Type 1 diabetes, metabolism and nutrition
Esther Muschel, MD
Cynthia Abraham, MD
Robert Karp, MD
SUNY-Downstate Medical Center
Brooklyn, NY
PRETEST
Q1. Insulin deficiency causes which of the following?
a. Glycogen synthesis, glycogenolysis, protein synthesis and lipid synthesis.
b. Glycogenolysis, gluconeogenesis, proteolysis and lipolysis.
c. Ketogenesis, gluconeogenesis, lipid synthesis and glycogen synthesis.
d. Proteolysis, ketogenesis, glycogen synthesis and gluconeogenesis.
Q2. Which of the following is the most important determinant of blood sugar?
a. Glycemic index of food (e.g. qualitative aspects of carbohydrate).
b. Carbohydrate content of food (e.g., quanitiative aspects).
c. Types of polysaccaride, disaccharide and monosaccharides consumed.
d. Cooking and processing of food elements.
Q3. Diabetic patients should consume:
a. Less protein than the general population
b. More protein than the general population
c. The same amount of protein as the general population
Q4. Children with diabetes who have good glycemic control are expected to achieve
a. A decreased height when compared to their peers and an increased BMI.
b. A similar height to their peers and an increased BMI.
c. A similar height to their peers and a similar BMI.
d. An increased height when compared to their peers and a decreased BMI.
Q5. Type 1 diabetics:
a. Should never perform rigorous physical activity.
b. Can always exercise if their blood sugar is very high in order to decrease blood sugar.
c. Should always eat a carbohydrate before exercising.
d. Should eat a carbohydrate before exercising if blood sugar is below 100 mg/dl.
Q6. Which of the following is an acute complications of T1DM?
a. nephropathy
b. retinopathy
c. diabetic ketoacidosis
d. A & B
OBJECTIVES:
At the conclusion of this module residents and physicians will
1. Understand the underlying metabolic defect of insulin depletion.
2. Be able to evaluate a child with Type 1 Diabetes Mellitus (T1DM).
3. Appreciate specific the nutritional principles of the diabetic diet related to carbohydrate metabolism and links to the metabolic syndrome
4. Recognize the impact of T1DM on nutritional status during childhood and in adult life.
5. Recognize the impact of T1DM on nutritional status later in life.
FACILITATOR PREPARATION:
The facilitator should review Part III (the obesity cycle) in the Teacher's Guide and the section in the Pediatric Nutrition Notes on carbohydrate metabolism. The position statement of the American Diabetic Association provides basic principle "Nutrition principles and recommendations in diabetes (Position Statement) which was published by the American Diabetes Association in Diabetes Care (26,Suppl. 1:S51-S61, 2003)."
Also see
Pozzilli P, Manfrini S, Picardi A: Cow's milk and trials for prevention of Type 1 diabetes. Diabetic Medicine 2003;20(11): 871-872.
Mathieu C, Badenhoop K: Vitamin D and type 1 diabetes mellitus: state of the art. Trends Endocrinol Metab 2005;16(6): 261-6.
Donaghue KC, Kordonouri O, Chan A, Silink M: Secular trends in growth in diabetes: are we winning? Arch Dis Child 2003;88(2): 151-4.
INTRODUCTION:
Type 1 Diabetes Mellitus (DM) is a disease that is characterized by total insulin deficiency. The prevalence of Type 1 diabetes is 1.9 in 1000 school age children and the incidence in the U.S. is 12 to 15 cases per 100,000 per year. There are two peaks for presentation, the first between 5 and 7 years and the second at puberty. The first peak corresponds to increased exposure to various infectious agents that may trigger the beta cell destruction in predisposed individuals. The second peak corresponds to the increase in steroid hormones and growth hormones, which antagonize insulin action. (1)
The majority of patients with Type 1 DM have type 1A diabetes, which is an autoimmune destruction of the insulin producing cells. Development of this type of diabetes has been associated with a genetic predisposition. People with HLA DR3 or HLA DR4 have a 2-3-fold increase in risk. Genetic predisposition alone however is not sufficient to trigger the autoimmune process. Certain viruses have been thought to be the trigger in predisposed individuals. Various other triggers are under investigation. (1) Type 1B is a disease of unknown etiology characterized by severe insulin deficiency without any autoimmune markers.
Treatment of Type 1 DM includes exogenous administration of insulin, adequate diet, exercise and frequent monitoring of blood glucose levels. Achieving good glycemic control in children is necessary in order to obtain adequate growth and to prevent both acute and long-term complications. It is therefore necessary to properly educate patients about diet. The diabetic diet differs from that of the general population and strict carbohydrate monitoring must be practiced.
This chapter will discuss various topics related to metabolism and nutrition in Type 1 DM. It will cover the metabolic pathways affected by insulin deficiency. It will also discuss the ADA recommendations with regard to the diabetic diet. Additionally, this chapter will cover the importance of good glycemic control and the pathogenesis of microvascular disease in poorly controlled diabetics.
Pathophysiology of Diabetes
Before delving into the effects of insulin deficiency on metabolism in the type 1 diabetic patient, it is important to understand the function of insulin. Insulin is a key player in glucose metabolism and acts on the liver, muscle and adipose tissue. Below is a diagram that not only demonstrates the effect that insulin has on these organs but emphasizes the changes that occur in the high insulin (the feeding state) state versus the low insulin (the fasting state) state. (5) (6)
Esther: WHERE DID THIS COME FROM. BEWARE OF COPYRIGHT INFRINGEMENT
ESTHER, Cynthia created this from the liver, muscle fibers, etc and table on insulin and feeding state. Is this "kosher?" That is, are we putting together material from various sources. That would be if sources are named and credited.
FIGURE 1 INSULIN IMPACT DEPENDS ON FEEDING STATE.
HIGH INSULIN (FEEDING STATE) LOW INSULIN (FASTING STATE)
TEACHING CAPTION: As can be seen, Insulin has multiple effects, including in addition, those on alpha and delta cells, steroidogenesis, vasodilatation, fibrinolysis, and growth. (6)
With this overview of insulin's actions, we can now explore what happens in type 1 diabetes. In this disease, there is a progressive insulin deficiency, resulting eventually in complete insulin deficiency, leading to the effects seen on the right side of the above figure. Although deficiency is the primary defect, there are several secondary changes involving the stress hormones that worsen the metabolic decompensation. The stress hormones include epinephrine, cortisol, growth hormone, and glucagon. The chart below summarizes the how these stress hormones increase blood sugar levels. (1)
ESTHER WHERE DID THIS COME FROM. BEWARE OF COPYRIGHT INFRINGEMENT-needs reference put back in. We lost source.
TABLE 1: Counter regulatory effects resulting in elevations in blood sugar.
Glucagon Stimulates glycogenolysis by activating hepatic phosphorylase
(from alpha cells) Promotes gluconeogenesis
Decreases insulin stimulated glucose utilization
Growth hormone Increases hepatic glucose production
(from anterior pituitary) Stimulates lipolysis
Stimulates protein synthesis
Decreases insulin stimulated glucose utilization
Cortisol Increases hepatic glucose production
(from adrenals) Stimulates lipolysis
Protein breakdown
Decreases insulin stimulated glucose utilization
Epinephrine Increases hepatic glucose production
Inhibits insulin production
TEACHING CAPTION: GIVE CREDIT IN A TEACHING CAPTION:
In the type 1 diabetic person, the decrease in insulin and the increase in counter-regulatory hormones all cause increasing blood glucose levels. As the disease progresses the patient becomes progressively hyperglycemic until the blood glucose level exceeds the renal threshold and the patient will develop glycosuria. The osmotic diuresis leads to polyuria, electrolyte losses, dehydration and polydipsia, as has occurred in Sara. These will further cause stress hormone release, which will continue to exacerbate the metabolic decompensation. (1)
Furthermore, the insulin deficiency and stress hormone excess lead to an increase in lipolysis and hence increase free fatty acid availability. The free fatty acids are shunted to become ketones. The ketones formed are beta-hydroxybutyrate, acetoacetate and acetone. These ketoacids can be utilized as fuel by extra-hepatic tissues, primarily skeletal muscle and the heart. Under extreme conditions, the brain also utilizes ketone bodies for fuel. (1)
A note on the history of diabetes treatments: How diabetes was treated before the advent of exogenous insulin.
A New York Times magazine article (2) a few years back discussed the story of Elizabeth Hughes, daughter of New York governor Charles Evans Hughes. When Elizabeth was 11 years old she developed an insatiable hunger and an unquenchable thirst, but despite her increased consumption Elizabeth was wasting away. . She was diagnosed with diabetes and her parents were given the horrible news that Elizabeth was likely to die within 1-3 years.
Here's a chance to engage residents with regards to their knowledge of diabetes care preinsulin. Ask for an explanation before explaining.
In 1919 Elizabeth was taken to Dr. Fredrick Allen who was renounced for treating her condition and prolonging the life of many individuals with use of a starvation protocol. His reasoning behind this mode of treatment was that if high levels of glucose were being excreted one had to prevent glucose from being consumed. When Elizabeth began treatment she was nearly five feet tall and weighed 75 pounds. Her treatment regimen consisted of a very low calorie diet of 400-600 calories a day, with one day per week of complete fasting. Her diet included meat, eggs, lettuce, milk, few fruits, boiled vegetables and tasteless bran rusks, all of which were carefully weighed.
The starvation diet was especially cruel. When patients presented with worsening symptoms Dr. Allen further decreased food intake. Patients continued to follow this regimen because there was no alternative. The "Physiatric Institute" became a famine ward. One 12-year-old patient undergoing this starvation diet, who was blind from diabetes and bedridden due to severe weakness, was suspected of somehow cheating on his diet, as his urine was still positive for sugar. It was later found that the boy was so hungry he had consumed toothpaste and birdseed from a nearby birdcage.
Elizabeth was maintained on the strict starvation diet and was punished if she was found sneaking food. Elizabeth was slowly wasting away. One nurse described patients as "big stomachs, skin and bone necks, skull like faces...they looked like an old Flemish painter's depiction of a resurrection after famine..."
In 1922 Frederick Banting and Charles Best discovered insulin. When Elizabeth's parents took her to Toronto to begin insulin therapy she was three days short of her 15th birthday and weighed 45 pounds. She was started on an insulin regimen and a new diet, initially still devoid of sugar, but later with addition of carbohydrates. Over a period of a few short months Elizabeth gained weight and thrived. She weighed 105 pounds. Elizabeth had been brought back from the brink of death. Elizabeth lived to the age of 74 when she died of a heart attack, more than 43,000 insulin injections later. (2)
Evaluating the Child with Type 1 Diabetes
CASE STUDY:
Sara G. is a five-year-old girl from an Italian America family who has no significant PMH. She is brought to the clinic by her mother who is concerned because Sara seems to be urinating excessively. Mrs. G first began to notice the frequent urination about one month ago, when Sara began wetting her bed for the first time in 2 years. Mrs. G first thought that perhaps Sara is having difficulty adjusting at her new school and therefore has begun to wet her bed, however she began to notice that Sara seems to be urinating frequently during the day as well. She is urinating at a frequency of about twice every hour. She also began to notice that Sara is drinking a tremendous amount of milk and juice and has been complaining of being hungry often. Mrs. G also reports that despite Sara's increase in appetite, she appears to be losing weight. In the clinic Sara is examined and examination is normal except for a 9 lb. weight loss since her well visit two months ago.
Q1. What is the differential diagnosis?
A1. Have students break into triplet: One person is the pediatrician, the other is the mother or father, while the third is an observer who gives fee back on discussion. Spend 5 minutes brainstorming Sara herself will enter the case ass she matures.
The differential diagnosis of a patient who presents with polyuria includes UTI, secondary enuresis, diabetes mellitus and diabetes insipidus. In a patient who has glycosuria the differential diagnosis includes renal disorders such as Fanconi syndrome, inborn errors of metabolism (cystinosis), and renal tubular damage (heavy metal intoxication, certain drugs). However, all of the above disorders can be ruled out by the presence of hyperglycemia. (1)
Given Sara's presentation the differential diagnosis is limited to the different types of diabetes. Polyuria, polydipsia, polyphagia and weight loss are the classic presentation for Type 1 Diabetes Mellitus (Type 1 DM). However clinical presentation is not the best way to diagnosis Type 1A diabetes. A better method is testing for the presence of anti-islet auto-antibodies. (3)
The Case continues:
Sara undergoes several lab studies. Her blood stick glucose from 2 hours after her last meal was 300mg/dl. A stat BMP showed glucose of 250mg/dl, CO2 of 20 and Na of 133. Urinalysis showed 2+ glucose and small ketones.
Q2. What other initial lab tests would you order for Sara and why?
A2. Let residents list before telling them
TEACHING CAPTION: Supportive tests are helpful in determining cause and duration of diabetes.
Further explanation:
" C-peptide levels determine how much endogenous insulin is still being produced.
" GAD 65 antibodies, islet cell and insulin antibodies are markers of autoimmunity. They are positive in >90% of non-Hispanic white Type 1A diabetics.
" Hgb A1c levels supply information about the average glycemia over the previous 3 months.
" Fructosamine test supplies information about the average glycemia over the previous 2 weeks.
" Thyroid antibodies (thyroperoxidase antibodies and thyroglobulin antibodies), free T4, TSH, and Tissue transglutaminase antibodies are performed to rule out autoimmune diseases such as celiac disease and thyroiditis. The rationale behind performing theses tests is that type 1 diabetics are at increased risk for other autoimmune diseases as well.
Q3. Does Sara have diabetes mellitus?
A3. Criteria for diagnosis of diabetes mellitus and impaired glucose tolerance:
WHERE DID THIS COME FROM. BEWARE OF COPYRIGHT INFRINGEMENT
Table 2. Normal glucose tolerance Impaired glucose tolerance Type 1 Diabetes mellitus
(any ONE of the following)
Fasting Plasma Glucose <100 mg/dl
100 and 125 mg/dl
126 mg/dl
2 hr postprandial
Glucose
<140 mg/dl 140 and 199 mg/dl 200 mg/dl
Polyuria, polydipsia, polyphagia, weight loss AND random plasma glucose of
200 mg/dl
------ ------ Present
TEACHING CAPTION: GIVE CREDIT HERE :As indicated by the chart above, the classic definition of diabetes mellitus includes symptoms of polyuria, polydipsia, polyphagia and weight loss with a random blood glucose >200mg/dl. Sara has all of the above and therefore has diabetes mellitus.
The Case continues:
After learning of Sara's diagnosis Mrs. G is visibly upset and asks to speak to you. She wonders whether she could have somehow prevented the disease. She asks whether if Sara's diet had been better the disease could have been prevented. She reports that Sara was breast fed as an infant and until recently has been eating pretty well but has had a significant "sweet tooth".
Q4. How do you respond to Mrs. G?
A4. Let's break into your three-some again and role play out the physician, Mrs. G and let the third person be Mr. G. Assumptions about ethnicity (e.g., stereotypes) are often incorrect, but for this child assume that you have an Italian American family that is within memory of immigration. There's an Italian born grandmother still in the picture. Try working this through with (again a stereotype) a suburban established American family.
You reassure Mrs. G that there was no way for her to prevent Sara's disease as the disease is an autoimmune destruction of the insulin producing cells, unlike in type 2 diabetes, where diet may play a role. Sara's form of diabetes could not have been prevented nutritionally. [Show Empathy and attempt engagement in your response]
Q5. Can early exposure to cow's milk be a trigger for type 1 diabetes in predisposed individuals?
A5. It has been suggested that early exposure to dairy products may increase the risk of developing Type 1 DM in predisposed individuals due to a component of cow's milk that may trigger the autoimmune response in type 1 diabetes. The immune response may be triggered by a mechanism of molecular mimicry between some cow milk protein and islet cell proteins. The proteins that may be involved are bovine serum albumin or beta casein. In one study of newly diagnosed type 1 diabetics, exposure to bovine beta casein led to proliferation of T cells in 51 % of patients with Type 1 DM but not in non diabetic subjects. There is also a correlation between beta casein consumption and Type 1 DM in an epidemiologic study.
Q6. Are there any protective nutrients?
A6. These are not well established. Research on Vitamin D supplementation in early infancy shows that it may be protective (9) Active vitamin D, 1 alpha, 25(oh)(2)d(3), has been found to modify T-cell differentiation and dendritic cell action and induce cytokine secretion. These effects on the immune system lead to tolerance and anergy rather than immune activation. Vitamin D has also been found to affect beta cell function. Animal studies show reduced insulin secretion in animals with deficient vitamin D or defective vitamin D receptor. Additional studies are necessary. Despite the above discussion though, there are currently no nutritional recommendations for prevention of T1DM. (9)
The Diet and Insulin Regimen of the Child with Type 1 Diabetes
The Case continues:
Mrs. G and Sara are sent to a nutritionist for education about the diabetic diet. The nutritionist gives them the guidelines below. These indications are based on the ADA position statement (10) on the nutrition principles and recommendations in diabetes.
The goals of medical nutrition in the treatment for Type 1 DM are:
1. Provide sufficient energy to allow normal growth and development.
2. Maintain optimal metabolic control, so as to prevent and reduce the risk for complications. This includes maintaining good blood glucose levels, achieving good lipid values, and maintaining favorable blood pressure.
3. Treat and prevent the worsening of complications.
4. Improve overall health by making healthy food choices and incorporating physical activity into lifestyle.
5. Accomplish all of the above in a way that suits the lifestyle and culture of the individual.
Table 4. Diet Composition
Take 5: Another exercise for our triplets: Tale these recommendations and apply them to the food culture(s) of your own family.
Carbohydrates and the glycemic response
The actual amount of carbohydrates and monosaturated fats is determined by the patient's need for weight loss. For instance, if the patient needs to lose weight, more carbohydrates and less monosaturated fat should be consumed. (10) Factors that influence the glycemic response include the amount of carbohydrate ingested, type of sugar, glycemic index, cooking and processing of food, and other components in food that may influence digestion. However studies demonstrate that the only factor that plays a significant role in glycemic response is the amount of carbohydrate ingested. Therefore it is important for patients to learn how to appropriately adjust their pre-meal insulin to match the amount of carbohydrates in their meal. It is recommended to include carbohydrates from whole grains, fruits, vegetables and low fat milk in the diabetic diet. See Assessment of Nutritional status for more on the Glycemic Index.
Proteins
In the average American diet, protein makes up 15-20% of calories throughout all age groups. Studies in type 1 diabetics treated with insulin have shown an increase in protein catabolism and it is therefore essential to ensure adequate protein intake. However, diabetics are not advised to increase their protein consumption because the average American consumes at least 50% more protein than necessary and therefore there is no need to consume extra protein. This amount of protein does not appear to increase the rate of diabetic nephropathy. However the long term effects of ingesting protein in amounts greater than 20% of total calories has not yet been established. Therefore it is recommended that protein intake not exceed 20% of calories. (10)
Fats
In patients with LDL levels greater than 100mg/dl consumption of less than 7% of calories from saturated fat is recommended. (10) Trans-fatty acids are found in baked goods and fried foods. Trans-fatty acids have been shown to elevate LDL and decrease HDL. Therefore trans-fatty acid consumption should be limited. (10)
Cholesterol
Diabetics appear to be more sensitive than the rest of the population to cholesterol. As in the general population the dietary goal for fat intake in diabetics is to limit cholesterol and saturated fat intake. When deciding whether to replace saturated fat with carbohydrates or with monosaturated fats one needs to take into account the whether the patient needs to lose weight. Diets low in saturated fats and high in carbohydrates and diets low in saturated fats and enriched in monounsaturated fats both decrease LDL levels. Polyunsaturated fats appear to lower LDL but not to the same degree as monounsaturated fats. Cholesterol intake should be less than 300 mg/day and in persons whose LDL levels are greater than 100 mg/dl, a diet containing less than 200 mg/dl is advised. (10)
Fiber
Diabetics (and everyone else) are encouraged to eat fiber rich foods including whole grains, fruits and vegetables. Some studies in type 1 diabetics show some benefit to consuming large amounts of fiber with regard to glycemic control. Others show mixed results with regard to glycemia and lipids. It is still recommended that diabetics consume the normal amount of fiber. (10) See Nutrition Notes and Fiber module.
Micronutrients
There is no real evidence of benefit from vitamin or mineral supplementation in patients with diabetes unless there is evidence of deficiency. The exceptions are folate and calcium/Vitamin D. (10) [Have to explain this]
Remember. There is an important consideration of weight gain. Tight glycemic control via intensive insulin therapy is often associated with weight gain, which can adversely affect blood sugar, lipids and blood pressure. Therefore attention should be paid to the total amount of calories in addition to the total carbohydrates. (10)
Case Continued:
As discussed above Sara meets with the dietician to come up with an appropriate meal plan. She weighs 36 kg and her height is 108 cm. The dietician decides that an exchange meal plan is the most appropriate diet for Sara. She calculates Sara's caloric need to be 1500 calories per day.
Meal Plans
There are three types of meal plans: constant carbohydrate, carbohydrate counting and the exchange diet. All three meal plans are equally effective and no individual plan was found to be superior to the others in terms of adequate control of blood sugar. (11) The following discussion will explain these meal plans.
The constant carbohydrate meal plan
With this meal plan the same amount of carbohydrate is consumed for each meal and snack from day to day and the amount of insulin is kept relatively constant from day to day. Consistency is a very important part of this meal plan. (11)
The carbohydrate counting meal plan
This plan is similar to the carbohydrate meal plan in so far as that emphasis is placed on carbohydrate intake. However it differs in that varying amounts of carbohydrates are consumed with appropriate adjustments to insulin. This plan therefore allows for flexibility. (11)
This meal plan simply means counting the total amount of carbohydrate to be consumed during a meal and taking the appropriate amount of insulin. The patient or parent must learn to read food labels. Most packaged foods have the amount of total carbohydrate and the serving size written on the label. For example, a label on a box of cheerios will show 22 g of carbohydrates for one cup (the serving size).
Patients who practice carbohydrate counting are on a flexible insulin regimen. The patient's doctor needs to assign an appropriate insulin to carbohydrate ratio. This varies between people. For example some patients may need 1 unit of insulin to cover 10g of carbohydrate whereas others may need 1 unit of insulin per 15 g of carbohydrates.
Additionally some patients may require a different insulin to carbohydrate ratio for different meals (ex: 1unit per 15g at breakfast, 1 unit per 30 g at lunch and 1 unit per 10 g at dinner). Patients can also adjust for planned exercise and current blood sugar. For example some people will decrease their insulin by 1 unit if their blood sugar is below 70mg/dl and increase 1 unit if their blood sugar is greater then 200mg/dl. (11)
A Case example
A patient has an insulin to carbohydrate ratio of 1 unit to 10 grams of carbohydrates. He would like to eat 1 ½ cups of cheerios with 1 ½ cups of milk. 1 cup of cheerios has 22 grams of carbohydrates and 1 cup of milk has 12 grams of carbohydrates. How many units of insulin must he take for this meal?
Give the problem to our triplets and let them have a try. They will need the instructions printed out
The desired total amount of carbohydrates needs to be calculated. 1 ½ cups of cheerios has 33 grams of carbohydrate (22+11=33 grams). 1 ½ cups of milk has 18 grams of carbohydrates (12+ 6= 18 grams). Therefore total carbohydrates to be consumed are 51 grams (33+18=51). Divide the total carbohydrates by the insulin to carbohydrate ratio to obtain the units of insulin necessary. 51/10=~5 units. The patient needs 5 units of insulin for this meal.
This meal plan requires some thinking and requires basic math skills. However while it may seem complicated starting out, it becomes very simple and automatic with some experience. Carbohydrate counting may be an appropriate type of diet for Sara once she is a little older. However at this point the exchange meal plan is more appropriate and will be discussed below.
Exchange meal plan:
In this plan, one is allowed to have only a certain number of items from each of six food groups (meat, bread, fat, fruit, milk) for each meal (breakfast, lunch, dinner). The number of items can range from 0 on upwards. Depending on the patients weight an appropriate number of calories is chosen. Most children under 14 years need 1000 calories plus 100 calories for each year of life per day. For example, a 5 year old child needs 1500 calories. The dietician then decides on an exchange plan to fit this number of calories. For example, for breakfast, a patient like Sara with a 1500 calorie requirement can have 1 item from the bread group, 2 items from the fruit group and 1 milk item. Because the items in each food group have a similar number of calories, carbohydrates, protein and fat, one food in a group can be exchanged for another. Many newly diagnosed patients are initially placed on this meal plan and later switch another plan. (11)
The exchange system takes some time to learn, however it has helped many diabetics stick to a healthy diet. The patient can get exchange lists from their doctor or dietitian and with practice will learn the various exchanges. (13)
Remember: Timing of the meals is important. Insulin has peaks and therefore meals and snacks need to be scheduled around those peaks. In addition, if a meal is delayed too long after injection the patient can experience hypoglycemia. (13)
Insulin regiments
Fixed dosage of insulin: insulin divided into 2 or 3 injections per day.
Flexible system: 1 unit of insulin is used to cover a pre-set amount of carbohydrates.
The flexible type allows patients to decide what to eat and take insulin accordingly, as opposed to the fixed insulin regimens that necessitate fixed carbohydrate consumption according to their dose of insulin. Therefore a fixed insulin regimen requires either a constant carbohydrate diet or an exchange meal plan, whereas a flexible insulin regimen requires carbohydrate counting.
The Case continues:
During Sara's follow up visit 2 months after diagnosis Mrs. G asks about Sara's growth potential. She wants to know whether Sara will grow as tall as her peers.
Q7. Do children with T1DM grow as tall as their healthy peers?
A7. They do with good control. A retrospective study was conducted comparing the growth patterns of children diagnosed with diabetes between the years 1974 and 1990 and those diagnosed between 1991 and 1995 found that height loss was related to higher HbA1C levels and fewer insulin injections (poorer control of diabetes). As diabetes management improved with home blood sugar monitoring and human insulin, and better glycemic control maintained, linear growth increased. The children diagnosed between 1974 and 1990 were shorter than those diagnosed between 1991 and 1995. Additionally those diagnosed between 1974 and 1990 had an increase in BMI, whereas the latter group did not. With tighter glycemic control there was concern for an increase in BMI however this study has been reassuring, showing no overall increase in the obesity trend in the later diagnosed group. This is possibly due to the increased educational programs focusing on physical exercise as an important factor in diabetes care. Therefore it is important to reassure Mrs. G that with her current care Sara will likely achieve a normal height. (14)
The Case continues:
Two years after diagnosis Sara presents for an office visit. She is doing well on her current therapy. She tests her own blood sugar and can administer her own insulin. She is compliant with her diet. She seems to be well adjusted and has just returned from a diabetic summer camp. Sara asks her mother if she can take gymnastics lessons at a nearby gym. Mrs. G would like to know if Sara can participate in competitive sports and how this would affect her blood glucose levels. She also wants to know if any adjustments should be made in Sara's care when participating in a strenuous sport.
Q8. Can Sara participate in rigorous sports and what modifications to therapy should be done during these sports?
A8. Type 1 diabetics who have good blood glucose control and have no complications can perform all levels of physical activities, ranging from leisure activities to professional sports. Therefore Sara can take gymnastics lessons but she must collect blood glucose data of her response to exercise and adjust her insulin and nutrition accordingly.
The following are the general ADA guidelines that may help in regulating the blood glucose response to exercise:
TEACHING CAPTION: Check blood glucose before exercise: <100 g/dL? Give carbohydrate; >250g.dL. Do not exercise. Adjust insulin does.
The Case continues:
Sara is currently 12 years old and is managing her diabetes very well. She is a seventh grader and is an honor student. She continues to be active in gymnastics and practices several times a week. In the fall Sara has competed in several regional meets. You are called to evaluate Sara in the ER after her mother brings her in. Sara complains of abdominal pain and vomiting since this morning. Finger stick reveals blood sugar of 410 mg/dl and urine is positive for ketones. Sara is admitted to the hospital for management of DKA. This is her first episode of DKA and her first hospital admission. During her hospital stay you try to assess a possible trigger for the episode. Sara denies any triggers but later reluctantly admits that she has been somewhat stressed over the past few weeks. She states that at a recent meet a judge commented that her 5 ft, 105 lb frame was slightly too heavy for gymnastics. Sara admits that she has been trying to lose weight and has occasionally omitted her insulin injections for this purpose.
Q9. Are diabetic children at higher risk of developing an eating disorder?
A9. Put your threesome together. What does the "Sara" character have to say?
In adolescent diabetics, in addition to the cultural push to be thin, the focus on diet and the weight gain sometimes associated with good glycemic control has raised the concern that diabetics may be more susceptible to eating disorders (16) Several studies have tried to asses the frequency of eating disorders in type 1 diabetics but these studies have shown conflicting results. Some have shown an increase in the rate of anorexia and bulimia in type 1 diabetics. Others have found that type 1 diabetics have a similar rate of anorexia and bulimia to that in the general population. A more recent case controlled study (17) has shown an increased rate of mild or sub-threshold eating disorders in preteen and teenage diabetics.
Q10. What are the risks of insulin omission?
A10. Diabetics who intentionally omit insulin are more likely to have poor glycemic control and may be at higher risk for acute and chronic complications such as DKA, retinopathy and neuropathy.
The Case continues:
Mrs. G would like to know what the long term complications of poor glycemic control are.
Q11. What are the long term effects of poor glycemic control?
A11. The risk of developing microvascular complications, 1) retinopathy, 2) nephropathy and 3) neuropathy, have been shown to be associated with increasingly poor glycemic control. The risk increases at any Hgb A1C above the non diabetic range but is highest above 12 percent. Tight glycemic control was found to be the most effective approach in the prevention of diabetic vascular complications.
Q12. What is the pathogenesis of microvascular complications due to poor glycemic control?
A12. There are several theories that have been proposed based on various studies to explain how poor glycemic control predisposes to microvascular disease. These include advanced glycosylation end products (AGEs), sorbitol pathway, generation of reactive oxygen species, and induction of flux through the hexosamine pathway, PKC activation and altered expression and function of growth factors.
Post-Test
REFERENCES:
1. Sperling MA: Diabetes Mellitus. In Sperling: Pediatric Endocrinology. 2nd ed. Sperling MA, Eds. ?, W.B. Saunders Company, 2002, p. 327-340, 6972.
2. Eisenbarth GS, Polonsky KS, Buse JB: Type 1 diabetes mellitus. In Williams Textbook of Endocrinology. 10th ed. Williams RH, Larsen PR, Kronenberg HM, Melmed S, Polonsky KS, Eds. ?, W.B. Saunders Company, 2002, p. 1486-1487
3. American Diabetes Association: Diagnosis and Classification of Diabetes Mellitus (position statement). Diabetes Care 29 (suppl 1):S43-S48, 2004
4. Champe PC, Harvey RA: Metabolic effects of insulin and glucagons. In Lippincott's Illustrated reviews: Biochemistry. 2nd ed. Winters R, Schott J, Caputo GR, Eds. Philadelphia, PA: Lippincott Williams and Wilkins, 1994, p273-274, 291-294
5. Up To Date: Insulin Action [ Can't use this unaccredited - go to source]
6. Pozzilli P, Manfrini S, Picardi A: Cow's milk and trials for prevention of Type 1 diabetes. Diabetic Medicine 20(11): 871-872, 2003
7. Up To Date: Pathogenesis of type 1 diabetes mellitus [ Can't use this unaccredited - go to source]
8. Mathieu C, Badenhoop K: Vitamin D and type 1 diabetes mellitus: state of the art. Trends Endocrinol Metab 2005;16(6): 261-6.
9. American Diabetes Association: Nutrition principles and recommendations in diabetes (Position Statement). Diabetes Care 26 (Suppl. 1):S51-S61, 2003
10. Chase HP: Food management and diabetes. In Understanding Insulin Dependant Diabetes. 9th ed. Publisher??, 1999, p 93-108??
11. www.diabetes.org [non specific - needs something else]
12. American Diabetes Association: Physical activity/exercise and diabetes (Position Statement). Diabetes Care 27 (Suppl. 1):S58-S62, 2004
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ANNOTATED PRETEST ANSWERS:
A1. B; In insulin deficiency the body goes into a state of starvation and therefore goes into a catabolic state. Proteins and lipids are broken down to amino acids and fatty acids. Glycogen is broken down into glucose. Additionally, the liver does not sense insulin and therefore "assumes" blood sugar is low and therefore produces glucose via gluconeogenesis. The free fatty acids are shunted into the ketogenic pathways. Glycogen synthesis, protein synthesis, and lipid synthesis all occur when insulin is high (fed state).
A2. B; While all of the above answers affect glycemic response and hence blood sugar, total carbohydrate content of food is the most significant determinant of glycemic response. In other words, when choosing a carbohydrate it is most important to know the grams of carbohydrate to be consumed. It is better for a diabetic to eat a food with a higher glycemic index and less total carbohydrates than a food with a lower glycemic index and more total carbohydrates.
A3. C; Diabetics should consume 15-20% of their calories in the form of proteins, as is the recommendation for the rest of the population. It is essential for diabetics to ensure adequate protein intake because diabetics have an increased protein catabolism, but the average American consumes 50% more protein than necessary. There is no increased risk of diabetic nephropathy with 15-20% of calories from protein, however long-term effects of consuming greater than 20% protein is still unknown. Therefore it is best for the diabetic to consume the recommended 15-20% protein.
A4. C; Diabetic children with good glycemic control are expected to achieve a similar height and BMI to their healthy peers. When glycemic control is poor, children were found to be shorter than their peers and have a higher BMI. When glycemic control improved there was no significant difference in height or BMI. This is despite the concern that tighter glycemic control will cause weight gain.
A5. D; Type 1 diabetics with good blood sugar control and no complications can perform rigorous physical activities. It is important for these patients to monitor blood glucose prior to exercising. A carbohydrate should be added before exercise if blood sugar is below 100 mg/dl. If it is greater than 100 mg/dl eating the extra carbohydrate is unnecessary, although carbohydrates should be readily available throughout exercise. The patient should avoid exercising if blood sugar is greater than 250 mg/dl and ketosis is present.
A6. C; Diabetic ketoacidosis is an acute complication that most often occurs secondary to missed insulin treatments. Nephropathy and retinopathy are chronic complications that have been shown to be associated with increasingly poor glycemic control. The risk increases at any Hgb A1C above the non diabetic range but is highest above 12 percent.
