severe forms of diabetic nerve disease are a major contributing cause of lower-extremity amputations. Diabetes is the leading cause of:

• New cases of blindness in adults age 20 to 74 years • Diabetic retinopathy in 4.2 million (28.5%) people with diabetes age 40 years or older • Kidney failure, accounting for 44% of all new cases in 2008

In 2013, the American Diabetes Association estimated that the total national cost of diagnosed

diabetes in the U.S. was $245 billion (including $176 billion in direct costs [hospital and ambulatory care] and $69 billion in indirect costs [disability, work loss and premature mortality]).

There is some good news. Although the cure for diabetes is not within reach, diagnosis is reliable

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and relatively simple, and care and treatment have been refined; those with diabetes can lead normal lives with modifications in eating and activity, and access the plethora of diabetes medications now available.

Technological advances and insurance reimbursement have made blood glucose monitoring nearly foolproof, as well as more available and affordable. New oral and injectable glucose-lowering medications have made optimal glucose control more achievable, and a multitude of meal-planning options allow for more individualization, flexibility and control.

However, science and technology are only as good as the practitioner. Diabetes education and treatment is by far the best means of controlling diabetes and minimizing its impact. Diabetes educators, physicians, nurses, dietitians and pharmacists must tailor their practice constantly to account for individual needs and scientific advances.

The purpose of this course is to give nutritionists, dietitians, and other healthcare practitioners a practical guide to the nutritional management of diabetes, which is the greatest challenge, but has the potential for greatly improving quality of life and decreasing complications.

References 1. Diabetes Report Card 2012: National and State Profile of Diabetes and its complications. Centers for

Disease Control and Prevention Web site. http://www.cdc.gov/diabetes/pubs/reportcard.htm. Accessed February 9, 2015.

2. Overweight and obesity. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/obesity/data/index.html. September 9, 2014. Accessed February 9, 2015.


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Chapter One: Classification, Diagnosis

and Pathogenesis

istorically, the term diabetes mellitus was used to describe a disorder characterized by the passage of sweet-smelling urine; excessive urination, thirst and hunger; and weight loss. A more correct definition, however, would be to describe diabetes mellitus as a chronic disorder rather

than a disease. It is characterized by hyperglycemia — a high level of sugar in the blood resulting from defects in insulin secretion, insulin action or both. Diabetes is progressive and associated with long-term damage and failure of organs, especially the eyes, kidneys, nerves, heart and blood vessels. Diabetes results from the body’s inability to use and store food properly. During normal digestion, foods are broken down into nutrients that the body uses for energy. These nutrients are:

• Protein, which is broken down into amino acids • Carbohydrate, which is broken down into glucose • Fat, which is broken down into fatty acids

Insulin, a hormone produced by the pancreas, regulates the body’s use of these nutrients. It is released into the bloodstream when glucose increases and binds itself to cells at sites called receptors. Once bound to receptors, insulin allows glucose from food to move from the bloodstream into the cells where it is broken down for energy.

The cells use glucose as their main energy source. Those with diabetes either make little or no insulin or are unable to use insulin properly. As a result, glucose stays in the blood instead of entering cells, and the cells starve. High levels of glucose in the blood are characteristic of uncontrolled diabetes.

Classification

Diabetes is classified into several clinical categories, including type 1 diabetes, type 2 diabetes and

gestational diabetes mellitus. Older terms used to classify type 1 diabetes were “insulin-dependent diabetes mellitus” or “juvenile-onset diabetes.” For type 2 diabetes, these older terms were “non-insulin-dependent diabetes mellitus” or “adult-onset diabetes.”1

Another important category is prediabetes. This population has glucose levels that are higher than normal but do not meet the criteria for diabetes, including impaired fasting glucose levels or impaired glucose tolerance. Prediabetes is the preferred term for IFG and IGT because it indicates the high risk of future development of diabetes.

Type 1 Diabetes Mellitus

Type 1, immune-mediated diabetes is the complete or near-complete inability of the body to make insulin, usually referred to as insulin deficiency. It results from an autoimmune destruction of the beta cells of the pancreas.1 To survive, those with type 1 diabetes depend on multiple, daily injections of insulin. They may have wide daily swings in blood sugar levels and be prone to two very different disorders: ketoacidosis and hypoglycemia.

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Classification, Diagnosis and Pathogenesis

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Ketoacidosis is marked by high levels of glucose and ketoacids (fat breakdown products, also called ketones) in the blood, caused by a lack of insulin. Hypoglycemia is low blood sugar.

Type 1 diabetes is usually characterized by an abrupt onset of symptoms commonly referred to as the “3 Ps”:

• Polyphagia: increased hunger • Polydipsia: increased thirst • Polyuria: increased urination

Those with newly diagnosed type 1 diabetes are usually lean, and often have experienced recent weight loss. Typically, type 1 diabetes develops in those younger than age 40. Half of all people diagnosed with type 1 diabetes are younger than age 20. Type 1 diabetes is more common among whites than members of other racial groups, and accounts for 5% to 10% of all known cases of diabetes mellitus.

Type 2 Diabetes Mellitus

Type 2 diabetes includes insulin resistance and a relative, rather than absolute, insulin deficiency.1 It is a condition in which the body still makes insulin, but cannot produce an adequate supply or cannot use the insulin properly (insulin resistance). Insulin levels may be normal, depressed or elevated.

This type of diabetes often goes undiagnosed for many years because high blood glucose levels develop gradually; initially, it does not present with any of the classic symptoms (“3 Ps”) of diabetes. Insulin secretory loss starts on average about 10 years before the diagnosis of type 2 diabetes and insulin deficiency likely occurs about 10 to 12 years after diagnosis.2 Most people with type 2 diabetes are obese, and excessive intake of calories leading to weight gain and obesity can cause insulin resistance. These obese people may be able to control blood glucose levels with a meal and exercise plan for weight control; if this is not successful, an oral glucose-lowering agent or insulin may be prescribed.

Type 2 diabetes can occur at any age, but is usually diagnosed after age 30. It accounts for approximately 90% to 95% of diabetes cases in the U.S. Prevalence of type 2 diabetes is increased markedly among Native-American, African-American and Hispanic-American populations. Prevalence also increases with age, degree of obesity and lack of physical activity. It occurs more frequently in women who were diagnosed with gestational diabetes and in those with hypertension or dyslipidemia. It is often associated with a genetic predisposition, even more than in type 1 diabetes. With the onset of childhood obesity, type 2 diabetes is diagnosed increasingly in children and adolescents.1 Data from the SEARCH for Diabetes in Youth study indicate that the prevalence of type 2 diabetes increased by 21% in American young people between 2001 and 2009. The onset of type 2 diabetes in children usually occurs in mid-puberty and beta cell (cells in the pancreas that produce, store and secrete insulin) failure occurs faster than in adults, with a mean transition time from prediabetes to diabetes of 2.5 years compared with 10 years in adults.3

Gestational Diabetes Mellitus

GDM is used to describe glucose intolerance that has its onset or is first detected during pregnancy. Women with known diabetes mellitus before conception are not part of this category.

Approximately 7% of all pregnant women in the U.S. are diagnosed with GDM, with 200,000 new cases diagnosed each year. Prevalence varies from 1% to 14% of all pregnancies, depending on the ethnic population and method of diagnostic testing.4 The risk of developing GDM is influenced by several factors, including excess body weight, inactivity, older age, history of GDM, previously large-for-gestational-age infant, family history of diabetes and high-risk ethnicity.5


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Risk estimates for developing diabetes — usually type 2 diabetes, after GDM — vary widely from 2% to 70%, depending on the population studied, criteria used for diagnosis and length of follow-up. Studies that focus on the immediate postpartum period (i.e., six-week postpartum follow-up glucose screening) have estimated the risk of glucose intolerance to be as high as 36%, and diabetes to be 2% to 16%. Cumulative incidence of type 2 diabetes increases markedly in the first five years after delivery, and appears to plateau after five years.6

Prediabetes

Prediabetes is a term used to distinguish people who are at increased risk of developing diabetes. They may have IFG, IGT or both:

• IFG is fasting plasma glucose levels higher than normal (100 mL/dL to 125 mL/dL), but lower than the diagnostic threshold for diabetes mellitus.

• IGT is blood elevated glucose level (140 mg/dL to 199 mg/dL) after a two-hour oral glucose tolerance test, but not high enough to be classified as diabetes.

The National Health and Nutrition Examination Survey cross-sectional health and nutrition survey from 2005-2006 reported a combined prevalence of 34.6% of U.S. adults with IFG and IGT. Prediabetic subjects in this cohort tended to be older, male, Mexican American, hypertensive and hyperlipidemic, with a substantially greater overall 10-year cardiovascular risk.7

Those who have IFG and IGT, and an A1C of 5.7% to 6.4%, should be informed of their increased risk for diabetes and counseled about effective lifestyle strategies to lower their risk.

Diagnosis Type 1 and Type 2 Diabetes

A diagnosis of diabetes can be made in the following ways:1 • A1C >6.5%. The test should be performed in a laboratory using a method that is certified

and standardized. • Fasting plasma glucose >126 mg/dL. Fasting is defined as no caloric intake for at least

eight hours. • Two-hour postprandial glucose >200 mg/dL during an OGTT. This test should be

performed using a 75-g glucose load. • Symptoms of diabetes plus random plasma glucose levels of >200 mg/dL. The classic

symptoms of diabetes include polyuria, polydipsia and unexplained weight loss. To confirm the diagnosis of diabetes using plasma glucose levels, each of the first three testing

methods should be repeated on different days. The A1C test has advantages when compared to the FPG test because of convenience (fasting not required), analytical stability and less day-to-day variation. However, these advantages must be balanced by the greater cost, limited availability of A1C in certain regions of the developing world and incomplete correlation between A1C and average glucose based on race/ethnicity.1,4

GDM

The onset of GDM is usually without symptoms, so maternal screening during pregnancy is necessary for diagnosis and treatment. In 2011, the American Diabetes Association for the first time recommended that all pregnant women not known to have prior diabetes undergo a 75-g OGTT (one-step approach) at 24 to 28 weeks’ gestation based on an International Association of Diabetes and


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Pregnancy Study Groups consensus meeting.8 Since this recommendation, the National Institutes of Health completed a consensus development conference and recommended continuation of the “two-step” approach for GDM screening.9 In January 2014, the U.S. Preventive Services Task Force recommended universal screening for all pregnant women at 24 weeks’ gestation.10

At the current time, two approaches can be used for screening and diagnosis of GDM: • “One-step” approach recommended by the IADPSG. Involves a 75-g OGTT. Blood glucose

levels are measured at fasting, and at one- and two-hours postprandial. The OGTT should be performed in the morning after an overnight fast.

• “Two-step” approach recommended by NIH. Involves an initial 50-g oral glucose challenge test (blood glucose result at one hour should be <140 mg/dL). If the test is positive, a three-hour OGTT with 100-g oral glucose is completed on a separate day. The diagnosis of GDM is made when the plasma glucose level measured three hours after the test is >140 mg/dL.1,4

GDM should be diagnosed between the 24th and 28th week of gestation. Women at high-risk should be screened preferably at the initial prenatal visit. If a high-risk woman is diagnosed with diabetes during the first trimester, a diagnosis of overt diabetes, not GDM, should be used. Women with a history of GDM who develop prediabetes should receive lifestyle intervention and/or metformin (Glucophage) to prevent diabetes.1

Pathogenesis

To understand diabetes mellitus, it is important to understand the pancreas, which is a complex

comma-shaped organ about 6 in. (15 cm) long, located just below and behind the stomach. The pancreas performs two major functions in humans. It produces many of the enzymes needed

for digestion and it also produces hormones to regulate the use of body fuels (nutrients), mainly glucose. Insulin, the primary hormone of the pancreas, is produced in the pancreas by clusters of cells called the Islets of Langerhans. These islets, which are scattered throughout the pancreas, contain several different types of cells (beta cells produce insulin).11

Normal Nutrient Metabolism

To explain the hormonal role of the pancreas, it is first necessary to explain the normal metabolism of carbohydrate, protein and fat. For normal metabolism of these fuels to occur, the body must maintain:11

• Plasma glucose within narrow limits • An adequate supply of emergency fuel in the form of glycogen • An adequate supply of protein for enzymes and structural body tissues • Protein stores during periods of fasting by drawing on fat reserves

Insulin and glucagon are hormones involved in metabolism of these nutrients. They work together with other hormones, including catecholamines, steroids and growth hormone, to coordinate storage and mobilization of nutrients.

Normally, a high level of circulating insulin marks the fed state, and a high level of circulating glucagon marks the fasted state. The ingestion of food immediately stimulates insulin secretion by beta cells, which causes increased glucose use and decreased glucose production, and promotes fat deposition and incorporation of amino acids into muscle tissue (body is in an anabolic, or building, state).


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Action of Insulin Insulin Promotes Insulin Inhibits

Entry of glucose into the cells Storage of glycogen Storage of fat Storage of protein

Synthesis of glucose Breakdown of glycogen Breakdown of fat Breakdown of protein

In the fasted state, the overall metabolic process is reversed, resulting in increased endogenous

(internal) glucose production. This process is often referred to as glycogenolysis (conversion of glycogen into glucose in body tissues) and gluconeogenesis (the formation of glucose from noncarbohydrate sources such as proteins and fats). Glucagon and insulin are biological antagonists. In the nondiabetic state, the metabolic effects of insulin balance those of glucagon so fluctuations in the plasma glucose level (i.e., fed vs. fasted state) are prevented.11

Nutrient Metabolism in Diabetes

In many ways, diabetes can be compared to the fasting state. Both conditions are characterized by a decrease in insulin activity, elevated plasma concentration of glucagon, increased glycogenolysis, gluconeogenesis and lipolysis (breakdown of fat). When an effective amount of insulin is not available, there is a loss of the mechanisms whereby insulin and glucagon maintain constant equality between the amount of glucose leaving and entering the circulation. The degree to which the insulin effect is lost determines the seriousness of the diabetes.

Pathogenesis of Type 1 Diabetes

Type 1 diabetes is, in part, an inherited disorder. Geneticists discovered that certain genetic markers are often found in children who develop type 1 diabetes. Multiple genes are reported to influence the risk of type 1 diabetes, but histocompatibility locus antigen alleles have the largest effect.

HLA are glycoproteins present on all human cell membranes, including the pancreatic beta cells. Normally, antigens identify a person’s own cells as “self” and the immune system understands not to destroy them. If immune cells destroy self cells, autoimmune diseases result (body attacks itself). The understanding of type 1 diabetes as an autoimmune disease is a breakthrough. There is an increased risk with type 1 diabetes to develop other autoimmune diseases, most commonly thyroiditis and celiac disease.

Research has shown that certain gene combinations seem to make some people especially prone to diabetes. But genes do not cause diabetes on their own. Other environmental factors have to occur to make diabetes emerge. The best evidence for environmental influences include the hygiene hypothesis; pregnancy and perinatal factors, including preeclampsia, neonatal respiratory disease and jaundice; the role of viruses, such as Coxsackie virus and enteroviral infections; and the role of diet, including cow’s milk (particularly the role of a milk protein, beta-casein).12-15

Although viruses seem to be involved in some cases of type 1 diabetes, and although some families have more than one person with diabetes, diabetes is not contagious, and cannot be transmitted from person to person. The best explanation of why diabetes “runs” in some families is that the family members share genes that make them prone to diabetes.


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Pathogenesis of Type 2 Diabetes Type 2 diabetes is caused by a combination of varying degrees of insulin resistance and relative

insulin deficiency. Its development most likely represents a complex interaction among environmental factors and genetics, which vary among populations and individuals.

Environment plays a major role in the pathogenesis of type 2 diabetes. The combination of a sedentary lifestyle with an increased caloric intake, leading to weight gain and the development of obesity, is the primary factor in the development of insulin resistance and, ultimately, type 2 diabetes. Inflammatory responses of tissue to excess nutrients may contribute to the insulin resistance found in type 2 diabetes.

Genetic factors are more prominent in the development of type 2 diabetes than in type 1 diabetes. A number of genes that contribute to the risk have been identified. The genetic risk is produced by an interaction of multiples genes. The genes that predispose someone to type 2 diabetes have been selected likely through evolution. Possessing genes that allow for efficient accumulation and storage of nutrients offers advantages during chronic food shortage. These so-called “thrifty genes” aren’t adaptive to our current food-rich society. Observations that demonstrate a genetic influence include:

• Prevalence of type 2 diabetes varies remarkably between ethnic groups living in the same environment. Type 2 diabetes is two to six times more prevalent in African Americans, Native Americans, Pima Indians and Hispanic Americans in the U.S. than in the white population.

• Thirty-nine percent of patients with type 2 diabetes have at least one parent with the disease.

• Among monozygotic twin pairs with one affected twin, approximately 90% of unaffected twins eventually develop the disease.

• The lifetime risk for a first-degree relative of a person with type 2 diabetes is five to 10 times higher than that of age- and weight-matched subjects without a family history of diabetes.16

Being overweight does not cause diabetes, but there is a strong association between excess energy expenditure and insulin resistance. With a continued oversupply of nutrients, the progressive increase in insulin resistance cannot be compensated adequately for from increased insulin secretion, resulting in impaired glucose tolerance and eventually, type 2 diabetes.16 It has been suggested that weight loss decreases insulin resistance. Exercise has been shown to make available insulin more effective. Thus, weight loss and exercise both play an important role in the treatment of type 2 diabetes.

Indeed, not every obese person develops diabetes. The capacity to secrete adequate amounts of insulin appears to be diminished in the obese with the genetic propensity to develop diabetes. Only after beta cells begin to exhaust themselves does diabetes develop in obese people.


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Review Questions 1. What is the primary difference between type 1 and type 2 diabetes? 2. Why do some people with a genetic predisposition or family history of diabetes get

diabetes while others don’t?

Answer 1: Those with type 1 diabetes lack the ability to make insulin, resulting in insulin deficiency, while those with type 2 diabetes initially have high circulating levels of insulin but lack the ability to use it effectively. This is called insulin resistance.

Answer 2: People who are susceptible to type 1 diabetes because of a genetic predisposition develop the disease after it is triggered by an environmental stress factor. People who are susceptible to type 2 diabetes because of a genetic predisposition develop the disease in combination with environmental factors (primarily obesity, inactivity and stress).

References 1. American Diabetes Association. Position Statement. Diagnosis and classification of diabetes mellitus.

Diabetes Care. 2014;37(Suppl 1):81-90.

2. Turner RC, Cull CA, Frighi V, Holman RR. Glycemic control with diet, sulfonylurea, metformin, or insulin in patients with type 2 diabetes mellitus: progressive requirement for multiple therapies. UK Prospective Diabetes Study (UKPDS) Group. JAMA. 1999;281(21):2005-2012.

3. Dabelea D, Bell RA, D’Agostino RB Jr., et al. Incidence of diabetes in youth in the Unites States. JAMA. 2007;297(24):2716-2724.

4. American Diabetes Association. Standards of medical care in diabetes — 2014. Diabetes Care. 2014;37(Suppl 1):S14-S80.

5. American Diabetes Association. Gestational diabetes mellitus. Diabetes Care. 2004;27(Suppl 1):S88-S90.

6. Kim C, Newton KM, Knopp RH. Gestational diabetes and the incidence of type 2 diabetes: a systematic review. Diabetes Care. 2002;25(10):1862-1868.

7. Metzger BE, Gabbe SG, Persson B, et al. International association of diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care. 2010;33(3):676-682.

8. Karve A, Hayward RA. Prevalence, diagnosis, and treatment of impaired fasting glucose and impaired glucose tolerance in nondiabetic U.S. adults. Diabetes Care. 2010;33(11):2355-2359.

9. Vandorsten JP, Dodson WC, Espeland MA, et al. NIH consensus development conference: diagnosing gestational diabetes mellitus. NIH Consens State Sci Statements. 2013;29(1):1-31.

10. Gestational diabetes mellitus, screening. U.S. Preventive Services Task Force Web site. http://www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/gestational-diabetes-mellitus-screening?ds=1&s=diabetes. Accessed February 9, 2015.

11. Stachura ME. Pathophysiology. In: Powers MA, ed. Handbook of Diabetes Medical Nutrition Therapy. Gaithersburg, MD: Aspen Publishers; 1996.

12. Bach JF. The effect of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med. 2002;347(12):911-920.

13. Dahlquist GG, Patterson C, Soltesz G. Perinatal risk factors for childhood type 1 diabetes in Europe. The EURODIAB Substudy 2 Study Group. Diabetes Care. 1999;22(10):1698-1702.

14. Dotta F, Censini S, van Halteren AG, et al. Coxsackie B4 virus infection of beta cells and natural killer cell insulitis in recent-onset type 1 diabetic patients. Proc Natl Acad Sci USA. 2007;104(12):5115-5120.


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15. Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE. Type 1 (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption. Diabetologia. 1999;42(3):292-296.

16. Burant CF. Medical Management of Type 2 Diabetes. 7th ed. Alexandria, VA: American Diabetes Association; 2012.


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Chapter Two: Treatment Options

he purpose of diabetes management is to help prevent the long-term problems due to uncontrolled diabetes and to promote self-management of diabetes. The treatment goals for optimal diabetes medical nutrition therapy are:1 • Promote and support healthy eating patterns through nutrient-dense foods in appropriate

portions to attain individualized metabolic outcomes (blood glucose, lipids, hypertension, achievement and maintenance of weight goals, and delay or prevention of diabetes complications)

• Address individual nutrition needs based on personal and cultural preferences, health literacy, access to healthy foods, willingness/ability to make behavior changes and barriers to change

• Maintain the pleasure of eating by providing positive messages and limiting food choices only when indicated by scientific evidence

• Provide practical day-to-day meal planning rather than focusing on nutrients or single foods

The major treatment tools used to manage diabetes include nutrition therapy to promote healthy eating, physical activity, medication (if necessary), self-monitoring of blood glucose, education and problem-solving skills. Treatment effectiveness is measured by blood glucose, lipid and blood pressure responses to therapy:2

• Hemoglobin A1C measures the average blood glucose level during the four to eight weeks before the test. When blood glucose levels are high, some of the glucose attaches to hemoglobin molecules in red blood cells. The glucose stays attached for the remaining life of the red blood cell (approximately 120 days). This test is an indicator of the overall glucose control during the past one to two months. It is more helpful than a single glucose level in terms of making adjustments with insulin and other treatment changes, such as meal planning and exercise.

• Postprandial glucose goals should be based on duration of diabetes, age, comorbid conditions and hypoglycemia unawareness; it can be targeted as a primary glycemic control indicator if A1C goals are not met, especially if preprandial glucose is at goal.

• In patients with overt cardiovascular disease, a low-density lipoprotein cholesterol goal of <70 mg/dL using a high dose of a statin is an option.

• Based on patient characteristics and response to lifestyle change/medication therapy, lower systolic blood pressure targets may be appropriate.

• More or less stringent glycemic goals may be appropriate for certain patients.

T

Treatment Options

12

Glucose, Lipid and Blood Pressure Measurements2

Test Recommendation

Glucose

Hemoglobin A1C Fasting/pre-meal plasma glucose Peak post-meal glucose

<7% 70 mg/dL to 130 mg/dL <180 (mg/dL)

Lipids

LDL <100 mg/dL

Blood Pressure

Systolic Diastolic

<140 <80

Evaluating other parameters such as associated diabetes complications, psychosocial issues (i.e.,

lifestyle, attitudes about healthcare and satisfaction with life) and personal characteristics (i.e., body weight, age and previous treatment history) allows the treatment regimen to be individualized further to enhance effectiveness.

Nutrition Therapy Because diabetes is related directly to how well the body uses food, nutrition therapy is an

important component in the management of type 1 and type 2 diabetes. Understanding basic nutrition and specific meal-planning guidelines for diabetes — and making better and healthier food choices — enables the person with diabetes to:

• Better control the amount of glucose in the blood • Improve the body’s ability to use insulin, as meal timing and the amount of food eaten at

each meal affects the way the body uses insulin • Control weight by monitoring caloric intake • Feel better and improve overall health through more nutritious meals and eating habits

Physical Activity

Physical activity is also an important tool in managing diabetes by:3 • Maintaining or improving cardiovascular fitness to prevent or minimize long-term

cardiovascular complications of diabetes • Improving flexibility, which decreases with aging because of changes in the elasticity of soft

tissue • Improving muscle strength, which may deteriorate as a result of neuropathy • Allowing those with type 1 diabetes to participate in and enjoy physical and/or sport

activities safely • Assisting in weight control and management in patients with type 2 diabetes


13

Realistic and achievable goals are crucial to success in increasing physical activity, and are best implemented by referring the person with diabetes to support resources such as physical therapy, personal training or an aerobic fitness program. Even less strenuous activity, such as walking, will help.

Exercise for patients with diabetes has many benefits; for most, benefits outweigh risks. Although exercise has not been shown to improve glycemic control in type 1 diabetes, these patients should be encouraged to exercise to improve cardiovascular fitness and for psychological well-being and recreation.2

In patients with type 2 diabetes, exercise is as important as nutrition to improve glycemic control, reduce cardiovascular risk factors, contribute to weight loss and increase psychological well-being. Furthermore, regular exercise may prevent type 2 diabetes in those at high risk.4

Benefits of Exercise for Those with Diabetes2 Benefit Type 1 Type 2

Improved cardiovascular and overall fitness • Flexibility, endurance and muscle strength

X X

Improved glucose control • Decreased blood glucose, increased insulin sensitivity

X

Adjunct to meal planning for weight control and maintenance X

Decreased cardiovascular risk factors • Hyperlipidemia, hypertension • Obesity

X X

Slowing the decline of mobility in the overweight X

Increased sense of well-being and quality of life X X

Preventing type 2 diabetes in those at high risk X Hypoglycemia is more common in those taking insulin who exercise and whose medication dose is

not altered or carbohydrate intake is not adjusted. If pre-exercise glucose levels are <100 mg/dL, carbohydrate should be taken.5 Hypoglycemia is more common after exercise (up to 24 to 36 hours) than during exercise, due to repletion of liver glycogen. Muscle can be sensitive to insulin for up to 24 hours after exercise.6,7 There is also replacement of liver and muscle glycogen stores that have been used during exercise.

Treatment Options

14

Risks of Exercise2 • Hypoglycemia during or after exercise in those taking insulin • Increased hyperglycemia in poorly controlled diabetes and underinsulinized

diabetes with pre-exercise blood glucose levels of 250 mg/dL to 300 mg/dL • Cardiovascular autonomic neuropathy is an independent risk factor for

cardiovascular death and silent myocardial ischemia • Possible worsening of microvascular diabetes complications, particularly

retinopathy • Damage to soft tissue and joints, especially if peripheral neuropathy is present

In type 1 diabetes, monitoring for hypoglycemia, supplementation with carbohydrate-containing

food or beverage, and reducing the insulin dose are three important management issues during exercise.

Exercise should not be done if blood glucose values are greater than 250 mg/dL to 300 mg/dL and urine ketones are present.3 When there is insufficient insulin, glucose use by muscle is decreased, and the liver will produce or release stored glucose to make up the anticipated muscle deficit, resulting in a further increase in blood glucose. Exercise of higher intensity may also lead to hyperglycemia.7 This type of exercise is stressful, causing counter-regulatory hormones to release glucose from glycogen stores.

Exercise may also present additional risks in people with chronic complications associated with diabetes. For example, those with proliferative retinopathy are at increased risk for retinal or vitreous hemorrhage or retinal detachment during certain types of strenuous exercise, although stationary cycling, swimming and walking can be encouraged.

Patients with neuropathy have an increased risk of foot injury, including soft-tissue and joint injury. Although these people should avoid activities that involve pounding of the lower extremities, they may be able to engage in non-weight-bearing activities, such as swimming, stationary cycling and arm exercises.

People who have autonomic neuropathy should avoid all strenuous activities, which could cause decreased or otherwise abnormal cardiovascular response.

Exercise Recommendations

There are several factors that affect the blood glucose response to exercise:7 • Type, amount and intensity of exercise • Timing and type of the previous meal • Timing and type of the insulin injection or oral diabetes agent • Pre-exercise blood glucose level • Person’s fitness level

For type 1 diabetes, a uniform recommendation for preventing hypoglycemia and improving the metabolic response to exercise cannot be made. Rather, self-monitoring of blood glucose should be incorporated into the exercise program to provide the information necessary to adjust food intake and/or insulin dosage.3,7 The exercise recommendation for children with type 1 diabetes is the same as for all children — 60 minutes of physical activity each day.2


15

An exercise program for people with type 2 diabetes should focus on improving lifestyle activity for health initially, and then progress to structured exercise for fitness. The specific recommendations for exercise include:2,7

• At least 150 min/week of moderate-intensity aerobic physical activity (50% to 70% of maximum heart rate), spread over at least three days/week with no more than two consecutive days without exercise, is recommended.

• In the absence of contraindications, people with type 2 diabetes should be encouraged to perform resistance training three times per week.

Timing the exercise session in those with type 2 diabetes may be used as an advantage. It appears that exercise performed after 4 p.m. may reduce hepatic glucose output and decrease fasting glycemia. Exercise after eating may reduce postprandial hyperglycemia commonly observed in type 2 diabetes.3

Recommending intermittent exercise (in the form of brisk walking) in 10-minute sessions after breakfast, lunch and dinner may be more realistic for people with type 2 diabetes who have a history of sedentary lifestyle, with very beneficial effects on postprandial glucose levels.

Also, asking patients to wear a pedometer to establish daily baseline steps is a good technique for initiating exercise. Individualized goals can be established to increase activity. Using a tracking form to record progress is a useful tool for patients, and can assist in promoting success with exercise goals.

Sample Lifestyle Diary

Circle the start date and mark progress every day with a check or number.

Mon Tue Wed Thu Fri Sat Sun

Mon Tue Wed Thu Fri Sat Sun Mon Tue Wed Thu Fri Sat Sun Mon Tue Wed Thu Fri Sat Sun

Date Achievements

Challenges

People with type 2 diabetes taking oral medications or insulin should self-monitor blood glucose to determine their glycemic response to exercise.

Treatment Options

16

When starting an exercise program, patients should:4 • Receive a complete medical evaluation or medical clearance from a physician. • Monitor blood glucose before and after exercise, as this is key to safety and understanding

how exercise effects blood glucose levels. (Self-monitoring of blood glucose is important in deciding when to exercise, as well as identifying potential hypoglycemia. Exercise may require a decrease in insulin dose.)

• Ingest adequate fluids. • Use proper footwear. • Inspect feet after exercise. • Avoid exercise in extreme heat or cold. • Avoid exercise during periods of poor glucose control. • Carry identification and a source of carbohydrate when exercising (if taking insulin or oral

diabetes agents). The decision regarding the need for and type of additional food intake before or during exercise

should be based on:4 • Blood glucose level • Intensity and duration of exercise • Preference for or tolerance of solid food vs. liquid • Other nutritional factors (osmolality, fiber and electrolyte supplementation)

Exercise can accelerate absorption of insulin into exercising limbs, especially when it is begun immediately after the insulin injection. Inject insulin into a non-exercising area, such as the abdomen, to minimize the effect of exercise on insulin absorption.

The response to exercise is so variable and multifactorial that adjustment in medication and food should be based on individual responses. Blood glucose monitoring is important in understanding response patterns and tailoring an exercise program.

Medication There are a variety of antihyperglycemic agents that can be used to lower blood glucose (i.e., orals

and injectables, including insulin). Those with type 1 diabetes need daily injections of insulin to counteract the insulin deficiency. The aim of insulin replacement in the treatment of type 1 diabetes is to mimic normal (non-diabetic) fluctuations in plasma insulin.

Those with type 2 diabetes may also use insulin. Early in the development of type 2 diabetes — when insulin resistance is the primary abnormality — nutrition therapy and exercise should be initial treatment. The results of nutrition therapy are usually evident by six weeks to three months.8

If the glucose abnormalities cannot be reduced or corrected, an antihyperglycemic agent(s) may be necessary to normalize blood glucose levels. In the later stages of type 2 diabetes, when progression leads to insulin deficiency, insulin will be a necessary part of the therapy.9

In 2012, the American Diabetes Association and the European Association for the Study of Diabetes developed a position statement with recommendations for the use of antihyperglycemic agents in type 2 diabetes.9 A patient-centered approach is promoted, and cost and adverse effects of each class of agents (including effect of body weight and hypoglycemic risk) are discussed. In the position statement, the most common oral antihyperglycemic agent, metformin (Glucophage), is recommended as the preferred initial agent primarily because of its efficacy, safety record and low cost. In addition, it may reduce the risk of cardiovascular events. With each new class of noninsulin agents added to initial therapy, A1C is lowered around 1%.


17

Insulin Insulin was derived originally from bovine or porcine pancreas. Commercial preparations contain

either beef or pork insulin, or a combination of the two. In the past decade, human insulin has been produced commercially by recombinant DNA technology and by changing the structure of pork insulin to the human chemical structure. Human insulin is produced commercially by recombinant DNA technology and by changing the structure of pork insulin to the human chemical structure.2

Insulin preparations are characterized by source and duration of action:10,11 • Rapid-acting (insulin aspart [NovoLog], insulin glulisine [Apidra] or lispro-insulin analog

[Humalog]) • Short-acting (insulin regular [Humulin R, Novolin R]) • Intermediate-acting (insulin NPH [Humulin N, Novolin N] or lente insulin [Humulin L,

Novolin L]) • Long-acting basal (detemir [Levemir] or glargine [Lantus])

Insulin combinations include: • 70% NPH/30% regular • 70% insulin aspart-protamine suspension/30% insulin aspart • 70% insulin lispro-protamine suspension/25% insulin lispro • 50% NPL/50% insulin lispro

Time Courses of Action of Insulin12

Such variation in duration makes it possible to inject insulin in a pattern that is close to normal

insulin activity. Such an individualized regimen allows insulin to be adjusted to the food intake pattern, rather than adjusting food intake to the insulin dose.

Reaching target blood glucose goals with only one injection of insulin per day is not possible in those with type 1 diabetes, and almost impossible in those with type 2 diabetes who are no longer controlled with antihyperglycemic oral agents.

Rapid-acting(aspart, gluli-sine, lispro)

Short-acting(Regular)

Intermediate-acting(NPH, Lente)

Long-actingbasal (Detemir, Glargine)

0 2 4 6 8 10 12 14 16 18 20 22 24 26 28Hours

Treatment Options

18

There are two types of physiological insulin secretion: basal and bolus (mealtime or prandial). Basal insulin secretion restrains hepatic glucose production, keeping it in equilibrium with basal glucose use by the brain and other tissues. Bolus insulin secretion — often referred to as the mealtime dose — stimulates glucose use and storage while inhibiting hepatic glucose output, thereby limiting the meal-related glucose rise.

Patients with type 1 diabetes lack both basal and bolus (mealtime) insulin secretion. Basal insulin is given in the following combinations:

• Intermediate-acting insulin (NPH) at bedtime and as a small morning dose before breakfast

• Long-acting basal insulin (detemir or glargine) given usually at bedtime, but sometimes before dinner; also, can be combined with a small dose before breakfast

• Part of a continuous subcutaneous insulin infusion program (insulin pump) Bolus insulin is best duplicated by a preprandial injection of a rapid-acting insulin analog (aspart,

glulisine or lispro) before each meal.2 The bolus insulin dose is adjusted individually to provide insulin appropriate to current blood glucose and the carbohydrate content of the meal.

Multiple Daily Injection Regimens12

Regimen Before

Breakfast Before Lunch

Before Dinner

Before Bedtime

Advantages

Disadvantages

1 NPH + rapid or regular

Rapid or regular

Rapid or regular NPH

More flexible with meal times and sizes

Requires 4 injections and mixing insulin

2 Rapid or regular

Rapid or regular

Rapid or regular + basil insulin*

–

More flexible with meal times and sizes

Requires 3 injections and mixing insulin

3 Rapid or regular

Rapid or regular

Rapid or regular

Basil insulin*

More flexibility

Requires 4 injections

*Basil insulin may also be given as a combined injection with rapid- or regular-acting insulin before breakfast as well as an injection before dinner or bedtime.

An alternative to multiple daily injections of insulin is the use of an insulin pump. Insulin is

administered by very frequent pumping of small amounts of rapid- or short-acting insulin through a subcutaneous catheter every few minutes to establish a steady basal insulin level. Bolus insulin doses are given before meals through the same catheter.

Although pump therapy is more expensive than other regimens, it provides another option for flexible, optimal diabetes management.12

Another alternative is the use of an amylin mimetic called pramlintide (Symlin). (Amylin is a protein produced by the pancreas that slows down the movement of food through the stomach, preventing blood sugar from rising too high after a meal.) Pramlintide is an injectable medication used with mealtime insulin to control blood glucose in adults with type 1 or type 2 diabetes. Pramlintide reduces A1C levels by 0.6 to 0.7 percentage points. In patients with type 1 diabetes, pramlintide is usually given in addition to meal insulin, when insulin alone will not control blood sugar levels. The main adverse effect of pramlintide is hypoglycemia.11


19

In type 2 diabetes, insulin is initiated after a combination of oral agents fails to achieve glycemic control because of worsening insulin deficiency. It is most commonly added as a basal insulin at bedtime in combination with an oral agent. Mealtime insulin could also be used initially, although in general it is not used because the risk of hypoglycemia is greater than using basal insulin, and it would need to be taken three times daily before meals instead of once daily. Mealtime insulin may eventually be needed. An A1C level >8.5% indicates a need to add either meal insulin or an injectable incretin (non-insulin drugs that reduce blood sugar).

Antihyperglycemic Agents Approximately 60% of people with type 2 diabetes achieve glycemic control by using medication

(antihyperglycemic agents or insulin), often to supplement the preferred treatment methods of nutrition, physical activity and lifestyle modifications. The effectiveness of oral diabetes agents is linked closely to residual beta cell function.

Because type 2 diabetes is associated with insulin resistance and resultant impairment of the action of insulin, antihyperglycemic agents are useful in lowering blood glucose levels. They are ineffective in lowering blood glucose in those with a reduction or loss of functioning beta cells.

The use of antihyperglycemic agents should be based on duration of action, range of dose, the client’s overall health and potential adverse effects. A low dose of oral diabetes agents is prescribed initially for people with type 2 diabetes who cannot achieve blood glucose goals through lifestyle modifications. The timing and amount of antihyperglycemic agents can be varied to improve glycemic control. If blood glucose is not controlled on the initial dose, it can be increased every one to two weeks until the maximum dose or desired blood glucose control is obtained. If the maximum dosage is used and elevated blood glucose levels continue, insulin should be considered.

Eight groups of oral diabetes agents are available: sulfonylureas, biguanides, thiazolidinediones, alpha-glucosidase inhibitors, meglitinides, gut hormone-based therapy (dipeptidyl peptidase 4 inhibitors and glucagon-like peptide), sodium-dependent glucose transporters and other drugs. Sulfonylureas

The most significant mechanism of action of sulfonylureas is to enhance basal and meal-stimulated insulin secretion. By reducing serum glucose and correcting “glucotoxicity,” sulfonylureas indirectly decrease the overproduction of hepatic glucose and increase the rate of glucose uptake by the muscle.11

Because type 2 diabetes is a disorder in which insulin secretion does not overcome insulin resistance, sulfonylureas are used to control hyperglycemia; however, they are ineffective in lowering blood glucose in those with minimal or no insulin production. Those with diabetes who are most likely to respond to sulfonylureas include:11

• More recent diagnosis (made in the previous five years) • Age >30 • Normal weight or overweight • Fasting blood glucose of <300 mg/dL • Willingness to comply with an individualized nutrition and exercise program • Not 100% insulin deficient

The second-generation sulfonylureas (glyburide [Micronase], glipizide [Glucotrol], glimepiride [Amaryl]) have all but replaced the first-generation sulfonylureas (tolbutamide [Orinase], chlorpropamide [Diabinese], tolazamide [Tolinase]) because of their increased potency, decreased adverse effects and less frequent interactions with other agents. Sulfonylureas are a popular choice because they are relatively inexpensive, and work well alone or in combination with biguanides

Treatment Options

20

(metformin) or basal insulin therapy. In addition to weight gain and rashes, they carry a risk of hypoglycemia.

Biguanides

Metformin remains the most common initial antihyperglycemic agent offered. The United Kingdom Prospective Diabetes Study showed that its use as a monotherapy can reduce mortality, myocardial infarction and weight gain in overweight patients.13 It was developed in France in 1959, approved for use by the U.S. Food and Drug Administration in January 1995 and has been used worldwide.

It has a different mode of action from sulfonylureas in that it works via the liver to decrease hepatic glucose production and on the muscle to increase glucose uptake. It does not work on the pancreas to stimulate insulin secretion.

The proposed benefits of using metformin include modest weight loss, decreased risk of hypoglycemia, decreased plasma triglycerides, decreased LDL-cholesterol, modest elevation of high-density lipoprotein cholesterol and decreased insulin levels.

The adverse effect of biguanides experienced by up to 30% of patients involves the gastrointestinal system; it may include abdominal bloating, cramping, feeling of fullness and diarrhea, as well as nausea. Contraindications for metformin use include acute kidney injury or significant fluctuations in renal status (monitor with estimated glomerular filtration rate), hepatic disease, alcohol abuse, history of lactic acidosis, cardiac insufficiency and other hypoxic conditions.14

Because metformin favorably affects the lipid profile and is not associated with weight gain, it is ideally suited for those who are obese, who have dyslipidemia or type 2 diabetes, and who do not have any contraindications to the drug.14 Metformin is used commonly with other antihyperglycemic agents, particularly sulfonylureas (glyburide), glitazones and DPP-4 inhibitors.

Thiazolidinediones

The two thiazolidinediones available in the U.S. are pioglitazone (Actos) and rosiglitazone (Avandia). Thiazolidinediones are sensitizing agents that improve the glycemia, dyslipidemia, inflammation and hypercoagulability associated with insulin resistance. These medications appear to work by enhancing insulin action in the liver, muscle and adipose tissue, thereby reducing insulin resistance. They do not affect insulin secretion. They bind to receptors on the cell nucleus, leading to actions that are similar to those of insulin.

Because insulin resistance is lowered, these compounds may be useful in the treatment of dyslipidemia, hypertension and even polycystic ovary disease. Pioglitazone and rosiglitazone have been approved for monotherapy, and combination use with sulfonylureas, metformin and insulin.15

The FDA has restricted use of rosiglitazone to patients with type 2 diabetes because of increased risk of cardiovascular morbidity and mortality. Pioglitazone effectively lowers A1C levels by as much as 1% to 1.5% (less in those with insulin resistance and diminished insulin secretory reserves).

The most common reported adverse effects in those with type 2 diabetes are weight gain and fluid retention. In older patients, there may be the potential for high fracture risk, particularly in those with osteopenia or osteoporosis.16

Alpha-Glucosidase Inhibitors

Acarbose (Precose) and miglitol (Glyset) are inhibitors of alpha glucosidase, a digestive enzyme that facilitates the breakdown of starch and disaccharides to glucose in the small intestine. These drugs have been approved by the FDA for use in people with insulin-requiring type 2 diabetes.


21

When ingested with the first bite of a meal, alpha-glucosidase inhibitors cause a slower and smaller rise in blood glucose levels postprandially; however, because carbohydrate breakdown continues at more distal parts of the small intestine, glucose continues to be absorbed and total glucose absorption is unchanged. As there is no decrease in caloric absorption, weight loss does not occur.

Adverse effects of acarbose and miglitol are caused by the malabsorption of a small amount of carbohydrate, with subsequent metabolism of the carbohydrate by intestinal bacteria. The most common adverse effects are increased flatulence and abdominal bloating. Some may experience diarrhea. Because of these adverse effects, these agents are less popular than other antihyperglycemic agents. Acarbose and miglitol are most effective when given with a high-fiber, high-carbohydrate meal plan.17 Hypoglycemia does not occur when they are used alone.

Meglitinides

In 1998, repaglinide (Prandin) received FDA approval as the first drug of a new class of beta-cell

stimulators called meglitinides. In 2000, another meglitinide, nateglinide (Starlix), received FDA approval. This class of oral diabetes agents stimulates the release of insulin from the beta cells of the pancreas in a glucose-dependent fashion. Nateglinide improves mealtime and mean glycemic control by restoring the early insulin secretion phase, which is useful in protecting against post-meal glucose spikes.18 Nateglinide may be especially effective in combination with metformin. The effect of metformin on the fasting glucose level and the effect of nateglinide on the mealtime glucose level improve the overall A1C level, and the fasting and postprandial hyperglycemia.19 However, the lack of data showing improved clinical outcomes with meglitinides, in addition to their cost and more frequent dosing, has limited widespread use.

Gut Hormone Therapy (Incretin-Based Therapy)

Incretins are gut hormones that facilitate insulin release with food ingestion. There are two classes of medication:

• Incretin enhancers (DPP-4 inhibitors), which restore low glucagon-like peptide-1 to more normal levels

• GLP-1 analogs (receptor agonists), which directly bind to GLP-1 receptors DPP-4 inhibitors, a new class of antihyperglycemic agents (FDA approved in 2006), augment

secretion of insulin from the beta cell and inhibit glucagon release from the alpha cell. The drugs include sitagliptin (Januvia), saxagliptin (Onglyza) and linagliptin (Tradjenta). They emphasize postprandial control of glucose levels and have been shown to reduce A1C by 0.6% to 1.4%. They can be used as monotherapy or in combination with metformin, pioglitazone and sulfonylureas. In January 2013, the FDA approved a fourth DPP-4, alogliptin (Nesina). Reported adverse effects include nasopharyngitis, urinary tract infections and headaches. There should be an adjustment dose (usually a 50% reduction), as measured by GFR for patients with renal dysfunction.20

GLP-1 analogs or incretin mimetics (injectable medications) bind to the receptor and appear to restore the glucose sensitivity of the pancreatic beta cells. Their specific actions are appetite suppression that can result in moderate weight loss, and delayed gastric emptying that blunts or delays meal-related hypoglycemia. Exenatide (Byetta), a receptor agonist, is a synthetic injectable analog of the Gila monster salivary compound, and is typically taken twice a day. Liraglutide (Victoza), another receptor agonist, is a human GLP-1 with a relatively long half-life and is taken as a once-daily injection. GLP-1 analogs commonly cause transient nausea and require dose titration as a result.

Treatment Options

22

Gut Hormone Therapy (Amylinomimetics) Amylin is a neuroendocrine hormone co-secreted with insulin by the beta cells. It slows down the

transit of food from the stomach, preventing large rises in blood glucose levels after a meal. Amylin deficiency is evident in type 1 diabetes, and amylin levels are high in the fasting state in type 2 diabetes, but the levels do not increase with meals. Pramlintide was developed as an amylin analog for use in type 1 diabetes and insulin-treated patients with type 2 diabetes. Mild nausea is the most common adverse effect, and is minimized by titrating the dose.

Sodium-Dependent Glucose Cotransporter 2 Inhibitors

The action of sodium-dependent glucose cotransporters is to transport glucose in an active manner into renal tubular cells. This results in improved serum glucose levels by excretion of glucose into the urine, creating an osmotic diuresis-like effect.21 Recently, the FDA approved canagliflozin (Invokana); several other drugs are in phase III studies. In addition to reductions in A1C levels of up to 0.9%, other benefits may include weight loss and a reduction in systolic blood pressure. Urinary infections were more common with SGLT-2 inhibitors. Another reported adverse effect has been hyperkalemia, suggesting caution for patients on blood pressure medication (angiotensin-converting enzymes inhibitors or angiotensin-receptor blockers).

Other Glucose-Lowering Agents

Two additional classes of medications that have been reported to lower blood glucose levels but whose mechanism of action is unknown are colesevelam (WelChol), which is a bile acid sequestrant, and bromocriptine (Cycloset), which is a dopamine agonist.11

Colesevelam is used in treatment of hypercholesterolemia, but has also been reported to lower A1C level by 0.5% to 0.7% in type 2 diabetes. It may have adverse effects (constipation) and may increase triglyceride levels with pre-existing dyslipidemia. Bromocriptine has been approved for use in type 2 diabetes and has been shown to improve A1C levels by about 0.7%. It improves insulin sensitivity by positively impacting central dopaminergic activity. The major adverse effect is nausea.


23

Time Activity of Antihyperglycemic Agents10,11 Medication Brand Name Dose Ranges Usual Maintenance Dose

First-Generation Sulfonylureas

Chlorpropamide Diabinese 100 mg/day to 500 mg/day 250 mg/day

Second-Generation Sulfonylureas

Glyburide Glipizide Glimepiride

DiaBeta, Micronase Glynase Glucotrol Glucotrol XL Amaryl

1.25 mg/day to 20 mg/day 0.75 mg/day to 12 mg/day 5 mg/day to 40 mg/day 2.5 mg/day to 20 mg/day 1 mg/day to 8 mg/day

1.25 mg/day to 10 mg/day 6 mg/day 20 mg/day 2.5 mg/day to 10 mg/day 1 mg/day to 4 mg/day

Biguanides

Metformin

Glucophage Glucophage XR Riomet Fortamet Glumetza

500 mg/day to 2,550 mg/day 500 mg/day to 2,000 mg/day 500 mg/day to 2,550 mg/day 500 mg/day to 2,550 mg/day 1,000 mg/day to 2,000 mg/day

500 mg/day to 2,000 mg/day 1,000 mg/day 1,500 mg/day 1,500 mg/day 1,500 mg/day

Thiazolidinediones

Pioglitazone Rosiglitazone

Actos Avandia

15 mg to 45 mg bid 2 mg to 4 mg bid

30 mg/day to 45 mg/day 4 mg to 8 mg tid

Alpha-Glucosidase Inhibitors

Acarbose Miglitol

Precose Glyset

25 mg to 100 mg tid 25 mg to 100 mg tid

50 mg tid 50 mg tid

Meglitinides

Repaglinide Nateglinide

Prandin Starlix

0.5 mg/day to 16 mg/day 120 mg tid

4 mg tid 120 mg tid

DPP-4 Inhibitors (Incretin Enhancer)

Sitagliptin Saxagliptin Linagliptin Alogliptin

Januvia Onglyza Tradjenta Nesina

100 mg/day 2.5 mg/day to 5.0 mg/day 5 mg/day 25 mg/day

100 mg/day 2.5 mg/day to 5 mg/day 5 mg/day 25 mg/day

GLP-1 Analogs (Incretin Mimetics)

Exenatide Liraglutide

Byetta Victoza

5 mcg/day to 10 mcg/day 0.6 mcg/day to 1.8 mcg/day

Amylinomimetics

Pramlintide Symlin 15 mcg/day to 60 mcg/day (type 1 diabetes) 60 mcg/day to 120 mcg/day (type 2 diabetes)

SGLT-2 Inhibitors

Canagliflozin Invokana 100 mg/day to 300 mg/day 100 mg/day to 300 mg/day

Other Agents

Colesevelam Bromocriptine

WelChol Cycloset

3,750 mg/day or 1,875 mg/twice daily 1.6 mg to 4.8 mg

Treatment Options

24

Combination Therapy Because the available antihyperglycemic agents have different mechanisms of action, combination

therapy using different types of these agents is possible. Advantages of this treatment approach include delaying the need for insulin therapy, decreasing the dose of each drug to reduce the incidence of adverse effects, and improving metabolic control (both lipids and glucose).

For patients with central obesity and insulin resistance, especially those who still have some endogenous insulin secretion, a combined insulin resistance approach (metformin plus a thiazolidinedione [pioglitazone] or an incretin mimetic [exenatide or liraglutide]) is an effective therapy. An oral incretin enhancer (DPP-4) is also popular because of its beneficial weight-loss effects in obese patients in combination with thiazolidinediones or metformin.

If monotherapy using one oral diabetes agent does not achieve treatment objectives in three months, then a second oral diabetes agent can be added. The most commonly used combination of oral agents is metformin with sulfonylureas. In obese patients and as described above, combinations of metformin and thiazolidinedione, metformin and incretin mimetics, metformin and DPP-4, or thiazolidinedione and DPP-4 are commonly used.

If the initial fasting glucose levels remain greater than 250 mg/dL to 300 mg/dL after eight to 12 weeks of any of the above combinations of antihyperglycemic agents, a combination of an oral agent and insulin therapy should be initiated. The most common and effective use of insulin with antihyperglycemic agents includes:

• Metformin and glargine insulin at bedtime • Twice-daily exenatide (or once-daily liraglutide) with glargine insulin

If, after eight to 12 weeks of any of the above combinations of oral diabetes agents and insulin, the initial fasting glucose levels are >400 mg/dL, the person with type 2 diabetes should be started on insulin.22 A basal or long-acting insulin (glargine or detemir) is the most frequent type of insulin added initially, and is generally taken once/day at bedtime to lower fasting glucose levels and is initiated with 10 units or 0.2 units/kg. Insulin can be increased by 2 units every three days until fasting levels are in the target range of 70 mg/dL to 130 mg/dL. The American Diabetes Association and the European Association for the Study of Diabetes have developed a consensus algorithm for the initiation and adjustment of therapy in type 2 diabetes.22

Self-Monitoring of Blood Glucose The purpose of SMBG in patients with diabetes is to identify treatment needs and then to evaluate

the effectiveness of the treatment (see Appendix 1). SMBG is used to:10,11 • Promote diabetes self-management and allow for near-normal glucose levels • Provide immediate feedback on blood glucose control • Prevent hypoglycemia • Adjust diabetes medications • Adjust food choices and/or meal plan • Adjust physical activity

As the first goal of diabetes medical nutrition therapy is to achieve glycemic control, SMBG is imperative. Every time blood glucose is tested, the level should be entered on a record so results can be reviewed, evaluated and used by the diabetes care team to determine the person’s food, insulin and exercise needs. Reviewing glucose records or logbooks to determine blood glucose patterns is the best method for evaluating the effects of diabetes medical nutrition therapy on blood glucose control. The diabetes care team should work with each client to establish target blood glucose goals. Monitoring


25

glucose records or logbooks can help evaluate whether goals are being met, whether existing goals should be revised and whether new goals should be developed. Out-of-target blood glucose results are not always caused by eating indiscretion; stress, illness, infection, change in exercise and incorrect medication dosage should be considered. If the cause is food-related, the diabetes care team should consider management changes to accommodate the change in food consumption.

The frequency of monitoring depends on the type of diabetes and each person’s overall therapy. Monitoring up to seven times a day seems excessive, but may be appropriate for the person with newly diagnosed type 1 diabetes or for the pregnant woman.

Blood glucose levels are monitored typically before meals; one to two hours after meals; at bedtime; in the middle of the night (3 a.m.); before, during and after exercise; when hypoglycemia is suspected; and before driving. ADA recommendations regarding glucose monitoring are:10,11

• For those using multiple insulin injections or insulin pump therapy, SMBG should be carried out three or more times daily.

• For those using less frequent insulin injections, noninsulin therapies or medical nutrition therapy alone, SMBG may be useful as a guide to the success of therapy.

• To achieve postprandial glucose targets, postprandial SMBG may be appropriate. • Patients using SMBG need to receive adequate instruction regarding techniques, how to

use glucose data to adjust therapy, routine follow-up, and evaluation to monitor technique and adjust therapy based on glucose pattern management.

• Continuous glucose monitoring may be a useful tool to improve glucose control for patients on intensive insulin regimens and for patients with hypoglycemia unawareness and/or frequent hypoglycemic episodes.

Because of rapid technological advances, most glucose meters are upgraded almost annually. It is important that those with diabetes consult with their physician and/or diabetes educator to make sure the meter they choose is suited to their needs.

Type 1 Diabetes

• Test before each meal and at bedtime.

• If necessary or when hypoglycemia is suspected, test one to two hours after meals and in the middle of the night (2 a.m. to 4 a.m.).

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Type 2 Diabetes • Ideally, test in pairs (pre- and post-meals or bedtime/fasting) because this is helpful to

determine the effect of meals and specific foods on blood glucose levels. If testing once daily, test at random times (e.g., before breakfast Sunday; two hours after breakfast Monday; before lunch Tuesday; two hours after lunch Wednesday; before dinner Thursday; two hours after dinner Friday; and before bedtime Saturday). Random testing is important to determine a 24-hour profile of blood glucose levels. At a minimum, test once or twice a week at random times.

With the addition of antihyperglycemic agents and/or insulin, it becomes even more important to test regularly and at consistent times to determine glucose patterns and to make self-adjustments in food, activity and/or medication.

Testing for Type 1 and 2 Diabetes

Additional testing/monitoring is indicated in the following situations: • Schedules change • Exercise is adjusted • Illness occurs • A new non-diabetes medication is initiated that will affect blood glucose

(e.g., prednisone [Cortan]) or will affect the ability to recognize low blood glucose (e.g., beta blockers)

• Diabetes medication is adjusted • Effect of a certain kind or amount of food is being determined • Effect of weight loss and/or exercise is being determined

Pattern Management

SMBG records should be examined at each visit to identify patterns. Medical, nutritional and lifestyle therapy can be adjusted to meet the identified goals based on these patterns. Ultimately, patients should be taught how to identify patterns and to make their own adjustments in food, activity and medication.


27

Blood Glucose Pattern Management23 Step 1: Establish target pre-meal and post-meal blood glucose levels. • Fasting: 90 mg/dL to 130 mg/dL • Post-meal: <180 mg/dL • Before bedtime: 110 mg/dL to 150 mg/dL

Step 2: Document blood glucose data • Fasting • Pre-meal • Postprandial • HS (hour of sleep or before bedtime) • 3:00 a.m. (if indicated)

Step 3: Assess types of patterns* • All blood glucose levels high • Highs and lows in same day • Pattern of blood glucose high/low at one time of day

Step 4: Assess variables • Food intake (carbohydrate consistency, high/low carbohydrate intake, accuracy of portion

size, delayed/skipped meals, +/- snack) • Activity (time of day, intensity, frequency, duration, +/- usual) • Illness/stress • Medications o Oral: type, dose and time o Insulin: type, dose and time o Injection site o Skipped meal

Step 5: Take action • Fix low blood glucose first • If blood glucose is always high o Add another oral diabetes agent and/or insulin o Increase the dose

• If fasting blood glucose is high o Consider bedtime insulin dose

• If blood glucose is high after meals o Adjust the food/activity variable (less carbohydrate, increase fiber, exercise after meals) o Try a different oral medication

• Tips o Change only one insulin at a time o Change the dose by 10% to 20% o Adjust insulin every three days if blood glucose is less stable o Adjust insulin every seven days if blood glucose is relatively stable

* Pattern = Three high blood glucose levels or two low blood glucose levels taken at the same time of day

Adjustment of therapy should be based on a pattern, rather than a single test result, and changes in

medication need to be gradual. There are numerous solutions to any management problem; the best answer may not be a changed eating plan.

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Common Blood Glucose Patterns Example: High Blood Glucose Pattern

Breakfast Lunch Dinner HS

Monday Tuesday Wednesday Thursday

240 236 202 284

204 192 211 198

193 220 305 220

285 264 —

214

Example: Low Blood Glucose Pattern



64 58 50 36

191 262 201 66

114 204 47

306

67 135 103 132

Example: Not Enough Information



122 — 47 75

— 96 — —

234 —

390 83

— — — —

Red = low glucose reading; blue = high glucose reading; black = normal glucose reading.

Education Ongoing education about diabetes and diabetes management will provide the knowledge, skills and

confidence to use meal planning, physical activity and medication effectively, as well as how to take action based on results from SMBG and urine ketone levels. Each management tool must be combined into a well-balanced, daily routine to manage diabetes successfully.24

Reimbursement

While it is well accepted that successful self-management of diabetes involves knowledge and skills in the areas of nutrition, exercise, medication and SMBG, a hurdle to providing all of these aspects for those with diabetes has been the lack of reimbursement or insurance coverage. Although hurdles still exist, the situation has improved due to the passage of federal and state laws as well as the recognition by some insurance companies that coverage of this service is clinically and economically effective.

In the U.S., the payer mix for diabetes is broken down as follows:25 • 43%: Private insurance • 37%: Medicare • 5%: Medicaid • 3%: Other • 11%: Uninsured


29

Effective February 2001, the Centers for Medicare and Medicaid Services reimburse for diabetes self-management education when provided by a program that meets national standards and is recognized by ADA or other approval bodies. Effective January 2002, Medicare reimburses for medical nutrition therapy provided to patients with diabetes and renal disease. A referral from a physician is necessary for medical nutrition therapy reimbursement. Medical nutrition therapy is reimbursed for three hours in the first year and two hours in subsequent years. The medical nutrition therapy reimbursement process involves many rules and it is necessary to understand how both the Medicare system and private payer systems work. (For information, see the Coding, Coverage and Compliance section of the Academy of Nutrition and Dietetics website, at http://www.eatright.org/coverage.)

Medicare/Medicaid Reimbursement for DSMT • Of the 10 hours allowed for initial training, 1 hour is allowed for individual training, which

can be used for any part of the training, including insulin training.

• DSMT must be provided in a group setting, unless no group training is available within two months of the date ordered for training, or the physician documents a special need (severe vision, hearing, language limitations or special conditions that hinder learning in a group setting).

• The initial 10 hours of training must be provided within a 12-month period.

• During subsequent years, two hours of follow-up DSMT are covered per year, either as group or individual training.

Reimbursement for Diabetes Education American Association of Diabetes Educators http://www.diabeteseducator.org (click on Policy & Advocacy) American Diabetes Association http://www.diabetes.org (click on Advocacy)

Suggested Reading Mensing C. The Art and Science of Diabetes Self-Management Education. 2nd ed. Chicago, IL: American Association of Diabetes Educators; 2010.

Glucose Meter Resource List Diabetes Forecast. Special Issue: Consumer Guide 2014. January 2014. Diabetes Health. Product Reference Guide. December 2013/January 2014.

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Review Questions 1. What are the recommended clinical outcomes for glucose, blood pressure and lipids for

patients with diabetes? 2. Outline the exercise recommendations for type 2 diabetes. 3. Differentiate the medication options for type 1 diabetes and type 2 diabetes. 4. What are the primary metabolic effects of using antihyperglycemic agents in patients with type

2 diabetes? Answer 1:

• A1C: <7% • Fasting plasma glucose: 70 mg/dL to 130 mg/dL • Post-meal plasma glucose: <180 mg/dL • Blood pressure: 140/80 • LDL: <100 mg/dL; 70 mg/dL, if overt diabetes with cardiovascular disease

Answer 2: • Perform at least 150 min/week of moderate-intensity aerobic physical activity (50% to 70%

of maximum heart rate). • In the absence of contraindications, people with type 2 diabetes should be encouraged to

perform resistance training three times per week.

Answer 3: • Those with type 1 diabetes require insulin to live because of an insulin deficiency; therefore,

insulin is the primary treatment tool. • People with type 2 diabetes, ideally, should be treated by first making changes in eating

(usually to promote weight loss) and increasing physical activity; if these options are unsuccessful, then antihyperglycemic agents can be initiated. Insulin therapy is the last option used in treating patients with type 2 diabetes.

Answer 4:

• Sulfonylureas and meglitinides: to increase insulin secretion • Biguanides: to decrease hepatic glucose production • Thiazolidinediones: to increase insulin action in liver, muscle adipose tissue • Alpha-glucosidase inhibitors: for malabsorption of carbohydrate • DPP-4 inhibitors: to increase insulin secretion and inhibit glucagon release • GLP-1 analogs: suppress appetite (weight loss); delay gastric emptying (delay meal-related

hypoglycemia) • Amylinomimetics: replace amylin that is deficient in type 1 diabetes and in low levels

postprandially in type 2 diabetes • SGLT-2 inhibitors: transports glucose into renal tubular cells, thereby increasing glucose

excretion in the urine


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References 1. Evert AB, Boucher JL, Cypress M, et al. Nutrition therapy recommendations for the management of adults

with diabetes. Diabetes Care. 2014;37(Suppl 1):S120-S143.

2. American Diabetes Association. Standards of medical care in diabetes – 2014. Diabetes Care. 2014;37(Suppl 1):S14-S80.

3. Sigal RJ, Kenny GP, Wasserman DH, Castaneda-Sceppa C. Physical activity/exercise in type 2 diabetes. Diabetes Care. 2004;27(10):2518-2539.

4. Colberg SR, Sigal RJ, Fernhall B, et al. Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement. Diabetes Care. 2010;33(12):e147-e167.

5. American Diabetes Association. Physical activity/exercise and diabetes. Diabetes Care. 2004;27(Suppl 1):S58-S62.

6. Mitchell TH, Abraham G, Schiffrin A, Leiter LA, Marliss EB. Hyperglycemia after intense exercise in IDDM subjects during continuous subcutaneous insulin infusion. Diabetes Care. 1988;11(4):311-317.

7. Shugart C, Jackson J, Fields KB. Diabetes in sports. Sports Health. 2010;2(1):29-38.

8. Pastors JG, Franz MJ, Warshaw H, Daly A, Arnold MS. How effective is medical nutrition therapy in diabetes care? J Am Diet Assoc. 2003;103(7):827-834.

9. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient-centered approach: position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care. 2012;35(6):1364-1379.

10. Kaufman FR, ed. Medical Management of Type 1 Diabetes. 6th ed. Alexandria, VA: American Diabetes Association; 2012.

11. Burant CF, Young LA, eds. Medical Management of Type 2 Diabetes. 7th ed. Alexandria, VA: American Diabetes Association; 2012.

12. Wolfsdorf JI, ed. Intensive Diabetes Management. 4th ed. Alexandria, VA: American Diabetes Association; 2009.

13. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998;352(9131):854-865.

14. Lipska KJ, Bailey CJ, Inzucchi SE. Use of metformin in the setting of mild-to-moderate renal insufficiency. Diabetes Care. 2011;34(6):1431-1437.

15. Einhorn D, Rendell M, Rozenweig J, et al. Pioglitazone hydrochloride in combination with metformin in the treatment of type 2 diabetes mellitus: a randomized, placebo-controlled study. The Pioglitazone 027 Study Group. Clin Ther. 2000;22(12):1395-1409.

16. Grey A. Thiazolidinedione-induced skeletal fragility — mechanisms and implication. Diabetes Obes Metab. 2009;11(4):275-284.

17. Van de Laar FA, Lucassen PL, Akkermans RP, Van de Lisdonk EH, De Grauw WJ. Alpha-glucosidase inhibitors for people with impaired glucose tolerance or impaired fasting blood glucose. Cochrane Database Syst Rev. 2006(4):CD005061.

18. Hanefield M, Bouter KP, Dickinson S, Guitard C. Rapid and short-acting mealtime insulin secretion with nateglinide controls both prandial and mean glycemia. Diabetes Care. 2000;23(2):202-207.

19. Horton ES, Clinkingbeard C, Gatlin M, et al. Nateglinide alone and in combination with metformin improves glycemic control by reducing mealtime glucose levels in type 2 diabetes. Diabetes Care. 2000;23(11):1660-1665.

20. Barnett A. DPP-4 inhibitors and their potential role in the management of type 2 diabetes. Int J Clin Pract. 2006;60(11):1454-1470.

21. Basile J. A new approach to glucose control in type 2 diabetes: the role of kidney sodium-glucose co-transporter 2 inhibition. Postgrad Med. 2011;123(4):38-45.

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22. Nathan DM, Buse JB, Davidson MB, et al. Management of hyperglycemia in type 2 diabetes; a consensus algorithm for the initiation and adjustment of therapy: a consensus statement form the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 2009;32(1):193-203.

23. Pastors JG, et al. Blood Glucose Pattern Management. Virginia Center for Diabetes Professional Education, Charlottesville, VA; 2002.

24. Funnell MM, Brown TL, Childs BP, et al. National standards for diabetes self-management education. Diabetes Care. 2010;33(Suppl 1):S89-S96.

25. Fitch K, Iwasaki K, Pyenson B. Improved management can help reduce the economic burden of type 2 diabetes: a 20-year actuarial projection. Milliman Client Report. Milliman Web site. http://publications.milliman.com/publications/health-published/pdfs/improved-management-can-help.pdf. Published April 28, 2010. Accessed on February 15, 2015.


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Chapter Three: Nutrition Recommendations

ietary manipulation, usually through starvation diets, was the primary treatment tool for diabetes before the discovery of insulin in 1921. After that, nutrition management began to take a lower priority due to the newness and simplicity of insulin therapy. From 1921 to 1986,

the recommended percentage of calories from fat decreased and the percentage of calories from carbohydrate increased because of the association between macrovascular disease and diabetes. Until 1994, the recommendations identified an “ideal” diet with percentages of carbohydrate, protein and fat.

The 1994 nutrition recommendations shifted the emphasis of medical nutrition therapy to focus on metabolic outcomes, treatment goals and a patient-centered approach. These recommendations also focused on the total amount of carbohydrate in the diet, rather than carbohydrate type. The nutrition recommendations published in 2002 and again in 2008, are based on evidence-based principles. Evidence-based nutrition recommendations are categorized according to the following criteria:1

• Strong evidence: two or more well-done clinical studies report similar outcomes • Some evidence: one well-done clinical study or multiple studies report different outcomes

by weight of evidence to support a particular view • Limited evidence: consensus of experts based on limited clinical evidence • No evidence: consensus of experts based on clinical experiences without supporting

evidence The 2008 nutrition recommendations focused on:1

• Primary prevention (prediabetes) • Secondary prevention (management of diabetes) • Tertiary prevention (prevention or control of diabetes complications)

Nutritional research during the past several years has promoted a renewed interest in nutritional

intervention, such as glycemic responses of various food nutrients, soluble fiber versus insoluble fiber, monounsaturated fats, caloric sweeteners, fat substitutes and very low-calorie diets.

The nutrition recommendations released this year emphasize the need for individualization to achieve a healthy eating pattern. To accomplish this, practical tools for meal planning should be used instead of focusing on nutrients, percent of nutrients in the diet or single foods.1

D

Nutrition Requirements

34

2014 Nutrition Recommendations and Interventions

The goal of nutrition therapy for everyone with diabetes is to be engaged actively in self-management, education and treatment planning, which includes collaborative development of an individualized eating plan.4 The specific goals of nutrition therapy for adults with diabetes are:4

• Promote and support healthful eating patterns, emphasizing a variety of nutrient-dense foods in appropriate portion sizes to: o Attain individualized glycemic, blood pressure and lipid goals:

§ A1C: <7% § Blood pressure: <140/80 mmHg § LDL cholesterol: <100 mg/dL § Triglycerides: <150 mg/dL § HDL cholesterol: >40 mg/dL for men and >50 mg/dL for women

• Achieve and maintain body weight goals. • Delay or prevent the development of chronic complications of diabetes. • Individualize nutritional needs based on personal and cultural preferences, healthy literacy,

access to healthy food choices, willingness and ability to make behavioral changes, and barriers to change.

• Maintain pleasure of eating by providing positive messages about food and limiting food choices only when based on scientific evidence.

• Provide practical tools for meal planning instead of focusing on nutrients or single foods.

Nutrient Composition of Diabetes Diets1-3 Distribution of Calories (%)

Year Carbohydrate Protein Fat

Before 1921 Starvation Diets

1921 20% 10% 70%

1950 40% 20% 40%

1971 45% 20% 35%

1986 50% to 60% 12% to 20% 30%

1994 A 10% to 20% B

2002 A 10% to 20% B

2006 C 15% to 20% D

A: Based on nutrition assessment B: <10% saturated fat

C: Individualized (includes carbohydrate sources from whole grains, legumes, fruits and vegetables, and low-fat milk)

D: <7% saturated fat


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Nutrition therapy has been shown repeatedly to be effective in improving metabolic outcomes. Randomized controlled trials and observational studies have documented improved glycemic outcomes of decreases in HbA1C of approximately 1% to 2%, depending on the type and duration of diabetes.2,5

In those with newly diagnosed type 2 diabetes, intensive nutrition therapy provided by RDs following nutrition practice guidelines decreased A1C levels by approximately 2%. Even with durations of type 2 diabetes averaging four years and without changes in medication, A1C levels decreased by approximately 1%.6 In those with type 1 diabetes who were taught to adjust mealtime insulin doses based on planned carbohydrate intake, A1C levels decreased by approximately 1% without a change in the total dose of insulin.7 Nutrition practice guidelines for type 1 and type 2 diabetes have been updated and published by the Academy of Nutrition and Dietetics.5

The evidence also suggests that, although nutrition therapy has the greatest impact at initial diagnosis, it continues to be effective at any time during the disease process. The benefit of nutrition therapy is known with clinical outcomes (i.e., weight loss, glycemic control, blood pressure and lipid improvement) between six weeks and three months. If no progress is made at six weeks, the RD needs to reassess and revise the nutrition care plan. If no clinical improvement is seen at three months, the RD needs to recommend a change in medication(s). Type 2 diabetes is a progressive disease, and as beta-cell function decreases, blood glucose-lowering medication needs to be combined with nutrition therapy to achieve blood glucose goals.

Energy, Overweight and Obesity

Of U.S. adults with diabetes, 75% are overweight; almost 50% are obese.8 Because of the effects of obesity on insulin resistance, weight loss is an important goal. Long-term weight loss is difficult for most people. In interventional studies of type 2 diabetes that were one year or longer, modest weight losses of approximately 2 kg to 8.5 kg were achieved.9,10 The Look AHEAD (Action for Health in Diabetes) study is a large multi-center trial to determine if long-term (up to 10 years) weight loss will improve glucose control and reduce risk for cardiovascular disease in those with type 2 diabetes. The goal of the intervention is to achieve and maintain a weight loss of at least 7% of initial body weight with the intervention including diet (decreased caloric intake and meal replacements), physical activity (175 minutes of moderate-intensity exercise/week), behavior modification, and group and individual meetings for support and education. At the 10-year study end, the mean weight loss was 6%.11,12

In a review of weight-loss intervention studies, those who achieved the greatest weight losses were those who were eating Mediterranean-style patterns (6.2 kg), and a comprehensive weight-loss program involving nutrition intervention (including meal replacements) and physical activity (8.4 kg). In a review of weight-loss studies that showed the greatest improvement in A1C levels, the Mediterranean-style eating pattern study (A1C declined 1.2%) and the Look AHEAD study (A1C declined 0.6%) reported the largest improvements.11,13

Structured, intensive lifestyle programs involving individualized education and counseling, reduced energy and fat, regular exercise and frequent contact are necessary to produce long-term weight loss.14 The challenge is implementing these types of programs in clinical practice. Third-party payers may not provide adequate reimbursement for the time and frequency necessary for achieving weight-loss goals.15

Many regain a portion of initial weight loss.16 Factors that contribute to weight regain include socioeconomic status, unsupportive environments and physiological.17

For the most beneficial effects on weight-loss interventions, the literature supports weight losses of >6 kg (7% to 8.5% of initial weight loss), regular physical activity and frequent contact with RDs.16

Other successful strategies include weekly self-weighing, regular consumption of breakfast, reduced intake of fast foods, reduced portion sizes and use of meal replacements.18


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Bariatric surgery is also an effective treatment for weight loss and can be considered in people with a body mass index >35. Surgery has been shown to be effective in normalizing blood glucose and reducing cardiovascular risk factors.19

Eating Pattern

A systematic review of macronutrients and eating patterns in the management of diabetes showed that several eating patterns may lead to improvements in glucose and cardiovascular disease risk factors. The eating patterns that were reviewed with evidence to support their use in diabetes include the Mediterranean-style eating pattern, vegetarian and vegan diets, a low-fat eating pattern, a low-carbohydrate eating pattern and the Dietary Approaches to Stop Hypertension eating plan.20 Personal preferences (e.g., tradition, culture, religion, health beliefs and goals, and economics) and metabolic goals should be considered when making recommendations about an eating pattern.4

Eating Patterns20

Mediterranean Style

• Includes fruits, vegetables, breads, other forms of cereals, beans, nuts and seeds

• Focuses on minimally processed, seasonally fresh, locally grown foods. • Fresh fruits for dessert; concentrated sugars or honey consumed for

special occasions • Olive oil as the primary fat source • Dairy products (mainly cheese and yogurt) in low to moderate amounts. • Fewer than 4 eggs/week • Red meat consumed in low amounts • Wine consumption in low to moderate amounts generally with meals

Vegetarian and Vegan

• Vegetarian diet excludes all “flesh” food, but includes egg and dairy products.

• Vegan diet excludes all “flesh” foods and animal-derived products. • Benefits of vegetarian and vegan diets include reducing the risk of

chronic disease through lower intakes of saturated fat and cholesterol, and higher intakes of fruits, vegetables, whole grains, nuts, soy, fiber and phytochemicals

Low Fat • Emphasizes vegetables, fruits, starches (bread/crackers, pasta, whole

grains, starchy vegetables), lean protein and low-fat dairy • Defined as total fat intake <30% and saturated fat intake <10%.

Low Carbohydrate

• Includes foods higher in protein (meat, poultry, fish, shellfish, eggs, cheese, nuts and seeds), fat (oils, butter, olives and avocado) and vegetables low in carbohydrate (salad greens, cucumber, broccoli and summer squash).

• Avoid sugar-containing foods and grains (e.g., pasta, rice, bread) • No consistent definition of low carbohydrate: range from very low (21

g/day to 70 g/day of carbohydrate) to moderate (30% to 40% of calories from carbohydrate)

DASH

• Emphasizes fruits, vegetables, low-fat dairy, whole grain, poultry, fish and nuts

• Reduces intake of sodium, saturated fat, red meat, sweets and sugar-containing beverages


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Quality and Quantity of Macronutrients There is no ideal percentage of calories from carbohydrate, protein and fat for all people with

diabetes. Macronutrient distribution should be based on individual preferences, current eating patterns and metabolic goals.4 It has been shown that people with diabetes eat approximately 45% of calories from carbohydrate, 36% to 40% from fat and 16% to 18% from protein.21 Carbohydrate

The amount of carbohydrate eaten is the primary predictor of glycemic response, although evidence is inconclusive for an ideal amount of carbohydrate. Reported studies are of short duration, and have small sample sizes and a low retention rate. For good health, the primary sources of carbohydrate should include fruits, vegetables, whole grain, legumes and low-fat milk. Monitoring carbohydrates through meal-planning intervention (carbohydrate counting and experience-based estimation) is an important strategy for achieving good glucose control. Glycemic Index and Load

Published studies of glycemic index and glycemic load are complex, and it is often difficult to differentiate between the effect of fiber compared with glycemic index or glycemic load on glucose control and other metabolic outcomes. Different definitions of low- and high-glycemic index exist, and the glycemic response to a particular food can vary among people and be affected by the overall mixture of foods.22 However, substituting low-glycemic load foods for higher-glycemic loads may improve glycemic control modestly.4 Fiber

Fiber intake goals for the general population are 14 g/1,000 calories, or about 25 g/day for adult women and 38 g/day for adult men.23 Those with diabetes should be encouraged to consume at least the same amount of fiber and whole grains recommended for the general population. This can be accomplished by choosing a variety of fiber-containing food, such as legumes, fiber-rich cereal (>5 g/serving), fruits, vegetables and whole grain products. Systematic reviews have found limited evidence that fiber significantly improves glucose control.20 To show a modest lowering of preprandial glucose or A1C (a decrease of 0.2% to 0.3%), fiber intakes greater than 50 g/day must be consumed, which is unrealistic for the majority of the population.24 Resistant Starch and Fructan

Resistant starch is a starch enclosed within intact cell structures. It is found in some legumes, raw potato and amylose modified by plant breeding. It is thought to decrease postprandial glycemia, prevent hypoglycemia and generally reduce hyperglycemia. Fructans are indigestible fiber. Fructan is added to processed foods in the form of chicory root.

There are no long-term studies in those with diabetes to show benefit from the use of resistant starch or fructan.25 Sucrose

Research studies have shown that substituting sucrose for starch (up to 35% of calories) does not affect glucose or lipid levels.5 Foods containing sucrose are generally high in calories with low-nutrient density; therefore, substituting isocaloric amounts of other carbohydrates for sucrose is recommended. Eating carbohydrates that are more nutrient dense to promote an overall healthful eating pattern should be the goal.4


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Fructose Fructose that occurs naturally in foods, such as fruit, may provide more benefit with glucose

control when compared with isocaloric amounts of sucrose and starch — if not consumed in excessive amounts.26 Fructose in sweetened beverages (containing high-fructose corn syrup) should be limited, or preferably avoided, to reduce risk of weight gain and cardiometabolic risk. It has been reported that approximately 33% of dietary fructose comes from fruits, vegetables and other natural sources in the diet; approximately 67% comes from food and beverages to which fructose has been added.27 Certainly, the amount of fruit recommended per meal should be individualized based on preferences and glucose patterns; a good general recommendation would be to limit to no more than 2 servings of fruit (30 g CHO)/meal.

Sweeteners

Nonnutritive sweeteners and alcohol sugars have been studied by the FDA, and approved for safety and consumption by the general public, including people with diabetes. They have the potential to reduce calories and carbohydrate, but only if they substituted for caloric sweeteners (e.g., sucrose and fructose). Systematic reviews have found little evidence that nonnutritive sweeteners and alcohol sugars lead to reductions in body weight.28

Protein

The Dietary Reference Intake range for protein is 10% to 35% of energy intake, with 15% to 19% being the average adult intake in the U.S. The Recommended Dietary Allowance for good quality protein is 0.8 g/kg body weight (approximately 10% of calories). For patients with diabetes who have normal renal function, there is insufficient evidence to recommend an optimal protein intake for glycemic control or to improve cardiovascular disease risk. For those with diabetic kidney disease, protein should not be lowered from usual intake because it does not affect glucose control or a decline in GFR.4

Protein does not increase plasma glucose levels. Many of us were taught that 50% to 60% of protein is converted to glucose. Current thinking suggests this percentage of protein does go through the process of gluconeogenesis, but does not enter into circulation.29 It is speculated that the glucose produced is stored in the liver as glycogen; when glycogen breaks down to glucose it is unknown if the original source of glucose was carbohydrate or protein. Protein is just as potent a stimulant of acute insulin release as is carbohydrate.4 In the ADA’s 2008 nutrition recommendations, it states: “Ingested protein can increase insulin response without increasing plasma glucose concentrations. Therefore, protein should not be used to treat acute or prevent nighttime hypoglycemia.”4

Fat

The primary goal for patients with diabetes is to improve the quality of fat to improve metabolic outcomes and reduce the risk of cardiovascular disease. Because of insufficient data, there is no ideal recommendation for fat intake; however, the Institute of Medicine defines an acceptable range for total fat intake as 20% to 35% of the total diet.30 A monounsaturated fatty acid-rich eating pattern may also benefit glucose control and reduce cardiovascular disease risk in those with diabetes. Consumption of omega-3 fatty acids from fish has been shown to reduce cardiovascular disease. Also, eating more fish (especially fatty fish), two or more times per week, is recommended for people with diabetes. The amount of saturated and trans fats, and dietary cholesterol recommended for people with diabetes is the same as the general public.4


39

The Dietary Guidelines for Americans recommendations include:23 • Saturated fat <10% of total calories

• Trans fat should be minimized or eliminated • Cholesterol intake <300 mg/dL

Plant Stanols and Sterols

For those with diabetes who have high lipid levels, plant stanols and sterols may reduce total and LDL cholesterol modestly. Evidence-based studies conclude that 1.6 g/day to 3 g/day is recommended (AND Evidence Analysis Library). Foods and beverages that contain plant stanols and sterols include spreads, dairy products, grain and bread products, and yogurt.31

Sodium

Those with diabetes are cautioned against excessive sodium intake, as is the general public. The recommendation for the general public is to reduce sodium to less than 2,300 mg/day. Sodium poses greater health risks to people with hypertension. Excess sodium ingestion may increase the severity of hypertension once it has developed in certain salt-sensitive patients. A lower intake should be individualized for those with diabetes and hypertension.4 There is a lot of debate by various healthcare groups about ideal sodium intake; however, there is agreement that the current average intake of 3,400 mg/day (excluding table salt) is too high and should be reduced.

Alcohol

The same precautions regarding alcohol use in the general public also apply to those with diabetes. An additional concern includes preventing hypoglycemia for the person with diabetes. If used, alcohol should be consumed in moderate amounts and with food — not more than 1 drink/day for adult women and 2 drinks/day for adult men. The type of alcoholic beverage doesn’t make a difference on blood glucose levels, if consumed in equivalent amounts. Patients consuming alcohol should be instructed that 1 oz of alcohol is contained in a 1.5 oz shot of distilled liquor, a 5 oz glass of wine, or a 12 oz glass of beer (see Appendix No. 2 for a table of alcoholic beverages and their nutrient composition).

Alcohol use can impair judgment, and an intoxicated person may forget to monitor blood glucose, eat meals according to schedule or administer medications at the proper time. Also, alcohol contributes calories as well as carbohydrates, and can interfere with glucose control. Large amounts of alcohol can exacerbate the symptoms of hypoglycemia or low blood glucose. In people treated with insulin, alcohol can predispose one to hypoglycemia, and blood glucose levels can fall to below fasting levels several hours after ingestion.

To reduce risk of hypoglycemia, alcohol should always be consumed with food. Advise those with the following conditions to avoid alcohol: 4

• History of alcohol abuse • Liver disease • Advanced neuropathy • High triglyceride levels • Pancreatitis • Pregnancy


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Vitamins and Minerals Evidence has shown that there is no clear benefit from vitamin and mineral supplementation in

those with diabetes unless vitamin and mineral deficiencies are identified. Patients such as the elderly, pregnant or lactating women, and strict vegetarians may benefit from multiple vitamin/mineral supplementation.

Antioxidants (such as vitamins E and C, and carotene) are not advised routinely because of long-term safety issues and uncertain efficacy — high dosages of antioxidants may lead to health problems, including diarrhea, bleeding and toxic reactions.32 Benefits from chromium, magnesium or vitamin D supplementation to improve glycemic control have not been demonstrated, and cannot be recommended.4

Review Questions 1. What specific strategies produce the most beneficial effects in overweight/obese

patients with type 2 diabetes? 2. What are the primary nutritional recommendations for carbohydrate, protein and fat? 3. What are the specific recommendations regarding use of simple sugars?

Answer 1: • Modest weight loss (7% to 8.5% of body weight) • Regular physical activity • Frequent contact with an RD

Answer 2: • Carbohydrate: focus on the total amount rather than type of carbohydrate; include

carbohydrate food sources from whole grains, legumes, fruits, vegetables and low-fat milk; and monitor carbohydrate amounts to achieve improved glucose levels.

• Protein: no optimal protein intake for patients with diabetes; no lower than usual protein intake (15% to 19% of intake) for those with diabetes kidney disease.

• Fat: focus on quality of fat to improve metabolic outcomes and reduce cardiovascular risk; limit trans fat, reduce saturated fat to less than 10% of calories and decrease dietary cholesterol <300 mg/day.

Answer 3:

• Substitute for other carbohydrates in the meal (fructose or starch) rather than just adding foods with simple sugar as an “extra.” It’s also important to consider nutritional value and extra caloric contribution in addition to the amount of carbohydrate. Often there are extra calories from fat in candy and desserts, in addition to simple sugar, and these choices generally contain minimal nutrition (usually calories from simple carbohydrate and fat, and no vitamins, minerals or fiber).


41

References 1. American Diabetes Association, Bantle JP, Wylie-Rosett J, et al. Nutrition recommendations and

interventions for diabetes: a position statement of the American Diabetes Association. Diabetes Care. 2008;31(Suppl 1):S61-S78.

2. Pastors JG, Warshaw H, Daly A, Franz M, Kulkarni K. The evidence for the effectiveness of medical nutrition therapy in diabetes management. Diabetes Care. 2002;25(3):608-613.

3. American Diabetes Association. Standards of medical care for patients with diabetes. Diabetes Care. 1994;17(6):616-623.

4. Evert AB, Boucher JL, Cypress M, et al. Nutrition therapy recommendations for the management of adults with diabetes. Diabetes Care. 2014;37(Suppl 1):S120-S143.

5. Franz MJ, Powers MA, Leontos C, et al. The evidence for medical nutrition therapy for type 1 and type 2 diabetes in adults. J Am Diet Assoc. 2010;110(12):1852-1889.

6. Monk A, Barry B, McClain K, et al. Practice guidelines for medical nutrition therapy provided by dietitians for persons with non-insulin-dependent diabetes. International Diabetes Center. J Am Diet Assoc. 1995;95(9):999-1006.

7. Kulkarni K, Castle G, Gregory R, et al. Nutrition Practice Guidelines for Type 1 Diabetes Mellitus positively affect dietitian practices and patient outcomes. The Diabetes Care and Education Dietetic Practice Group. J Am Diet Assoc. 1998;98(1):62-70.

8. Ali MK, Bullard KM, Saaddine JB, et al. Achievement of goals in U.S. diabetes care, 1999-2010. N Engl J Med. 2013;368(17):1613-1624.

9. Wolf AM, Conaway MR, Crowther JQ, et al. Translating lifestyle intervention to practice in obese patients with type 2 diabetes: Improving control with activity and nutrition (ICAN) study. Diabetes Care. 2004;27(7):1570-1576.

10. Krebs JD, Elley CR, Parry-Strong A, et al. The Diabetes Excess Weight Loss (DEWL) Trial: a randomised controlled trial of high-protein versus high-carbohydrate diets over 2 years in type 2 diabetes. Diabetologia. 2012;55(4):904-914.

11. Pi-Sunyer X, Blackburn G, Brancati FL, et al. Reduction in weight and cardiovascular disease risk factors in individuals with type 2 diabetes: one-year results of the look AHEAD trial. Diabetes Care. 2007;30(6):1374-1383.

12. Look AHEAD Research Group, Wing RR, Bolin P, et al. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med. 2013;369(2):145-154.

13. Esposito K, Mairorino MI, Ciotola M, et al. Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy in patients with newly diagnosed type 2 diabetes: a randomized trial. Ann Intern Med. 2009;151(5):306-314.

14. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346(6):393-403.

15. Mayer-Davis EJ, D’Antonio AM, Smith SM, et al. Pounds off with empowerment (POWER): a clinical trial of weight management strategies for black and white adults with diabetes who live in medically underserved rural communities. Am J Public Health. 2004;94(10):1736-1742.

16. Franz MJ, VanWormer JJ, Crain AL, et al. Weight-loss outcomes: a systematic review and meta-analysis of weight-loss clinical trials with a minimum 1-year follow-up. J Am Diet Assoc. 2007;107(10):1755-1767.

17. Warshaw HS. Nutrition therapy for adults with type 2 diabetes. In: Franz MJ, Evert AB, eds. American Diabetes Association Guide to Nutrition Therapy in Diabetes. Alexandria, VA: American Diabetes Association; 2012:117-142.

18. Raynor HA, Jeffery RW, Ruggiero AM, et al. Weight loss strategies associated with BMI in overweight adults with type 2 diabetes at entry into the Look AHEAD (Action for Health in Diabetes) trial. Diabetes Care. 2008;31(7):1299-1304.

19. Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA. 2004;292(14):1724-1737.


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20. Wheeler ML, Dunbar SA, Jaacks LM, et al. Macronutrients, food groups, and eating patterns in the management of diabetes: a systematic review of the literature, 2010. Diabetes Care. 2012;35(2):434-445.

21. Oza-Frank R, Cheng YJ, Narayan KM, Gregg EW. Trends in nutrient intake among adults with diabetes in the United States: 1988-2004. J Am Diet Assoc. 2009;109(7):1173-1178.

22. Franz MJ. Diabetes mellitus nutrition therapy: beyond the glycemic index. Arch Intern Med. 2012;172(21):1660-1661.

23. Dietary Guidelines. U.S. Department of Health and Human Services and U.S. Department of Agriculture Web site. http://www.health.gov/dietaryguidelines. Accessed February 15, 2015.

24. Post RE, Mainous AG 3rd, King DE, Simpson KN. Dietary fiber for the treatment of type 2 diabetes mellitus: a meta-analysis. J Am Board Fam Med. 2012;25(1):16-23.

25. Bonsu NK, Johnson CS, McLeod KM. Can dietary fructans lower serum glucose? J Diabetes. 2011;3(1):58-66.

26. Sievenpiper JL, Carleton AJ, Chatha S, et al. Heterogeneous effects of fructose on blood lipids in individuals with type 2 diabetes: systematic review and meta-analysis of experimental trials in humans. Diabetes Care. 2009;32(10):1930-1937.

27. Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr. 1993;58(5 Suppl):737S-747S.

28. Wiebe N, Padwal R, Field C, et al. A systematic review on the effect of sweeteners on glycemic response and clinically relevant outcomes. BMC Med. 2011;9:123.

29. Franz MJ. Macronutrients and nutrition therapy for diabetes. In: Franz MJ, Evert AB, eds. American Diabetes Association Guide to Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association; 2012:19-40.

30. Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. Washington, D.C.: National Academies Press; 2002.

31. Disorders of lipid metabolism (DLM) and plant stanols and sterols. Academy of Nutrition and Dietetics Evidence Analysis Library Web site. http://andevidencelibrary.com/template.cfm?key=2986&auth=1. Accessed February 15, 2015.

32. Institute of Medicine. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium and Carotenoids. Washington, D.C.: National Academies Press; 2000.


43

Chapter Four: Key Differences in Nutritional

Management of Diabetes

ecause the characteristics of type 1 and type 2 diabetes are varied, there are significant differences in the nutritional recommendations for each type of diabetes.

Type 1 Diabetes

Approximately 1.89 per 1,000 children and youth have diabetes; more than 80% is type 1 diabetes, primarily in non-Hispanic white youth. Type 1 diabetes has been increasing 3% to 4% per year in youth, and even more in children younger than age 5. The incidence of type 1 diabetes decreases after the age of 20.1

Because children have their own agendas about food, involving fads, peer pressure, immature tastes and psychological issues, the challenge to the diabetes educator is great. It is important for children to have an interest in nutrition and meal planning to establish lifelong healthy eating habits, and doing so involves a great degree of creativity and patience. There is no “good” age to make eating habit changes, and there will always be obstacles to change.

Insulin Regimen

Insulin therapy should be integrated into food and exercise patterns. Those with type 1 diabetes who take bolus supplements of rapid- or short-acting insulin before meals or through an insulin pump should adjust meal insulin based on the carbohydrate content of meals. The Dose Adjustment for Normal Eating Study demonstrated that people can learn how to use glucose testing to match insulin to carbohydrate intake. In the study, improvements were seen in A1C levels without significant hypoglycemia, and there were improvements in quality of life, satisfaction with treatment and overall psychological well-being.2

For those with type 1 diabetes on fixed daily insulin doses, consistency of carbohydrate with respect to time and amount of food is very important. The more consistent the physical activity and eating — both timing of meals and snacks, and amounts of food eaten — the easier it is to manage and control blood glucose levels. In children with type 1 diabetes, consistency in amounts of food can be hard to maintain because of variability in daily energy intake.1

B

Key Differences in Nutritional Management of Diabetes

44

Nutrition Therapy for Type 1 Diabetes1

Food intake should be matched with the anticipated rise and fall of insulin levels. Normally, blood

glucose level rises in response to food eaten at meals. The body responds by releasing insulin into the bloodstream at meals to allow glucose to enter the cells and lower the blood glucose levels.

For planned exercise, insulin doses can be adjusted. For unplanned exercise, extra carbohydrate may be needed.

With intensive insulin therapy, there is more flexibility with the decision about when, what and how much to eat for snacks and/or meals, and exercise. This flexibility in eating and exercise must be matched with increased responsibility in self-management, particularly with SMBG and insulin dose adjustment, as keeping a record of blood glucose values makes it easier to adjust insulin doses.

Energy Requirements

Patients with type 1 diabetes need sufficient calories to reach and maintain reasonable weight as adults, and normal growth and development rates in children. Targeting the appropriate energy requirement can be challenging, as energy needs may vary tremendously, especially with children during growth spurts or in adults whose activity level varies. Some suggest that external regulation of intake by healthcare professionals, rather than internal regulation via appetite, is a major reason for poor diet compliance in children.

Generally, the child’s usual food intake is a better measure of energy need than theoretical estimates. This can be obtained by a thorough nutrition history and/or true food intake recorded by the child/parent when the child is allowed to eat to appetite. Adequate energy intake for normal growth and development is of primary importance; insulin should be adjusted to allow for appropriate nutritional intake.

Combining Nutrition and Insulin Therapy

Management of carbohydrate intake is one of the most important strategies in achieving glucose control. For those with type 1 diabetes and those who require insulin, it is important to have a thorough knowledge of the carbohydrate content of food and its effects on blood glucose levels and insulin requirements. Monitoring the amount of carbohydrate and adjusting meal insulin will assist in

Integrate insulin w/eating & exercise habits

Synchronizefood

w/insulin

Eatconsistently,adjust insulin

Integrateinsulin into

lifestyle

Adjust insulinto compensate

for lifestyle

Conventionaltherapy

Intensivetherapy


45

regulating postprandial glucose levels. Using a meal-planning approach, such as advanced carbohydrate counting (using insulin:carbohydrate ratios and blood glucose correction factors), with type 1 diabetes can result in improved glycemic control. Glucose variability occurs frequently in type 1 diabetes. A flexible nutrition therapy intervention with self-adjustment of insulin will help reverse postprandial hyperglycemia and reduce glycemic variability.3

In the Diabetes Control and Complications Trial, those who chose a lower carbohydrate intake (approximately 37%) and higher fat intakes (approximately 45%) had higher A1C values at year 5 compared to those who chose a higher carbohydrate intake (approximately 56%) (7.5% vs. 7%, respectively).4 The authors note that high-fat meals have been shown to interfere with insulin signaling, which can increase insulin resistance, and that lower-fat intakes can improve insulin sensitivity in type 1 diabetes. These results suggest that those who choose a lower carbohydrate intake should ideally use monounsaturated fats as the fat of choice and pay particular attention to total calorie intake.5

Type 2 Diabetes

A primary goal for those diagnosed early in the disease process with type 2 diabetes is lifestyle intervention, including nutrition, exercise, behavior change and ongoing support. Lifestyle intervention will assist in achieving modest weight loss of 5% to 7% that can improve metabolic outcomes (glucose, lipids and blood pressure).

Evidence suggests that nutrition intervention, especially lifestyle modification and promotion of modest weight loss, is most effective early on in the disease process (ideally, should be done with those who are prediabetic and before diagnosis of type 2 diabetes). Improved metabolic outcomes are seen mostly between six and 12 weeks after changes are made.

Because type 2 diabetes is a progressive disease, nutrition therapy is important at all stages of the disease process. As type 2 diabetes progresses, the addition of medication, and eventually insulin, will be necessary. When insulin therapy is initiated — especially fixed doses of insulin — consistency of carbohydrate content and timing of meals becomes more important. With intensive insulin therapy (basal-bolus regimen), a more flexible food intake and lifestyle is possible. SMBG can be used to determine whether adjustments in foods and meals is sufficient to achieve blood glucose goals or if medication(s) needs to be combined with nutrition therapy.

An increase in physical activity can assist in improving glucose control, decreasing insulin resistance, and reducing cardiovascular risk. As previously discussed, at least 150 minutes/week of moderate-intensity aerobic physical activity is recommended, combined with resistance training to increase muscle strength.

A variety of eating patterns can be successful for managing type 2 diabetes, including the Mediterranean-style eating pattern, vegetarian and vegan diets, a low-fat diet, a low-carbohydrate diet and the DASH diet. Personal preferences and metabolic goals should be considered when making a decision about the most appropriate eating pattern, with emphasis on individualization.6

Key Differences in Nutritional Management of Diabetes

46

Nutrition Therapy for Type 2 Diabetes7

Clinical trials in type 2 diabetes have compared low carbohydrate/high total fat and saturated fat

intakes with high carbohydrates/lower total fat and saturated fat intakes. Both high- and low-carbohydrate diets lead to similar improvements in glycemic control (A1C) and body weight — total caloric intake appears to be a more important factor than nutrient distribution. High-carbohydrate/low-fat diets tend to have more favorable effects on total and LDL cholesterol, and low-carbohydrate/high-fat diets have beneficial effects on triglycerides and HDL cholesterol. Based on the results of these clinical trials, the best recommendation may be an eating pattern with moderate amounts of carbohydrate (approximately 45% carbohydrate) that includes fruits, vegetables, whole grains and low-fat dairy foods in appropriate amounts and portion sizes.3

Monitor blood glucose,

add meds if needed

Increase physical activity

Space meals

Modify fat intake

Improvefood choices

Restrict kcal for moderateweight loss

Learn new behaviors

Glucose Control


47

Review Questions 1. How do the priorities with medical nutrition therapy differ in those with type 1 and type 2

diabetes? 2. What are the primary differences in meal-planning strategies between type 1 and type 2

diabetes? 3. What is the current recommendation for carbohydrate intake in those with type 2 diabetes?

Answer 1: • Type 1 diabetes: glycemic control is achieved by integrating insulin therapy with

carbohydrate intake and physical activity. • Type 2 diabetes: improved metabolic outcomes (glucose, lipids and blood pressure) are

achieved using lifestyle modification to decrease caloric intake and increase physical activity.

Answer 2: • Type 1 diabetes: Matching carbohydrate intake and insulin using advanced

carbohydrate counting (carbohydrate: insulin ration and blood glucose correction factor) to achieve optimal glycemic control

• Type 2 diabetes: Lifestyle modification focusing on nutrition intervention with calorie and fat restriction, physical activity, behavior modification and group support to achieve modest weight loss of 5% to 7%

Answer 3: • Moderate carbohydrate (45%) with attention to lower-energy intake and emphasis on

food choices from vegetables, fruits, whole grains and low-fat dairy.

References 1. Kaufman FR, ed. Medical Management of Type 1 Diabetes. 6th ed. Alexandria, VA: American Diabetes

Association; 2012.

2. DAFNE Study Group. Training in flexible, intensive insulin management to enable dietary freedom in people with type 1 diabetes: dose adjustment for normal eating (DAFNE) randomised controlled trial. BMJ. 2002;325(7367):746.

3. American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Alexandria, VA: American Diabetes Association; 2012.

4. Delahanty LM, Nathan DM, Lachin JM, et al. Association of diet with glycated hemoglobin during intensive treatment of type 1 diabetes in the Diabetes Control and Complications Trial. Am J Clin Nutr. 2009;89(2):518-524.

5. Strychar I, Cohn JS, Renier G, et al. Effects of a diet higher in carbohydrate/lower in fat versus lower in carbohydrate/higher in monounsaturated fat on postmeal triglyceride concentrations and other cardiovascular risk factors in type 1 diabetes. Diabetes Care. 2009;32(9):1597-1599.


7. Burant CF, ed. Medical Management of Type 2 Diabetes. 7th ed. Alexandria, VA: American Diabetes Association; 2012.


49

Chapter Five: Specific Nutrient Guidelines

ach of the macronutrients — carbohydrate, protein and fat — is important in diabetes nutritional management. It is crucial to understand specifically what each macronutrient is, as well as its metabolism and rationale for recommended intake.

Carbohydrate

Carbohydrate can be classified as digestible or indigestible carbohydrate. Digestible carbohydrate is subdivided further into complex and simple carbohydrate; indigestible carbohydrate is also called dietary fiber.

Simple carbohydrate refers to monosaccharides, disaccharides and oligosaccharides. Monosaccharides, the simplest form of carbohydrate, serve as building blocks of complex carbohydrates. The three most important monosaccharides are glucose, fructose and galactose.

Disaccharides are simple sugars made by the linkage of two monosaccharides. Examples are: • Sucrose, which is glucose + fructose • Maltose, which is glucose + glucose • Lactose, which is glucose + galactose (lactose is the sugar found in milk)

Oligosaccharides contain between three and 10 monosaccharide units. The oligosaccharides

stachyose and raffinose occur in small amounts in legumes, such as kidney beans and lentils. Metabolically, bacteria in the lower small intestine and colon act on stachyose and raffinose, causing increased flatus production in certain people. The digestion of complex carbohydrates begins in the mouth with hydrolysis by salivary amylase. Very little digestion takes place in the stomach, with the bulk of carbohydrate digested by pancreatic enzymes in the upper intestine. Complex carbohydrate is reduced to simple carbohydrate and absorbed across the plasma membrane into the intestinal mucosa and transported to the liver.

Complex carbohydrate (also known as polysaccharide or starch) refers to carbohydrates comprised of a large number of monosaccharide molecules. Polysaccharides or starch consist of amylose (straight chains) and amylopectin (branched chains), both of which yield glucose on digestion. Starch is the major constituent of cereals, with wheat, rice and corn being used in the largest quantities. Potatoes and legumes, including a variety of beans and peas, are also rich in starch.

All carbohydrate is metabolized into glucose eventually. It is used for immediate energy needs, stored as glycogen in the liver and muscle for future energy needs, or converted to fat and stored as adipose tissue. The digestion and metabolism of carbohydrate is affected by many factors, including the intake of protein, fat, fiber, fluid and sodium, as well as hormonal and neurological factors.

Because all digestible carbohydrate is metabolized to glucose, it becomes the primary nutrient of consideration in diabetes and its effect on postprandial glucose levels. Although total amount of carbohydrate is more important than source of carbohydrate on glycemic control, debate remains about what amount of carbohydrate is best to facilitate the best glycemic control. As has been stated, a carbohydrate intake similar to the general public, which is considered a modest amount of carbohydrate

E

Specific Nutrient Guidelines

50

(43% to 45%), is easiest for patients with diabetes to achieve and does not affect glucose control negatively.

Sucrose

Scientific evidence does not justify the long-held belief that sugars should be restricted in the diets of those with diabetes. The belief was that sugars increase blood glucose by virtue of the fact that they are digested and absorbed more rapidly than starches. The AND Evidence Analysis Library has reviewed 15 studies in which sucrose was substituted for complex carbohydrates with no adverse effect on glycemia. The AND concluded:1

If persons with diabetes choose to eat foods containing sucrose, the sucrose-containing food can be substituted for other carbohydrate foods. Sucrose intakes of 10% to 35% of total energy do not have a negative effect on glycemic or lipid level responses when substituted for isocaloric amounts of starch.

Knowing the total amount of carbohydrate in foods, including sugars, can assist people with diabetes to make appropriate food choices they enjoy while promoting glucose control. The American Diabetes Association nutrition recommendations concluded:2

Sucrose can be substituted for other carbohydrate sources in the meal plan or, if added to the meal plan, adequately covered with insulin or other glucose-lowering medications. Intake of other nutrients ingested with sucrose, such as fat, need to be considered to avoid excess energy intake.

Sucrose and sucrose-containing foods must be substituted for other carbohydrates and not just added to the meal plan. It is also important to remember that many sucrose-containing foods (desserts such as pie, cake and cookies) also contain high percentages of fat and provide a significant contribution to the total caloric content of these types of foods (fat calories must be considered/substituted). The other option for those with diabetes on insulin and/or for whom weight control is not an issue, is to cover the intake of sucrose and sucrose-containing foods with extra insulin.

Fructose

Fructose is a monosaccharide found naturally in fruits, vegetables and honey, and provides 4 kcal/g, just like all other carbohydrates. It is also a component of added sugars found in beverages and processed snacks (namely, high-fructose corn syrup). High-fructose corn syrup, commonly used by the beverage industry for sweetening, is composed of either 42% or 55% fructose, and is similar in composition to sucrose. It does not differ from sucrose in its effects on glucose, insulin and triglycerides as long as intake doesn’t exceed 12% of total caloric intake.3 However, because it is primarily in beverages and sweet snacks, it has the potential to promote weight gain. Large amounts of fructose, >100 g/day, may have adverse effects on LDL cholesterol and triglycerides.4 The ADA nutrition recommendations state that fructose should be consumed as “free fructose” (naturally occurring in foods). It is not recommended as a sweetening agent, particularly in sugar-sweetened beverages, to reduce risk of weight gain and cardiometabolic risk.2,5


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Sugar Alcohols and Nonnutritive Sweeteners Sugar alcohols (erythritol, isomalt, lactitol, maltitol, sorbitol, mannitol, xylitol, tagatose and starch

hydrolysates) have the potential to reduce overall calorie/carbohydrate intake if substituted for other sugars that contain calories, such as sucrose and fructose. They produce lower postprandial glucose responses, primarily because they contain fewer calories (about 2 kcal/g) than other nutritive sweeteners. They are often less sweet than sugar but give a sweet taste and add bulk to food. Excessive amounts of sugar alcohols may result in gastrointestinal discomfort or have a laxative effect, especially in children.2 The availability of nonnutritive sweeteners (sugar substitutes) in American food dates back more than 100 years to the discovery of saccharin.

There are five FDA-approved low-calorie sweeteners on the market: saccharin, aspartame, acesulfame-K, sucralose and neotame. Stevia, another nonnutritive sweetener, is an extract of an herb with intense sweetness that has been approved as generally recognized as safe.6,7

Saccharin Saccharin is a petroleum derivative and the oldest sugar substitute. It is not metabolized by the

body and is excreted unchanged by the kidneys. Saccharin’s relative sweetness is 300 times that of sucrose, and it is quite stable when exposed to heat or solution. Saccharin can possess a bitter aftertaste at high concentrations.

In 1977, the FDA proposed a ban on saccharin in light of research that implicated saccharin as a weak carcinogen in animals. Public opposition to the ban led Congress to pass the Saccharin Study and Labeling Act that permitted continued use of the sweetener, pending further safety studies.

To date, the saccharin moratorium has been extended seven times, and saccharin is available in the U.S. on an interim basis as a food additive. Most researchers agree that any carcinogenic effects are weak. Consumption of saccharin has dropped dramatically since the approval of aspartame in 1981.

Aspartame

Aspartame, best known as NutraSweet, is a protein-based nonnutritive sweetener. It is the dipeptide of L-aspartic acid and L-phenylalanine methyl ester. Due to its protein structure, it is metabolized in the intestine to aspartate, phenylalanine and methanol. Aspartame is 180 to 220 times sweeter than sucrose. In 1981, aspartame was approved by the FDA as a tabletop sweetener and for several dry applications. In 1983, aspartame was approved for carbonated beverages, which accounts for the majority of its consumption, and in 1996 it was approved by the FDA as a general use sweetner.8

One drawback to aspartame is its lack of stability when exposed to heat for prolonged periods. In its present formulation, aspartame cannot withstand baking. The NutraSweet Company has developed a method to encapsulate aspartame to protect it from heat exposure until near the end of the cooking or baking process. This product is available to the food industry only for incorporation into prepared products.

Acesulfame-K

Acesulfame-K is the potassium salt of a cyclic sulfonamide. Discovered in 1967, ace-K is 200 times sweeter than sucrose and classified as a nonnutritive sweetener. Like saccharin, it is not metabolized and is excreted unchanged by the kidneys. Sunette is the trade name for ace-K marketed as a sweetening ingredient; two tabletop sweeteners with ace-K are Sweet One and SwissSweet. In July 1998, it was approved for use in liquid beverages. In 2003, the FDA approved ace-K for use in any food or beverage, except meat or poultry.9


52

Ace-K’s chief asset is its long-term stability. It can withstand heat without alteration in sweetness and may be blended with other sweeteners. This blending of two or more sugar substitutes can accentuate their individual sweetnesses, yielding a much sweeter food than if the same amount of a single sweetener were used. This synergy is important to food manufacturers that blend artificial sweeteners in smaller amounts to achieve a desired degree of sweetness. A negative aspect of ace-K is its bitter aftertaste at high concentrations.

Sucralose

Sucralose is a trichloro derivative of sucrose produced by selective chlorination of hydroxyl groups. In April 1998, the FDA approved it for use in 15 food categories, and it is marketed under the brand name Splenda. Sucralose is 600 times as sweet as sucrose, and has excellent stability, solubility in solution and the ability to be used in baking applications.

Neotame

Neotame is approved as a general-purpose sweetener and is 8,000 times sweeter than sucrose. It is marketed as a sweetener with a clean sweet taste without bitter metallic or off flavors. It is partially absorbed in the small intestine, rapidly metabolized by esterases, and excreted in urine and feces. The FDA reports that neotame is structurally similar to aspartame, and it is approved as a general use sweetener.

Stevia

Stevia is derived from a shrub in the chrysanthemum family. It has been sold since the late 1990s as a dietary supplement. A highly purified form of Stevia, rebaudioside A, has entered the marketplace in the form of several new, nonnutritive sweeteners: PureVia, Truvia and Stevia in the Raw. In 2008, the Joint Food and Agriculture Organization/World Health Organization Expert Committee on Additives reviewed the research on highly purified Stevia and approved it as meeting specific purity criteria and safe for intended use as a general purpose sweetener.10

Use of Nonnutritive Sweeteners

It should not be assumed that a non-caloric sweetener is necessary for patients with diabetes. They were developed originally because of earlier recommendations to avoid simple sugars. The current recommendations are to be more flexible with the amount of sugar allowed in the diet, based on research and widespread use of self-monitoring of blood glucose. In fact, the use of added sweeteners or “sweets” may serve to stimulate the desire for sugar. The desire for sugar may diminish if an attempt is made to enhance other flavors in foods, and if sugar is not considered an absolutely forbidden food.

Although nonnutritive sweeteners do not affect glycemic responses, some food products that contain nonnutritive sweeteners contain calories and carbohydrate from other sources that need to be considered. There is also limited evidence to suggest that use of nonnutritive sweeteners leads to reductions in body weight.7


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Fiber Dietary fiber refers to the components of food (plant polysaccharides and lignin) that are resistant

to hydrolysis by the digestive enzymes of man. These components have complex chemical structures. Dietary fiber is found in plant foods, cereal grains, legumes, and fruits and vegetables.

Other foods, not usually thought of as containing fiber, may be sources because of fiber additives; for example, some ice cream may contain guar gum as a stabilizer, and alginates may be used in pudding, ice cream and beer. The amounts, however, are usually minimal.

One of the functions of dietary fiber is water retention (its hydrophilic property); therefore, dietary fiber is often referred to by its solubility. The water-insoluble fibers, such as cellulose, lignin and most hemicelluloses, are poorly metabolized and have an effect on increasing stool volume. They increase the rate of gastric emptying and decrease intestinal transit time.

A lack of insoluble fiber has been associated with several gastrointestinal disorders, including colon cancer, constipation and diverticular disease. These disorders may be related to the effect fiber has as a bulking agent and to its effect on decreasing transit times throughout the gastrointestinal tract. Examples of foods that contain a large portion of water-insoluble fiber include wheat, in the form of flour, cereals and bran.

In contrast, water-soluble fibers, such as pectins, gums, storage polysaccharides and a few hemicelluloses, ferment in the colon to gases and short-chain fatty acids, and contribute little to fecal bulk. They contribute to colon health as a food source for “good” bacteria found in the colon. Soluble fibers prolong stomach-emptying time so glucose is released and absorbed more slowly. Examples of foods containing higher percentages of the water-soluble fibers include fruits (especially citrus and apples), oats, barley and legumes.

A report by the AND Evidence Analysis Library that reviewed 15 clinical trials concluded:1

While diets containing larger amounts of fiber (44 g/day to 50 g/day) improved glucose levels (preprandial glucose and A1C) in persons with diabetes, usual fiber intakes (up to 24 g/day) have not shown any glycemic improvements. Fiber in amounts of 25 g/day to 30 g/day are recommended, with emphasis on soluble fiber sources (7 g/day to 13 g/day), which can have a beneficial effect on lipids.

The ADA recommends that people with diabetes choose a variety of fiber-containing foods because

these foods provide vitamins, minerals and other substances (phenolic compounds, phytoestrogens) for good health. These substances may be important for those at risk for cardiovascular disease.6

Glycemic Index and Glycemic Load

The glucose response to carbohydrate foods has been studied, and a glycemic index was developed to classify more than 600 foods based on potential to increase blood glucose.11,12 The formal definition of the glycemic index is the incremental area under the blood glucose curve after the consumption of 50 g of carbohydrate from a test food divided by the area under the blood glucose curve after eating a similar amount of a control food, generally white bread or glucose.13 In general, refined grain products and potatoes have a higher glycemic index, legumes and unprocessed grains have a moderate glycemic index, and nonstarchy fruits and vegetables have a lower glycemic index.

The glycemic load is a calculation of the physiological effects of carbohydrate. It combines the glycemic index and the carbohydrate content of an average serving of a food, meal or daily intake, and is defined as the weighted mean of the dietary glycemic index multiplied by the percentage of total


54

energy from carbohydrate. The glycemic index cannot capture the entire glucose-raising potential of carbohydrate from foods because blood glucose response is influenced by the glycemic index values of a food and the amount of carbohydrate in food. The concept of GL attempts to incorporate both quality and quantity of carbohydrate consumed.14

Glycemic Index vs. Glycemic Load15

Food Serving Size Carbohydrate Glycemic

Index Glycemic

Load

Pizza White rice Potatoes Orange juice White bread Carrots Milk

1 slice 1 cup 1 6 oz 1 slice ½ cup 8 oz

78 g 45 g 37 g 20 g 13 g 8 g

11 g

86 102 102 75

100 131 46

68 46 38 15 13 10 5

It is interesting to note how closely the GL corresponds to the grams of carbohydrate in a serving

of food and not the glycemic index. Substituting low GL foods for higher GL foods may modestly improve glucose levels, with A1C decreases of 0.2% to 0.5%.2

Determining the benefit of using a tool such as the glycemic index or GL is complex because responses to food vary. People generally consume foods as meals with a variety of nutrients in a mixture of foods, making it difficult to pinpoint metabolic benefits of a particular food on metabolic outcomes, such as glucose and lipids. Separating the effect of fiber from the glycemic index or GL of the food or meal is difficult.2,16

Protein The primary function of dietary protein is to provide amino acids required for tissue growth and

maintenance. Dietary proteins serve two major metabolic functions: the carbon skeletons of their amino acids can be oxidized to yield energy, and the carbon and nitrogen atoms may be used to synthesize nitrogen-containing cellular constituents.

Protein and amino acids are not stored by the body. In a 75-kg adult, the amount of protein synthesized daily is approximately 300 g to 400 g. This amount represents a daily turnover of protein that is three times the intake of the average diet. After a normal mixed meal, protein yields amino acids that are used in the synthesis of new proteins or are broken down through the same pathways as glucose to provide energy.

The dietary protein requirement is based on the need for amino acids that are not synthesized by the body. Nine amino acids are essential in the human diet.


55

Amino Acids17 Essential Nonessential

Branched chain Valine (G) Leucine (K) Isoleucine (B)

Aromatic Phenylalanine (B) Tryptophan (B)

Basic Lysine (B) Histidine (B)

Other Threonine (B) Methionine (B)

Alanine Arginine Asparagine Aspartic acid Cysteine Glutamic acid Glutamine Glycine Proline Serine Tyrosine

G = glucogenic; K = ketogenic; B = both (glucogenic and ketogenic). All nonessential amino acids are considered glucogenic.

Since the discovery of insulin, many healthcare providers have advocated a high-protein diet.

Because most amino acids are gluconeogenic, protein was believed to help stabilize blood glucose levels by providing a substrate for glucose production when needed.

For some time, it was thought that about half of ingested protein was converted to glucose; therefore, protein should have one-half the effect of carbohydrate on blood glucose levels. In those with type 2 diabetes, protein intake results in increased insulin and glucagon responses, but only a minimal effect on postprandial glucose. If diabetes is well-controlled, minimal amounts of hepatic glucose are released into the general circulation after the ingestion of protein.18

Studies in type 1 diabetes and protein intake are limited, but it appears that postprandial glucose and increased prandial insulin requirements are affected only if large amounts of protein are consumed.

Evidence does not support the concepts that protein slows absorption of carbohydrate, contributes to a sustained elevation of glucose or is helpful in the treatment of hypoglycemia.18

The average protein intake in the U.S. for all age groups is 15% to 19% of total calories. The current RDA for adults for protein is 0.8 g/kg of body weight (about 10% of energy intake). This translates to about 60 g/day for a 75-kg (165-lb) man and 44 g/day for a 55-kg (121-lb) woman. For those with diabetes and normal renal function, protein intake should be the same as for the general population because of insufficient evidence to suggest that usual protein intake should be modified.2

Fat Fats can be classified chemically into three types: simple, compound and derived. Simple fats

include fatty acids and glycerides; compound fats include phospholipids and lipoproteins; and derived fats include sterols and the fat-soluble vitamins, A, D, E and K.

Chemically, fatty acids are comprised of linear chains of carbon atoms with hydrogen atoms attached. The chain length (i.e., the number of carbons) and the degree of saturation with hydrogen


56

atoms (number of double bonds) are different for each particular fatty acid. Dietary triglycerides are made up of one glycerol and three fatty acids. They comprise 98% to 99% of most natural fats. Most are long-chain triglycerides, containing between 12 and 20 carbon atoms. The number of double bonds between the carbon atoms determines the degree of hydrogen saturation. All animal fats are saturated. Fish and shellfish contain minimal amounts of saturated fats. Animal fats, meats, hydrogenated shortenings, some vegetable oils (palm, coconut and cocoa butter), whole-milk dairy products and commercial baked goods are the major sources of saturated fat in the diet (see Appendix 3 for a listing of the fat content and fatty acid composition of various foods).

Monounsaturated fats are derived predominantly from oleic acid. Major dietary sources include canola oil, olive oil and peanut oil. They are not essential fatty acids and are synthesized endogenously. Linoleic, linolenic and arachidonic acids are polyunsaturated fatty acids that cannot be synthesized by the body, and are essential fatty acids. Of these, linoleic is the most commonly found in food. The major sources of PUFA in the U.S. diet are vegetable oils, shortenings and partially hydrogenated margarines.

Types of Fats in Common Oils19

Fat metabolism can be described most simply by a diagram that shows the metabolism of dietary

fat and cholesterol into chylomicrons, and their breakdown in the liver to free fatty acids, glycerol, cholesterol and phospholipids. These compounds combine with protein to form the various lipoproteins (i.e., very-low-density lipoprotein, LDL and HDL).

The Cell, Nutrients and Energy

32

function and prevent unnecessary inflammation. Presently, Americans and Europeans eat foods with a higher omega-6 PUFA content and not enough omega-3 PUFA, creating an imbalance.2 To improve the ratio, more foods containing omega-3 PUFA need to be eaten, such as fish, canola oil, flaxseed and English walnuts; and omega-6 PUFA foods, such as vegetable oils (corn, sunflower and safflower), should be avoided.

Types of Fats in Common Oils3

A common question is: “What’s the best oil to use?” Take a look at canola oil; it’s only about 5%

saturated. That’s good, because saturated fat raises serum cholesterol. It’s also very high in monounsaturated fats, not that high in polyunsaturated fats and contains about 10% omega-3 fatty acids. Notice that soybean oil also contains some omega-3 fatty acids (about 7%). Flaxseed has the highest amount of omega-3 PUFA of all the oils. Palm kernel and coconut oils, on the other hand, are very high in saturated fat, and tend to raise serum cholesterol.

Increasing oils with omega-3 fatty acids and decreasing the oils high in omega-6 fatty acids will help reduce inflammation. Decreasing inflammation is important in people with inflammatory diseases such as arthritis, lupus and other autoimmune diseases. Inflammation is also at the root of obesity, making it easier to gain weight and harder to lose. In certain diseases (e.g., heart disease), it is preferable to decrease blood clotting to reduce the likelihood of a clot blocking an artery, which can cause a heart attack or stroke. Inflammation of the arteries is implicated in heart disease because it causes plaque to

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Saturated Fat Trans Fat Monounsaturated Fat Polyunsaturated Fat


57

Fat Metabolism Simplified20

Dietary fat intake and lipid metabolism are important considerations in diabetes because coronary

heart disease, stroke, cardiac failure and peripheral artery disease are common complications. Mortality from atherosclerosis is two to three times more common among people with diabetes than those without diabetes, with an expected lifespan of five to seven years. In studies comparing diabetic and non-diabetic populations, serum total cholesterol was higher in the diabetic population.21

Total Fat The primary goal regarding dietary fat in patients with diabetes is to improve the quality of fat in

the diet. The Dietary Guidelines for Americans recommend that saturated fat be limited to less than 10% of the total caloric intake. Intake of trans fat should be minimized, and cholesterol intake should be less than 300 mg/dL. Eating two or more servings per week of fish, which contains omega-3 fatty acids, is recommended.2,22

Cholesterol There are limited long-term, clinically controlled research studies to base a recommendation for

optimal dietary cholesterol intake. One large, prospective cohort study in women with type 2 diabetes found a 37% increase in cardiovascular disease risk for every 200 mg cholesterol/1,000 kcal increase in cholesterol consumption.23

Dietary Fat / Dietary Cholesterol

Intestines

Chylomicrons

LIVER

Very Low-Density Lipoproteins (FLDL)

Intermediate-Density Lipoproteins (IDL)

Low-Density Lipoproteins (LDL)

LDL Receptors in Tissue

(Digested to free fatty acids, glycerol, and phospholipids that combine with protein to form chylomicrons)

(Absorbed into lymph and transported to blood)

(Chlomicrons catabolized to free fatty acids, glycerol, cholesterol, & phospholipids that combine w/protein to form lipoproteins)

(Some catabolized by muscle or adipose tissue for energy)

Bile

Lipoprotein Lipase (LPL)

LIVER High-Density Lipoproteins (HDL)

LPL

Fatty Acids


58

The ADA recommends the same cholesterol guidelines for the general population as for those with diabetes. The Dietary Guidelines for Americans recommend aiming for <300 mg of cholesterol/day.

Saturated Fat

Again, few long-term, clinically controlled research studies have confirmed a relationship among saturated fat, glycemic control and cardiovascular disease risk in people with diabetes. A three-week study that compared a low-saturated fat diet (8% of total calories) to a high-saturated fat intake (17% of total calories) found no significant difference in glycemic control or cardiovascular disease risk measures.24 As with cholesterol, the 2014 ADA nutrition recommendations suggest that saturated fat intake should remain the same for people with diabetes and the general population. The Dietary Guidelines for Americans recommend consuming less than 10% of calories from saturated fat to reduce cardiovascular disease risk.

When removing saturated fats and trans fats from the diet, PUFAs and monounsaturated fatty acids are recommended as replacements.22 The Dietary Guidelines for Americans 2010 committee reviewed 12 studies published (after 2000) and concluded that a 5%-calorie substitution of PUFAs or MUFAs for saturated fatty acid decreases risk of cardiovascular disease and type 2 diabetes in healthy adults. It also improves insulin responsiveness in those with insulin-resistant type 2 diabetes.22

PUFA/Omega-3 Fatty Acids There are two categories of PUFA that play an important role in lipid-lowering diets:

• Omega-6 fatty acid series: found mainly in linoleic acid • Omega-3 fatty acid series: present mainly in fish oils, but also found in plant sources such

as flax and walnuts Both are essential in the diet. The role of omega-6 and omega-3 fatty acids in the prevention of

diabetes and in the prevention of complications in people with diabetes is controversial. To date, there has not been sufficient evidence that increasing omega-3 fatty acids in the diet can prevent the onset of diabetes, although it does have other benefits.25

There is limited evidence as to the effects of omega-6 PUFAs on those with diabetes and complications from diabetes. Controversy also exists on the best ratio of omega-6 to omega-3 fatty acids; there is no recommended ratio. It should be noted that the typical U.S. diet contains high amounts of omega-6 PUFA, mainly from vegetable oils used for cooking and added to foods.

The omega-3 fatty acids, eicosapentaenoic acid and docosahexaenoic acid, are the two most common fish oils, and have antiinflammatory properties.

Studies in people with diabetes have used primarily fish oil supplementation and not dietary intake to determine the metabolic effects of omega-3 fatty acids and on the risk for cardiovascular disease. In patients with type 2 diabetes, supplementation with omega-3 fatty acids did not improve glycemic control, but higher-dose supplementation decreased triglycerides. Evidence does not support recommending omega-3 supplements for people with diabetes for the prevention of cardiovascular disease.24

In studies in which foods containing both fish-derived and plant-derived omega-3 fatty acids were used, no detrimental effects on glucose measures were reported; both diets improved insulin sensitivity and lipid levels.26 As is recommended for the general public, an increase in foods containing omega-3 fatty acids is also recommended for persons with diabetes because of their beneficial effects on lipids and insulin sensitivity.1 At least two servings of fish (particularly fatty fish) per week is recommended as a better alternative to fish oil supplements.2


59

The recommended two servings of fish would be approximately 6 oz/serving, and has been calculated to have approximately 500 mg to 1 g of omega-3 fatty acid/serving. Good food sources of omega-3 fatty acids include non-predator, fatty meat fish, such as salmon, mackerel, sardines and herring; and plant sources, such as flaxseed, soybeans and walnuts. Although fish is a positive addition to the diet, a balance of omega-6 and omega-3 fatty acids is needed. For most, the best way to achieve a balanced ratio of fatty acids is to increase consumption of omega-3 fatty acids. Aim for a minimum daily amount of omega-3 fatty acids, decrease consumption of omega-6 fatty acids and don’t worry about ratios.

MUFAs

MUFAs are recommended substitutes for saturated or trans fats.22 Evidence from a systematic review of randomized controlled trials indicates that diets high in MUFA are associated with improved glycemic control and improved cardiovascular disease risk; foods high in MUFA improve glycemic control and/or blood lipids when substituted for carbohydrate and/or saturated fat.27 Foods that contain MUFA are recommended in a Mediterranean-style diet, and have been studied in patients with type 2 diabetes.

The AND Evidence Analysis Library found that a 5% energy replacement of saturated fatty acids with MUFA improves insulin responsiveness in those with type 2 diabetes who are insulin resistant.28

Trans Unsaturated Fatty Acids

Trans fats are created through the process of hydrogenation that solidifies liquid oils. Trans fats are found in many foods (vegetable shortenings, margarines, potato chips, crackers, cookies, cakes, pies and doughnuts), as well as convenience and restaurant foods (e.g., fried foods, such as chicken, fish and potatoes). Most trans fats in foods come from processed foods; only about one-fifth of trans fats come from unprocessed animal sources, such as meat and dairy products.

According to the FDA, hydrogenation helps manufacturers increase the shelf life and flavor stability of vegetable oils. Studies indicate that consumption of trans fats contributes to increased LDL-cholesterol and decreased HDL-cholesterol levels, which increase the risk for heart disease. Trans fats also affect the inflammatory process and interfere with fat metabolism.29

The ADA recommends limiting trans fat as much as possible in those with diabetes (same recommendation as the general population). People can lower their intake of trans fat by decreasing total fat and saturated fat intake. Total fat can be decreased especially from commercial foods, such as margarine, cookies, crackers, frozen convenience foods and restaurant foods that have been deep-fat fried. Instead, use a margarine low in trans fats, such as a liquid or a tub margarine.

The use of trans fat has decreased steadily since 2006 when identification on food labels was required. Intake decreased from 4.6 g/day in 2003 to 1 g/day in 2012.30 Many manufacturers have been removing trans fats voluntarily from foods because consumers want foods free of trans fat. In 2013, the FDA announced its preliminary determination that artificial trans fats are not GRAS. If the decision is finalized, trans fat will be considered a “food additive,” and will need regulation before it will be allowed in food.30

Natural trans fats are present in meat, milk and milk products, and eliminating them is not recommended.6


60

Plant Stanols and Sterols As more Americans adopt diets lower in calories and fat, food technology is challenged to keep up

with consumer demands for tasty products that meet dietary guidelines. A wide range of foods and beverages are enriched with plant stanols or sterols, including many spreads, dairy products, grain and bread products, and yogurt. These products do contain calories, so overweight people with diabetes should substitute them for comparable foods to avoid weight gain.

Plant sterol and stanol esters block the intestinal absorption of dietary cholesterol. The AND Evidence Analysis Library reviewed 28 studies that showed no adverse effects with plant stanol/sterol consumption.31 The beneficial effects of these products in four randomized controlled trials using both people with type 1 and type 2 diabetes was to lower total and LDL cholesterol.32

Based on these studies, the ADA recommends the use of plant stanols and sterols in those with diabetes who have dyslipidemia to reduce total and LDL cholesterol modestly. An amount of 1.6 g/day to 3 g/day is the suggested intake.2

Carbohydrate/Fat Controversy

Tradition suggests that simple sugars should be limited in the diets of those with diabetes, and carbohydrates should be complex carbohydrates or starches.

The assumption was that complex carbohydrates were digested and absorbed slowly, and were preferred carbohydrates for patients with diabetes; whereas the more rapidly digested and absorbed simple carbohydrates or sugars were to be avoided. Interest was refocused on this issue in the 1970s when studies of starch foods of similar macronutrient content (baked potato, boiled white rice, kernel corn and white bread) found unexpected differences in post-ingestion insulin and glucose responses.33

Subsequent studies found a relationship between the rate of digestion and the postprandial blood glucose response to a food.13,34 Studies of different simple carbohydrates also demonstrated widespread variations in blood glucose response, with fructose ingestion resulting in a markedly flattened glycemic response compared to glucose or sucrose, when given alone or in test meals.35 Additional studies have found that blood glucose response to different complex and simple carbohydrate foods varies so greatly that in general the two groups cannot be distinguished on the basis of glycemic response.10,13

The glycemic response to different carbohydrates under physiological conditions cannot be predicted consistently and accurately. Much remains to be learned about the effects on metabolism of differently processed and prepared foods.

Investigators are examining the mechanisms underlying the differences in postprandial glucose response to different foods, to elucidate the factors that determine the glycemic response and to define foods that yield unusually low blood glucose responses.

Factors that affect the glycemic response to foods are dietary fiber content, food form and processing, cooking, rate of meal ingestion, antinutrients (e.g., natural enzyme inhibitors, pectins, phytates and tannins), and the starch/protein/fat interactions. In simple terms, foods with the following characteristics will decrease glycemic response:6

• High in water-soluble fiber • In whole form (instead of pureed, mashed or chopped) • Raw (instead of cooked) • Eaten slowly • High in antinutrients (such as legumes) • Eaten in a mixed nutrient food source (e.g., a combination of carbohydrate, protein and fat

[cookies] vs. a single nutrient [hard candy])


61

A big dilemma regarding the carbohydrate-fat controversy has been the short-term, controlled nature of many of the previously published studies. Few long-term studies have compared nutrition guidelines for people, especially with type 2 diabetes, in free-living situations.

In the first edition of this manual in 1992, the authors proposed that 1990s nutritional recommendations would include a decrease in carbohydrate to <50%. Because people with diabetes simply cannot adhere to a high-carbohydrate (>55% carbohydrate), high-fiber (>40 g) diet on a long-term basis, incorporating a meal plan with a lower percentage of carbohydrate (45% to 50%) would be more realistic and practical. Current research regarding the beneficial effects on lipid levels by substituting MUFAs provides a workable complement to decreasing carbohydrate level. By decreasing carbohydrates to 45% to 50%, fat could be increased from 30% to 35%, primarily from MUFAs.

In 1994, 2005, 2008 and again in 2014, the ADA published nutrition recommendations for people with diabetes.2 Since 1994, the committee has not established specific recommendations for total dietary carbohydrate and fat. Rather, it recommends that the distribution of calories for carbohydrate and fat be dependent on the glucose, lipid and weight goals of each person with diabetes, as well as evidence for specific nutrient recommendations. And in 2014, even more emphasis was placed on individual metabolic outcomes and personal preferences through use of meal-planning tools and eating patterns.

The recommended percentage of calories from fat and carbohydrate should be based on achieving desired glucose, lipid and weight outcomes, with the focus being to improve the quality rather than the amount of fat and carbohydrate. The final decision about the distribution of calories from fat and carbohydrate should be individualized based on a comprehensive nutrition assessment and treatment goals, which are negotiated between the healthcare provider and the person with diabetes. In most cases, this will result in moderate changes in both the amount of carbohydrate and fat.


62

Review Questions 1. List the classifications of carbohydrate and the components of each. 2. How have beliefs about protein changed as it relates to diabetes? 3. List the three types of fatty acids, food sources and the primary effects on lipid levels

of each.

Answer 1: • Digestible carbohydrate:

o Monosaccharides (glucose, fructose [fruit sugar] and galactose) o Disaccharides (sucrose [table sugar] = glucose + fructose; lactose [sugar in milk]

= glucose + galactose; maltose = glucose + glucose) o Oligosaccharides (raffinose, stachyose): kidney beans, lentils, navy beans

• Indigestible carbohydrate: dietary fiber o Water-insoluble fibers (cellulose, lignin and hemicelluloses): whole-wheat flour,

whole-grain cereal and bran o Water-soluble fibers (pectins, gums and storage polysaccharides): apples, citrus,

barley, oats and legumes Answer 2:

• It was thought that half of ingested protein was converted to glucose and had half the effect of carbohydrate on blood glucose levels. It now appears that protein goes through the process of gluconeogenesis, but minimal amounts are released into circulation after ingestion of protein. If eaten in recommended amounts, protein has a minimal effect on increasing blood glucose levels.

Answer 3:

• Saturated fatty acids o Sources: animal fats, hydrogenated shortening, palm and coconut oils, and

whole-milk dairy products o Effects: increase total blood cholesterol

• MUFAs o Sources: canola oil, olive oil and peanut oil o Effects: decrease total cholesterol and LDL levels without decreasing HDL levels

• PUFAs o Sources: vegetable oils, shortening and partially hydrogenated margarines; and

fish oils o Effects: Omega-6 decrease total cholesterol levels; omega-3 decrease

triglyceride levels (fish oil supplements may increase LDL levels)


63

References 1. Type 1 and type 2 diabetes evidence-based nutrition practice guidelines for adults, 2008. Academy of

Nutrition and Dietetics Evidence Analysis Library Web site. http://www.andeal.org/topic.cfm?cat=3251. Accessed February 15, 2015.


3. Sievenpiper JL, Carleton AJ, Chatha S, et al. Heterogeneous effects of fructose on blood lipids in individuals with type 2 diabetes: systematic review and meta-analysis of experimental trials in humans. Diabetes Care. 2009;32(10):1930-1937.

4. Zhang YH, An T, Zhang RC, et al. Very high fructose intake increases serum LDL-cholesterol and total cholesterol: a meta-analysis of controlled feeding trials. J Nutr. 2013;143(9):1391-1398.

5. Kelishadi R, Mansourian M, Heidari-Beni M. Association of fructose consumption and components of metabolic syndrome in human studies: a systematic review and meta-analysis. Nutrition. 2014;30(5):503-510.

6. Franz MJ, Evert A. American Diabetes Association Guide to Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association; 2012.

7. Nutritive and nonnutritive sweeteners (2010-2011). Academy of Nutrition and Dietetics Evidence Analysis Library Web site. https://www.andeal.org/topic.cfm?menu=4100. Accessed February 15, 2015.

8. Fitch C, Keim KS, Academy of Nutrition and Dietetics. Position of the Academy of Nutrition and Dietetics: use of nutritive and nonnutritive sweeteners. J Acad Nutr Diet. 2012;112(5):739-758.

9. Department of Health and Human Services, Food and Drug Administration (FDA). Food additives permitted for direct addition to food for human consumption; acesulfame potassium. FDA Web site. http://www.fda.gov/ohrms/dockets/98fr/03-32101.htm. December 31, 2003 (Volume 68, No. 250). Accessed February 15, 2015.

10. Warshaw H. What’s new in non-nutritive sweeteners? Stevia, of course! NutriZine Web site. http://www.presentdiabetes.com/ezines/index.php?action=viewPublication&nopopout=true&confirm Off=true&SearchText=&id=243&keepThis=true&TB_iframe=true&height=700&width=768&full=true. Published February 2009. Accessed February 15, 2015.

11. Wolever TM, Katzman-Relle L, Jenkins AL, et al. Glycemic index of 102 complex carbohydrate foods in patients with diabetes. Nutr Res. 1994;14(5):651-669.

12. Foster-Powell K, Brand-Miller JB. International tables of glycemic index. Am J Clin Nutr. 1995;62(4):871S-890S.

13. Jenkins DT, Wolever TM, Taylor RH, et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr. 1981;34(3):362-366.

14. Pi-Sunyer FX. Glycemic index and disease. Am J Clin Nutr. 2002;76(1):290S-298S.

15. Foster-Powell K, Holt SH, Brand-Miller JC. International tables of glycemic load values: 2002. Am J Clin Nutr. 2002;76(1):5-56.

16. Franz MJ. Diabetes mellitus nutrition therapy: beyond the glycemic index. Arch Intern Med. 2012;172(21):1660-1661.

17. Fürst P, Stehle P. What are the essential elements needed for the determination of amino acid requirements in humans? J Nutr. 2004;134(6 Suppl):1558S-1565S.

18. Franz MJ, Bantle JP, Beebe CA, et al. Evidence-based nutrition principles and recommendations for the treatment and prevention of diabetes and related complications. Diabetes Care. 2002;25(1):148-198.

19. Common oils in fats. Department of Veterans Affairs Web site. http://www.nutrition.va.gov/docs/PatientEducation/CommonOilsandFats.doc. Accessed February 15, 2015.

20. Powers MA, ed. Handbook of Diabetes Medical Nutrition Therapy. Burlington, MA: Jones and Bartlett; 1996.


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21. 2011 National Diabetes Fact Sheet. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/diabetes/pubs/factsheet11.htm. Updated October 2013. Accessed February 15, 2015.

22. Dietary Guidelines for Americans, 2010. U.S. Department of Health and Human Services Web site. http://www.health.gov/dietaryguidelines. Accessed February 15, 2015.

23. Tanasecu M, Cho E, Manson JE, Hu FB. Dietary fat and cholesterol and the risk of cardiovascular disease among women with type 2 diabetes. Am J Clin Nutr. 2004;70:999-1005.


25. Xun P, He K. Fish consumption and incidence of diabetes: meta-analysis of data from 438,000 individuals in 12 independent prospective cohorts with an average 11-year follow-up. Diabetes Care. 2012;35(4):930-938.

26. Karlström BE, Järvi AE, Byberg L, et al. Fatty fish in the diet of patients with type 2 diabetes: comparison of the metabolic effects of foods rich in n-3 and n-6 fatty acids. Am J Clin Nutr. 2011;94(1):26-33.

27. Schwingshackl L, Strasser B, Hoffman G. Effects of monounsaturated fatty acids on glycaemic control in patients with abnormal glucose metabolism: a systematic review and meta-analysis. Ann Nutr Metab. 2011;58(4):290-296.

28. Recommendations Summary. Disorders of lipid metabolism (DLM) and major fat components. Academy of Nutrition and Dietetics Evidence Analysis Library Web site. http://andevidencelibrary.com/template.cfm?template=guide_summary&key=2984#supportevidence. Accessed February 15, 2015.

29. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285(19):2486-2497.

30. FDA takes further steps to reduce trans fats in processed foods. Food and Drug Administration Web site. http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm373939.htm. Released November 7, 2013. Accessed February 15, 2015.

31. Disorders of Lipid Metabolism and Plant Stanols and Sterols. Academy of Nutrition and Dietetics Evidence Analysis Library Web site. http://andevidencelibrary.com/template.cfm?key=2986&auth=1. Accessed February 15, 2015.

32. Hallikainen M, Kurl S, Laakso M, Miettinen TA, Gylling H. Plant stanol esters lower LDL cholesterol level in statin-treated subjects with type 1 diabetes by interfering the absorption and synthesis of cholesterol. Atherosclerosis. 2011;217(2):473-478.

33. Crapo PA, Reaven G, Olefsky J. Postprandial plasma-glucose and –insulin responses to different complex carbohydrates. Diabetes. 1977;26(12):1178-1183.

34. O’Dea K, Snow P, Nestel P. Rate of starch hydrolysis in vitro as a predictor of metabolic responses to complex carbohydrate in vivo. Am J Clin Nutr. 1981;34(10):1991-1993.

35. Crapo PA, Kolterman OG, Olefsky JM. Effects of oral fructose in normal, diabetic, and impaired glucose tolerance subjects. Diabetes Care. 1980;3(5):575-582.


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Chapter Six: Process of Diabetes

Medical Nutrition Therapy

iabetes medical nutrition therapy is a four-step model that includes assessment of metabolic, nutrition and lifestyle parameters; identification and negotiation of nutrition goals; intervention designed to achieve individualized goals; and evaluation of outcomes.

Diabetes medical nutrition therapy allows those with diabetes to acquire and maintain the knowledge, skills, attitudes, behaviors and commitment to meet the challenges of daily diabetes self-management successfully. This is not accomplished with one counseling session, but occurs during a longer period, using the process of diabetes medical nutrition therapy.

Promoting changes in eating habits constitutes a great challenge in diabetes self-management training. One reason clients have difficulty with “diet-related issues” may be because they are not referred to RDs or diabetes educators for diabetes nutrition self-management training. Instead, they may experience one of the following scenarios:

• They are given a “diet sheet” that provides very basic information about food exchanges, a meal plan and a sample menu.

• They are given a list of “good” and “bad” foods. • They are told to avoid sugar or limit fat, and to lose weight. • They are given an exchange list booklet for a prescribed calorie level with minimal

education or individualized instruction just before hospital discharge. Without adequate nutrition advice, or an individualized meal plan based on the client’s lifestyle,

“dietary nonadherence” will continue to be a primary inhibitor to optimal blood glucose control. For medical nutrition therapy to be effective, it must be implemented in a standardized process that involves a comprehensive assessment, individualized care, and the monitoring and evaluation of nutrition therapy interventions to meet treatment goals.1

Even though assessment is the initial step of the four-step model, beginning the relationship and establishing a rapport with the client is an important preliminary step. Nutrition Assessment

Nutrition assessment is the most crucial step in diabetes medical nutrition therapy. The main purpose of an assessment is to gather information needed to assist in the development of individual nutrition goals and establish an appropriate nutrition intervention.2

The major components of a nutrition assessment are collection of clinical data, nutrition history, weight history, physical activity history, monitoring of psychosocial and economic information (stress and social supports), diabetes knowledge and skill level, and readiness to change.

Information from all components must be obtained, and used to develop achievable goals and workable interventions appropriate to the person with diabetes. Assessment is ongoing, and must be modified and updated.

D

Process of Diabetes Medical Nutrition Therapy

66

The amount of time for an assessment varies, depending on the educator, client and other factors, such as the client’s ability to provide information, as well as the complexity of the information needed.

Initial Nutrition Assessment Components Assessments

Clinical data • Anthropometrics: height, weight, BMI, waist circumference • Lab data: fasting, random, post-meal glucose; A1C, lipids,

microalbuminuria

Nutrition history

• Current diabetes medical nutrition therapy (if not available from preliminary data)

• Who does food preparation/shopping • Frequency/choices for dining out • Alcohol intake • Use of vitamins, minerals and nutrition supplements • Eating disorders • Nutrition history (using any/all of the following methods: 24-

hour recall, usual food intake, food frequency or food records) • Energy intake and macronutrient composition (type and

amount)

Physical activity history

• Activity types and frequency • Energy expenditure • Limitations that hinder exercise • Willingness and ability to become more physically active

Monitoring

• Knowledge of target blood glucose levels • SMBG method/frequency of testing • Other types of record keeping (food, physical activity, etc.) • Client benefits from monitoring

Psychosocial/economic information

• Living situation, finances, educational background and employment

Knowledge and skill level • Survival or continuing education knowledge level

Expectations and readiness to change • Willingness to change

Clinical Data

Clinical data include both anthropometrics (such as height, weight, BMI and waist circumference) and pertinent lab or physical exam data (such as fasting, random or post-meal glucose values; A1C; lipids; microalbuminuria; blood pressure; and eye and foot exam). Nutrition History

A nutrition history identifies the client’s personal food choices and eating habits, and allows for determination of nutrition needs and an appropriate approach for tailored meal planning. Specific information that should be collected includes:

• Past nutrition intervention • Previous meal-planning methods, and self-assessment of comprehension and compliance


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• Household/family situation • Food preparation/shopping • Issues with eating away from home • Alcohol intake • Intake of nutrition supplements • Issues with compulsive eating

[A completed nutrition history is provided in the Case Study in the Appendix section.] It is important to collect information about common trends in the client’s food intake. This can be

done using several different methods (24-hour recall, usual food intake, food frequency or food record). After collecting a nutrition history and typical food intake information, the educator should

evaluate energy intake, and type and amount of macronutrient composition. Several methods can evaluate nutritional adequacy, including software programs, apps and exchange lists for meal planning. Weight History Information specific to weight includes:

• Usual weight, weight history and healthy weight goals • Assessment of interest or readiness to change or lose weight • Expectations regarding weight change

The Case Study (in the Appendix section) includes a completed weight history form (part of the Lifestyle Questionnaire). This form is most useful for those in whom weight loss is the primary desired clinical outcome. These components could also be incorporated into a nutrition history form. Physical Activity History

Because exercise or physical activity is an important component of diabetes management, it should be addressed when completing an assessment. The educator should ask the client questions concerning previous and current activity levels, readiness to become more physically active, limitations that might hinder exercise and physical activities of interest (see the Case Study for use of a typical physical activity record). Monitoring

An assessment of the client’s monitoring practice could include a written log of SMBG, food and/or physical activity (see Appendix 1). It is important to assess previous and/or current practices as well as the interest level regarding SMBG, to determine the level of complexity of the management plan and to promote participation in self-monitoring.

Some glucose meters allow events (e.g., eating or exercising) to be entered, and have software programs that allow downloading data to a computer. Electronic printouts can document blood sugar trends over time, and are most helpful in those who test frequently and use intensive insulin treatment.

The use of smartphone applications (apps) has been shown to be a good method for accurately logging and managing SMBG results. SMBG data logged on a smartphone app can be reviewed easily with healthcare practitioners to make recommendations about exercise, diet or medications. Smartphones or devices, such as the iPod Touch and the iPad (iOS devices), offer a variety of diabetes apps that may be helpful in managing other aspects of diabetes care, such as exercise, carbohydrate counting and medication adherence.3


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Psychosocial and Economic Information Psychosocial and economic information includes the living situation, finances, educational

background, employment status, ethnic or religious beliefs, family/social support and level of stress. This could be included on a nutrition history form; often, it is included in a medical chart or a general diabetes assessment form (the Case Study includes a form that could be used to assess the history of stress for a person with diabetes). Knowledge and Skill Levels

Many educators have developed their own checklists or surveys to assess a client’s knowledge of nutrition. Another method to assess knowledge is to compare client information collected from nutrition questionnaires or a verbal nutrition history with established goals and standards for education. Diabetes Self-Management Education and Support

In 2011, a joint task force of the American Association of Diabetes Education and the ADA updated the National Standards for Diabetes Education, first published in 2007, based on relevance, scientific evidence and expert consensus, known as AADE7 Self-Care Behaviors. It is designed to define quality diabetes self-management education and support, and to assist educators in providing evidence-based education and self-management support.4

The AADE Outcome Standards for Diabetes Education specify behavior change as the key outcome and provide a useful framework for assessment and documentation. The AADE7 lists seven essential factors:

• Physical activity • Healthy eating • Taking medication

• Monitoring blood glucose • Diabetes self-care-related problem solving • Reducing risks of acute and chronic complications • Psychosocial aspects of living with diabetes

Readiness to Change

The Transtheoretical Model for behavioral change provides a framework for assessing readiness to change using a five-stage model:5

• Precontemplation: No intention to change in the foreseeable future • Contemplation: Aware that a problem exists; thinking about making a change • Preparation: Decision making; seriously considering change in the near future • Action: Making changes • Maintenance: Working to prevent relapse

These stages of change may be applied to a variety of health behavior interventions, including fat reduction, exercise, smoking cessation, alcohol treatment, SMBG and weight management.6 Movement through the five stages often involves a move in either direction. Focusing intervention to the appropriate stage can facilitate tailoring intervention to the client’s needs to improve the likelihood of success. Assessment of readiness to change can guide the educator in negotiations to establish behavior change goals.

http://www.diabeteseducator.org/ProfessionalResources/AADE7


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Collection of Assessment Data The two barriers most commonly faced in clinical practice for obtaining assessment data are time

limitations and reluctance of the client to provide information. Some solutions that may help use time more efficiently include:

• Use data previously collected by other staff • Focus on assessment information that is the most pertinent to the person with diabetes • Prioritize information by obtaining the most crucial information first

In an ambulatory care setting, you may wish to consider providing the client with forms or questionnaires to be completed before or in conjunction with the appointment. For example, at the initial appointment, provide forms to be completed before the next scheduled appointment; mail forms before the first appointment and ask the client to bring completed forms to the initial appointment; or have the client complete the forms while waiting for the appointment.

In the inpatient setting, because of time constraints and limited patient contact, the use of forms or questionnaires may not be possible or efficient. Instead, the forms or questionnaires can be used to record nutrition assessment information collected verbally from the patient. To maximize the information provided by the person with diabetes:

• Take time to develop a rapport and establish trust • Be nonjudgmental when asking questions and reacting to responses (there are no wrong

answers) • Respect the client’s emotional state, which may require waiting to obtain comprehensive

assessment data Nutrition assessment serves an educational purpose for both the educator and client because it

can improve the client’s awareness of health status, treatment options and lifestyle factors that affect his or her health. Nutrition assessment also provides the educator with an opportunity to establish the tone of the relationship with the client.

Ideally, the educator and client should develop a working partnership. The educator should ask for information, reactions, feelings and thoughts about the information being discussed. This is a natural progression into the next step of the four-step model of diabetes medical nutrition therapy — goal setting. Goal Setting and Diagnosis

Lifestyle change goals are an important aspect of the management and education plan. The purpose of setting goals is to establish realistic target behaviors to evaluate success in making positive lifestyle changes.

Diabetes management goals are the clinical or metabolic outcomes of treatment intervention. They may include lipid levels, blood glucose levels and body weight, and are necessary in making a nutrition diagnosis for intervention. Goals are established by mutual agreement between the educator and the client. This contributes to the likelihood that the client will “own” the goals and become committed to self-care behaviors that will enable him or her to reach and maintain them.


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Negotiating Goals To negotiate goals, educators need to be sensitive to clients’ needs for flexibility and structure.

While educators should respond to requests for guidance, they need to encourage development of a realistic degree of independence in self-care. These questions can assist in developing behavioral goals:

• What goals are most likely to help you develop a healthier lifestyle? • What behavior would you like to change? • What changes can you make in your current lifestyle? • What obstacles do you see to making these changes? • What benefits do you see as a result of these changes? • What are you willing to do right now?

The way goals are set affects the tone of the relationship between the educator and the client. The nature of the relationship will have a strong influence on the outcome of treatment.

Goals are not permanent. As time passes, the client’s health, lifestyle and attitudes can be expected to change; at this point, goals will need to be reassessed and renegotiated. The educator should view goal setting as a continuous process. (Two resources discussed in the Case Study, the Eating Behavior Diary and the Behavioral Goals form, can assist the educator and the person with diabetes in goal setting. The diary provides the person with experience in monitoring eating behaviors to become more aware of factors that influence eating. The goals form is a tool to assist in recording and tracking behavior goals to assess and make improvements in lifestyle behaviors.)

Intervention Intervention refers to activities that facilitate or support the client’s nutrition self-management

plan. Effective nutrition intervention requires the educator to act as information provider and counselor. The role of information provider is part of the traditional information-centered approach to diabetes management. The role of counselor is based on the client-focused trend in healthcare.

As a counselor, an educator can help the client understand what having diabetes means personally and support the client in an effort to cope responsibly with the disease. Often, in the counselor role, educators think their responsibility is to motivate the person with diabetes; however, this is false. The educator’s role is to serve as a guide to help clients discover how they are motivated and to help them use their motivation to create positive changes in eating behavior.

Both roles are part of an essential balance that expands the role of the educator and contributes to quality healthcare. Components of Nutrition Intervention

Nutrition intervention specifically refers to the basic and in-depth education stages of the nutrition intervention process. Basic education is providing primary information about nutrition and nutrient requirements, discussing the diabetes nutrition management guidelines and introducing other survival skills information that may be important to the specific-type of diabetes. In-depth education is selecting an appropriate meal-planning approach for achieving individually determined goals.


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Nutrition Intervention Resources Intervention includes the use of education resources for the development of meal-planning skills

and strategies for behavior change. When choosing the type of intervention resources to use, take into consideration:

• The client’s ability and/or willingness to learn • The client’s level of motivation to make needed changes in eating habits • The nutrition goals established by the client and the educator • The type and amount of insulin or oral glucose-lowering medication used • The client’s current activity level • The client’s lifestyle (job/school schedule, current eating habits, favorite foods,

religious/ethnic food beliefs, and social and economic factors) Some education materials may not be appropriate for certain clients. Instead, you may want to

develop your own materials or choose not to give any printed material. Another strategy may be to write down short-term eating behavior goals with a client, and use the list as an education resource. It is important to choose from a variety of materials. The backgrounds, lifestyles, needs and interests of clients differ vastly, and as do their educational needs.

Nutrition Therapy Timeframes7 • A series of three to four sessions lasting from 45 to 90 minutes with an RD

• Sessions should begin at diagnosis of diabetes (or first referral) and be completed within three to six months

• RD should determine if additional nutrition therapy sessions are needed

• At least one follow-up session annually to reinforce lifestyle changes, and evaluate and monitor outcomes

Evaluation

Evaluation refers to the activities of the educator and client that enable them to determine the effectiveness of a plan, identify its strengths and weaknesses, and reinforce changes to be implemented. The educator evaluates whether behavioral goals have been met, and if specific clinical outcomes have improved. Adjustments in goals or educational interventions should be negotiated jointly.

Evaluation is a continuous and cyclical process. For clients to learn and maintain new behaviors, the four-step model of diabetes medical nutrition therapy must be reinforced. Over time, reassessment, establishment of new or revised goals, and new or revised interventions should be tried.

Follow-up should be both immediate and long-term. After the second or third visit, it should be possible to determine whether the client is progressing toward the goals. If no progress is evident, the client and educator need to reassess and, perhaps, revise the plan for intervention. Clients need to understand diabetes is a chronic disease and they should return to their nutrition educator at least annually for follow-up.


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References 1. Green Pastors J, Franz MJ. Effectiveness of medical nutrition therapy in diabetes. In: Franz MJ, Evert AB,

eds. American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Alexandria, VA: American Diabetes Association; 2012.

2. Green Pastors J. Nutrition assessment for diabetes medical nutrition therapy. Diabetes Spectrum. 1996;9(2):99-103.

3. Tran J, Tran R, White JR. Smartphone-based glucose monitoring and applications in the management of diabetes. Clin Diabetes. 2012;30(4):173-178.

4. Haas L, Maryniuk M, Beck J, et al. National standards for diabetes self-management education and support. Diabetes Care. 2014;37(Suppl 1):S144-S153.

5. Prochaska JO, DiClemente CC, Norcross JC. In search of how people change. Applications to addictive behaviors. Am Psychol. 1992;47(9):1102-1114.

6. Prochaska JO, Ruggiero L, eds. Readiness for change: application of the transtheoretical model to diabetes. Diabetes Spectrum. 1993;6:22-60.

7. Type 1 and type 2 diabetes evidence-based nutrition practice guidelines for adults, 2008. Academy of Nutrition and Dietetics Evidence Analysis Library Web site. http://www.andeal.org/topic.cfm?cat=3251. Accessed February 15, 2015.


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Chapter Seven: Nutrition Intervention:

Basic and In-depth

here is substantial agreement among healthcare professionals and clients with diabetes that “diet” constitutes the biggest problem in diabetes care. Comments such as, “e is noncompliant with his diet,” or “She’s just not motivated,” are routine among healthcare professionals. Unfortunately,

clients are often blamed for “diet failure.” But what has failed? Is it really “the diet?” The primary focus in diabetes nutrition therapy should

be achieving and maintaining blood glucose, lipid and blood pressure levels in the normal range; preventing or reducing the rate of complications; and addressing individual nutrition needs using a variety of eating patterns, while maintaining the pleasure of eating. It should not focus on the provision of a “diabetic diet” or a calorie level to address weight loss.

A large percentage of people with diabetes do not receive any structured diabetes education or nutrition therapy. National data indicate that about 50% of those with diabetes report receiving some type of diabetes education; even fewer see an RD.1 This is particularly unfortunate, as it is during this initial stage of newly developed diabetes that nutrition/weight control, exercise and behavioral change may be the most effective in achieving normoglycemia, improving hyperlipidemia and hypertension, and preventing or delaying the need for oral medication and/or insulin.

Two widely publicized studies — the Diabetes Prevention Program in subjects who are at high risk for diabetes and the Look AHEAD trial in those with type 2 diabetes at risk for cardiovascular disease — have shown that type 2 diabetes can be prevented or improved by lifestyle interventions.

The Diabetes Prevention Program showed that type 2 diabetes could be prevented or delayed.2 The DPP was a 27-center randomized trial involving more than 3,200 adults who were older than age 25 and at increased risk for developing type 2 diabetes (i.e., blood glucose higher than normal but less than diabetes diagnostic criteria of 126 mg/dL, overweight and family history of type 2 diabetes). The study involved three groups:

• A control group that received standard care plus a placebo pill • An intervention group that received intensive lifestyle modification, including moderate

weight loss (7% of body weight) and regular physical activity (150 minutes/week) with dietary strategies to reduce intake of fat and calories

• An intervention group that received standard care plus an oral anti-hyperglycemic agent (metformin [Glucophage])

The major study findings indicate that participants who made lifestyle changes reduced their risk of

getting diabetes by 58% compared to the medication intervention group who reduced their risk by 31%.2 A follow-up to this study, the U.S. Diabetes Prevention Program Outcomes Study, showed a sustained reduction in the rate of conversion to type 2 diabetes (34% at 10 years).3

The results of the Look AHEAD trial demonstrated improvements in cardiovascular risk factors. The Look AHEAD trial was a 16-center randomized controlled trial with 5,145 overweight or obese patients who participated in either an intensive lifestyle intervention program that promoted weight

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loss through decreased caloric intake and increased physical activity (intervention group) or diabetes support and education (control group).

At the end of the 10-year study, mean weight loss from baseline was 6%, and A1C levels improved by 0.64%. Other statistically significant improvements included less medication for glycemic control/management of cardiovascular disease risk factors, reduced sleep apnea and depression, and improved quality of life.4 Strategies reported in the study associated with weight loss/weight maintenance included weekly self-weighing, consumption of breakfast and reduced intake of fast foods.5

These studies confirm the importance of nutrition and exercise therapy as a primary intervention in preventing type 2 diabetes, and as the primary treatment after the initial diagnosis of diabetes is made.

False Premises

Several standard premises and accepted practices for nutritional management of diabetes are FALSE.

If you have diabetes, you should avoid foods with sugar and not eat sweets.

It is now known that it is the total amount of carbohydrates (both starches and sugars) eaten that

raise blood glucose levels, not whether the carbohydrate is from bread, potato or candy. Those with diabetes can fit sweets into their food choices as long as they substitute sweets for other carbohydrate-containing foods.

If you take diabetes medicines, you don’t need to worry about what you eat.

Taking care of diabetes and controlling blood glucose levels requires eating healthy, being

physically active and taking diabetes medication. Healthy food choices and a regular eating schedule help diabetes medication to better control blood glucose levels.

Those who have diabetes need a highly structured meal plan.

A meal plan should not be considered a diet, but rather a guide to healthy eating. Because diabetes

is a chronic disease, nutrition recommendations should be able to be incorporated on a long-term basis. There is no one diabetic or ADA diet. Medical nutrition therapy for clients with diabetes should be individualized, with consideration given to usual eating habits and other lifestyle factors.

Not everyone needs structure to make healthy food choices; for some, too much structure may lead to noncompliance. Given that most people with type 2 diabetes are overweight and older than age 40 they are a population with long-established habits and patterns of eating.

An individualized meal plan means more than making adjustments for food preferences and distributing the calories based on usual eating patterns. Selecting an appropriate eating pattern and meal-planning approach based on a client’s educational and nutritional needs, and willingness to control diabetes, are the keys to individualizing the meal plan.

When the client understands how to plan meals, nutritional needs can be attained more easily, and diabetes can be managed better.


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All people with diabetes should use the same meal plan. A meal-planning approach is used by the practitioner to teach the client how much to eat and how

to plan meals, and needs to be individualized. A variety of meal-planning approaches are available, and the approach should take into consideration:

• The client’s ability and/or willingness to learn • The client’s level of motivation to make needed changes in eating habits • Clinical goals (e.g., target blood glucose and lipid goals) • Nutrition therapy goals established by the client, RD and other members of the diabetes

care team (e.g., decrease saturated fat and calories, increase physical activity) • Type and amount of insulin or oral diabetes agent used (if any) • Activity level • Lifestyle (job/school schedule, current eating habits, favorite foods, religious/ethnic food

beliefs, social and economic factors)

Differentiating Between an Eating Pattern and a Meal Plan A meal plan provides information about how much to eat. It can be more basic by suggesting

portion sizes or numbers of servings of foods/food groups or more in-depth by providing specific calories, carbohydrate choices or grams of carbohydrate, fat or calories.

One of the primary goals of the ADA 2014 Nutrition Therapy Recommendations is to promote and support a variety of healthful eating patterns to improve overall health. An eating pattern is defined as a combination of different foods or food groups. The recommendations suggest that personal preferences (e.g., tradition, culture, religion, health beliefs and goals, economics) and metabolic goals should be considered when recommending an eating pattern.6 Types of eating patterns include Mediterranean, vegetarian and vegan, low-fat, low-carbohydrate and DASH patterns with specifics about the combinations of foods and food groups.

Selecting a Meal-Planning Approach When selecting a meal-planning approach, a dietetics/nutrition professional or diabetes educator

needs to consider the long-term nature of diabetes education and the likelihood that a combination of different meal-planning approaches and resources may be needed.7 Ideally, nutrition intervention should be conducted in stages, and based on a comprehensive nutrition assessment and establishment of individualized goals.

Basic intervention includes providing basic information about nutrition and nutrient requirements, discussing diabetes nutrition management guidelines, providing guidance in making initial changes in selection of food choices and introducing other beginning information that may be important specific to the type of diabetes. The meal-planning approaches can be referred to as basic meal plans. Examples of these eating or meal plans include the U.S. Department of Agriculture MyPlate Method, DASH Eating Plan, the Mediterranean Diet Pyramid and the Vegetarian/Vegan Eating Plan.

In-depth intervention includes selecting a more structured meal-planning approach for achieving individually determined goals and providing continuity of care. This more structured plan includes a specific number of calories, grams of carbohydrate or fat. An individualized plan of eating can use a variety of in-depth meal-planning approaches, including carbohydrate counting, fat and/or calorie counting, exchange lists or individualized menus.


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Basic Meal Plans The practitioner needs to conduct a comprehensive nutrition assessment and establish individual

goals to make a nutrition diagnosis, and introduce nutrition and meal planning. Basic meal plans provide a foundation of basic nutrition information and can be used as an assessment tool to determine nutrient adequacy. If used as stand-alone resources for diabetes nutrition education, they are a good choice for starting the education process.

Using basic meal plans will allow the RD/diabetes educator to individualize education based on each client’s knowledge, interest and ability to make changes in current eating patterns. Specific ideas for improvements in meal planning can be made without having to provide large amounts of detailed information.

Basic meal plans lack structure or specificity of nutrient percentages or amounts, and may be less effective in achieving the degree of glucose control desired, especially for those who are fine-tuning glucose control (i.e., giving particular attention to carbohydrate intake) and for those who need to lose weight (i.e., those who would benefit from a structured eating plan with an emphasis on calories and decreased fat intake).

Basic meal plans will provide consistency in food intake, but primary emphasis is on making healthier food choices without weighing and measuring foods; using exchanges; or counting points, calories, fat or carbohydrate.

USDA MyPlate Method

The MyPlate Method for meal planning can help clients select meals with acceptable food portions more easily. Serving sizes are estimated without measuring to promote consistency of carbohydrate of meals. This method is useful, particularly for teaching simplified meal planning, basic portion control, and for those who have poor reading or math skills, or who do not speak English.

When reviewing the plate method graphic with the client, highlight the following tips: • Build a healthy plate. • Cut back on foods high in solid fats, added sugars and salt. • Eat the right amount of calories for you. • Be physically active.

The tips for healthy eating can be compared with the client’s usual intake and individualized goals established for gradual improvement of his or her eating plan.

It may also be helpful to introduce a standard meal pattern. Use the sample plate format to plan a day’s meals and snacks. The sample meal plan shown provides about 45 g to 60 g of carbohydrate at each meal (three to five carbohydrate servings). Calories can vary based on food choices. Serving sizes for snacks are the same as for meals.


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Sample Meal Plan for MyPlate Method8 Breakfast Lunch or Dinner

1/4 to 1/2 plate bread or cereal An 8-oz glass of milk Piece of fruit or 1/2 cup fruit juice, or

1/2 cup dried fruit Optional 1/2 plate of meat or protein If client does not, or should not, drink

milk at all meals, you can increase bread/cereal portion

1/4 plate bread, grain or starchy food (rolls, rice, crackers, cereal, potatoes, corn, winter squash and legumes)

1/4 plate meat, fish or poultry 1/2 plate nonstarchy vegetables (broccoli, green beans,

carrots, mushrooms, tomatoes, cauliflower, spinach, peppers and salad greens)

An 8-oz glass of milk A piece of fruit If client does not, or should not, drink milk at all meals,

you can increase bread/cereal portion

Print materials and videos from the USDA are available at www.choosemyplate.gov.

Mediterranean Meal Plan The Mediterranean-style eating pattern from the Mediterranean region of the world has been

observed to improve cardiovascular disease risk factors and has achieved improvements in glycemic control.9 The Mediterranean eating pattern includes:9

• Plant food sources, including fruits and vegetables, potatoes, bread and grains, beans, and nuts and seeds

• Minimally processed foods; emphasis is on seasonally fresh and locally grown food • Olive oil is primary fat, replacing other fats and oils (including butter and margarine) • Total fat ranging from 25% to 35% of total energy, with saturated fat no more than 7% of

calories • Low-to-moderate amounts of cheese and yogurt • Twice-weekly consumption of fish and poultry; approximately seven eggs/week (including

those used in cooking and baking) • Fresh fruit as daily dessert; sweets only a few times/week • Red meat a few times/month (limited to 12 oz to 16 oz per month) • Regular physical activity to promote a healthy weight, fitness and well-being • Moderate consumption of wine, normally with meals; approximately two glasses/day for

men and one glass/day for women For more information see the Mediterranean Diet Pyramid from Oldways, as well as explanations

of the differences between the Mediterranean Diet Pyramid and the Healthy Eating Plate from Harvard University School of Public Health.

Vegetarian/Vegan Meal Plan

A plant-based meal plan is an excellent source of necessary nutrients for optimal health, especially when a wide variety of foods are eaten. There are ethical, nutritional (including food sustainability) and cultural reasons why people choose a plant-based diet. In studies of vegetarian and low-fat vegan diets, there was no significant benefit of a vegetarian or vegan diet to improved glycemic control or reduced cardiovascular disease risk, except when energy intake was reduced and weight was lost.10

http://oldwayspt.org/resources/heritage-pyramids/mediterranean-diet-pyramid

http://www.hsph.harvard.edu/nutritionsource/pyramid-questions/


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A vegetarian pattern of eating includes all plant-based food sources, in addition to milk and egg (lacto-ovo)-based products. A vegan pattern of eating includes only plant-based food sources, and is free of all flesh foods, milk and egg products. Vegetarian-vegan meal plans have been developed using food groups and a plate method.11

Vegetarian-Vegan “Power” Plate

Courtesy of Physicians Committee for Responsible Medicine. See website for a four-page brochure to be used with clients.

DASH Meal Plan

The DASH eating plan was developed based on studies by the National, Heart, Lung, and Blood Institute to show that blood pressure can be reduced by decreasing the amount of sodium consumed and following an eating plan that is low in saturated fat, cholesterol and total fat, and that emphasizes fruits, vegetables, whole grain products, low-fat milk and milk products, nuts, fish and poultry. It reduces red meat, sweets and sugar-containing beverages. Studies have found that reducing sodium to 2,300 mg/day can lower blood pressure and that an even lower level of sodium (1,500 mg/day) can further reduce blood pressure (see Appendix 4 for a DASH eating plan of 2,000 calories that includes the number of daily servings of various food groups). The number of servings will vary, depending on caloric need. Additional eating plans with other calorie levels can be obtained on the NHLBI website describing the DASH eating plan to lower blood pressure.12

In-Depth Meal-Planning Approaches

The in-depth stage of the nutrition intervention process provides more information about meal planning. In-depth nutrition education is information that provides more structure to the process of meal planning and/or provides specific nutrient (e.g., carbohydrate, fat) or calorie information to assist with meal planning.

Do I need to advance everyone from the basic to the in-depth stage of education?

Many people do well with guideline information and do not need more structured information

about meal planning. This is not based solely on intellect or literacy level; many well-educated people may need or want only basic information. They may not have time to use a more in-depth system of meal planning, or don’t need it to adopt a healthy eating plan and meet their diabetes-nutrition therapy goals. Conversely, those not able to comprehend an in-depth approach (a system of counting, exchanges or menus) may need only the basic stage of nutrition education; however, this does not

http://www.nhlbi.nih.gov/health/health-topics/topics/dash/followdash.html


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mean they need only one education session or that follow-up sessions should be review of information. The challenge is to present new information using techniques that are individualized to their particular needs. Information should empower them to make gradual changes in their lifestyle and eating behaviors that are permanent.

What nutrition education resources should I use?

It is important to choose from a variety of resources rather than always disseminating standardized

educational resources. Clients’ backgrounds, lifestyles, needs, interests and diabetes management goals are different, and as a result, their educational needs will differ considerably. The goal should be to individualize education and counseling sessions for each client rather than use the same procedure for everyone.

Should I provide an educational resource to every person with diabetes?

You may decide that the educational material you usually use and that is available to you may not

be appropriate for certain clients. Instead, you may want to develop your own resources or choose not to give any printed material.

What are the in-depth meal-planning approaches?

For purposes of simplification, the in-depth meal-planning approaches that will be discussed have

been placed into subcategories based on their similarities. The subcategories and meal planning approaches include:

• Counting o Carbohydrate counting

§ Carbohydrate consistency (choices or grams) § Advanced carbohydrate counting (insulin:carbohydrate ratio and blood glucose

correction factor) o Calorie counting o Fat counting

• Exchange lists • Individualized menus

Carbohydrate-Counting Approach

Teaching carbohydrate counting is one of the most commonly used methods of diabetes meal planning. It is supported by research that shows carbohydrate is the primary nutrient affecting postprandial blood glucose levels and insulin requirements, and all sources of carbohydrate (monosaccharides, disaccharides or polysaccharides) affect blood glucose levels similarly when eaten in the same amounts.13

The DCCT reported that carbohydrate counting was the most successful meal-planning approach used by clients with type 1 diabetes.14 It has been found that monitoring carbohydrate by counting can improve postprandial glucose control. Evidence shows that the total amount of carbohydrate eaten is the primary predictor of glycemic response.15 The ADA nutrition recommendations emphasize the importance of focusing on the total amount of carbohydrate eaten, rather than the specific source of carbohydrate.13


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In its simplest form, carbohydrate counting can help clients become more aware of carbohydrate in foods and focus on the consistency of food consumption at meals and snacks. At a more advanced level, the focus will be on adjustment of food, medication and activity, based on patterns from daily food and blood glucose records.

To use an advanced level of carbohydrate counting, it is essential that both the educator and client understand intensive insulin therapy (i.e., how to make food and/or insulin adjustments based on blood glucose monitoring results).

Basic Carbohydrate Counting

Count Your Carbs: Getting Started is a booklet developed by the ADA and the AND (released in 2008 and updated in 2010) to teach clients the basics of carbohydrate counting. It provides guidance on how much carbohydrate to eat, record keeping and where to find carbohydrate information.

Function of carbohydrate. Review the importance of carbohydrate as an energy source, the brain’s dependence on glucose and storage of excess carbohydrate in the liver as glycogen for use as needed.

Types of carbohydrate. Discuss the types of carbohydrate: starches, which are long chains of 10+ sugar molecules; sugars, which are short, simple chains of <10 sugar molecules; and fiber, which is non-digestible carbohydrate. The most common sugars in foods are sucrose (table sugar), fructose (sugar in fruits) and lactose (sugar in milk).

Effect of carbohydrate on blood glucose. Define the major macronutrients in foods that contain calories (carbohydrate, protein and fat). Review that carbohydrate has the most pronounced effect on blood glucose and that most carbohydrates have a similar effect on blood glucose when eaten in similar quantities.

Sources of carbohydrate. Those with diabetes need to develop an awareness of the primary sources of carbohydrate. Foods that contain carbohydrate include:

• Breads, crackers and cereals • Pasta, rice and grains • Starchy vegetables, such as potatoes, corn and peas • Nonstarchy vegetables, such as broccoli, salad greens and carrots • Milk and yogurt • Fruits and juices • Sweets and desserts

Nutrient density. Many sweets and desserts provide a significant amount of calories from fat and do not contribute vitamins and minerals, so discussion of nutrient density or quality of food choices is important.

Measuring carbohydrate. Carbohydrate is measured is grams. One carbohydrate serving is a portion of food that contains 15 g of carbohydrate (1 carbohydrate serving = 15 g).

For basic carbohydrate counting, it is easier to begin by teaching carbohydrate servings rather than counting grams. One carbohydrate serving = one serving of grain, dried beans, starchy vegetables, fruit, milk or sweet/dessert, which in the standard serving size listed is equal to 15 g of carbohydrate. One serving of non-starchy vegetables equals 5 g of carbohydrate, which would be considered “free.” If three or more “free” servings are eaten in a meal, count them as 1 carbohydrate serving.

Those with diabetes should practice estimating and measuring portions using various methods (food scale, measuring cups and measuring spoons).


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Label reading. The Nutrition Facts panel from food labels is the preferred source of carbohydrate information. Steps to using a food label for counting carbohydrate are:

• Find the standard “Serving Size” and the grams of “Total Carbohydrate” for one standard serving of food on the label. Remind clients that sugars are included in the total grams of carbohydrate.

• Compare the standard “Serving Size” of food from the label to the portion being eaten. Remind clients that many packages contain more than one “serving” of food. Increase grams if the portion eaten is larger than the standard serving; decrease grams if it is smaller.

• Calculate the number of carbohydrate servings. Divide the total carbohydrate in the portion of food being eaten by 15 g of carbohydrate per “carbohydrate serving.”

• I f a food has >5 g of fiber per serving, subtract the grams of fiber from the total grams of carbohydrate before calculating carbohydrate servings.

• If a food has >10 g of sugar alcohols (which have about half the caloric value of other carbohydrates and a smaller effect on blood glucose) per serving, half the amount of sugar alcohol can be subtracted before calculating carbohydrate choices.

Calculating caloric needs and amount of carbohydrate. The last component of teaching basic carbohydrate counting is addressing how much carbohydrate to eat. Amount of carbohydrate should be individualized, based on usual carbohydrate intake and nutrition goals set by the client and RD, considering the client’s therapeutic regimen. Clients should be provided with a meal plan with individualized carbohydrate goals.

If a dietitian is not available to provide an individualized meal plan or complete a comprehensive assessment, a reasonable recommendation is to use three to five carbohydrate servings at each of three meals and one to two carbohydrate choices at snacks, if they are appropriate or desired.

The following steps are important to teach with basic carbohydrate counting: Step 1: Learn which foods contain carbohydrate Step 2: Understand how to measure carbohydrate in food

• 1 carbohydrate choice = 15 g carbohydrate Step 3: Learn the grams of carbohydrate in common foods

• Learn how to use food labels for carbohydrate counting • Learn how to determine 1 carbohydrate choice

Step 4: Learn to estimate portion sizes and how much carbohydrate you are eating Step 5: Learn how to determine carbohydrate needs

• To lose weight: women, 2 to 3 servings/meal; men, 3 to 4 servings/meal • To maintain weight: women, 3 to 4 servings/meal; men, 4 to 5 servings/meal • For active people: women, 4 to 5 servings/meal; men, 5 to 6 servings/meal


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Carbohydrates in a Typical Meal Plan Based on 1,500 calories with 50% of calories from carbohydrate

Meal Carbohydrate Choices Grams

Breakfast 3 45

Lunch 3 15

Snack 1 15

Dinner 4 60

Snack 1 15

Advanced Carbohydrate Counting Advanced Carbohydrate Counting is a booklet developed by the ADA and the American Dietetic

Association (published in 2003; updated in 2012) to teach how to use food records to create personalized insulin/carbohydrate ratios to improve blood glucose control and allow increased flexibility of food choices and timing of meals and snacks.

Record keeping is the first component of advanced carbohydrate counting. A client must keep and study several weeks of detailed records of food, medication, physical activity and blood glucose levels. Records (print or electronic from a computer download or app) should be reviewed with feedback provided, whenever possible. Initially, the diabetes care team will make insulin adjustments; however, as time passes, the client will assume responsibility for making adjustments, with appropriate coaching.

To learn the effects of carbohydrate intake on blood glucose, it is necessary for the client to check blood glucose levels before and two hours after the start of some meals to see trends in blood glucose levels. Information necessary to track advanced carbohydrate counting and pattern management are meal time, amount and type of food eaten, estimate of carbohydrate per food item, and total amount of carbohydrate for each meal and snack. Recording insulin doses is important, as well as any unusual circumstances such as illness, stress or menstrual cycle.

Pattern management is a systematic approach to identifying patterns in blood glucose reading to determine if changes are needed in medical management to improve blood glucose control. The benefits of using pattern management, which is an anticipatory approach, instead of the commonly used Sliding Scale method (blood sugar is tested, and based on the amount of glucose in the blood, a set amount of insulin is administered), is a compensatory approach.


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Pattern Management vs. Sliding Scale16 Pattern Management Sliding Scale

Adjusts insulin therapy based on patterns of blood glucose over several days

Addresses the cause of the problem (e.g., schedule, carbohydrate, activity, insulin dose)

Problem-solving approach Patterns reflect previous insulin dose

Adjusts insulin to correct a single blood glucose at the moment

Lag time/time of day/cause of problem not considered

Quick-fix approach Asks insulin to “work backward” Requires hyperglycemia or hypoglycemia

before action

Ratio and correction factor calculation. An insulin:carbohydrate ratio tells the client how much

rapid- or short-acting insulin is needed to “cover” the carbohydrate that is eaten at a meal or snack. Knowing how to match insulin doses with what the client eats allows greater flexibility of lifestyle along with improved glucose control.

The preferred method of figuring an insulin:carbohydrate ratio is to use several days of food records, blood glucose records and total daily dose of insulin. In general, about half of the TDD is background (basal) insulin and half is mealtime (bolus) insulin. Insulin:carbohydrate ratios can vary from meal to meal, active days vs. sedentary days, or because of illness or stress. It may be necessary to use a different insulin:carbohydrate ratio for different meals or from day to day, depending on activity level.

To calculate the insulin:carbohydrate ratio, divide the number of grams of carbohydrate eaten at the meal by the units of pre-meal insulin. For example, if a client with diabetes uses 5 units of pre-meal insulin and is eating 75 g of carbohydrate, the insulin:carbohydrate ratio is 75 divided by 5, or 15, which equals 1 unit of insulin per 15 g of carbohydrate — a 1:15 ratio.

This calculation assumes the pre-meal blood glucose is in the target range. If the pre-meal blood glucose is above or below the target range, an additional correction bolus is needed.

Two other methods used to calculate an insulin:carbohydrate ratio are the “weight method” and the “450 to 500” rule. These methods are not as accurate as food records because they don’t take individual amounts of carbohydrate eaten at meals into account.

The 450 to 500 rule uses the following formula for calculating the insulin-to-carbohydrate ratios: Divide the total daily insulin into 450 (for regular insulin) or 500 (for rapid-acting insulin — lispro [Humalog] or aspart [NovoLog]). For example, if the total daily insulin dose is 50 units and the patient is using rapid-acting insulin, the insulin:carbohydrate ratio would be 10 (500/50).


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Insulin:Carbohydrate Ratio7 Weight (lb) Ratio

120 to 129 130 to 139 140 to 149 150 to 159 170 to 179 180 to 189 190 to 199

200+

1:15 1:14 1:13 1:12 1:11 1:10 1:9 1:8

An additional component of calculating an insulin:carbohydrate ratio is calculation of a correction

factor. This factor is used to correct a high or low blood glucose level before a meal. A correction factor is added (or subtracted) to the pre-meal bolus insulin dose. A correction factor of 1,800 is used for rapid-acting insulin and 1,500 for regular insulin. The formula is 1,800 or 1,500 divided by the TDD of insulin.

For example, if a client uses 50 units of total daily insulin and Humalog insulin before meals, the correction factor would be 36 (1,800 divided by 50). This means that 1 additional unit of insulin will lower blood glucose approximately 36 mg/dL. If a client’s blood glucose level is 169 mg/dL before lunch, and target blood glucose range is <130 mg/dL, an additional unit of insulin is needed to correct for pre-meal high blood glucose (169 – 130 = 39). This extra unit of insulin would be added to the pre-meal bolus insulin dose calculated using the lunch insulin:carbohydrate ratio.

If the lunch insulin:carbohydrate ratio is 10, and the client plans to eat 60 g of carbohydrate, he/she would take 6 units of rapid-acting insulin to cover the meal, plus 1 additional unit of rapid-acting insulin to compensate for the initial high blood glucose — 7 units total.

[See Appendixes 6 and 7 for more information on mealtime or bolus insulin supplement/advanced carbohydrate counting.]

Fat- and/or Calorie-Counting Approach

A low-fat eating (25% to 30% fat) pattern, using either fat- and/or calorie-counting meal plans, was used as a strategy to lose weight and/or improve cardiovascular health in both the DPP and Look AHEAD research trials.2,5 Lowering total fat intake, and thereby, total calories, did not consistently improve glycemic control or cardiovascular disease risk factors. Improvements were more likely seen when calories were reduced and weight loss occurred. Many online and print educational resources are available for low-fat and/or low-calorie meal plans (see Appendix 5 for a list of resources).

Exchange Lists for Meal Planning The concept of “exchange” or “substitution” of different foods acceptable for use by clients was

developed by the American Dietetic Association and the ADA in 1950. Before their development, meal-planning approaches in the U.S. were chaotic, with no agreement on educational and meal-planning approaches among the major organizations involved with diabetes and nutrition. The goal was to develop an educational tool that would provide uniformity in meal planning and allow a wider variety of foods to be included.


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Exchange lists for meal planning originally grouped foods into six lists called exchange lists. Each list was a group of measured foods of approximately the same nutritional value; therefore, foods on each list could be substituted or “exchanged” with other foods in the same list.

The six exchange lists were: • Starch/bread • Meat/meat substitutes • Vegetables • Fruits • Milk • Fat

Within each food group, one exchange or choice was approximately equal to another in calories, and in the amount of carbohydrate, protein and fat it contained.

In 1995, a work group of the American Dietetic Association and the ADA Nutrition Education Resources Steering Committee revised the Exchange Lists for Meal Planning. In 2008, the lists were revised again, and the title was changed to Choose Your Foods: Exchange Lists for Diabetes. The exchange lists have been divided into three food groups:

• Carbohydrate Group: includes the Starch List, Fruit List, Milk List, Other Carbohydrate List and the Vegetable List

• Meat and Meat Substitutes Group: contains four meat categories based on the amount of fat they contain and represents the major source of protein in the lists

• Fat Group: contains three fat categories, based on the main type of fat they contain (saturated, polyunsaturated and monounsaturated)

Choose Your Foods: Exchange Lists for Diabetes also alerts consumers to foods that are good sources of dietary fiber, and foods that contribute significant amounts of sodium. Foods on the fruit, vegetable, and whole grain bread and cracker lists contribute an average of about 2 g of dietary fiber per exchange serving; however, a fiber symbol is next to foods that have ≥3 g of fiber/serving.

A sodium symbol is next to foods that contain ≥400 mg of sodium per exchange serving; however, another symbol is next to foods that will also contribute ≥400 mg of sodium per serving when two or more exchanges are eaten in one day. In addition, a yield symbol identifies foods that contain extra fat or are prepared with added fat.

Choose Your Foods: Exchange Lists for Diabetes can be used for either type 1 or type 2 diabetes. For those with type 1 diabetes, the list can be used to emphasize the need for consistency in the timing of food intake and to identify the amount of food to be eaten at meals and snacks while providing for needed variety and flexibility. For those with type 2 diabetes, they can be used to teach caloric and fat values of foods.

When used with appropriate clients, the Choose Your Foods: Exchange Lists for Diabetes can provide a framework for grouping foods that takes into account the calorie, carbohydrate, protein and fat content of foods. Also, the exchange lists emphasize important nutritional management concepts such as calorie control, fat modifications, fiber content and an awareness of high-sodium foods.

Choose Your Foods: Exchange Lists for Diabetes can teach those with diabetes and healthcare professionals the amount of carbohydrate, protein, fat and calories contributed by foods. With an understanding of the basis of the exchange lists, clients and professionals can use nutrient values from food labels and can incorporate a wider variety of foods into the meal plan.


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Menu Approach The menu is the basis of all meal-planning approaches. It is the written description of what can and

should be eaten. Ideally, the RD will incorporate some degree of menu planning into whatever nutrition counseling approach is chosen. In fact, the RD should write out at least one sample menu to illustrate how meals can be designed to fit a client’s individual nutrition care plan.

An individualized menu is a method of meal planning whereby the RD works with the client to prepare menus that specify the foods (and appropriate quantities) that should be eaten over a period of days that reflect the individualized nutrition goals. Menus can be specific or involve choices. The client is not expected to follow the menus indefinitely, but will learn how to select foods and determine appropriate portion sizes.

RDs traditionally discourage the use of preprinted menus because they are not individualized. However, there may be situations in which preprinted menus could be developed specifically for a certain population (and be individualized to the eating style of that group). They can be useful for the dietitian when counseling time is very limited and there will be an opportunity at a later time to follow up with a more customized approach.

The simplicity of this approach is its major advantage. Those who have routine eating habits and eat at consistent times/places are likely to do better than those without a routine. However, this method may be good for those without routines, as it forces structure and discipline, while allowing freedom of choice regarding menu selection. The disadvantage with this approach is that individualized menus may be too restrictive or monotonous in regard to food choices.

Meal Planning There is no right or wrong method, and not every client needs a complex system of meal planning.

Any method, technique or teaching tool that supports the nutrition management goals of achieving or maintaining desirable body weight, determines the appropriate serum glucose and lipid levels, promotes good nutrition and is realistic and workable for the client with diabetes is acceptable.

Selection of Meal-Planning Approaches Category (Diabetes) Type 1 Type 2: Non-obese Type 2: Obese

Basic Meal Plan Approaches

Plate Method X X X

Mediterranean X X X

Vegetarian/Vegan X X

DASH X X

Meal Plan Approaches

Basic carbohydrate counting X

Advanced carbohydrate counting X

Calorie counting X

Fat counting X

Exchanges X X X

Menus X X Note: This table represents the author’s experience with meal planning approaches. Readers may modify the table.


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Nutrition educators should be flexible and creative. Boredom can set in with any regimen and can lead to noncompliance. It is the responsibility of the RD to promote continuity of learning by introducing new ideas and concepts and altering the learning environment. Taking the time to listen to clients and hear what they are saying, and providing them with new possibilities will promote more permanent behavior changes than giving them a standardized or structured tool for meal planning.

There are many educational resources available to teach meal planning. The important issue is to individualize the resource to the client, and employ an effective method of education and counseling that will promote positive changes in eating behavior. Gradual change is often the key to incorporating changes into lifelong eating habits. Education and counseling about meal planning and eating behaviors is a continual process!

Review Questions 1. What behaviors indicate a need for structured meal planning? 2. Which meal-planning approaches are best for teaching healthy eating and glucose/weight

control? Answer 1:

• Frequent meal skipping; variable calorie intake; making inappropriate food choices; unsuccessful previous weight-loss attempts; no improvement in blood glucose level after eating changes; interest in more information.

Answer 2: • Healthy eating: MyPlate method, DASH eating plan, Mediterranean eating plan and

vegetarian/vegan eating plan • Glucose/weight control: fat and/or calorie counting; basic and/or advanced

carbohydrate counting

References 1. Ali MK, Bullard KM, Saaddine JB, et al. Achievement of goals in U.S. diabetes care, 1999-2010. N Engl J

Med. 2013;368(17):1613-1624.

2. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346(6):393-403.

3. Diabetes Prevention Program Research Group, Knowler WC, Fowler SE, et al. 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study. Lancet. 2009;374(9702):1677-1686.

4. Look AHEAD Research Group, Wing RR, Bolin P, et al. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med. 2013;369(2):145-154.

5. Raynor HA, Jeffery RW, Ruggiero AM, et al. Weight loss strategies associated with BMI in overweight adults with type 2 diabetes at entry into the Look AHEAD trial. Diabetes Care. 2008;31(7):1299-1304.


7. Green Pastors J, Waslaski J, Gunderson H. Diabetes meal planning strategies. In: Diabetes Medical Nutrition Therapy and Education. Chicago, IL: American Dietetic Association; 2005:201-217.

8. ChooseMyPlate. United States Department of Agriculture Web site. http://www.choosemyplate.gov. Accessed February 16, 2015.


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10. Barnard ND, Cohen J, Jenkins DJ, et al. A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled 74-wk clinical trial. Am J Clin Nutr. 2009;89(5):1588S-1596S.

11. Craig WJ, Mangels AR. American Dietetic Association. Position of the American Dietetic Association: vegetarian diets. J Am Diet Assoc. 2009;109(7):1266-1282.

12. U.S. Department of Health and Human Services. Your guide to lowering your blood pressure. National Heart, Lung, and Blood Institute Web site. http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf. Revised April 2006. Accessed February 16, 2015.

13. Bantle JP, Wylie-Rosett J, Albright AL, et al. Nutrition recommendations and interventions for diabetes—2006: a position statement of the American Diabetes Association. Diabetes Care. 2006;29(9):2140-2157.

14. Delahanty LM, Halford BN. The role of diet behaviors in achieving improved glycemic control in intensively treated patients in the Diabetes Control and Complications Trial. Diabetes Care. 1993;16(11):1453-1458.

15. Thomas D, Elliott EJ. Low glycemic index, or low glycaemic load, diets for diabetes mellitus. Cochrane Database Syst Rev. 2009;1:CD006296.

16. Pearson J, Bergenstal R. Fine-tuning control: pattern management versus supplementation. Diabetes Spectr. 2001;14(2):75-78.


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Chapter Eight: Special Topics for Meal Planning

here are special concerns that clients need to understand, including use of alcohol, dining out (especially at fast food restaurants) and snacking. The most important issues to address with those with type 1 diabetes are the treatment of hypoglycemia and sick-day management.

Alcohol

Alcohol is absorbed rapidly by the stomach and small intestines, and appears in the bloodstream within five minutes after ingestion. Alcohol concentration in the blood reaches its highest level 30 to 90 minutes after ingestion. Foods high in fat and protein may slow down the alcohol absorption rate by delaying gastric emptying. In 75% of people with no chronic exposure, alcohol is metabolized by the liver, primarily by the alcohol dehydrogenase pathway. The initial step in the alcohol dehydrogenase system is the conversion of alcohol to acetaldehyde by an enzyme, alcohol dehydrogenase. Acetaldehyde is reduced further by another enzyme, acetaldehyde dehydrogenase, to carbon dioxide, water and acetyl coenzyme A. Both carbon dioxide and water are eliminated from the body, whereas acetyl-CoA is converted subsequently to fatty acids stored by the body.1

Because alcohol and fats are metabolized through common intermediates — two carbon units and acetyl-CoA — calories from alcohol can be substituted for fat in a diabetes meal plan.

Moderate alcohol intake of one to two drinks/day (drink equals 12 oz of regular beer, 5 oz of dry wine or 1.5 oz of distilled liquor) with a meal does not have detrimental effects on blood glucose levels in type 2 diabetes; however, in type 1 diabetes, there are minimal acute effects on glucose levels and insulin needs.2

With type 1 diabetes, there is a risk of late-onset hypoglycemia with alcohol use. Self-monitoring of blood glucose before and after alcohol intake allows for prediction of potential hypoglycemia and prevention.3 Another concern is the impact of alcohol and potential hypoglycemia on cognitive function with driving.

For those with type 2 diabetes, a risk of alcohol-induced acute hypoglycemia is modest.3 Moderate intake of alcohol is associated with reduced risk of cardiovascular disease in type 2 diabetes. The mechanism may be related to improvements in insulin sensitivity.4

Some research has suggested that alcohol intake may increase triglyceride levels, increase blood pressure and promote weight gain. It appears this is only with excessive intakes of alcohol; with moderate levels of consumption, there is no evidence that this increases risk of congestive heart disease or mortality.3 In those with diabetes, a limited number of studies examined the effect of alcohol intake on triglycerides, blood pressure and weight.

Nutritional Composition of Alcoholic Beverages Alcohol is a concentrated source of calories, yielding 7 kcal/g, compared to carbohydrates and

protein, which yield 4 kcal/g, and fat, which yields 9 kcal/g. Alcohol provides energy but no essential nutrients. Calorie and carbohydrate content of liquors should not be overlooked; otherwise, total daily calorie intake can be underestimated.

T

Special Topics for Meal Planning

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Alcoholic beverages vary in carbohydrate content; distilled spirits have virtually no carbohydrate content, whereas sweet wines, beers and cordials may contain considerable quantities. Because of their carbohydrate content, mixers can be an additional source of calories (see Appendix 2 for information on alcoholic beverage composition).

If a client with diabetes is planning to incorporate alcohol into the meal plan, the type of alcohol and quantity should be calculated. One alcohol equivalent is equal to 1.5 oz of distilled liquor, 5 oz of wine or 12 oz of beer. Dry wines and low-calorie wines that are lower in carbohydrate should be recommended in place of sweeter wines, as should reduced-calorie beer. Labels on distilled liquor indicate the proof, which is equal to twice the alcohol percentage.

Carbonated beverages used in mixed alcoholic beverages can add significant calories and carbohydrate, and increase blood glucose level. Calorie-free mixers can be used in place of the more calorically dense mixers. For some, occasional ingestion of an alcoholic beverage will probably not cause problems. Clients should be educated in responsible drinking rather than have alcohol forbidden altogether. In addition, they should have a clear understanding of what constitutes responsible drinking, and not be left uncertain and feeling guilty every time they have a drink.

Clients who should be advised to abstain from alcohol use include alcohol abusers; those who have pancreatitis, gastritis, frequent hypoglycemic reactions, and certain types of kidney and heart disease; women with gestational diabetes; and pregnant women with type 1 or type 2 diabetes. Alcohol can interact with barbiturates, tranquilizers and numerous other drugs. Clients with diabetes should check with their physician to see if any contraindications apply to them.

If diabetes is well controlled, moderate use of alcohol is unlikely to affect blood glucose adversely; however, it is important to verify this through blood glucose monitoring. Those who take insulin should limit intake to no more than two drinks/day. In the fasting state, alcohol may produce hypoglycemia. This is because alcohol cannot be converted to glucose, inhibits gluconeogenesis and augments or increases the effects of insulin by interfering with the counter-regulation of insulin-induced hypoglycemia.3

If alcohol is consumed, it should not be counted as part of the meal plan, but in addition to the meal plan. Even though extra calories are consumed, total food intake should not be reduced. In cases where caloric intake is restricted (if weight loss is indicated), alcohol is best substituted for fat (one drink equals two fat exchanges, or about 100 kcal that would have been consumed as fat).

General guidelines for alcohol use are: • For insulin users:

o Limit to two drinks/day for men and one drink/day for women. o Drink only with food. o Do not reduce food intake.

• For non-insulin users: o Limit to two drinks/day for men and one drink/day for women.

• Substitute for fat calories: o Limit to promote weight loss or maintenance. o Limit if triglycerides are elevated (>500 mg/dL).

• Abstain: o If there is a history of alcohol abuse o During pregnancy and lactation


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Eating Out Following a meal plan at home prepares people with diabetes to enjoy eating out. They can eat out

with less hesitation if they know which foods they should eat, portion sizes and how to substitute appropriately. Teaching clients with diabetes to be assertive and curious regarding the foods they order prepares them to make appropriate food selections. Suggestions such as calling the restaurant in advance to obtain more information about the menu and how the food is prepared may make the actual eating out experience easier.

Eating out usually results in a higher fat intake. It may be helpful to recommend that your clients save their fat calories for the day and use them at the meal they plan to eat out. Restaurant-prepared foods are often high in saturated fat, salt and sugar, and low in fiber.

Reducing Fat When Dining at Restaurants5,6 • Order salad dressing, butter, margarine and sour cream on the side, and control the

amount used. • Order reduced-calorie or fat-free salad dressing, or vinegar and a small amount of

oil. • Request that entrées be prepared with minimal fat (broiled, grilled or baked entrées

prepared with a minimal amount of oil or butter). • Request that vegetables be cooked in reduced amounts or without

butter/margarine. • Order “free foods” (lettuce, salad, raw vegetables). • Share an entrée to reduce portion size, and order a side salad or vegetable.

More restaurants offer healthier dessert selections. Examples of dessert choices that would be

acceptable would be fresh fruit, frozen yogurt, a plain piece of pumpkin pie, custard, pudding or plain cake (e.g., order carrot cake and remove the icing).

Fast-Food Guidelines The key to reducing calories and fat in a fast-food restaurant is to buy small portions and eat only

at meal times. The average fast-food meal contains 685 kcal, which is not outrageously high for a meal, but is usually too many calories for a snack. Words on a menu like “jumbo,” “giant” or “deluxe” should signal caution. Larger serving sizes mean additional calories as well as more fat, cholesterol and sodium.

Advise clients to choose wisely; order items without toppings; ask about preparation methods; and avoid sauces, cheese and mayonnaise, which add calories.

The American Diabetes Association publishes helpful resources on restaurant dining and eating out at fast-food restaurants, including Guide to Healthy Restaurant Eating and The American Diabetes Association Guide to Healthy Fast-Food Eating. The guides contains nutrition information for more than 50 fast food chains and gives tips for how to eat out and stay on a meal plan.5,6


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Snacking For children, adolescents and adults requiring insulin, snacks may help prevent fluctuations in

blood glucose levels. The timing of meals and snacks, and nutrient distribution needs to be individualized, rather than

patterned using the antiquated practice of dividing food into three meals and three snacks, with the snacks each containing one-ninth of the total carbohydrate. Those using rapid-acting insulin by injection or on an insulin pump should adjust meal and snack insulin doses based on the carbohydrate content of the meals and snacks.2 To promote optimal metabolic control and to meet caloric needs, most children with type 1 diabetes require snacks throughout the day. Using a basal-bolus insulin regimen is recommended so children do not have to follow a fixed schedule of meals and snacks.

When children reach adolescence, conformity with peers is of utmost importance and may provide additional challenges in coordinating the insulin schedule with meal/snack patterns. Insulin adjustments must be made to accommodate desired changes in eating patterns. For example, the morning regular insulin can be decreased to allow for omission of the morning snack. Individualized food/meal plans and insulin regimens can provide flexibility to accommodate irregular meal times and schedules, varying appetites and varying activity levels. Blood glucose monitoring data can be used to integrate insulin into meal/snack and exercise schedules.

A controversial issue with snacking and diabetes is the necessity of including a protein-containing bedtime snack, particularly for clients requiring insulin. Limited research has been done on the question of protein in bedtime snacks. In one study, four bedtime snacks were tested.7 They did not test a carbohydrate-only bedtime snack. The authors concluded that the need for a bedtime snack depends on bedtime glucose, such that no snack is necessary at blood glucose levels >180 mg/dL. At levels between 126 mg/dL and 180 mg/dL, any snack is advised; at <126 mg/dL, a standard snack is recommended. Logically, it is likely that an all-carbohydrate snack would have worked just as well. One protein serving contains 7 g of protein, and even if 60% were converted to glucose and enter the circulation, this would be about 4 g of glucose. It is difficult to believe that 4 g of glucose ingested at bedtime is going to prevent hypoglycemia 5+ hours later.

One study examined using protein to the treat hypoglycemia. The treatments compared were 15 g of carbohydrate from bread, or 15 g of carbohydrate from bread and 2 oz of meat. Response to both treatments was identical, and the rate of redevelopment of hypoglycemia also did not differ. The authors concluded that adding protein to the treatment of hypoglycemia merely adds calories rather than prolonged protection against subsequent hypoglycemia.8

Encouraging clients with diabetes to monitor blood glucose before bedtime, especially if prone to hypoglycemia, may be the best advice in making the decision about the amount and composition of the snack.9

For clients with type 2 diabetes, snacking should be discouraged if it is not needed for blood glucose control, as they have a delayed response to insulin secretion. A four- to five-hour period after meals is usually needed to return glucose levels to baseline, and snacking between meals prevents normalization of glucose levels during the day. Also, most clients with type 2 diabetes are overweight, and recommending an eating pattern of three meals per day generally encourages healthier food choices and lower caloric intake. Individualization is important in promoting permanent behavior change, especially for clients who have a long history of snacking. When clients are not willing to change their usual pattern of eating, snacks that contain less than 20 kcal would be recommended.


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Snacks and Beverages <20 Kcal Beverages Foods

Club soda with 2 Tbsp of fruit juice Diet soda Iced tea w/artificial sweetener Coffee or hot tea (use artificial sweetener,

and skim or 1% milk if desired) Hot chocolate (use hot water and half a

packet of sugar-free hot cocoa mix) Fat-free broth or bouillon

Raw vegetables (e.g., celery, cucumber, green and red pepper, broccoli, cauliflower, lettuce and mushrooms)

7 pretzel sticks 1 cup of air-popped popcorn 3 mini rice cakes

Hypoglycemia Hypoglycemia is defined as an abnormally low blood glucose level, and is also referred to as insulin

reaction, insulin shock and low blood sugar. It can result from the administration of excessive insulin or oral diabetes agents, too little food intake, delayed or missed meals or snacks, exercise or other physical activity, or alcohol intake without food. A blood glucose level of ≤70 mg/dL indicates hypoglycemia.10

Hypoglycemia usually occurs in those with type 1 diabetes and in insulin-treated clients with type 2 diabetes. Signs and symptoms, treatment and prevention of hypoglycemia should be reviewed with clients who take insulin.

Symptoms. Initial symptoms are anxiety, irritability, light-headedness and shakiness. Advanced symptoms include headache, blurred vision, lack of coordination, confusion, anger and numbness in the mouth.

Prevention of hypoglycemia is an important component of diabetes self-management. SMBG and use of a continuous glucose monitor in those at high risk for or with continuous episodes of hypoglycemia are key tools to detect hypoglycemia and evaluate medication therapy. Clients with diabetes who are on insulin should understand that certain behaviors can increase the risk of hypoglycemia —intense exercise, meal skipping or not eating when sick, when fasting for tests or procedures, and, possibly, during sleep. Providing education about insulin adjustment, glucose pattern management, use of insulin:carbohydrate ratios for managing carbohydrate intake, treatment during intense exercise and sick-day management can be helpful to prevent hypoglycemia.

Treatment. Hypoglycemia must be treated immediately with glucose. Fifteen grams of simple carbohydrate is recommended for treatment; this amount raises the blood glucose level by 30 mg/dL to 45 mg/dL in 15 to 30 minutes. The response to the carbohydrate varies from person to person, and is influenced possibly by how low blood glucose actually is and the cause of the reaction.

The treatment procedure described is often referred to as the “15/15 rule” — take 15 g of carbohydrate and test blood glucose in 15 minutes. If blood glucose levels remain low (<70 mg/dL), treatment should be repeated, even if not symptomatic. A meal or snack should be eaten within the next hour to prevent further reduction of blood glucose levels.


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15-g Carbohydrate Sources for Treating Hypoglycemia11

3 to 4 glucose tablets 8 to 10 Lifesaver candies 2 Tbsp of raisins 4 oz of nondiet soft drink 4 oz of fruit juice 1 cup of nonfat milk

General guidelines for treating hypoglycemia are:11

• Wait 15 minutes after initial treatment and test blood glucose level to determine if additional treatment is needed.

• Treat using blood glucose level as a guide, rather than continuing to eat until symptoms disappear.

• High-fat foods will delay peaking of glucose levels from carbohydrate intake and should be avoided (e.g., treatment of hypoglycemia with chocolate bars).

• Clients who use insulin should always carry a simple carbohydrate for emergency treatment of hypoglycemia; glucose products should be available at the bedside during periods of sleep, as well as in the car while driving.

• Clients who take insulin should always wear diabetes identification. Over-treatment of hypoglycemia can occur very easily if a person relies only on symptoms and not

on blood glucose results. Over-treatment with additional food can cause post-treatment hyperglycemia. Using commercially available, portion-controlled glucose products can help avoid overtreatment.

Sick-Day Management

The main rules for sick-day management are: • Take diabetes medication (insulin or antihyperglycemic agent) • Self-monitor blood glucose • Test urine ketones, if on insulin • Eat the usual amount of carbohydrate, divided into smaller meals and snacks if necessary; if

blood glucose is 250 mg/dL or higher, all of the usual amount of carbohydrate is not necessary

• Drink fluids frequently • Call the diabetes care team

Ketones in the urine and an elevated blood glucose level indicate that additional insulin, particularly regular or short-acting insulin, may be needed. When the body is unable to use glucose, it breaks down fats for energy, and the byproducts of the fat breakdown are ketones. Along with elevated blood glucose levels, the presence of ketones in the urine indicates the potential for diabetic ketoacidosis.

Blood glucose levels should be monitored very closely, as blood sugar can rise due to changes in hormones and metabolism during an illness. If the blood glucose level is 250 mg/dL or higher continuously for 24 hours, the physician should be informed. Those with type 2 diabetes may lapse


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into coma without any sign of ketones in their urine due to the potential of hyperosmolar hyperglycemic state (also known as hyperosmolar hyperglycemic nonketotic coma).

Consuming fluids and taking an adequate dose of insulin are critically important during an illness. Soft, semisolid foods in small amounts are better tolerated during an illness.

Vomiting and diarrhea cause loss of fluid as well as the electrolytes potassium and sodium. Adequate rehydration is extremely important because it helps restore and maintain the depleted vascular volume, and it enhances the kidneys’ ability to excrete glucose, thus lessening hyperglycemia.12 Broth or bouillon and tomato juice help replace some of the lost sodium. If unable to tolerate solids or semisolid foods, the person should drink liquids with appropriate amounts of calories and carbohydrate.

A list of sick-day foods, including sugar-containing items (e.g., soft drinks, gelatins) not routinely purchased by those with diabetes, should be provided.

High-Protein, Low-Carbohydrate Diet Recommendations

The high-protein, low-carbohydrate diet has resurfaced in popularity. Weight loss and improved blood lipids, including triglycerides, VLDL triglyceride, VLDL cholesterol, total cholesterol and HDL cholesterol, have been demonstrated in several studies of high-protein, low-carbohydrate diets.13 Weight loss in these studies confounds the interpretation of the results — is it the low-carbohydrate or the low-calorie intake that causes weight loss? There is no consistent definition of “low carbohydrate.” In research studies, carbohydrate ranges varied from very low (21 g/day to 70 g/day) to moderately low-carbohydrate (<30% to 40% of calories).14 If weight is lost, insulin needs may drop, and blood glucose and lipid levels may improve.

The reason these diets assist with weight loss is most likely because they eliminate a whole category of nutrients and, as a result, are lower in calories. Carbohydrates alone aren’t to blame for weight gain, but rather, consuming too many calories from any source and burning too few. Also, with a high-protein intake and strict limitation of carbohydrate, water stored from glycogen is released — this is the primary reason for the initial, rapid weight loss. The effect of ketone development with these diets also results in weight loss from decreased appetite.9,15

There is insufficient evidence to support one specific amount of carbohydrate intake in diabetes. It is increased physical activity, caloric restriction and/or moderate weight loss, and controlling fat intake that have been shown to improve insulin sensitivity, not changes in the protein-to-carbohydrate ratio.16,17 High-protein, low-carbohydrate diets restrict whole grains, fruits and vegetables — foods that are linked to prevention of cancer and heart disease. To replace carbohydrates, they encourage meat substitutes such as cheese and fats (e.g., butter and cream), foods that are high in saturated fat that may increase the risk of coronary artery disease, in particular, increasing LDL cholesterol levels. Foods high in saturated fat have also been shown to increase the risk of some types of cancer.

Those with diabetes, high blood pressure, heart disease and kidney disease should be careful. Kidneys have to work hard to process waste from the breakdown of proteins. The high-protein, low-carbohydrate diet may not be harmful for a short period, but long-term improvements in health can be sacrificed for only temporary weight loss.


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Review Questions 1. What are recommendations for alcohol use in clients with diabetes? 2. What are the differences in snacking between those with type 1 and type 2 diabetes? 3. What are early and advanced clinical symptoms of hypoglycemia? 4. How can hypoglycemia be prevented? 5. What are the main rules for sick-day management? 6. What are the primary concerns with a high-protein, low-carbohydrate diet?

Answer 1:

• Alcoholic beverages should be used in moderation and allowed only if diabetes is well controlled.

• For clients with type 1 diabetes at normal weight, one to two equivalents (one for women and two for men) can be used as an “extra”; food should not be omitted.

• For clients with type 2 diabetes whose weight is a concern, calories from alcohol should be counted in the meal plan. Two equivalents of alcohol is equal to 90 kcal. Meals and snacks should still be eaten on time. Alcohol should not be consumed on an empty stomach; rather, it should be used with meals.

• Drinks should be sipped slowly; symptoms of alcohol intoxication are similar to hypoglycemia. Alcoholic drinks that contain simple sugar should be avoided. Those with diabetes should wear visible identification.

Answer 2:

• Type 1 diabetes: snacking helps to prevent fluctuations in blood glucose level. Snacking may be needed to correspond with peak insulin activity/physical activity.

• Type 2 diabetes: snacking is discouraged because of delayed insulin reaction and to encourage weight loss for the overweight person with type 2 diabetes.

Answer 3:

• Early symptoms include anxiety, irritability, lightheadedness and shakiness.

• Advanced symptoms include headaches, blurred vision, lack of coordination, confusion, anger and numbness of the mouth.

Answer 4:

• Educate patients about effects of omitting meals or snacks, treatment for intense exercise with appropriate insulin adjustment or food intake, and treatment of sick days. Be knowledgeable about the onset, peak and duration of the insulin dose and use of insulin:carbohydrate ratios to balance insulin with carbohydrate intake. Do SMBG as part of the daily regimen.

Answer 5:

• Take insulin or oral diabetes agent.

• Self-monitor blood glucose.

• Test urine for ketones.

• Try to eat usual amounts of carbohydrate.

• Drink frequent fluids.

• Call the diabetes care team. Answer 6:

• Lack of definition of a low-carbohydrate diet

• Temporary weight loss

• Low-nutrient intake from lack of fruits and vegetables

• High-saturated fat intake leading to increased lipid levels


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References 1. Zakhari S. Overview: how is alcohol metabolized by the body? Alcohol Res Health. 2006;29(4):245-254.


3. Franz MJ. Alcohol and diabetes. In: Franz MJ, Evert AB, eds. American Diabetes Association Guide to Nutrition Therapy for Diabetes. 2nd ed. Alexandria VA: American Diabetes Association; 2012.

4. Bantle AE, Thomas W, Bantle JP. Metabolic effects of alcohol in the form of wine in persons with type 2 diabetes mellitus. Metabolism. 2008;57(2):241-245.

5. Warshaw H. Guide to Healthy Fast-Food Eating. 2nd ed. Alexandria, VA: American Diabetes Association; 2009.

6. Warshaw H. American Diabetes Association Guide to Healthy Restaurant Eating: What to Eat in America’s Most Popular Chain Restaurants. 4th ed. Alexandria, VA: American Diabetes Association; 2009.

7. Kalergis M, Schiffrin A, Gougeon R, Jones PJH, Yale JF. Impact of bedtime snack composition on prevention of nocturnal hypoglycemia in adults with type 1 diabetes undergoing intensive insulin management using Lispro insulin before meals: a randomized, placebo-controlled, crossover trial. Diabetes Care. 2003;26(1):9-15.

8. Gray RO, Butler PC, Beers TR, Kryshak EJ, Rizza RA. Comparison of the ability of bread versus bread plus meat to treat and prevent subsequent hypoglycemia in patients with insulin-dependent diabetes mellitus. J Clin Endocrinol Metab. 1996;81(4):1508-1511.

9. Franz MJ. Protein controversies in diabetes. Diabetes Spectrum. 2000;13(3):132-142.

10. Cryer PE. Hypoglycemia in Diabetes: Pathophysiology, Prevalence, and Prevention. Alexandria, VA: American Diabetes Association; 2009.

11. Sisson EM, Cornell S. Pharmacotherapy for glucose management. In: Mensing C, ed. The Art and Science of Diabetes Self-Management Education Desk Reference. 2nd ed. Chicago, IL: American Association of Diabetes Educators; 2011:417-458.

12. Kaufman FR. Medical Management of Type 1 Diabetes. 6th ed. Alexandra, VA: American Diabetes Association; 2012.

13. Kirk JK, Graves DE, Craven TE, et al. Restricted-carbohydrate diets in patients with type 2 diabetes: a meta-analysis. J Am Diet Assoc. 2008;108(1):91-100.


15. Green Pastors J, Arnold MS, Daly A, et al. Diabetes Nutrition Q & A for Health Professionals. Alexandria, VA: American Diabetes Association; 2003.

16. Mayer-Davis EJ, Monaco JH, Hoen HM, et al. Dietary fat and insulin sensitivity in a triethnic population: the role of obesity. The Insulin Resistance Atherosclerosis Study (IRAS). Am J Clinc Nutr. 1997;65(1):79-87.

17. Mayer-Davis EJ, D’Agostino R Jr, Karter AJ, et al. Intensity and amount of physical activity in relation to insulin sensitivity: the Insulin Resistance Atherosclerosis Study. JAMA. 1998;279(9):669-674.


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Chapter Nine: Special Management Concerns

regnancy presents special problems for those with diabetes. It is important for women with diabetes to understand the impact of diabetes on pregnancy so they can make informed choices, as well as manage diabetes appropriately.

Pregnancy

Before insulin was available, few women with diabetes could conceive. If pregnancy occurred, perinatal mortality rate was high — it has been estimated at 42%. Since 1921, the outlook is considerably brighter, and if diabetes is diagnosed and well controlled, the rate of maternal complications approaches that of the normal population. Perinatal mortality has decreased as well.

Uncontrolled diabetes, however, can have devastating consequences.

Complications of Women With Preexisting Diabetes Who Become Pregnant1

Maternal Complications Fetal Complications

Before Pregnancy During Pregnancy

Progression of retinopathy Progression of nephropathy Hypertension

Blood sugar control is difficult

Hypertension Hypertensive disorders of

pregnancy (preeclampsia, eclampsia and chronic hypertension)

Diabetic ketoacidosis Progression of retinopathy Progression of nephropathy Cesarean delivery

Stillbirths Neonatal deaths Macrosomia Prematurity Traumatic deliveries Hypoglycemia Polycythemia Polyhydramnios Jaundice Respiratory distress syndrome Congenital anomalies Hypocalcemia

Several studies conducted during the last 10 years have compared the percentage of anomalies in

infants born to mothers who had undergone preconception counseling and had achieved optimal blood glucose control with those in infants of mothers who had not received such counseling and who had poor control.2 In every study, a larger percentage of anomalies occurred in infants of mothers with poor metabolic control.

Ideally, a woman with type 1 diabetes should have begun to receive preconception counseling at the onset of puberty; it should continue throughout her childbearing years. The blood glucose goals for preconception counseling are to achieve A1C levels as close to normal as possible (<7%).3

P

Special Management Concerns

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Pathophysiology of Diabetes in Pregnancy Pregnancy alters metabolism. The main energy source used by the fetus is glucose (amino acids are

supplied to the fetus for some energy, but mostly for protein needs). The mother’s metabolism makes adjustments to provide for the needs of the fetus, as well as supplying her own needs. To do that, the mother begins to burn fat as her energy source.

The changes in metabolism include lower fasting blood glucose (10 mg/dL to 20 mg/dL less than non-pregnant women), increased fatty acids (higher during normal pregnancy), elevated plasma ketones and lower plasma insulin.4

Two to three times as much insulin is needed during pregnancy to maintain glucose homeostasis. This insulin resistance is a result of the hormones produced for pregnancy (estrogen and progesterone). Another hormone, human placental lactogen, is a potent insulin antagonist. HPL enhances fat mobilization, and reduces maternal glucose use and protein degradation so the fetus has a plentiful supply of glucose and amino acids. Insulinase, produced by the placenta, degrades insulin, reducing its supply even further.5

Diabetes causes additional metabolic abnormalities in pregnancy. The mother experiences a relative insulin deficiency due to resistance of tissues, and decreased production and increased degradation of insulin. Elevation in plasma glucose, free fatty acids, triglycerides and branched-chain amino acids results from the insulin deficiency.

If diabetes is uncontrolled during pregnancy, metabolic abnormalities can cause potentially serious harm to the mother and fetus — specifically, alterations in the amount of energy fuels available and hyperinsulinemia.

Prior Onset of Type 1 and 2 Diabetes

As a result of hormonal changes during the first trimester of pregnancy, blood glucose levels are often erratic for women with preexisting diabetes, which makes glucose control difficult. There is an increased risk of hypoglycemia because of overall lowering of basal glucose and an increased sensitivity to insulin. Hypoglycemia and its treatment should be discussed; the importance of between-meal snacks should be emphasized.

Gastrointestinal upsets may occur at any time, and can make blood glucose control a challenge. Sick-day guidelines should be followed when nausea and vomiting are present. Liberal fluid intake should be encouraged to prevent dehydration. Insulin adjustments will be likely, and more frequent blood glucose monitoring is essential.

Insulin demands increase during the second and third trimesters. Insulin requirements peak at two to three times the prepregnancy level at 38 to 40 weeks’ gestation in response to elevated glucose levels caused by increased production of pregnancy-associated hormones.2

This increased insulin need must be met with exogenous insulin. Meal-plan adjustments are necessary to provide the additional calories to support growth of the fetus. Regular follow-up is needed to monitor calorie and nutrient intake, weight gain and blood glucose control to prevent starvation ketosis.

The general goal for glycemic management in the preconception period and during the first trimester for pregnant women with diabetes should be to obtain the lowest A1C level possible, without undue risk of hypoglycemia. Levels that are as close to normal as possible are desirable.3


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Gestational Diabetes GDM is defined as any degree of glucose intolerance with onset during the present pregnancy. This

definition applies whether or not exogenous insulin is used, and whether or not the condition persists post-pregnancy.6

Awareness of glucose intolerance in pregnancy has improved, and screening finds many more women with GDM. It was once felt that only women with risk factors for diabetes needed to be screened for diabetes. However, research indicates that 35% of all women had no previously identifiable risk factors before diagnosis. There are certain factors, listed below, that place women at low risk for development of glucose intolerance during pregnancy. However, testing should be considered in all women, especially those who are overweight (BMI >25) and have additional risk factors. In January 2014, the U.S. Preventive Services Task Force recommended universal screening for all pregnant women at 24 weeks’ gestation.7 Factors that place women at low risk for GDM are:3

• Age <25 years • Normal body weight • No first-degree relatives with diabetes mellitus • Not of an ethnic group at increased risk for type 2 diabetes mellitus • No history of abnormal glucose tolerance • No history of poor obstetric outcome

Approximately 7% of all pregnant women in the U.S. will be diagnosed with GDM, with 200,000 new cases diagnosed each year.8 The risk of developing GDM is influenced by several factors, including excess body weight, inactivity, older age, history of GDM, previously large-for-gestational-age infant, family history of diabetes and high-risk ethnicity (i.e., African American, Hispanic, Native American).8

The onset of GDM is usually without symptoms, so maternal screening during pregnancy is necessary for diagnosis and treatment. GDM is usually diagnosed between the 24th and 28th week of gestation, but those at high risk should be screened during the first trimester, preferably at the first prenatal visit. Women who have been diagnosed with GDM should be screened for diabetes at 6 to 12 weeks’ postpartum and have lifelong screening for diabetes every three years. If diagnosed with pre-diabetes, they should receive lifestyle intervention and metformin (Glucophage), if needed, to prevent diabetes.3 There are two methods approved for screening GDM:

• “One-step” method approved by the IADPSG based on the results of the Hyperglycemia and Adverse Pregnancy Outcomes study9

• “Two-step” method approved by the NIH based on a consensus development conference10

Screening and Diagnosis of GDM3,9,10

(at 24 to 28 weeks’ gestation in women not previously diagnosed with diabetes)

One-Step Method Two-Step Method

Perform a 75-g OGTT after an overnight fast of at least 8 hours with a plasma glucose measurement at fasting, 1 hour and 2 hours. The diagnosis of GDM is made when any of the following plasma glucose values are exceeded:

• Fasting: >92 mg/dL • 1 hour: >180 mg/dL • 2 hour: >153 mg/dL

Perform a 50-g non-fasting OGTT with plasma glucose measurement at 1 hour. If the plasma glucose level measured at 1 hour is >140 mg/dL, a 100-g fasting OGTT should be performed. Perform a 100-g fasting OGTT. The diagnosis of GDM is made when plasma glucose level is:

• 3 hours: >140 mg/dL

http://www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/gestational-diabetes-mellitus-screening?ds=1&s=gestational diabetes


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Nutritional Management of Diabetes in Pregnancy The goals of nutrition during pregnancy are to provide adequate maternal and fetal nutrition, to

assist in appropriate maternal weight gain and to assist with normalization of maternal blood glucose levels, especially minimizing blood glucose excursions.1

High blood glucose levels need to be evaluated and treated to prevent potential complications for the mother and baby. Blood glucose levels must be monitored regularly at home — particularly fasting and postprandial glucose levels. These results can be recorded and used to make changes and to share with the healthcare provider. Other parameters for evaluation include weight changes, ketone levels and food selection. The most important clinical outcomes for GDM and preexisting diabetes include:

• Achieving and maintaining normoglycemia (recommended glucose levels should be maintained at the following levels):1 o GDM:

§ Fasting plasma glucose: <95 mg/dL § 1-hour postprandial: <140 mg/dL § 2-hour postprandial: <120 mg/dL

o Preexisting diabetes: § Pre-meal, bedtime and overnight glucose: 60 mg/dL to 99 mg/dL § Peak postprandial glucose: 100 mg/dL to 129 mg/dL § A1C: <6%

• Consumption of adequate energy to promote appropriate weight gain and to avoid maternal ketosis o Weight gain recommendations for pregnancy:11

§ Underweight client (BMI <19.8): 28 lb to 40 lb gain § Normal-weight client (BMI 19.8 to 26): 25 lb to 35 lb gain § Overweight client (BMI >26 to 29): 15 lb to 25 lb gain § Obese client (BMI >29): 11 lb to 20 lb gain

• Consumption of food providing nutrients necessary for maternal and fetal health Risk estimates for developing diabetes (usually type 2 diabetes), after GDM vary widely from 2% to

70%, depending on the population studied, criteria used for diagnosis and length of follow-up. Studies that have focused on the immediate postpartum period (i.e., the six-week postpartum follow-up glucose screening) have estimated the risk of glucose intolerance to be as high as 36%; risk of diabetes is 2% to 16%. Cumulative incidence of type 2 diabetes increases markedly in the first five years after delivery and appears to plateau after five years.6

Recent studies have confirmed that the greatest predictors of early postpartum development of type 2 diabetes in women with GDM are:6

• Elevated fasting plasma glucose during pregnancy (>121 mg/dL during pregnancy increases the risk of developing diabetes within four months’ postpartum 21-fold)

• Use of insulin therapy during pregnancy • BMI >35 before or during pregnancy


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Nutrition Recommendations for Preexisting Diabetes and GDM During Pregnancy12

Energy

Adequate energy levels for appropriate gestational weight gain, achievement and maintenance of normoglycemia, and absence of ketones: • In general, there are no additional energy requirements during the

first trimester • Caloric needs increase about 340 kcal/day to 450 kcal/day during

second and third trimesters. Include three small to moderate-sized meals and two to four snacks. Space

snacks and meals at least 2 hours apart A bedtime snack is recommended to diminish the number of hours fasting

and to prevent accelerated ketosis overnight

Carbohydrate

Approximately 45% of energy from carbohydrate has been shown to prevent hyperglycemia (acceptable range for carbohydrate is 45% to 65%)

General carbohydrate guidelines are: 15 g to 45 g at breakfast; 45 g to 75 g at lunch and evening meal; and 15 g to 45 g for snacks.

Blood glucose is often difficult to control after the breakfast meal because of insulin resistance associated with higher hormone levels; carbohydrate is restricted to 15 g to 45 g, and use of highly processed breakfast cereals, sweet drinks including fruit juice and fast foods is discouraged

Recommendations should be modified based on individual assessment and blood glucose monitoring test results

High-sucrose Foods

Emphasize reduction of large amounts of simple carbohydrates, such as desserts and sweetened drinks with low-nutrient density

Recommendations should be individualized based on the client’s ability to maintain blood glucose goals and nutritional adequacy of the diet

Protein

Protein foods do not raise post-meal blood glucose levels Add protein to meals and snacks to help provide enough calories and to

satisfy appetite. Meet the RDA for protein for adult women (0.8 g/kg desirable BW) + 25 g/day

to meet additional protein needs of the fetus

Fat Focus on leaner choices Limit saturated and trans fats

Sodium Not routinely restricted

Fiber Whole grains, and raw fruits and vegetables Activity and fluids help to relieve constipation

Nonnutritive Sweeteners

Generally safe in pregnancy; use in moderation

Vitamins and Minerals

Preconception folate (600 mg/day) Assess for individual needs: adequate calcium, iron, folate, vitamin D and

magnesium are especially important in pregnancy

Fish Avoid mercury-contaminated fish Eat two servings of low-mercury fish per week

Alcohol Avoid alcohol.


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The National Diabetes Education Program is promoting a GDM Diabetes Prevention Initiative, and has a newly revised brochure (Did You Have Gestational Diabetes When You Were Pregnant? What You Need To Know) to help women with a history of GDM (and their families) lower the risk of type 2 diabetes.13 The following actions have been recommended:

• Get tested for diabetes 6 to 12 weeks after your baby is born and every three years thereafter.

• Breastfeed: it may lower your child’s risk for developing type 2 diabetes. • Being overweight puts you at higher risk for type 2 diabetes. • Talk to your healthcare provider about what changes you can make to lose weight and how

to get additional assistance. o Make healthy food choices such as fruits and vegetables, fish, lean meats, dry beans,

whole grains, and low-fat or skim milk and cheese. o Cut down on fatty, fried and processed foods. o Drink water, or sugar-free sodas and fruit drinks. o Eat smaller portions.

• Choose an activity you enjoy and be active at least 30 minutes, five days/week, to burn calories and lose weight.

• Talk to your physician or healthcare provider: o About test results o What you can do to stay healthy o If you plan to become pregnant again (consultation and planning)

Postpartum educational interventions that offer continued support for healthy eating, regular physical activity, weight reduction and breastfeeding are of high importance for all women with GDM after delivery. Postpartum interventions for women with GDM who are at high risk for developing type 2 diabetes need to be developed and incorporated in settings such as WIC clinics and diabetes education programs throughout the country.

Individualization of the meal plan, and use of food and blood glucose records to monitor glycemic control cannot be emphasized enough; however, for some, it may be helpful to have specific nutrition recommendations when getting started. Nutrition recommendations specific to type 1 and type 2 diabetes can be used initially with alterations made based on the individual nutrition history, weight gain, glucose and urine ketone records, and personal needs and preferences.


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Review Questions 1. What are the glycemic goals for pregnant women with prior onset of type 1 or type 2

diabetes? 2. What criteria are used to determine if a woman is at high risk for GDM? 3. What are the greatest risks for women who have had GDM in developing type 2 diabetes? Answer 1:

• Obtain the lowest hemoglobin A1C level possible without undue risk of hypoglycemia to the mother; usually, a level that is <1% above the normal range (i.e., <6%) or approximately 7% is desirable.

Answer 2:

• Older than age 25 • Overweight • First-degree relative with diabetes • Ethnic group at high risk for diabetes (e.g., Hispanic, African American and Native

American) • History of abnormal glucose tolerance • History of poor obstetrical outcome

Answer 3:

• An elevated fasting plasma glucose during pregnancy • Use of insulin therapy during pregnancy • BMI >35 before or during pregnancy

References 1. Reader DM. Pregnancy with Diabetes. In: Mensing C, ed. The Art and Science of Diabetes Self-

Management Education: A Desk Reference for Healthcare Professionals. 2nd ed. Chicago, IL: American Association of Diabetes Educators; 2011:621-658.

2. Coustan DR, Laptook AR, Homko CJ, Biastre S, Daley JM. Medical Management of Pregnancy Complicated by Diabetes Mellitus. 5th ed. Alexandria, VA: American Diabetes Association; 2013.

3. American Diabetes Association. Standards of medical care in diabetes – 2014. Diabetes Care. 2014;37(Suppl. 1):S14-S80.

4. King JC. Physiology of pregnancy and nutrient metabolism. Am J Clin Nutr. 2000;71(5 Suppl):1218S-1225S.

5. Forbes K, Westwood M. Maternal growth factor regulation of human placental development and fetal growth. J Endocrinol. 2010;207(1):1-16.

6. Metzger BE, Buchanan TA, Coustan DR, et al. Summary and recommendations of the Fifth International Workshop-Conference on Gestational Diabetes Mellitus. Diabetes Care. 2007;30(Suppl 1):S251-260.

7. U.S. Preventive Services Task Force recommends screening all pregnant women for gestational diabetes in final statement. U.S. Preventive Services Task Force Web site. http://www.uspreventiveservicestaskforce.org/Page/Topic/recommendation-summary/gestational-diabetes-mellitus-screening?ds=1&s=gestational%20diabetes. Published January 14, 2014. Accessed February 16, 2015.


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8. American Diabetes Association. Gestational diabetes mellitus. Diabetes Care. 2003;26(suppl 1):S103-S105.

9. HAPO Study Cooperative Research Group, Metzger BE, Lowe LP, et al. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med. 2008;358(19):1991-2002.

10. Vandorsten JP, Dodson WC, Espeland MA, et al. NIH consensus development conference: diagnosing gestational diabetes mellitus. NIH Consens State Sci Statements. 2013;29(1):1-31.

11. Institute of Medicine. Weight Gain During Pregnancy: Reexamining the Guidelines. Washington, DC: National Academies Press; 2009.

12. Reader DM. Nutrition therapy for pregnancy, lactation, and diabetes. In: Franz MJ, Evert AB, eds. American Diabetes Association Guide to Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association; 2012:181-203.

13. Did You Have Gestational Diabetes When You Were Pregnant? What You Need to Know. National Diabetes Education Program Web site: http://ndep.nih.gov/publications/PublicationDetail.aspx?PubId=93. Accessed February 16, 2015.


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Chapter 10: Complications of Diabetes

he complications of diabetes mellitus can be divided into two categories: acute and chronic. The acute complications are related to rapid changes in metabolism and include diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS) (also known as HHNK coma) and severe

hypoglycemia. These complications are mostly preventable and require immediate clinical intervention. It is important to lower plasma lipid and glucose levels, and to control hypertension, the latter being particularly important in terms of its benefits for reducing risks of microvascular and macrovascular disease.

The chronic complications of diabetes account for far more morbidity and mortality than do acute complications, and are divided into two categories based on the size of the vessel damage:1

• Microvascular: primarily retinopathy, nephropathy and neuropathy • Macrovascular: coronary artery disease, cerebrovascular disease and peripheral vascular

disease; less directly related to metabolic changes

Acute Complications

DKA DKA is a life-threatening but reversible complication characterized by severe disturbances in

protein, fat and carbohydrate regulation. The two best clinical indicators for evaluating DKA are a high level of blood glucose (>250 mg/dL) and presence of ketones in the urine.2

The onset of DKA is usually sudden, especially when combined with an illness (i.e., colds, flu and infections), causing dehydration and ketosis, electrolyte imbalance and acidosis. The most common precipitating factors leading to the development of DKA are any major stress, and deliberate or inadvertent omission of insulin. Infections such as pneumonia, meningitis, gastroenteritis and influenza are some of the types of illnesses and infections that provide stress to the system. Other warning symptoms might include nausea and vomiting, stomach pains, thirst and fruity breath.

DKA occurs because of an absolute or relative deficiency of insulin that is antagonized by elevated levels of counter-regulatory hormones (i.e., glucagon, epinephrine, cortisol and growth hormone). The imbalance usually occurs because of failure to take insulin or because of an excess of these counter-regulatory hormones that occurs with stress (usually physical, such as from infection, tissue injury or surgery, but may be psychological).

The degrees of insulin deficiency and insulin/counter-regulatory hormone imbalance needed to cause DKA are usually found only in those with type 1 diabetes. As a result of this imbalance, amino acids and free fatty acids are mobilized into the tissues, and delivered to the liver for gluconeogenesis and lipid metabolism.

T


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Diabetic Ketoacidosis3 • Life-threatening, but reversible • Usually found in type 1 diabetes • Onset usually sudden • Warning symptoms:

o Nausea, vomiting, stomach pains, thirst and fruity breath • Diagnostic indicators:

o Blood glucose >250 mg/dL o Ketones in urine o Metabolic acidosis

• Cause: insulin deficiency relative to counter-regulatory hormones o Failure to take insulin o Excess hormones due to stress from infection, tissue injury and

surgery The result is an increased output of glucose by the liver combined with decreased metabolism of

glucose by insulin-deficient tissues, resulting in hyperglycemia. Glucose that spills into the urine increases osmosis, causing urinary sodium and water losses that lead to dehydration and further increases in blood glucose levels. Nausea and vomiting (perhaps due to ketosis) further worsen the state of dehydration and hyperglycemia.

The initial goal of therapy should be to correct the life-threatening abnormalities (i.e., dehydration, insulin deficiency or electrolyte imbalance [potassium, phosphorus and magnesium]).3 Dehydration is present in almost all cases of DKA. There are many routes of water and/or electrolyte loss, including polyuria, hyperventilation, and vomiting and diarrhea. The best index of dehydration is acute weight loss.

Other clinical indices to monitor include orthostatic hypertension, dry mucous membranes, decreased tissue turgor and thirst. A decrease in urine output is less reliable because of persistent osmotic diuresis with hyperglycemia. Adequate rehydration is extremely important in initial therapy because it helps restore and maintain depleted vascular volume, and it enhances the kidneys’ ability to excrete glucose, thus lessening hyperglycemia. Isotonic saline is usually the initial choice of rehydrating fluid.

Insulin should be provided in all patients with DKA because its cause includes absolute or relative insulin deficiency. Although rehydration by itself will reduce ketone bodies, insulin is required for suppression of keto acid production, and is necessary to correct acidosis.

Those with DKA are depleted in total body potassium, even though most have a normal or even elevated serum potassium level. The reasons for this are complex, but include the catabolic state, potassium wasting in urine secondary to polyuria, inability of the kidney to conserve potassium, and the effects of vomiting and/or diarrhea.

Once insulin infusion is begun, potassium replacement should be initiated. Insulin tends to lower serum potassium by enhancing its movement back into cells. If potassium levels fall too low, hypokalemia-induced death from cardiac arrhythmia may result.2

Most often, DKA can be prevented, given appropriate education and prompt physician attention. Those with diabetes must contact their physicians when ill, especially if nausea and vomiting, fever, persistent hyperglycemia or ketonuria is present. If caught early, DKA can be treated successfully with frequent injections of short-acting insulin and oral administration of fluids. For those with diabetes who have repeated episodes of DKA, psychological consultation should be considered to assist patients


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in understanding why they are having difficulty maintaining the regimen and taking care of themselves, as well as how to correct that problem.

Hyperosmolar Hyperglycemic State (HHS)

The four major clinical features of HHS are: • Severe hyperglycemia (blood glucose >600 mg/dL) • Absence of or slight ketosis • Plasma hyperosmolality • Profound dehydration

HHS is most common in older patients with type 2 diabetes. The precipitating factors include use of medication or procedures that cause an increase in blood sugar, as well as other acute and chronic diseases, particularly infections.

A question often asked is why there is no ketosis in this type of acute complication. Because it occurs primarily in those with type 2 diabetes, they are not totally insulin deficient. However, the presence of ketonuria or mild ketonemia can be detected in some patients. A primary reason that “non-ketotic” was used in the acronym HHNK is to distinguish it from DKA, the primary presenting feature of which is the presence of ketones. Another reason is that the primary issue with HHS is hyperglycemia, fluid depletion and an osmolar imbalance that needs correction, rather than ketonemia.

Treatment involves correcting dehydration, hyperglycemia and the hyperosmolar condition with use of appropriate fluids, insulin and potassium.4

Severe Hypoglycemia

Severe hypoglycemia is usually precipitated by excessive medication (usually insulin), decrease in or absence of food intake, excessive exercise or overconsumption of alcohol. Severe hypoglycemia should be suspected in those who present with altered mental or neurological function (changes in behavior, coma or seizure).2

Severe hypoglycemia can cause acute harm to the client as well as others, especially if it causes motor vehicle accidents, falls or other injury. Severe hypoglycemia occurs when the patient is not able to self-treat. Glucagon, a counter-regulatory hormone that stimulates hepatic glucose production, should be prescribed for those with diabetes taking insulin who are at significant risk. It produces hyperglycemia, but its effects are short-lived. Follow-up treatment with liquid carbohydrate needs to be given after the patient is able to swallow to maintain normoglycemia.

Family members and/or caregivers should be instructed how to administer glucagon and taught how to cope with episodes of severe hypoglycemia as well as what to expect in terms of behavior (e.g., possible resistance and stupor). If coworkers, friends and teachers are unable or unwilling to treat hypoglycemia, 911 should be called. The following guidelines should be used to treat severe hypoglycemia:1

• If the person is able to swallow and not at risk of aspiration, glucose gel, honey or syrup can be placed inside the cheek.

• If unable to swallow, glucagon should be given by SC or IM injection: o 20 mg for adults and children who weigh >20 kg o 0.5 mg for children who weigh <20 kg

Glucagon can cause nausea and vomiting. Frequent blood glucose monitoring is needed during the next several hours to detect if blood glucose levels continue to fall, or to detect hyperglycemia due to overtreatment.5


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Microvascular Complications Microvascular complications include retinopathy, nephropathy and neuropathy of the small blood

vessels. Major risk factors for microvascular complications of diabetes are hypertension, hyperlipidemia, hyperglycemia, lack of exercise and smoking. Most of these risk factors are more prevalent in type 2 diabetes.

Eye Disease: Retinopathy

The prevalence of retinopathy is related strongly to the duration of diabetes. After 20 years of diabetes, nearly all patients with type 1 diabetes and more than 60% of those with type 2 diabetes have some degree of retinopathy. Other factors associated with retinopathy include chronic hyperglycemia, nephropathy and hypertension.6 The DCCT demonstrated that improved metabolic control can delay significantly the development of diabetic retinopathy as well as progression from less to more severe forms of retinopathy.7 The process by which diabetes results in retinopathy is not fully understood; however, what is known is that diabetes causes retinal capillaries to become less functional. The course of diabetic retinopathy is as follows:6

• Formation of microaneurysms (outpouchings of capillary walls) • Increased vascular permeability of retinal capillaries • Closure of retinal capillaries and arterioles • Proliferation of new vessels and fibrous tissues • Contraction of fibrous tissue and hemorrhage and/or retinal detachment due to traction

To provide further specificity to the definition, retinopathy is usually subdivided: • Nonproliferative diabetic retinopathy: retinal microaneurysms, occasional blot

hemorrhages, hard exudates and one or two soft exudates • Proliferative diabetic retinopathy: new vessels on the disc, new vessels elsewhere on the

retina, preretinal or vitreous hemorrhage and fibrous tissue proliferation Laser photocoagulation has proved to be successful in delaying or preventing progression from pre-

proliferative to proliferative retinopathy. A vitrectomy can also be performed to remove vitreous material that contains hemorrhage and scarring. Antivascular endothelial growth factor is indicated for diabetes macular edema. This is a recombinant monoclonal neutralizing antibody that can improve vision and reduce the need for laser photocoagulation.8 Those with type 1 diabetes of more than three to five years’ duration, and those with type 2 diabetes should have an annual dilated and comprehensive eye examination by an ophthalmologist or optometrist experienced in diagnosing diabetic retinopathy and knowledgeable about its management.8

Kidney Disease: Nephropathy

Diabetic nephropathy represents a distinct clinical syndrome characterized by albuminuria, hypertension and progressive renal insufficiency. Diabetic nephropathy can lead to end-stage renal disease, where survival depends on either dialysis or kidney transplantation.

The first renal function changes in clients with type 1 diabetes is microalbuminuria, which is low, but abnormal, levels of albumin in the urine (>30 mg/24 hours). Diabetic nephropathy occurs in 20% to 40% of those with diabetes, and is the leading cause of end-stage renal disease. The new term “persistent albuminuria” (albuminuria >30 mg/24 hours) replaces the terms microalbuminuria (30 to 299 mg/24 hours) and macroalbuminuria (>300 mg/24 hours) to emphasize the continuous nature of albuminuria as a risk factor for kidney disease.8 Annual screening to quantitate urine albumin excretion will allow for early detection. Testing should begin five years after diagnosis in those with type 1 diabetes, and at diagnosis for those with type 2 diabetes.


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Improving glycemic control and aggressive treatment to control blood pressure are the most important recommendations for slowing the rate of progression of nephropathy in both type 1 and 2 diabetes.9 For those with urinary albumin excretion <30 mg/24 hours, either an ACE inhibitor or ARB is recommended.

For those with diabetes and diabetic kidney disease with albuminuria >30 mg/24 hours, reducing dietary protein below usual intake is NOT recommended, as it does not alter glycemic control, reduce risk of cardiovascular disease or further glomerular filtration rate decline. Dietary protein restriction might be considered when nephropathy is progressing, despite optimal glucose and blood pressure control, even with the use of an ACE inhibitor or ARB.10

Diseases of the Nervous System: Neuropathy

Those with diabetes who develop neuropathy may have no symptoms or may experience pain, sensory loss, weakness and autonomic dysfunction. Neuropathy may result in significant morbidity and contribute to other complications, such as lower extremity amputation. The most common types of diabetic neuropathy are distal symmetrical polyneuropathy and autonomic neuropathy.

Although its cause is unclear, distal symmetrical polyneuropathy is believed to result from abnormal neural metabolism, generalized neural ischemia or both. The onset and course of illness cannot be predicted, but increasing age, male sex, increasing height, longer duration of diabetes, poorer glucose control, hypertension, alcohol consumption and smoking may be independent risk factors. The primary clinical symptoms are burning pain and sensory loss (i.e., loss of temperature and pressure sensation). The pain often resolves with more rigorous attention to glucose control. If pain persists, there are several pharmacological agents available for treatment.

Conditions of autonomic neuropathy include hypoglycemia unawareness, orthostatic hypotension, gastroparesis, constipation, diabetic diarrhea, fecal incontinence, bladder dysfunction and sexual dysfunction.

Neurogenic Delayed Gastric Emptying11

Insulin injectionat mealtime

Delayedemptying

Stomachemptying

Time

Bloo

d G

luco

se

Con

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ratio

n


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Gastroparesis (slow emptying of the stomach) is a debilitating disease process that affects an estimated 4% of the population. The most common etiologies preceding the development of gastroparesis symptoms are diabetes (50%), status post-vagotomy or gastric resection and those reporting a viral episode before symptom development. However, before the diagnosis can be made, mechanical or structural disorders of the gastrointestinal tract must be ruled out.12

Clinically, patients with gastroparesis are at risk for fluid, electrolyte and nutrient deficits; patients with diabetes risk erratic glycemic control. Treatment is targeted at correcting fluid, electrolyte and nutritional deficiencies, reducing symptoms, and correcting the precipitating cause of gastroparesis, if possible.

In diabetes-caused gastroparesis, the most important goal is to achieve or maintain optimal glucose control. This is achieved more easily by frequent monitoring of blood glucose levels and self-adjustment of insulin given throughout the day. Nutritional intake is often variable due to symptoms of anorexia, early satiety, bloating and fullness, and can often be inconsistent from meal to meal and day to day.

Because the patient with diabetes with gastroparesis is often not able to tolerate regular meals or solid foods, this can compromise glucose control and produce fluctuating glucose levels throughout the day. Also, an increase in insulin requirements often occurs because of the need to add nutritional supplements (any are encouraged). Some steps can be taken to improve glucose control and nutritional adequacy.13

Patients should eat smaller, more frequent meals consistent in carbohydrate as much as possible. In general, a person needs approximately 14 to 16 choices of carbohydrate (210 g to 240 g of carbohydrate)/day. If six small meals were eaten throughout the day, each small meal should consist of approximately two to three carbohydrate choices (30 g to 45 g of carbohydrate). There is a strong relationship between pre-meal insulin dose and post-meal glucose response to carbohydrate content of the meal. The total carbohydrate in the meal does not influence the glucose response if the pre-meal insulin is adjusted for the carbohydrate content of the meal. For those receiving fixed doses of short- and intermediate-acting insulin, day-to-day consistency in the amount of carbohydrate is associated with lower A1C levels.

Solid foods may be better tolerated earlier in the day, with a switch to liquid meals later in the day if the patient begins to feel full. Monitor blood glucose levels before the small meal or snack is eaten, and adjust the insulin dose according to the blood glucose level and the anticipated amount of carbohydrate to be eaten.

An insulin regimen of a basal dose of insulin (NPH or a long-acting insulin such as glargine [Lantus] or detemir [Levemir]) at bedtime or in the evening, and a bolus or supplemental dose of insulin (short-acting, regular or rapid-acting such as aspart [NovoLog], lispro [Humalog] or glulisine [Apidra]) before the meal or snack, would be ideal to promote optimal glucose control. Some may need to take the bolus dose of insulin approximately a half hour after the meal, once they can tolerate solid food.

Treating patients with gastroparesis remains a very challenging task. Chronic nausea and vomiting not only can precipitate dehydration, electrolyte disturbances, hyperglycemia, malnutrition and inadequate medication delivery, but creates a serious impact on overall quality of life. Identifying and stratifying patients into level of nutrition risk will help the clinician determine those who would benefit from early nutrition support to restore nutrition and hydration status.13

Macrovascular Complications

Macrovascular disease is defined as arteriosclerotic, which is thickening and hardening of the blood vessel walls; and atherosclerotic, where material deposits in blood vessel walls. Atherosclerosis includes


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coronary artery disease, cerebrovascular disease and peripheral vascular disease. Sixty-five percent of deaths in diabetes are due to CAD or cerebrovascular events. People with diabetes are two to four times more likely to have a stroke, myocardial infarction or sudden death. Also, those with diabetes and peripheral vascular disease are more prone to limb ischemia and increased risk of amputation. Risk factor reduction includes improving glucose control, blood pressure and lipids; therapeutic lifestyle change; and smoking cessation.14

Coronary Artery Disease

CAD occurs earlier and is more extensive in people with diabetes, and usually presents as angina or acute myocardial infarction. Prevention of CAD involves reducing risk factors such as smoking, hypertension, and a high intake of total and saturated fat. Other conditions that may affect the etiology of cardiovascular disease in those with diabetes are obesity, inactivity and hyperinsulinemia.

Type 2 diabetes is associated with a two- to four-fold increased risk of CAD. The most common pattern of dyslipidemia in type 2 diabetes is elevated triglyceride levels and decreased HDL cholesterol levels. The LDL cholesterol level is not significantly different when compared to those without diabetes; however, people with diabetes tend to have smaller, denser LDL particles that are more atherogenic.8

Aggressive therapy of elevated lipid levels in those with diabetes will probably reduce the risk of heart disease. Priorities for treatment of dyslipidemia in those with diabetes are:8

• Lower LDL levels to <100 mg/dL in patients without overt cardiovascular disease; in those with overt cardiovascular disease, a lower LDL cholesterol goal (<70 mg/dL) is recommended. Nutrition intervention involves limiting the saturated fat intake to <10%, and either lowering total fat intake or increasing intake of monounsaturated fat. The first choice of medication therapy is usually an HMG-CoA reductase inhibitor (statin).

• Lower triglyceride levels <150 mg/dL, and raise HDL levels to >40 mg/dL in men and >50 mg/dL in women. Behavioral interventions directed toward weight loss, increased physical activity and smoking cessation may be useful.

• Lower triglyceride levels. Glycemic control is the first priority. • If combined hyperlipidemia, improve glycemic control and add a high-dose statin.

Cerebrovascular Disease

Atherosclerosis affecting the central nervous system is characterized by transient ischemic attack, cerebrovascular accident [stroke]) or vascular dementia.

The classic definition of TIA (sometimes called “mini stroke”) is the sudden onset of a neurological deficit that lasts less than 24 hours and is not associated with a permanent residual effect, but it requires urgent referral. TIA is caused by a decrease in blood supply, causing ischemia in the area of the brain that produces the symptoms. The symptoms can differ significantly depending on the area of the brain, but can include a migraine, syncope and seizure. Treatment can involve surgery or medical management, and is based on the severity of the stenosis, symptoms of the patient and whether the patient is a candidate for vascular surgery.

In cases of TIA and CVA/stroke, it is most important to focus on decreasing the cardiovascular risk factors by treating hypertension, dyslipidemia and hyperglycemia, as well as recommending smoking cessation. If the person is at high risk, antiplatelet therapy may be effective to reduce the risk of stroke.14

The best way to treat vascular dementia is to prevent stroke. The important risk factors are older age, recurrent stroke and dominant hemisphere stroke. Risk factor management, particularly hypertension and statin use, have been associated with decreased incidence of dementia.


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Peripheral Vascular Disease Peripheral vascular disease, commonly referred to as peripheral artery disease, refers to

atherosclerotic blockages found in the lower extremity obstruction of large arteries (not within the coronary vasculature or brain). More than 50% of those with diabetes diagnosed with peripheral artery disease are asymptomatic; one third have intermittent claudication (pain, weakness, numbness or cramping in muscles due to decreased blood flow); and one sixth have severe ischemia (lack of blood supply).14 A physical assessment to palpate pedis and tibial pulses and determine an ankle-brachial index (the ratio of systolic pressure at the ankle and brachial artery) is used to detect peripheral artery disease and its severity.

Those with peripheral artery disease have an elevated risk for cardiovascular events, and an estimated 20% risk of a coronary event in 10 years. There is a low risk that a person with claudication will develop severe ischemia and require amputation, but risk of death from coronary events is three to four times higher than in those without claudication. Of patients with intermittent claudication, about 7% will undergo lower extremity bypass surgery, 4% will undergo major amputations and 16% will experience worsening claudication.15 Treatment of peripheral artery disease is similar to the preventive measures for atherosclerotic disease including antihypertensive drugs, lipid-lowering drugs, glucose control, smoking cessation, antiplatelet therapy and exercise. Smoking cessation is the most important element of risk factor management in peripheral artery disease.14

Review Questions 1. What does treatment for DKA involve? 2. How does severe hypoglycemia differ from hypoglycemia? What are the treatment

differences? 3. What are the vascular complications of diabetes? 4. What are the important guidelines for those with diabetes and gastroparesis to improve

glucose control and nutritional adequacy?

Answer 1: • Correcting dehydration, insulin deficiency or potassium deficiency with fluid and

potassium replacement, and insulin administration. Answer 2:

• Severe hypoglycemia occurs when blood glucose is low enough that the person with diabetes loses cognition and is not able to self-treat. Treatment often involves use of glucagon (counter-regulatory hormone), which requires a subcutaneous injection.

Answer 3: • Microvascular: retinopathy, nephropathy and neuropathy • Macrovascular: coronary artery disease, cerebrovascular disease and peripheral vascular

disease Answer 4:

• Eat small, more frequent meals that emphasize carbohydrate consistency. • Eat solid foods earlier in the day; liquid foods at night. • Use a basal/bolus insulin regimen to improve glucose control.


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References 1. Abbate SL, Abbate AJ. Chronic complications. In: Mensing C, ed. The Art and Science of Diabetes Self-

Management Education Desk Reference. 2nd ed. Chicago, IL: American Association of Diabetes Educators; 2011:603-620.

2. Kaufman FR. Medical Management of Type 1 Diabetes. 6th ed. Alexandria, VA: American Diabetes Association, Inc.; 2012.

3. Trachtenbarg DE. Diabetic ketoacidosis. Am Fam Physician. 2005;71(9):1705-1714.

4. Burant CF. Medical Management of Type 2 Diabetes. 7th ed. Alexandria, VA: American Diabetes Association, Inc.; 2012.

5. Sisson EM, Cornell S. Pharmacotherapy for glucose management. In: Mensing C, ed. The Art and Science of Diabetes Self-Management Education Desk Reference. 2nd ed. Chicago, IL: American Association of Diabetes Educators; 2011:417-458.

6. ACCORD Study Group, Chew EY, Ambrosius WT, et al. Effects of medical therapies on retinopathy progression in type 2 diabetes. N Engl J Med. 2010;363(3):233-244.

7. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993;329(14):977-986.

8. American Diabetes Association. Standards of medical care in diabetes — 2014. Diabetes Care. 2014;37(Suppl 1):S14-S80.

9. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. UK Prospective Diabetes Study Group. BMJ. 1998;317(7160):703-713.

10. Hansen HP, Tauber-Lassen E, Jensen BR, Parving HH. Effect of dietary protein restriction on prognosis in patients with diabetic nephropathy. Kidney Int. 2002;62(1):220-228.

11. Vanormelingen C, Tack J, Andrews CN. Diabetic gastroparesis. Br Med Bull. 2013;105:213-230.

12. Gastroparesis. National Digestive Diseases Information Clearinghouse (NDDIC) Web site. http://digestive.niddk.nih.gov/ddiseases/pubs/gastroparesis. Updated June 15, 2012. Accessed February 16, 2015.

13. Parrish CR, Green Pastors JG. Nutrition management of gastroparesis in people with diabetes mellitus. Diabetes Spectrum. 2007;209(4):231-234.

14. Lorber D. Macrovascular diseases in diabetes. In: Mensing C, ed. The Art and Science of Diabetes Self-Management Education Desk Reference. 2nd ed. Chicago, IL: American Association of Diabetes Educators; 2011:659-698.

15. Shammas NW. Epidemiology, classification, and modifiable risk factors of peripheral arterial disease. Vasc Health Risk Manag. 2007;3(2):229-234.


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Case Study Delores is a 45-year-old woman with type 2 diabetes. She is referred to a diabetes outpatient clinic for diabetes medical nutrition therapy. Her family practice physician states in his referring letter that Delores has a long history of “dietary noncompliance,” and that if this course of nutrition intervention does not achieve the desired results, insulin therapy will be initiated.

She is 5 ft, 5 in. tall and weighs 223 lb (currently at maximum adult weight). A reasonable body weight would be 180 lb.

A review of her food record reveals that Delores is a frequent snacker, often including 4 to 5 snacks in her daily eating pattern. When asked, Delores says she snacks when she is lonely, bored or stressed. She is eating special products, such as diet carbonated beverages, sugar-free ice cream, low-fat dairy products and low-calorie frozen entrees, although she frequently chooses high-fat, high-calorie snacks (e.g., cheese and peanut butter crackers, potato chips with dip, and cookies). Her high calorie and total fat intake, low fiber intake, and infrequent consumption of fruits and vegetables are problem areas. Estimated calorie intake is 3,170.

Her current level of physical activity is low and consists primarily of housework once a week. She is interested in a walking program, but doesn’t like to exercise alone.

Delores also has hyperlipidemia. A recent lipid profile was completed:

• Total cholesterol = 218 mg/dL • HDL cholesterol = 27 mg/dL • LDL cholesterol = 148 mg/dL • Triglycerides = 278 mg/dL

Delores was diagnosed with type 2 diabetes approximately six years ago. She is being managed on the maximum dose of a second-generation oral glucose-lowering medication. She monitors her fasting blood glucose level. A review of her glucose log reveals fasting glucose levels ranging from 100 mg/dL to 258 mg/dL. Recent laboratory values sent with the physician referral letter indicate a glycosylated hemoglobin level of 13.2%.

Delores is a high school graduate, lives alone and does her own food shopping and preparation. She eats away from home at lunch and eats out once or twice a week for dinner, usually at a fast-food restaurant. Delores states she is interested in losing weight and doesn’t care how long it takes as long as “I don’t have to go on insulin!,” which is her primary concern.

She has received nutrition intervention in the past; two years ago, she lost 15 lb by “avoiding sweets and sticking to a 1,200 kcal exchange diet” and walking five days a week, but has gained it all back over the past year. She knows how important it is for her to lose weight, but doesn’t know how to lose it and keep it off. She is interested in learning to manage her weight, increase her level of physical activity and improve her glucose control.

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Case Study Delores was asked to complete the Lifestyle Questionnaire in the waiting room before her appointment. The dietitian reviewed the questionnaire with Delores and asked her to monitor her eating behavior by using the Eating Behavior Diary form. She was asked to bring three to five days of records to her return visit in one week to establish goals and determine initial nutrition intervention.

When the Eating Behavior Diary forms were reviewed with Delores, she said the major issues for her are snacking too much and eating in response to being alone. The Lifestyle Change Plan was used with her to identify eating behaviors to change, establish goals and develop an action plan for accomplishing her goals.

During the goal-setting session, Delores decided she would address the problem of snacking, increase fruit and vegetable consumption, and begin comprehensive monitoring for diabetes self-management using the following tactics: • Eat 5 to 7 servings of vegetables and fruits each day • Eat low-fat crackers, pretzels, popcorn or cookies for snacks • Explore alternative evening activities to decrease time spent alone • Use monitoring forms to record glucose levels, food intake and nutrient information • Test blood glucose results daily, but at random times during the day

Delores’s specific goals and action plans are described in the attached Lifestyle Change Plan. Delores was asked to sign it as a form of written agreement to work on these goals until her follow-up visit in one month.

Delores was provided with information on increasing intake of fruits and vegetables and with a handout from the National Cancer Institute on the Five-A-Day Program. Ideas for healthy snacks were also discussed.

She was given several copies of the Lifestyle Change: Food and Physical Activity Record and a copy of the Lifestyle Change: Summary Record to use in recording information about blood glucose monitoring results, nutrient information (i.e., total servings of fruits and vegetables) and physical activity, as well as instructions on how to complete the form. Delores agreed to bring in 3 to 4 complete Lifestyle Change: Food and Physical Activity Records to a clinic visit with the dietitian in one month.

A review of Delores’s Lifestyle Change: Food and Physical Activity Record shows a big improvement with fat intake and consumption of fruits and vegetables. She introduced new products into her daily eating pattern (e.g., low-fat crackers, frozen yogurt), primarily at snack time. Delores was able to increase her fruit and vegetable intake to 5 to 7 servings per day. Her weight decreased by 2 lb. Delores discussed her snacking problems with her cousin. They decided to join a local volleyball team to increase physical activity and social support levels. A return appointment was made for one month.

The dietitian continued to see Delores on a monthly basis until she met initial goals. They reviewed monitoring forms at each visit and continued to revise goals and action plans as necessary.


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Case Study: Lifestyle Questionnaire

Name: Delores Date: April 2014

Do you want to change your lifestyle? The time you take to provide this information will help your healthcare team work better for you. Thank you for taking an important step to manage your health.

• Have you made any changes in your lifestyle that you feel good about? ýYes ☐No

If yes, what changes have you made? _______________________________________________________ ________________________________________________________________________________________ • If you and your nutritionist discover changes you could make in your lifestyle to

improve your health (e.g., eating, exercise or self-monitoring plan), would you be open to the changes? ýYes ☐No

If yes, who will support and encourage you as you make these changes? Friends

at work If no, what would keep you from making these changes? _____________________________________ ________________________________________________________________________________________ • What important information would you like from the nutritionist? ☐ Meal planning ý Weight management ☐ Tips on eating out ý Exercise ☐ Food label reading/supermarket shopping ☐ Record keeping ☐ Eating less fat ☐ Other ______________________________ • What changes would you like to make? ☐ Improve my eating habits ☐ Get more information ☐ Improve my activity level ýFeel better about my health ý Improve my blood glucose control ýLearn how to manage my weight ý Lower my blood pressure ý Improve my energy level ☐ Improve my cholesterol, triglyceride levels ☐Control food cravings. ☐ Learn how to prevent high/low blood glucose levels ☐ Other______________________________________________ __________________________________ ______________________________________________________________________________

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Case Study: Lifestyle Questionnaire, continued


Nutrition History

• Have you ever wanted to make changes in what you eat? ýYes ☐No If yes, what advice have you been given? Lose weight, avoid sweets, eat more

fruits and vegetables.

• Are you following any type of meal plan, such as exchange lists, calorie counting, carbohydrate counting, low cholesterol, low fat or low sodium? ☐Yes ýNo

If yes, please describe. Not currently, have followed 1,200 calorie exchange list diet.

If yes, how much of the time are you able to follow your meal plan? ☐ Rarely ☐ Sometimes ☐ Often ☐ Usually

• How many people live in your household? Just myself Ages ________

• Who usually does the cooking? me

• How many times each week do you eat away from home? 6 - 7 a. Which meals are usually eaten away from home? lunch b. In which type of restaurant do you usually eat or carry out? (mark F for Frequently, O for Occasionally or N for Never) __F__ Fast food (hamburger, chicken, seafood, pizza, subs, tacos) __O__ Buffets/All-you-can-eat __O__ Sit-down restaurant (Types: Steakhouse) __O__ Sweets/Dessert shops

• Do you drink alcohol? Beer: ☐Yes ýNo Wine: ☐Yes ýNo Liquor: ☐Yes ýNo How often? ___________________________________ How much? __________________

• Do you take vitamins, minerals, herbs or any other food or nutritional supplement? ☐Yes ýNo

If so, please list: _____________________________________________________________

• Do you regularly skip meals? ☐Yes ýNo If yes, list which meals you skip most often and why: _____________________________

• Do you have “trigger” foods that often cause you to overeat? ýYes ☐No If yes, please list: sweets, especially chocolate

• Have you ever been on an extreme diet (such as fasting) or a fad diet? ☐Yes ýNo If yes, please explain: ________________________________________________________

• Do you eat for reasons other than hunger? ýYes ☐No If yes, please list: boredom, loneliness


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Food Record

• This food record can help you and your nutritionist better understand how food affects your health.

• Please write down everything you eat and drink from the time you wake up to the time you go to bed. Include meals, snacks and drinks. If you eat or drink anything when you wake up, that should be added to the list.

Time Type of Food/Beverage Amount

7:30 a.m. Cornflakes

Skim milk

1 cup

1/2 cup

10:00 a.m. Peanut butter/cheese crackers

Diet cola

1 package

1 can

noon Tossed salad (lettuce, tomato, carrots, red cabbage, onions)

Salad dressing – ranch

Cottage cheese – low fat (2%)

Diet cola

large

1/2 cup

2 Tbsp

1 cup

1 can

3:00 p.m. Twinkies

Slurpee

3

1 medium

5:30 p.m. Potato chips

Onion dip

4 oz

1/2 container

7:00 p.m. Lean Cuisine – chicken entree

Diet cola

1

1 can

9:30 p.m. Oatmeal-raisin cookie 4

10:00 p.m. Sugar-free ice cream 4 scoops

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122



Weight History

• Height: 5’5” Present weight: 223 lb Usual weight: over 200 • Has your weight changed any over the past year? ýYes ☐No If yes, please describe how: I gained back the 15 lb I lost 2 years ago. How do you feel about your weight now? I need to lose weight. I don’t want

to take insulin shots! • What has been your weight range as an adult? 180 – 223 lb • What would you consider to be a healthy weight for you? 180 lb Would you feel comfortable at that weight? ýYes ☐No • Have you ever tried to change your weight before? ýYes ☐No

If yes, what have you tried? Avoided sweets: “stuck to” 1,200 calorie exchange diet. Ate more fruits & vegetables, walked 5 days a week (with cousin for 1 year)

Have you been successful? No • Are you interested in working to change your weight?

ý Yes, right now. ☐ Yes, but I can’t right now. ☐ No, but I will think it over. ☐ No, not now. ☐ No, I’m not interested.


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Case Study: Lifestyle Questionnaire


Physical Activity History

• What types of activities do you do regularly, and how much time each week do you spend doing them?

Examples include walking, dancing, golf, tennis, biking, aerobics and swimming.

Activity Times/week Minutes/activity

None

None None

• Do you like to do these activities alone or with others? __________________________

• Do you perform other physical activities of daily living, such as housework, gardening, or climbing stairs? If yes, list type and amount. Housework, once a week for 2 hours

• Are you interested in becoming more physically active? ý Yes, right now. ☐ Yes, but I can’t right now. ☐ No, but I will think it over. ☐ No, not now. ☐ No, I’m not interested.

If yes, what type of physical activity could you see yourself doing regularly?

Walking, played volleyball in high school If no, why? _________________________________________________________________

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Stress History

• Have you had a significant change in life events (such as marriage, divorce, death of a family member, new home or change in employment) during the past year?

☐Yes ☐No If yes, please describe how: _______________________________________________ • How does stress affect you physically or emotionally (e.g., headaches, neck aches,

sleeping difficulties, eating too much or too little, fear, depression)? Overeat when stressed • How do you deal with stress (e.g., meditation, exercise, avoidance)? Avoidance

Record Keeping

• Do you keep food records? ☐Yes ýNo ______________________ • Do you keep blood glucose records? ýYes ☐No Daily • Do you keep exercise records? ☐Yes ýNo ______________________ • Do you keep other kinds of records? ☐Yes ýNo ______________________

(for example, blood pressure) Type _____________________________ • Who benefits from your record keeping? ý Self ☐ Family ý Physician ☐ Other ________________________________________________________________


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Case Study: Eating Behavior Diary Name: Delores Date: Monday. April 7, 2014

Time Location or

Place

Food/Beverage Consumed

Amount/Description Degree of Hunger1

Social Situation2

Comments3

7:30 a.m.

Home — kitchen

Cornflakes w/Equal — 1 cup

Skim milk — 1/2 cup

1 Home — alone

10:00 a.m.

Work – desk Peanut butter/cheese crackers — 1 pkg.

Diet cola — 1 can

2 Work — with friends

Noon Work — desk (brought lunch from home)

1 sandwich — ham & Swiss cheese, mustard, lettuce, whole wheat bread

2 Alone at desk

Busy at work trying to catch up

3:00 p.m.

Work – desk M&Ms — 1 pkg

Diet cola

2 Vending machine

Feel stressed at work

7:00 p.m.

Home — in front of TV

Cheeseburger — 2

French fries — large

Chocolate milkshake — large

3 Worked late,

stopped for fast food

Very hungry and tired!

9:00 p.m.

Home — in front of TV

Low-fat devil’s food cake cookie — 1 box

Diet cola — 1 can

3 Home — watching TV

Bored, depressed, TV

What did I learn about my eating habits? I snack too much! I eat in response to my emotions. __________________________________________________________________________

_____________________________________________________________________________________

_____________________________________________________________________________________

1. Use rating scale of: 1=not hungry, 2=moderately hungry, 3=very hungry

2. Who were you with? What were you doing?

3. Include feelings (e.g., sad, bored, angry), thoughts (e.g., eating out with friends) and concerns (e.g., stressed out at work).

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126

Case Study: Lifestyle Change Goals To improve my health, I will: (Write the behavioral goals you checked on the previous pages in the blank spaces

provided below, and track your weekly progress on the tracking form. Make notes about your successes and challenges.)

1. Eat 5-7 servings of fruits and vegetables each day

2. Eat low-fat crackers, pretzels, popcorn for snacks

3. Record blood glucose values: test once/day at random times





Date Successes

Date Challenges


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Case Study: Lifestyle Change

Food and Physical Activity Record

Name: Delores Date: Monday, May 5, 2014

Food Eaten Nutr. Info.

Food Eaten

Nutr. Info.

Food Eaten

Nutr. Info.

Time Day: Monday F V Time Day: Wednesday F V Time Day: Friday F V

7:30 a.m.

1 cup cornflakes 1 cup skim milk 1 banana

1

7:40 a.m.


1

7:15 a.m.


1

10:00 a.m.

15 LF cheese crackers

diet cola

10:00 a.m.

15 LF cheese crackers

diet cola

9:45 a.m.

1/2 bagel diet cola

12:00 p.m.

1 cup LF cottage cheese

1 tomato carrots & celery orange

1

1 1

12:15 p.m.

1 cup LF yogurt Turkey sandwich

w/2 slices rye bread, mustard, lettuce, tomato

1

12:00 p.m.

Chef salad w/half cup tuna, lettuce, tomato, cucumber, pepper

10 crackers 1 apple

1

1 1

3:00 p.m.

16 oz tomato juice

15 pretzels

1 3:30 p.m.

6 oz orange juice 3 LF devil’s food

cookies

1 3:15 p.m.

5 jelly beans 16 oz tomato juice 15 pretzels

1

6:00 p.m.

Lean Cuisine chicken

Tossed salad w/1 Tbsp LF dressing

1

6:30 p.m.

1 piece lasagna 2 slices French

bread w/diet margarine

fresh pineapple

1

1 6:30 p.m.

1 grilled chicken breast sandwich w/lettuce, tomato

corn on the cob watermelon

1

1 1

9:00 p.m.

1 cup LF vanilla yogurt

1/2 cup strawberries

2 Tbsp chocolate syrup

1

9:30 p.m.

1 cup LF chocolate yogurt

10:00 p.m.

1 cup LF vanilla yogurt

2 Tbsp chocolate syrup

Totals 3 4 3 2 3 5

Physical Activity

Type & Amount — — —

Other Information

Glucose: 179 mg/dL 7:20 a.m.

215 mg/dL 2:15 p.m.

182 mg/dL

9:00 p.m.

Instructions: F = fruit servings V = vegetable servings LF = low-fat Comments: I liked the low-fat crackers & pretzels – even the low-fat yogurt!

Nutr. = nutrition, w/ = with.


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Appendix 1 Diabetes Self-Care Daily Record

Date: Day of week:

Time

Medication

Blood Glucose Results

Food Intake

Nutrient Information

Physical Activity

Type Amount a.m. p.m. Type of

food/drink Amount Type Amount

Comments: Daily Totals:

Appendix

130

Appendix 2 Composition of Alcoholic Beverages

Beverage Serving (oz) Alcohol (g) Carbohydrate (g) Kcal

Beer Regular Light

12 12

13 12

13 5

150 100

Distilled Spirits (80 proof) Gin Rum Vodka Whiskey

1.5 1.5 1.5 1.5

14 14 14 14

Trace Trace Trace Trace

100 100 100 100

Wine Dry white Red or rosé

5 5

15 15

2

2.5

105 105

Source: Self Nutrition Data Web site. http://nutritiondata.self.com. Accessed February 16, 2015.


131

Appendix 3 Fat and Fatty Acid Composition

Food Total Fat

(%) Saturated

Fat (%) Unsaturated

Fat (%) Monounsaturated

Fat (%)

Linoleic Alpha-Linoleic (Oleic)

Oils

Canola Safflower Flaxseed Sunflower Corn Olive Soybean Peanut Cottonseed Lard Palm Butter Coconut

100 100 100 100 100 100 100 100 100 100 100 100 100

7 8 9

12 13 15 15 19 27 43 51 68 91

21 14 16 71 57 9

54 33 54 9

10 3 2

11 1

57 1 1 1 8

Trace Trace

1 Trace

1 0

61 77 18 16 29 75 23 48 19 47 39 28 7

Margarines

Stick (1 Tbsp) Tub (1 Tbsp)

100 100

19 14

3 18

28 9

48 56

Fish

Salmon (3 oz) Sardines (3.75 oz) Tilapia (3 oz) Trout (3 oz) Tuna (3 oz)

41 50

17.5 35 <1

15 13 39 28 29

8 31 11 5 1

32 13 9

21 26

33 34 39 30 20

Nuts/Vegetable

Almonds (1 oz) Peanuts (1 oz) Peanut butter

(1 Tbsp) Pecans (1 oz) Pistachio (1 oz) Avocado (1 oz)

78 78 76

93 71 82

1 14 17

9

13 15

26 33 32

30 32 12

0 Trace Trace

1.5

Trace 1

69 53 52

60.5 56 72

Sources: Canolainfo.org Web site. http://www.canolainfo.org/. Accessed February 16, 2015. Self Nutrition Data Web site. http://nutritiondata.self.com. Accessed February 16, 2015.

Appendix

132

Appendix 4 Following the DASH Eating Plan

The DASH eating plan is based on 2,000 calories/day (below). The number of daily servings in a food group may vary, depending on individualized caloric needs. Use this chart to help plan menus or while shopping as a guide.

Food Group Daily

Servings

Serving Sizes

Examples and Notes

Significance of DASH Eating

Plan

Grains* 6 to 8 1 slice bread 1 oz dry cereal† ½ cup cooked rice,

pasta, or cereal

Whole-wheat bread and rolls, whole-wheat pasta, English muffins, pita bread, bagel, cereals, grits, oatmeal, brown rice, unsalted pretzels, popcorn

Major sources of energy and fiber

Vegetables 4 to 5 1 cup raw, leafy vegetable ½ cup cut-up raw or cooked vegetable ½ cup vegetable juice

Broccoli, carrots, collards, green beans, green peas, kale, lima beans, potatoes, spinach, squash, sweet potatoes, tomatoes

Rich sources of potassium, magnesium and fiber

Fruits 4 to 5 1 medium fruit ¼ cup dried fruit ½ cup fresh, frozen or canned fruit ½ cup fruit juice

Apples, apricots, bananas, dates, grapes, oranges, grapefruit, grapefruit juice, mangoes, melons, peaches, pineapples, raisins, strawberries, tangerines

Important sources of potassium, magnesium and fiber

Fat-free or low-fat milk and milk products

2 to 3 1 cup milk or yogurt 1½ oz cheese

Fat-free (skim) or low-fat (1%) milk or buttermilk; fat-free, low-fat or reduced-fat cheese; fat-free or low-fat regular or frozen yogurt

Major sources of calcium and protein

Lean meats, poultry and fish

≤6 1 oz cooked meats, poultry, or fish 1 egg¶

Select only lean; trim away visible fats; broil, roast or poach; remove poultry skin

Rich sources of protein and magnesium

Nuts, seeds and legumes

4 to 5 per week

1/3 cup (1½ oz) nuts 2 Tbsp peanut butter 2 Tbsp or ½ oz seeds ½ cup cooked legumes (dry beans and peas)

Almonds, hazelnuts, mixed nuts, peanuts, walnuts, sunflower seeds, peanut butter, kidney beans, lentils, split peas

Rich sources of energy, magnesium, protein and fiber

Fats and oils§

2 to 3 1 tsp soft margarine 1 tsp vegetable oil 1 Tbsp mayonnaise 2 Tbsp salad dressing

Soft margarine, vegetable oil (canola, corn, olive, safflower), low-fat mayonnaise, light salad dressing

Study had 27% of calories as fat (in or added to foods)

Sweets and added sugars

≤5 per week

1 Tbsp sugar 1 Tbsp jelly or jam ½ cup sorbet, gelatin 1 cup lemonade

Fruit-flavored gelatin, fruit punch, hard candy, jelly, maple syrup, sorbet and ices, sugar

Low-fat sweets

*Whole grains are recommended for most grain servings as a source of fiber and nutrients. †Serving sizes vary between ½ cup and 1¼ cups, depending on cereal type. Check the product’s Nutrition Facts label. ¶As eggs are high in cholesterol, limit egg yolk intake to no more than four per week; two egg whites have the same

protein content as 1 oz of meat. §Fat content changes the serving amount for fats and oils. For example, 1 Tbsp of regular salad dressing equals 1 serving;

1 Tbsp of a low-fat dressing equals ½ serving; 1 Tbsp of a fat-free dressing equals zero servings.


133

Appendix 5 Resources for In-Depth Meal Planning Approaches

Carbohydrate, Fat and Calorie-Counting Resources

Booklets Count Your Carbs: Getting Started* Match Your Insulin to Your Carbs* Books Borushek A. The Calorie King Calorie, Fat, and Carbohydrate Counter. Costa Mesa, CA: Family

Health Publications; 2014. (available from www.calorieking.com/products/books) Hozmeister L. The Diabetes Carbohydrate and Fat Gram Guide. 4th ed. Alexandria, VA:

American Diabetes Association; 2010.* Warshaw HS, Bolderman KM. Practical Carbohydrate Counting: A How-To Teach Guide for

Health Professionals. 2nd ed. Alexandria, VA: American Diabetes Association; 2009.*

Exchanges List Resources

Booklets Choose Your Foods: Exchange Lists for Meal Planning (2007 revision)*

Organizations

International Diabetes Center http://www.idcpublishing.com Joslin Diabetes Center http://www.joslin.org

United States Department of Agriculture (USDA) http://www.choosemyplate.gov National Diabetes Education Program http://www.ndep.nih.gov

*Order from The Academy of Nutrition and Dietetics at www.eatrightstore.org or the American Diabetes Association at http://shopdiabetes.org/?loc=bb&source=bb-2014.

Appendix

134

Appendix 6 Mealtime or Bolus Insulin Supplement

Advanced Carbohydrate Counting

Practice Worksheet

The mealtime insulin supplement is composed of two boluses: the meal bolus and the blood glucose correction bolus. The meal bolus is the number of units of insulin needed to cover the food (carbohydrate) to be eaten at the forthcoming meal. The blood glucose correction bolus is the number of units of insulin needed to correct for pre-meal blood glucose levels that are outside of the target range. These boluses are determined arithmetically and combined, and the resulting mealtime insulin supplement is given before the meal.

Meal Bolus

The meal bolus is determined by first calculating the carbohydrate/insulin ratio, and then estimating the amount of carbohydrate that will be eaten at the meal. Calculating the Carbohydrate/Insulin Ratio A common starting place is to use:

• 1:10 ratio for type 2 diabetes • 1:15 ratio for type 1 diabetes

Estimating the Carbohydrate Intake The amount of carbohydrate eaten at meals can affect how high blood glucose level rises afterward. It is the balance between carbohydrate and insulin that determines how high blood glucose will rise after eating. Carbohydrate can be estimated or counted by either carbohydrate servings/choices or by carbohydrate grams (1 carbohydrate serving/choice = 15 g of carbohydrate). Carbohydrate grams can be found on the Nutrition Facts section of the food label or by using a food analysis website (www.nal.usda.gov/fnic/foodcomp) or reference book (The Calorie King Calorie, Fat, and Carbohydrate Counter or www.calorieking.com). It’s important to learn and recognize portion sizes.

Practice: Estimate the amount of carbohydrate in a pizza meal (2 slices of thin-crust veggie pizza, lettuce salad with 2 Tbsp of Italian dressing, diet cola) ______ g of carbohydrate

Practice: Estimate the amount of carbohydrate in a McDonald’s meal (Big Mac, medium French fries, chocolate milkshake) ______ g of carbohydrate

Determining the Meal Bolus The meal bolus is determined by dividing the estimated carbohydrate intake of the meal (in grams) by the carbohydrate/insulin ratio that has been calculated. This is the number of units of insulin supplement needed to cover the carbohydrate intake of the meal.

Practice: Assume a meal has an estimated carbohydrate amount of 60 g. Calculate the

meal bolus using a carbohydrate/insulin ratio of 15:1.

Grams of carbohydrate _____ divided by carbohydrate/insulin ratio ______ = ______ units


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Advanced Carbohydrate Counting

Blood Glucose Correction Bolus

The blood glucose correction bolus is used to correct for a pre-meal blood glucose level that is higher or lower than the target blood glucose goal. A common starting place for calculating a blood glucose correction bolus is to use a formula based on the type of diabetes, which is:

• 1 unit of insulin/50 mg of BG >150 for type 1 diabetes • 1 unit of insulin/30 mg of BG >150 for type 2 diabetes

Calculate the Blood Glucose Correction The blood glucose correction is calculated by subtracting the pre-meal blood glucose level from the target blood glucose level. Although the recommended pre-meal target blood glucose level is between the range of 90 mg/dL to 130 mg/dL, a target glucose level of 150 mg/dL is often used as a starting place when determining a glucose correction bolus to err on the side of safety.

Practice: Calculate the amount of glucose to be corrected based on an actual pre-meal blood glucose level of 300 mg/dL and a target glucose level of 150 mg/dL.

_______ (actual blood glucose) – _______

(target blood glucose) = _______ (blood glucose correction)

Determining the Blood Glucose Correction Bolus To determine the correction bolus, divide the blood glucose correction by the correction factor (30 or 50) to determine how many units of insulin are needed for the correction bolus.

Practice: Type 1 diabetes, a pre-meal blood glucose level of 250 mg/dL and a target blood glucose of 150 mg/dL. ____ (pre-meal BG) – _____ (target BG) = ______ mg/dL (BG correction) _____ (BG correction) divided by _____ (50) = _____ (correction bolus) Practice: Type 2 diabetes, a pre-meal blood glucose level of 50 mg/dL and a target blood glucose of 150 mg/dL. _____ (pre-meal BG) – _____ (target BG) = ______ mg/dL (BG correction) _____ (BG correction) divided by _____ (30) = _____ (correction bolus)

Combining the Meal Bolus and the Glucose Correction Bolus to Determine the Mealtime or Bolus Insulin Supplement

To determine the mealtime or bolus insulin supplement, you need to combine the meal bolus and the correction bolus. This information is used to calculate the amount of insulin needed to cover the meal (carbohydrate intake) and to determine the amount of insulin needed to correct for a high or low blood glucose level.

Appendix

136


Advanced Carbohydrate Counting Practice: Determine the mealtime insulin supplement using the following problems

sets: Meal Bolus information: Use a carbohydrate/insulin ratio of 15:1 for type 1 diabetes and 10:1 for type 2 diabetes, and the carbohydrate intake of the following lunch meal:

1 medium apple 30 g carbohydrate 1 carton of low-fat fruit yogurt 25 g carbohydrate 1 small bag of pretzels 20 g carbohydrate TOTAL 75 g carbohydrate

Blood Glucose Correction Bolus information: Target blood glucose = 150 mg/dL

ü Pre-meal BG: 150 mg/dL How much bolus insulin is needed to cover the meal and the blood glucose correction for

type 1 and type 2 diabetes? _____/_____ units


type 1 and 2 diabetes? _____/_____ units ü Pre-meal BG: 50 mg/dL How much bolus insulin is needed to cover the meal and the blood glucose correction for

type 1 and 2 diabetes? _____/_____ units

Source: Joyce Green Pastors, RD, MS, CDE, University of Virginia Diabetes Center.


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Advanced Carbohydrate Counting: Answers

Practice Worksheet

Meal Bolus

Estimating the Carbohydrate Intake

Practice: Estimate the amount of carbohydrate in a pizza meal (2 slices of thin-crust veggie pizza, lettuce salad with 2 Tbsp of Italian dressing, diet cola). Answer: 60 g of carbohydrate Practice: Estimate the amount of carbohydrate in a McDonald’s meal (Big Mac, medium French fries, chocolate milkshake). Answer: 145 g of carbohydrate

Determining the Meal Bolus

Practice: Assume a meal has an estimated carbohydrate amount of 60 g. Calculate the

meal bolus using a carbohydrate/insulin ratio of 15:1. Answer: Grams of carbohydrate (60) divided by carbohydrate/insulin ratio (15) = 4 units



Practice: Calculate the amount of glucose to be corrected based on an actual pre-meal blood glucose level of 300 mg/dL and a target glucose level of 150 mg/dL. Answer: 300 mg/dL (actual blood glucose) – 150 mg/dL (target blood glucose) = 150 (blood glucose correction)

Determining the Blood Glucose Correction Bolus

Practice: Type 1 diabetes, a pre-meal blood glucose level of 250 mg/dL and a target blood glucose of 150 mg/dL. Answer: 250 mg/dL (pre-meal BG) – 150 mg/dL (target BG) = 100 mg/dL (BG correction) 100 mg/dL (BG correction) divided by 50 (50) = 2 (correction bolus) Practice: Type 2 diabetes, a pre-meal blood glucose level of 50 mg/dL and a target blood glucose of 150 mg/dL. Answer: 50 (pre-meal BG) – 150 (target BG) = –100 mg/dL (BG correction) –100 (BG correction) divided by 30 (30) = –3 (correction bolus)

Appendix

138


Advanced Carbohydrate Counting: Answers

Combining the Meal Bolus and the Glucose Correction Bolus to Determine the Mealtime or Bolus Insulin Supplement

Practice: Determine the mealtime insulin supplement using the following problems sets.

Meal Bolus Info: 75 g carbohydrate

Blood Glucose Correction Bolus information: Target blood glucose = 150 mg/dL


type 1 and type 2 diabetes? Answer: 5/7.5 or 8 units


type 1 and 2 diabetes? Answer: 8/12.5 or 13 units ü Pre-meal BG: 50 mg/dL How much bolus insulin is needed to cover the meal and the blood glucose correction for

type 1 and 2 diabetes? Answer: 6/9.2 or 9 units


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Test 1. The clinical classifications of diabetes are:

a. Primary and secondary diabetes b. Type 1 diabetes and type 2 diabetes c. Juvenile-onset and maturity-onset diabetes d. Type 1 diabetes, type 2 diabetes, gestational diabetes and pre-diabetes

2. The initial defect in type 2 diabetes is:

a. Hypoglycemia b. Insulin resistance c. Diabetic retinopathy d. Insulin deficiency

3. What is needed to confirm a diagnosis of diabetes mellitus?

a. A1C ≥6.5% b. Fasting plasma glucose ≥126 mg/dL on two occasions c. Two-hour plasma glucose level >200 mg/dL during an oral glucose tolerance test d. All of the above

4. The treatment components for most persons with diabetes include:

a. Medication, meal planning and exercise b. Medication, meal planning, exercise, self-monitoring of blood glucose and education c. Medication, meal planning and SMBG d. Medication, meal planning, exercise and SMBG

5. The primary purpose of SMBG is to: a. Provide immediate feedback on blood glucose control and understand glucose patterns. b. Adjust diabetes medications. c. Adjust diet and activity. d. Diagnose hypoglycemia and determine need for treatment.

6. The exercise recommendations for type 2 diabetes should focus on:

a. Structured exercise for fitness b. Improving lifestyle activity for health c. Increasing aerobic activity d. Promoting weight loss

7. An intensive insulin regimen that most closely mimics a normal insulin profile is:

a. Rapid- or short-acting insulin before breakfast, lunch and dinner b. Rapid- or short-acting insulin before breakfast, lunch and dinner, and intermediate-acting

insulin at bedtime and before breakfast c. Long-acting insulin before breakfast, lunch and dinner d. Rapid- or short-acting insulin before breakfast, lunch and dinner, and long-acting insulin

once or twice daily


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8. What is the MOST common and preferred antihyperglycemic agent to use initially in type 2 diabetes?

a. Glyburide (DiaBeta) b. Metformin (Glucophage) c. Acarbose (Prandase) d. Sitagliptin (Januvia)

9. What is the PRIMARY nutrition goal for those with diabetes? a. Determine an individualized and appropriate calorie prescription. b. Collaborate and develop an individualized meal plan. c. Restrict the amount of carbohydrate at mealtimes. d. Emphasize a healthy and balanced meal plan with appropriate amounts of carbohydrate,

protein and fat. 10. What is the recommended nutrient distribution for those with diabetes?

a. 50% carbohydrate, 20% protein and 30% fat b. 40% carbohydrate, 20% protein and 40% fat c. 50% to 55% carbohydrate, 12% to 20% protein and <30% fat d. Recommendations are based on evidence, individualized assessment and clinical goals

rather than numerical percentages of nutrients. 11. What is the PRIMARY benefit of including whole-grain foods in the diet of those with diabetes?

a. Improves nutrition and general health b. Improves lipid levels c. Improves glucose levels d. Promotes satiety

12. Which statement about the use of nutritive sweeteners such as fructose and alcohol sugars

is MOST correct? a. Fructose is recommended as a sweetening agent if used in equivalent amounts to sucrose. b. Fructose in the form of whole fruit is highly encouraged in an eating plan. c. Alcohol sugars are the preferred substitute for sucrose in products such as candy, frostings

and baked goods. d. Because fructose and alcohol sugars contain more nutrients, they are recommended in place

of nonnutritive sweeteners. 13. The recommendation for use of alcohol is:

a. Never recommended for those with diabetes b. No more than 1 serving/day for women and 2 servings/day for men (if diabetes is well

controlled) c. Only for those with type 2 diabetes who are not taking insulin d. No more than 1 serving/day

14. Which BEST describes the metabolic effect of protein in persons with diabetes?

a. It does not increase plasma glucose levels. b. It raises plasma glucose levels and needs to be accounted for (i.e., carbohydrate). c. It slows the absorption of carbohydrates, and can be helpful in avoiding hypoglycemia,

particularly at night. d. Approximately 60% of protein is converted to glucose, so it has about half the effect of

carbohydrates on plasma glucose levels.


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15. The meal-planning strategy with the highest priority in obese persons with type 2 diabetes is: a. Fat and/or calorie modification b. Sucrose limitation c. Protein moderation d. Fiber modification

16. A newer class of antihyperglycemic agents, sodium-dependent glucose cotransporter

inhibitors should NOT be used in those with diabetes who are: a. Normal weight with moderately elevated glucose levels b. Hypertensive and obese c. Young and obese d. Using angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers

17. Which is MORE important to monitor for achieving good glucose control?

a. Glycemic index b. Glycemic load c. Total amount of carbohydrate d. Total calories from carbohydrate, protein and fat

18. The steps for diabetes nutrition therapy include:

a. Assessment, diagnosis and goal setting, intervention, and documentation b. Assessment, diagnosis and goal setting, intervention, and evaluation c. Assessment, intervention, communication and follow-up d. Assessment, intervention, documentation and reassessment

19. Basic nutrition intervention should focus on:

a. Providing a meal plan that promotes healthy eating b. Replacing the current diet with a new diet that is healthier c. Providing a list of foods not to eat d. Developing a nutrition prescription for calories, carbohydrate, protein and fat

20. What are the recommendations for weight loss in obese/overweight persons with type 2

diabetes? a. Modest weight loss (5% to 10% of body weight) b. Weight loss of 1 lb/week to 2 lb/week c. Weight loss to achieve ideal body weight d. Don't need to focus on weight loss

21. Which nutrition strategy would be MOST beneficial for the overweight/obese person with

type 2 diabetes? a. Consistency of carbohydrate b. Calorie limitation c. Fat modification d. Agreed upon and individualized

22. The in-depth education stage of nutrition intervention includes:

a. Selecting a more structured meal-planning approach b. Teaching food exchange lists c. Providing continuity of care d. Providing supplementary information


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23. Recent studies have suggested that type 2 diabetes can be prevented MOST effectively by: a. Initiating oral diabetes agents b. A high-fiber diet c. Weight loss through lifestyle intervention d. Screening for diabetes at an earlier age

24. Which meal-planning approach provides tight glucose control with some flexibility in eating patterns?

a. Exchange lists b. Carbohydrate counting c. Calorie/fat counting d. Menus

25. Which meal-planning approach is thought to be MOST effective for persons with diabetes?

a. Any approach that supports the nutrition goals and is realistic for persons with diabetes b. Carbohydrate counting c. An individualized meal plan using Exchange Lists d. A simplified meal plan that emphasizes no “concentrated sweets”

26. The primary emphasis with advanced carbohydrate counting is:

a. Teaching grams of carbohydrate instead of carbohydrate servings or choices b. Calculating an insulin:carbohydrate ratio and a correction factor c. Portion size d. Label reading

27. Which are the MOST important components of a nutrition assessment?

a. Nutrition, medication, physical activity and economic histories b. Nutrition, physical activity, weight and glucose monitoring histories c. Food record, psychosocial, physical activity and clinical histories d. Nutrition, physical activity, weight and psychosocial histories

28. What is the caloric contribution of alcohol?

a. 9 kcal/g b. 4 kcal/g c. 7 kcal/g d. 0 kcal/g

29. What is the primary reason a high-protein, low-carbohydrate diet is NOT recommended for

persons with diabetes? a. It is high in saturated fat that can increase total cholesterol and LDL levels. b. It restricts whole grains, fruits and vegetables. c. The improvements in weight, blood glucose and lipid levels are usually temporary. d. It is difficult to follow an eating pattern with extremes of low and high amounts of protein

and carbohydrate on a long-term basis. 30. What is the recommended treatment for hypoglycemia?

a. “15 /15” guideline b. High-protein diet c. Increased insulin dosage d. Fasting


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31. In addition to testing glucose and ketones, which is the MOST critical for treating an illness in patients with diabetes? a. Small frequent meals and changing diabetes medication b. Monitoring intake of carbohydrate and reducing medication c. Frequent fluids and continuing to take diabetes medication d. Eating enough calories for the medication

32. Diabetes and pregnancy is characterized by which metabolic change?

a. Decreased total cholesterol b. Increased insulin resistance c. Decreased serum ketones d. Decreased insulin resistance

33. In gestational diabetes, which strategy may be MOST effective in controlling blood glucose

levels? a. Eat small to moderate-size meals. b. Include a bedtime snack to decrease hours of fasting. c. Include snacks between meals. d. Avoid simple carbohydrates such as high-processed breakfast cereal and fruit juice at

breakfast. 34. How often should those with type 2 diabetes have a dilated eye exam?

a. Annually b. Every six months c. Every five years d. At every clinic visit

35. Which is a criterion for high risk of gestation diabetes?

a. Family history of diabetes b. Normal body weight c. <25 years of age d. White race

36. Which is the MOST common precipitating factor(s) for the development of diabetic

ketoacidosis? a. Too much food and not enough exercise b. Not taking insulin, and stress from infection or illness c. Taking too much insulin d. Poor glucose control

37. Hyperosmolar hyperglycemic state differs from DKA in which of the following ways?

a. Glucose levels are lower. b. There is a decrease in total body potassium. c. No dehydration is present. d. There is no ketosis.

38. The MOST correct diagnosis of hypoglycemia is a blood glucose level of:

a. <70 mg/dL b. <120 mg/dL c. <40 mg/dL d. <20 mg/dL


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39. What is the recommended treatment for someone with severe hypoglycemia in a semi-conscious state who is unable to take food or liquid by mouth? a. Administer glucose gel. b. Administer glucagon injections. c. Rush the person to the ED. d. Revive via inhalants, and give oral glucose.

40. What are the major microvascular complications of diabetes?

a. Vascular disease and neuropathic conditions b. Retinopathy, nephropathy and neuropathy c. Hypoglycemia and hyperosmolar hyperglycemic state d. Cardiovascular, cerebrovascular and peripheral vascular disease

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