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Vol. 13 •Issue 8 • Page 37
Sound the Alarm

Childhood Obesity and the Emergence of Type 2 Diabetes

An alarming number of newly diagnosed diabetes cases in children and adolescents are now the type 2 form.1 The American Diabetes Association estimates that between 8% and 45% of new cases of pediatric diabetes fall in this category. Because this is a new phenomenon, more definitive statistics aren't yet available.

Less than a decade ago, type 1 was the primary form of diabetes affecting children. In this manifestation of the disease, the pancreas cannot produce the insulin required to maintain proper body function.

In type 2 diabetes, the pancreas produces insufficient amounts of insulin or the body does not use what it produces. Until recently, type 2 diabetes was most common in middle-aged adults.

Running a parallel course to diabetes among children and adolescents is obesity. Table 1 shows how pediatric obesity soared between 1970 and 2000.2 Obesity can be determined by body mass index (Table 2). A patient is considered obese if he or she falls above the 85th to 95th percentile for age and gender.2

The National Health and Nutrition Examination Survey recommends using the 85th percentile as the cutoff between overweight and obese, while the Centers for Disease Control and Prevention advocates the 95th percentile as the cutoff.3

Risk Factors

The risk factors for type 2 diabetes are the same as for obesity. The link between obesity and type 2 diabetes is considered multifactorial, involving relationships among modifiable, nonmodifiable and environmental risk factors (Table 3).4 Factors that are nonmodifiable cannot be changed; they will exert their influence no matter what the person does.

Familial tendencies toward obesity and type 2 diabetes give significant credibility to the genetic predisposition theory. Studies of twins have demonstrated a definite link between genetics and the development of obesity and diabetes.5 A child of obese parents has a 30% to 40% probability of becoming obese. The children of a diabetic parent or parents have a 25% risk of developing the disease.6

Ethnic influences on obesity have been studied, but definitive conclusions have not been reached. Any influence may be associated with the immigration of ethnic cultures from impoverished countries into an environment that has an overabundance of nutrition.3 Populations that have shown an increased susceptibility to obesity and type 2 diabetes are listed in Table 4.6,7 The data about obesity is well documented, but because of misclassification or underdiagnosed type 2 diabetes in children, the exact prevalence of type 2 diabetes has not been determined.8,9

Pathophysiology of Diabetes

The mechanism of insulin release and utilization is primarily controlled by a system of supply and demand. In a normal physiologic state, the body produces insulin in response to a demand. Hyperinsulinism is a state with an overabundant supply compared with the demand, a common side effect of obesity.6 The resulting increase in the concentration of plasma glucose is partly due to the body trying to feed target cells that have become resistant to insulin. The production demand placed on the pancreatic beta cells by chronic overstimulation results in their ultimate failure.6

The distribution of adipose tissue — not general adiposity as previously believed — seems to be connected to type 2 diabetes.10 Visceral fat may have a greater influence on the development of insulin resistance, type 2 diabetes and cardiovascular disease. Visceral adipose cells may oversecrete certain factors directly linked to metabolism. Free fatty acids are released from visceral adipose cells, captured by the portal vein and delivered directly to the hepatic system. This in turn stimulates the hepatic system to produce glucose.10 Current research is attempting to establish the relationship between cytokines such as IL-6, TNF-alpha, adiponectin and resistin (all released by visceral adipose cells) and insulin resistance. Researchers are also exploring whether the collection of lipids within the skeletal muscle cell contributes to insulin resistance.10

Pathophysiology of Obesity

A complex hormone-regulating mechanism controlled by the hypothalamus interprets various messages from systems throughout the body and adjusts energy expenditures.3 Obesity can be defined as an alteration in energy expenditure and energy storage.3 Efforts are being made to identify the specific gene responsible for obesity, but it appears that several genes may contribute to the problem.4

Environment also plays a role in the development of obesity. The thrifty gene theory, which proposes that an increased plasma insulin level existed during the early stages of evolution to facilitate adipose tissue uptake of glucose, is also being explored. The so-called thrifty gene is theorized to have helped people in times of famine, when limited resources had to be maximized to preserve life.3

Other factors may influence the development of obesity and type 2 diabetes as well. Children with first- or second-degree relatives who have diabetes have an 80% to 90% risk of developing the disease.5,6

Children in the United States today are not as physically active as the previous generation thanks to increased television viewing, extensive computer and video game use, and a diet high in fat, carbohydrates and processed food. Children's expenditure of energy is not proportional to their intake, so the excess energy is stored for future use. The body stores this excess energy as adipose tissue. When body mass index reaches the 85th percentile, obesity is achieved.2,11 The socioeconomic influences of some minority populations may also promote conditions that are ripe for the development of obesity and type 2 diabetes in children.

Diagnosis

Diagnosis of obesity and diabetes begins with the proper identification and classification of the population at risk of developing the disease. A complete history provides clues about familial tendencies as well as insight into how the parents and child view obesity. Complete testing and screening information on diabetes is provided in the continuing education article in this issue of ADVANCE (Seley JJ, Wei E. Managing type 2 diabetes. Patient and NP as partners in care. ADVANCE for Nurse Practitioners. 2005;13[8]:22-33).

To diagnose obesity in children and adolescents, calculate BMI and consider the results in relation to the risk factors listed in Table 3. BMI should not be the only criteria used to diagnose obesity.

Treatment and Prevention

The goal of treatment for type 2 diabetes and obesity is the achievement of a normal glucose level and a decrease in body weight. This effort begins with lifestyle changes, diet control, physical activity, appropriate medication and proper follow-up. The biggest challenge is lifestyle change. Because weight reduction improves insulin sensitivity and secretion, weight loss should be a primary objective.12,13 Research shows that by kindergarten, children have a good idea of what they like to eat. Parents have control over what is presented to children at meals, so teaching parents to provide balanced, nutritious meals should be part of the treatment regimen. This can be accomplished through training sessions and counseling.14 Children should be educated about nutritious eating as well.

Physical activities for children should focus on unstructured activities because children tend to lack the ability for extended concentration.12 Activities that are short in duration and are fun will engage the child.14

To increase physical activity, television viewing should be decreased. TV promotes a sedentary lifestyle and increased food consumption, particularly of unhealthy foods. The average child watches television between 1.8 and 2.4 hours per night and consumes an average of 1.4 to 1.6 soft drinks per day.11

Nutrition education is an important intervention and shouldn't be overlooked. Socioeconomic restrictions might make it hard for some families to undertake a healthy lifestyle. When faced with choosing between healthier but more expensive food products and less healthy but less expensive foods, the impoverished tend to choose the latter. Children tend to choose what they eat according to what they have seen advertised or by peer influence.14,15

For the pharmacologic treatment of diabetes, the only medications approved by the FDA for the treatment of type 2 diabetes in children are metformin (Glucophage) and insulin. Metformin is the treatment of choice if the child is not in a severe hyperglycemic state.9 The side effect profile of metformin is limited to mild and self-limiting gastrointestinal complaints. Unlike some of the other antiglycemic agents currently on the market, metformin does not cause weight gain and its anorexic properties may prove beneficial in aiding patients who have a tendency to overeat.16

Metformin works primarily in the liver by decreasing glucose production. It also improves the sensitivity of target cells to insulin.5,16 Metformin alone cannot achieve a euglycemic state, and proper lifestyle change in combination with metformin increases the likelihood of success.16 Insulin requires close monitoring for the prevention of hypoglycemia. Its use is usually indicated in patients who present in a ketotic or severe hyperglycemic state. Once the crisis is over, the patients can be transitioned to oral agents.5

Other agents commonly used in the adult population have not been studied sufficiently to reach conclusions about pediatric use. The thiazolidinediones (Avandia, Actos) are second-generation agents and require more in-depth studies to determine toxicity levels. Side effects of this class include subcutaneous weight gain, edema and anemia.16

Alpha-glucosidase inhibitors (Precose, Glyset), which are taken with meals, work on the border of the intestine by decreasing the absorption of carbohydrates, thereby decreasing postprandial blood glucose. The unwelcome side effects of flatulence, abdominal cramping, diarrhea and distention decrease the likelihood that adolescents will comply with the prescribed regime.5,16

The meglitinides (Prandin, Starlix) must be taken within 30 minutes of meals. This class influences the pancreas by stimulating insulin release. Adolescents have unpredictable eating patterns, making it difficult to sustain a normal glycemic state.5

The sulfonylureas (Glucotrol, Amaryl, DiaBeta, Glucovance) are in the insulin secretagogue family. These agents exert their effect on specific receptor sites on the wall of the beta cells, thereby producing insulin release. The major drawback to these agents is the associated risk of hypoglycemia.16

Long-Term Monitoring

The goal of long-term monitoring is to reach a euglycemic state and prevent long-term complications of obesity and type 2 diabetes. Recommendations from the American Diabetes Association include once- to twice-daily self-monitoring of blood glucose levels.5 More frequent checks are needed if the treatment regimen needs adjustment.

Glycosylated hemoglobin (HbA1c) testing provides a measure of glucose control over time and should be performed every 3 months.5 This test is helpful in determining compliance with your prescribed treatment regimen.

Since hyperglycemia can cause microvascular compromise, neurological signs and blood pressure should be checked at every visit. Urine testing and a dilated eye exam should be performed every year.5 Diet control and physical activities should be reinforced, and positive gains should be acknowledged.

Improving Lives

Nurse practitioners have the opportunity to sound an alarm with parents and children. We can improve the lives of children with type 2 diabetes or obesity by intervening early and providing thorough education and appropriate treatment. Research is needed to identify preventive measures that are appealing to children and adolescents, to encourage compliance and long-term change. In addition, more diabetes medications appropriate for the pediatric population should be developed.

Educational and training modules for parents and children with diabetes and obesity are needed as well. The National Association of Pediatric Nurse Practitioners (NAPNAP) has developed a program to reduce overweight and obesity in children. Healthy Eating and Activity Together provides evidence-based guidance on nutrition and physical activity to encourage lifelong healthy habits.

The sidebar at left provides more information on this valuable program.

References

1. Goran MI, Ball GDC, Cruz ML. Obesity and risk of type 2 diabetes and cardiovascular disease in children and adolescents. The Journal of Clinical Endocrinology & Metabolism. 2003;88(4):1417-1427.

2. Ludwig DS, Ebbeling CB. Type 2 diabetes mellitus in children: primary care and public health. JAMA. 2001;286(12):1427-1430.

3. Burniat W, Cole T, Lissau I, Poskitt E. Child and Adolescent Obesity: Causes and Consequences, Prevention and Management. Cambridge, England: University Press; 2002.

4. Clément AK, Ferré P. Genetic and pathophysiology of obesity. Pediatric Research. 2003;53:721-725.

5. Aye T, Levitsky LL. Type 2 diabetes: an epidemic disease in childhood. Current Opinion in Pediatrics. 2003;15:411-415.

6. Silink M, Kida K, Rosenbloom AL. Type 2 diabetes in children and adolescents in North America. In: Imperatore G, Williams DE, Vinicor F. Type 2 Diabetes in Childhood and Adolescence: A Global Perspective. London, England: Martin Dunitz; 2003: 37-49.

7. Rosenbloom AL. Increasing incidence of type 2 diabetes in children and adolescents: treatment consideration. Pediatric Drugs. 2002;4:209-221.

8. Rocchini AP. Childhood obesity and a diabetes epidemic. NEJM. 2002;346:854-855.

9. Bloomgarden ZT. Type 2 diabetes in the young: the evolving epidemic. Diabetes Care. 2004;27:998-1010.

10. Goran MI, Ball GDC, Cruz ML. Obesity and risk of type 2 diabetes and cardiovascular disease in children and adolescents. The Journal of Clinical Endocrinology & Metabolism. 2003;88:1417-1427.

11. Giammattei J, Blix G, Marshak HH, Wollitzer AO, Pettitt DJ. Television watching and soft drink consumption: associations with obesity in 11- to 13-year-old school children. Archives of Pediatric and Adolescent Medicine. 2003;157:882-886.

12. American Diabetes Association. Type 2 diabetes in children and adolescents. Pediatrics. 2000;105:671-680.

13. Gumbiner B, Battiwalla M. Obesity and type 2 diabetes mellitus: a treatment challenge. The Endocrinologist. 2002;12:23-28.

14. Sothern MS, Gordon ST. Prevention of obesity in young children: a critical challenge for medical professionals. Clinical Pediatrics. 2003;42:101-111.

15. Rivera FP, Whitaker R, Sherman PM, Cuttler L. Influencing the childhood behaviors that lead to obesity: role of the pediatrician and health care professional. Pediatrics & Adolescent Medicine. 2003;157:719-720.

16. Freemark M. Pharmacologic approaches to the prevention of type 2 diabetes in high risk pediatric patients. Clinical Endocrinology & Metabolism. 2003;88:3-13.

André Roy is a family nurse practitioner who practices at First Medical Care Inc. in Decatur, Ga.

Turning up the HEAT on Pediatric Obesity

The Healthy Eating and Activity Together (HEAT) Initiative is a 5-year leadership initiative by the National Association of Pediatric Nurse Practitioners (NAPNAP) to combat childhood overweight through excellence in preventive efforts in primary care. This is the only national effort by a major nursing organization to address this critical health issue.

Mary Margaret Gottesman, NP, a past president of NAPNAP who is a faculty member at The Ohio State University and a member of the ADVANCE for Nurse Practitioners editorial advisory board, is chair of the project. HEAT's Steering Work Group of eight NAPNAP member leaders met over the past 2 years to carve out a strategic plan for the initiative. In alphabetical order, the members are Margaret Brady, NP, Christina Calamaro, NP, Barbara Deloian, NP, Karen Duderstadt, NP, Bonnie Gance-Cleveland, NP, Lynn Gilbert, NP, Linda Jonides, NP, and Carolyn Montoya, NP. The centerpiece of the initiative is the creation of the first clinical practice guideline developed by NAPNAP.

Data from a recent survey of pediatric nurse practitioners and pediatricians show that as few as 15% of primary care professionals routinely include all aspects of the history and physical exam recommended by the National Heart, Lung and Blood Institute (NHLBI) and the American Academy of Pediatrics when evaluating overweight children. Many respondents reported feeling unsure about various aspects of guidance for children and their families. At the same time, Cochrane reviews of intervention efforts for childhood overweight demonstrated only modest effectiveness that is seldom sustained. Based on this data, the HEAT Steering Work Group concluded that the initiative would focus on prevention from birth through adolescence.

The HEAT Preventing and Identifying Overweight in Children Clinical Practice Guideline, along with its accompanying Resource Kit, aim to provide a solid set of materials for preventive efforts by primary care providers. Echoing the age groupings of the Bright Futures materials, the guideline provides evidence-based recommendations for care during infancy, early childhood, school age and adolescence to achieve optimal practices in early identification, nutrition and feeding, physical activity, development and communication. Important features include specific suggestions to assure cultural acceptability of guidance efforts for Native American, African American and Hispanic populations, as well as the identification of advocacy interventions for children, teens, parents, teachers and health professionals.

The Steering Work Group released prototypes of the guideline and resource kit at NAPNAP's annual conference in March and the American Academy of Nurse Practitioners conference in June, testing the clarity and "doability" from the NP's point of view. The finalized guideline and resource kit will be released this winter.

NAPNAP acknowledges the generous support of several industry partners for this initiative. For more information about HEAT, contact the NAPNAP national office at 856-857-9700 or info@napnap.org.

–Mary Margaret Gottesman, NP

No More Tears: The Link Between Dry Eye and Diabetes

Patients with diabetes are at increased risk for dry eye syndrome. The condition is characterized by dryness, burning or sandy-gritty irritation in the eyes that worsens throughout the day.

In a 1994 study, more than half of patients with diabetes experienced dry eye, while 37% of diabetes patients in a Canadian survey reported the syndrome.1,2

Dry eye irritation occurs when the production of tears decreases. In patients with diabetes, the decreased production of tears is usually a result of impaired corneal sensation, or relative numbness of the eye surface, according to Jeffrey P. Gilbard, MD, a clinical assistant professor at Harvard Medical School and president of Advanced Vision Research, maker of TheraTears. Aside from diabetes, other factors that can impair corneal sensation include LASIK eye surgery, certain viral infections of the cornea and long-term wear of hard contact lenses.

The stinging and burning associated with dry eye syndrome result from a skewed water-salt balance in the tears.

"The first thing that happens when an eye becomes dry is that the tears lose water and become too salty," Gilbard says. "Just like when you throw salt on a wound and it causes stinging and burning, when your tears become too salty they cause stinging and burning of the eye surface. As the eyes become drier, this becomes a sandy—gritty irritation of the eyes."

Patients with dry eye syndrome can usually relieve symptoms with drops, omega-3 nutritional supplements or punctal plugs. Healthy lifestyle may also help ease symptoms and enable tear glands to perform at their best. Patients should eat dark, oily fish such as sardines, anchovies and salmon; reduce their intake of vegetable oil; and stay well hydrated by drinking water and avoiding excess alcohol, Gilbard advises.

References

1. Caffery BE, Richter D, Simpson T, Fonn D, Doughty M, Gordon K. CANDEES. The Canadian Dry Eye Epidemiology Study. Adv Exp Med Biol. 1998;438:805-806.

2. Seifart U, Strempel I. The dry eye and diabetes mellitus. Ophthalmologe. 1994;91:235-239.




     

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