Childhood Obesity, Part 1: Weight Evaluation and Comorbidity Screening

Childhood obesity has reached epidemic proportions. From 2003 to 2006, 16.3% of children and adolescents were identified as obese.1 This reflects a stabilization of the rise in childhood obesity previously described between 1999 and 2004.¹ Although genetic causes of obesity exist, the percentage of obese children whose excess weight can be attributed to a genetic disorder is quite low²; moreover, obesity interventions and comorbidity screenings for patients with genetic disorders are often limited to those recommended for patients with the more common exogenous obesity.³

Increased weight is associated with many comorbidities, including hyperlipidemia, hypertension, hepatic steatosis, polycystic ovary syndrome, insulin resistance, and type 2 diabetes mellitus. According to data from the third National Health and Nutrition Examination Survey (NHANES III) from 1988 to 1994, of all adolescents with diabetes mellitus (about 100,000 US adolescents aged 12 to 19 years), 29% had type 2 disease,⁴ a disorder traditionally associated with aging and obesity. During the 1990s, various local communities documented a 2- to 4-fold increase in type 2 diabetes diagnoses among children and adolescents^5.6. This represented a major new health issue for adolescents.

Obesity in childhood also augurs health problems later in life. Among girls who had body mass indexes (BMIs) above the 85th percentile in childhood and young adulthood, the probability of obesity continuing into adult life was 20% to 39.9%; for boys who had BMIs above the 85th percentile in childhood and young adulthood, the probability of obesity continuing into adulthood was less than 20%.⁷ Recently, high childhood BMIs (above the 95th percentile) have been associated with increased cardiovascular risk in adulthood.⁸ These data underscore the importance of obesity screening in children and adolescents.

In this article, I review how to screen children for obesity and when to screen for comorbidities associated with obesity. In a forthcoming article, I will provide an overview of obesity interventions.

WEIGHT EVALUATION

Overweight in children is defined as a BMI at the 85th to 94th percentile, whereas obesity refers to a BMI at or above the 95th percentile. ⁹ The weight and height data that have been used to construct these BMI percentile distributions come from multiple representative national surveys as well as some state- and region-specific measures. Of note, weight data from the NHANES III for children and adolescents aged 6 through 20 years were excluded when the BMI percentile distributions were developed.¹⁰ Thus, BMI scales do not demonstrate the secular trend of weight increases from 1988 to 1994.

Although BMI does not differentiate between increased weight attributable to lean mass and weight attributable to fat mass, it has been shown to correlate relatively well with calculations of fat mass as measured by dual-energy x-ray absorptiometry, ¹¹ underwater weighing,¹¹ and skin-fold thickness^.8 A BMI above the 99th percentile for a patient's age and sex is associated with an increased number of comorbidities. ⁸ Because BMI has a high predictive value for adult obesity^,8,12 it is useful in identifying high-risk children who require screening for comorbid conditions and in whom preventive measures are needed to avoid adult disorders (Algorithm). Waist circumference provides an index of visceral fat.¹³ Ethnic-specific standards are available for clinical use and are increasingly being employed in the routine evaluation of overweight and obese children.¹⁴

COMORBIDITY SCREENING

Hypertension. Blood pressure (BP) measurements are recommended for all children 3 years and older during each health care visit.¹⁵ BP values above the 90th percentile for a child's age and sex but below the 95th percentile are considered prehypertensive. BP values above the 95th percentile are hypertensive. However, a diagnosis of hypertension requires that multiple (3 or more) measurements be obtained over weeks to months to confirm the initial elevations.¹⁵ 

Lifestyle interventions are recommended for children who are prehypertensive. For those with confirmed hypertension, both lifestyle interventions and, in certain settings, pharmacotherapy are indicated after evaluation as outlined in the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents.¹⁵

Type 2 diabetes. A fasting blood sugar test is recommended in obese children 10 years or older (and in those younger than 10 if they experience precocious puberty) whose BMI is above the 85th percentile for their age and sex and who have 2 of the following high-risk criteria:

• Family history of type 2 diabetes mellitus.

• Race or ethnicity associated with an increased risk of diabetes.

• Clinical features of insulin resistance or disorders associated with insulin resistance (eg, hyperlipidemia, hypertension, polycystic ovary syndrome).¹⁶

Insulin resistance. Consider screening obese children for insulin resistance irrespective of the presence of acanthosis nigricans (Figure). Acanthosis nigricans is associated with decreased insulin sensitivity and is commonly considered a marker of insulin resistance; its presence typically obviates the need for insulin measurements. However, obese children without acanthosis nigricans may also have increased insulin resistance.¹⁷

Figure

The euglycemic hyperinsulinemic clamp is the gold standard test for measuring insulin resistance; however, because this is not a standard clinical test, proxy measures may be substituted. These include the homeostasis model assessment (HOMA)¹⁸ and the quantitative insulin sensitivity check index (QUICKI),¹⁹ which have been shown to correlate with clamp measures. The HOMA and QUICKI tests are based on fasting glucose and insulin measures. Both tests have shown in children a variable but significant correlation with the euglycemic hyperinsulinemic clamp, ranging from r = -0.49 to -0.51 for HOMA and r = -0.57 to-0.69 for QUICKI.^20,21

Some experts recommend simple fasting insulin measures, because values outside the range of normal, by definition, indicate insulin resistance. Fasting insulin values have been shown to correlate with clamp measures (r = -0.34 to-0.92) as well as HOMA and QUICKI do.^21,22 However, simple fasting measures of insulin cannot be routinely recommended because insulin assays are not uniform, and comparability between laboratories is poor.²³

Hyperlipidemia.

Screening obese children and adolescents with a fasting lipid profile is necessary and appropriate. The Bogalusa Heart Study demonstrated that lipid levels, particularly low-density lipoprotein (LDL) cholesterol levels, track from childhood into adulthood and can predict risk of cardiovascular abnormality (Table).²⁴

Table

Table

Until recently, the National Cholesterol Education Program had recommended routine pediatric screening for hypercholesterolemia based on family history and follow-up evaluation with a fasting lipid profile in patients with abnormal screening values^.25 The US Preventive Services Task Force has noted that this strategy could overlook 30% to 60% of children and adolescents with elevated total cholesterol or LDL cholesterol levels.²⁶ Moreover, this strategy does not involve first-line screening for triglyceride and highdensity lipoprotein (HDL) cholesterol abnormalities, which can be key to diagnosing metabolic syndrome. Review by the American Heart Association and the American Academy of Pediatrics has led to a revision of these guidelines, with the recommendation that targeted screening be expanded to include children with an unknown family history, those who are overweight, and those who have other cardiovascular risk factors; it is also now recommended that a fasting lipid panel be used as the screening method.²⁷

The new guidelines recommend dietary changes and other lifestyle interventions, such as increased physical activity, for children with elevated LDL cholesterol levels and increased cardiovascular risk. Consideration of pharmacological interventions is recommended for those 8 years and older whose LDL cholesterol level is higher than 190 mg/dL (or higher than 160 mg/dL with a family history of early heart disease or at least 2 additional risk factors, or higher than 130 mg/dL when diabetes is present).

Metabolic syndrome. Although no single set of diagnostic criteria have been established for metabolic syndrome,²⁸ the combination of hypertriglyceridemia and/or low HDL cholesterol with hypertension (usually BP at or above the 90th percentile²⁹) and increased waist circumference suggests the diagnosis. NHANES data indicate that 4.1% of 12- to 19-year-olds meet these proposed criteria for metabolic syndrome; among those with a BMI at the 95th percentile or higher, 28.7% fit this definition.³⁰

Measurement of waist circumference is a key component of the definition of metabolic syndrome based on criteria from the National Cholesterol Education Program.³¹ In prepubertal children, waist circumference measures have been shown to correlate with adverse lipid profiles and hypertension.³² Although it remains controversial whether waist circumference measures provide additional or more relevant information about cardiovascular risk than BMI alone,^33,34 Janssen and colleagues³⁵ suggest using waist circumference as a categorical variable (low, normal, high) in combination with BMI to identify the excess risk that visceral fat contributes to that of a diagnosis of obesity in childhood. Maffeis and coworkers³¹ agree that among overweight children, waist circumference or waist to height ratio does add additional information about metabolic and cardiovascular risk.

Hepatic steatosis. In a population- based autopsy series, the prevalence of fatty liver based on histological results was 9.3% in children aged 2 to 19 years.³⁶ Of those patients who were obese, the prevalence was as high as 38%. Elevated transaminase levels and an ultrasonographic increase in liver echogenicity have been considered clinical markers of fatty liver in the absence of biopsy and after exclusion of other known hepatic disorders. Although generally benign, fatty liver may progress to hepatic steatosis with inflammation and fibrosis.³⁷ Factors governing this progression are not clearly understood; however, weight loss and increased insulin sensitivity have been shown to result in both decreased liver enzyme levels and decreased liver echogenicity.³⁸ Because of the high prevalence of fatty liver, routine screening of obese children with liver transaminases and/or liver ultrasonogram has been recommended. When these abnormalities are detected, an aggressive effort should be made to encourage patients to adapt lifestyle changes; weight loss produces documented improvement in liver enzyme levels..

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