A) | single parent families. | ||
B) | increased body weight. | ||
C) | drug and alcohol abuse. | ||
D) | autoimmune dysfunction. |
Why has there been an escalation in the prevalence of type 2 diabetes in this previously unaffected population? The answer to this question appears to be closely related to features of our modern way of life. Increased body weight is strongly associated with type 2 diabetes in youth, pointing to lifestyle as a causative factor. Childhood obesity has more than tripled since the 1970s [14]. It is anticipated that obesity will affect the health of 91 million children worldwide by 2025 [15].
A) | less than 100 mg/dL. | ||
B) | 100–125 mg/dL. | ||
C) | 150–200 mg/dL. | ||
D) | greater than 200 mg/dL. |
Prediabetes is an asymptomatic condition and can only be detected by laboratory testing. Prediabetes includes any one of the following findings of increased risk for diabetes [20]:
Impaired fasting glucose (IFG), defined as fasting plasma glucose (FPG) 100–125 mg/dL
Impaired glucose tolerance (IGT), defined as a postprandial blood glucose 140–199 mg/dL
Hemoglobin A1c between 5.7% and 6.4%
A) | age of onset. | ||
B) | lean vs. obese body type. | ||
C) | whether or not the patient injects insulin. | ||
D) | the presence or absence of endogenous insulin. |
The presence or absence of endogenous, or internally produced, insulin in the body is the defining factor that differentiates type 1 and type 2 diabetes (Table 1). Type 1 diabetes is an autoimmune disease that leads to the destruction of the insulin-producing beta cells of the pancreas, resulting in a complete absence of endogenous insulin [26]. It has traditionally been associated with onset in people younger than 30 years of age. Until recently, it was the only type considered prevalent in children. In this type of diabetes, insulin therapy is required and is the only appropriate pharmacologic option. Without insulin therapy, the person with type 1 diabetes will develop ketoacidosis, a life-threatening condition characterized by high blood glucose levels and a buildup of acids in the blood that will result in death if not treated.
A) | 5 and 8 years of age. | ||
B) | 8 and 12 years of age. | ||
C) | 10 and 19 years of age. | ||
D) | 16 and 18 years of age. |
Because it is a relatively new phenomenon, there is still much to learn about the epidemiology and pathophysiology of type 2 diabetes in children. While it closely resembles that of adults, youth-onset type 2 diabetes displays unique aspects, such as rapidly progressive beta-cell decline and accelerated development of diabetes complications [20,27,28]. According to the CDC, type 2 diabetes in children is usually diagnosed between 10 and 19 years of age. Risk factors include obesity, having a family member with type 2 diabetes, and being born to a mother with gestational diabetes. After 10 years of age, being a member of minority populations, such as Hispanic, African American, Asian/Pacific Islander, and American Indian, greatly increases the risk for development of type 2 diabetes in youth [29]. Whether it occurs in adults or children, most cases of type 2 diabetes begin with insulin resistance. In this condition, the pancreas initially continues to produce insulin, but the tissues are unable to use it. This may be due to a scarcity of receptors on the cells or because the receptors do not function well. Reasons for poorly functioning receptors include adiposity, muscular inactivity, and genetic factors. The beta cells of the pancreas respond to insulin resistance by producing even more insulin in an attempt to compensate. However, much of the insulin remains unused and blood levels of insulin are temporarily high (hyperinsulinemia). After a period of manufacturing large amounts of insulin, the beta cells of the pancreas eventually become exhausted, the amount of endogenous insulin greatly declines, and clinical diabetes ensues. In some cases, type 2 diabetes can be managed with a combination of diet, exercise, and oral medications. Many times, insulin therapy is required to control blood glucose levels and to prevent long-term complications of the disease. Individuals with type 2 diabetes usually produce enough insulin to prevent ketoacidosis. Therefore, they are not truly "insulin dependent," even if they do use insulin therapy to control blood glucose.
A) | ketoacidosis. | ||
B) | dyslipidemia. | ||
C) | insulin resistance. | ||
D) | autoimmune dysfunction. |
Because it is a relatively new phenomenon, there is still much to learn about the epidemiology and pathophysiology of type 2 diabetes in children. While it closely resembles that of adults, youth-onset type 2 diabetes displays unique aspects, such as rapidly progressive beta-cell decline and accelerated development of diabetes complications [20,27,28]. According to the CDC, type 2 diabetes in children is usually diagnosed between 10 and 19 years of age. Risk factors include obesity, having a family member with type 2 diabetes, and being born to a mother with gestational diabetes. After 10 years of age, being a member of minority populations, such as Hispanic, African American, Asian/Pacific Islander, and American Indian, greatly increases the risk for development of type 2 diabetes in youth [29]. Whether it occurs in adults or children, most cases of type 2 diabetes begin with insulin resistance. In this condition, the pancreas initially continues to produce insulin, but the tissues are unable to use it. This may be due to a scarcity of receptors on the cells or because the receptors do not function well. Reasons for poorly functioning receptors include adiposity, muscular inactivity, and genetic factors. The beta cells of the pancreas respond to insulin resistance by producing even more insulin in an attempt to compensate. However, much of the insulin remains unused and blood levels of insulin are temporarily high (hyperinsulinemia). After a period of manufacturing large amounts of insulin, the beta cells of the pancreas eventually become exhausted, the amount of endogenous insulin greatly declines, and clinical diabetes ensues. In some cases, type 2 diabetes can be managed with a combination of diet, exercise, and oral medications. Many times, insulin therapy is required to control blood glucose levels and to prevent long-term complications of the disease. Individuals with type 2 diabetes usually produce enough insulin to prevent ketoacidosis. Therefore, they are not truly "insulin dependent," even if they do use insulin therapy to control blood glucose.
A) | retinopathy. | ||
B) | cardiovascular disease. | ||
C) | cerebral vascular disease. | ||
D) | peripheral vascular disease. |
Uncontrolled hyperglycemia over a number of years is known to cause damage to the small vessels that supply the retina of the eye (retinopathy), the nephrons of the kidney, and the motor, sensory, and autonomic nerves. There is evidence that these complications are especially aggressive in young people with type 2 diabetes; they are also highly prevalent [32,33,37]. The United Kingdom Prospective Diabetes Study demonstrated that intensive treatment of type 2 diabetes in adults can significantly lower the risk for developing diabetes-related eye, kidney, and nerve disease. The findings from this study included a 25% reduction of microvascular disease in subjects who maintained long-term glycemic control [38].
A) | triglycerides less than 150 mg/dL. | ||
B) | blood pressure greater than 130/85 mm Hg. | ||
C) | high-density lipoprotein cholesterol (HDL-C) greater than 50 mg/dL. | ||
D) | Both A and C |
A person has metabolic syndrome if he or she has any three of the following risk factors [39,40]:
In adults, waist circumference more than 40 inches for men or more than 35 inches for women, indicating excess visceral fat. This is known as the round or "apple" body shape.
Dyslipidemia (Table 2)
Triglycerides greater than 150 mg/dL
High-density lipoprotein (HDL) cholesterol less than 40 mg/dL in men or less than 50 mg/dL in women
Blood pressure greater than 130/85 mm Hg
FPG greater than 100 mg/dL
A) | pancreatitis. | ||
B) | neuropathic pain. | ||
C) | coronary artery disease. | ||
D) | kidney disease and failure. |
A person has metabolic syndrome if he or she has any three of the following risk factors [39,40]:
In adults, waist circumference more than 40 inches for men or more than 35 inches for women, indicating excess visceral fat. This is known as the round or "apple" body shape.
Dyslipidemia (Table 2)
Triglycerides greater than 150 mg/dL
High-density lipoprotein (HDL) cholesterol less than 40 mg/dL in men or less than 50 mg/dL in women
Blood pressure greater than 130/85 mm Hg
FPG greater than 100 mg/dL
A) | boys and young men. | ||
B) | those with a lean body type. | ||
C) | children younger than 10 years of age. | ||
D) | those who have at least one parent with the disease. |
Risk factors for the development of type 2 diabetes in young people have been identified. These include [7,30,41,42]:
Overweight or obesity: A clear correlation exists between the incidence of obesity and the development of type 2 diabetes in all age groups, including children and adolescents. Central adiposity, characterized by a concentration of fat in the torso and abdominal region, is also specifically associated with insulin resistance. Excess fat cells are believed to interfere with insulin utilization and cause insulin resistance.
Ancestry: Insulin sensitivity appears to vary among ethnic groups. Preliminary population studies on the incidence of type 2 diabetes in youth indicate that this disorder appears in significantly higher rates in Native Americans, African Americans, Hispanics, and Pacific Islanders.
Family history: Type 2 diabetes is more likely to occur in those who have a first- or second-degree relative with the disease. An estimated 45% to 80% of children with type 2 diabetes have at least one parent who also has the disease. Furthermore, obesity has a familial tendency.
Developmental stage: Most new cases of type 2 diabetes in young people are diagnosed after the onset of puberty, with a mean age of diagnosis of approximately 13.5 years. During normal adolescence, there is an approximate 50% decrease in insulin sensitivity. It is believed that this is related to the increased production of growth hormone during the pubescent years.
Gender: The occurrence of type 2 diabetes is more frequent in girls and young women than in boys and young men. Girls are typically more insulin-resistant than boys when controlled for body mass index.
In utero exposure to diabetes: Having a birth mother with pre-existing or gestational diabetes also increases the risk for diabetes.
A) | rosacea. | ||
B) | insulin resistance. | ||
C) | acanthosis nigricans. | ||
D) | polycystic ovary syndrome. |
Acanthosis nigricans is a skin condition characterized by brownish-black patches, usually found on the back of the neck, in the axillae, and on areas exposed to repeated friction. They are slightly raised lesions that feel velvety to touch. Presence of the condition is considered a marker of hyperinsulinemia, and it develops in some cases of type 2 diabetes in children. This sign is most frequently recognized in obese, dark-skinned individuals and occurs more frequently in Native Americans, African Americans, and Hispanics when compared to White or Asian-origin individuals [43]. Parents of children with this condition often mistake acanthosis nigricans for poor hygiene and attempt to treat it with vigorous scrubbing and topical medications or cleansers. Some schools have initiated screening procedures for acanthosis nigricans, as many obese children who go on to develop type 2 diabetes present with only this sign [31].
A) | acne. | ||
B) | low estrogen levels. | ||
C) | low androgen levels. | ||
D) | frequent menstruation. |
PCOS is a disorder of the female reproductive system and is closely associated with insulin resistance. It is characterized by chronic anovulation, resulting in scanty or infrequent menstruation. In patients with PCOS, estrogen levels are usually normal while androgen levels are high. The elevated androgen levels can result in acne and hirsutism [44].
A) | annually after 2 years of age. | ||
B) | annually after 10 years of age or onset of puberty. | ||
C) | every two years after 10 years of age or onset of puberty. | ||
D) | every three years after 10 years of age or onset of puberty. |
The American Diabetes Association (ADA) recommends the screening of asymptomatic high-risk youth for type 2 diabetes every three years, beginning at 10 years of age or the onset of puberty, whichever occurs first. For the purposes of screening criteria, the ADA considers children at high risk if they are overweight (BMI ≥85th percentile) or obese (BMI ≥95th percentile) and have one or more of the following additional risk factors [20]:
Family history of type 2 diabetes in a first- or second-degree relative
Native American, African American, Hispanic, Asian American, and/or Pacific Islander race or ethnicity
Signs of insulin resistance, including acanthosis nigricans, hypertension, dyslipidemia, small-for-gestational-age birth weight, or PCOS (as evidenced by menstrual irregularities and/or hirsutism)
Maternal history of diabetes or gestational diabetes during the child's gestation
A) | Middle Eastern ancestry. | ||
B) | Eastern European ancestry. | ||
C) | African American ancestry. | ||
D) | Northern European ancestry. |
The American Diabetes Association (ADA) recommends the screening of asymptomatic high-risk youth for type 2 diabetes every three years, beginning at 10 years of age or the onset of puberty, whichever occurs first. For the purposes of screening criteria, the ADA considers children at high risk if they are overweight (BMI ≥85th percentile) or obese (BMI ≥95th percentile) and have one or more of the following additional risk factors [20]:
Family history of type 2 diabetes in a first- or second-degree relative
Native American, African American, Hispanic, Asian American, and/or Pacific Islander race or ethnicity
Signs of insulin resistance, including acanthosis nigricans, hypertension, dyslipidemia, small-for-gestational-age birth weight, or PCOS (as evidenced by menstrual irregularities and/or hirsutism)
Maternal history of diabetes or gestational diabetes during the child's gestation
A) | weight loss through a strict calorie-controlled diet. | ||
B) | glucose control through the use of oral medications or insulin. | ||
C) | weight loss through the use of appetite-suppressing medications. | ||
D) | lifestyle management, including self-management education and weight loss through a healthy eating plan coupled with increased activity. |
The primary means for treating type 2 diabetes in youth is lifestyle management, which includes youth-oriented, culturally appropriate self-management education and support, and weight loss through a healthy eating plan coupled with increased daily physical activity [20]. Blood glucose monitoring is important in providing feedback to the individual on how these changes affect glycemia. Clinical practice guidelines from the American Academy of Pediatrics (AAP) recommend starting metformin in newly diagnosed patients with an A1c of 6.5% or greater [46]. This recommendation also is supported by the ADA [20].
A) | Adhering to a low carbohydrate diet | ||
B) | Achieving and maintaining reasonable body weight | ||
C) | Increasing the A1c level to 3% greater than normal | ||
D) | Attaining fasting blood glucose levels less than 200 mg/dL |
Achieving and maintaining a reasonable body weight is the major therapeutic goal in the management of type 2 diabetes in youth. Other goals of medical nutrition therapy include normalizing blood glucose (without excessive hypoglycemia) and maintaining healthy lipid and blood pressure values while allowing for normal growth and development [16,20].
A) | be realistic. | ||
B) | be outcome-oriented. | ||
C) | never have reward systems attached to them. | ||
D) | offer a comprehensive plan to change eating habits. |
Guidelines for facilitating healthy eating-related behaviors in youth include:
Help set realistic goals. Goals should be oriented to behavior rather than outcomes. An example of a behavior goal might be, "I will eat a piece of fruit every day as my after-school snack." Avoid outcome-oriented goals such as, "I will lose 5 pounds this month," which tend to be less supportive of behavioral change and less empowering for the individual.
Start slowly, focusing on two or three behavior changes at a time. A plan to make a comprehensive change in a person's eating habits tends to overwhelm and is more likely to result in failure.
If developmentally appropriate, ask the patient to keep a food diary and review this with the patient. This is often considered the first step in the behavior change. Parents can help younger patients with this.
Avoid the term "diet." Promote obesity management as a lifelong process. Focus on lifestyle changes that will improve glycemic control and long-term, overall health.
Focus on a general understanding of the principles of good nutrition instead of handing out food lists and diet sheets. General instructions might include recommendations to reduce portion sizes, reduce the intake of fatty and processed foods, and increase the intake of fiber and fresh produce.
Develop reward systems for appropriate behavior. Rewards could include earning a trip to an amusement park or getting a special toy. Reward charts can help track progress, providing feedback and a source of motivation.
A) | Miglitol | ||
B) | Glipizide | ||
C) | Metformin | ||
D) | Repaglinide |
Table 6 lists various medications used in the treatment of type 2 diabetes, although many are not labeled for use in children. Metformin and insulin are approved for children with type 2 diabetes[20,31]. In addition, the GLP-1 agonists dulaglutide, extended-release exenatide, and liraglutide are approved for use in children 10 years of age and older if glycemic targets are not met with metformin (with or without insulin) and if the child's medical and family history allow[20,60]. In metabolically stable patients, metformin, if not contraindicated and if tolerated, is the preferred initial pharmacologic agent for the treatment of type 2 diabetes[20].
A) | It may cause weight gain. | ||
B) | It may cause severe hypoglycemia. | ||
C) | It may help lower LDL-C and triglycerides. | ||
D) | It worsens symptoms of polycystic ovary syndrome. |
Metformin acts by decreasing the amount of glucose produced by the liver and improving insulin sensitivity. For adolescents using metformin, it is important to screen for alcohol abuse, including binge drinking, as this medication is contraindicated in those with moderate-to-heavy alcohol use. Besides being effective in lowering blood glucose levels, metformin has other advantages:
Metformin does not put the child at risk for hypoglycemia when used as the sole pharmacologic agent to treat diabetes. This is especially important in pediatric patients who typically do not appreciate the seriousness of hypoglycemia or respond appropriately to its symptoms.
Metformin has a beneficial effect on the lipid profile, potentially lowering both low-density lipoprotein cholesterol (LDL-C) and triglyceride levels.
Metformin may aid in weight loss.
Metformin may normalize ovulatory function in girls with PCOS.
A) | biannual lipid panel. | ||
B) | annual hemoglobin A1c test. | ||
C) | foot exam at every medical office visit. | ||
D) | screening for microscopic protein loss from the kidneys every two to three years. |
The prevention and control of long-term complications in young patients with diabetes is of vital importance due to the increased risks associated with earlier disease onset. The coexistence of obesity, hypertension, and dyslipidemia, which are common in children with type 2 diabetes, greatly increases the risk for cardiovascular disease. Because of the seriousness of these complications, hypertension and dyslipidemia must be aggressively treated and should be considered as important as blood glucose control. These comorbidities are often already present at the time of diagnosis. Therefore, the ADA recommends that blood pressure measurement, fasting lipid profile, microalbuminuria assessment, and dilated eye exam be performed at the time of diagnosis [20]. In addition to cardiovascular risk, hypertension is a risk factor for the development of eye and kidney disease. Routine preventive care can often delay or slow the progression of complications by ensuring early treatment. The routine preventive care schedule recommended for all patients with diabetes consists of [3,7,20]:
Annual dilated eye exam or less frequent monitoring when advised by an eye care professional
Annual screening for early, microscopic protein loss from the kidneys (microalbuminuria)
Annual lipid panel if lipids are abnormal, or if LDL-C levels remain less than 100 mg/dL, repeat lipid profile every five years
Blood pressure monitoring at each office visit
Foot exam at each office visit, including annual test for sensation using a mono-filament
Hemoglobin A1c test every three months
A) | learn how to make compromises within an overall healthy meal plan. | ||
B) | allow their child to forgo blood glucose monitoring if it seems too traumatic for the child. | ||
C) | tell the child that his or her blood glucose level is "bad" whenever results are out of range. | ||
D) | make sure the child understands the negative consequences of cheating on his or her meal plan. |
Some parents may cope by trying to achieve perfection in meeting therapeutic goals. This is manifested by rigid adherence to diet and unrealistically expecting blood glucose values to be within the target range all of the time. In these cases, parents should be educated that their child's self-esteem may be threatened by the overemphasis on treatment. They can also be educated that it is appropriate to make compromises in the meal plan as long as the overall eating pattern is healthy. For example, cake and ice cream for a birthday may add calories and raise blood sugar, but consumption of these types of food can occasionally be accommodated by working them into the entire day's meal plan and by maintaining or increasing physical activity.