Dennis M. Styne

Assessment of Child and Adolescent Overweight and Obesity

Accurate appropriate assessment of overweight and obesity in children and adolescents is a critical aspect of contemporary medical care. However, physicians and other health care professionals may find this a somewhat thorny field to enter. The BMI has become the standard as a reliable indicator of overweight and obesity. The BMI is incomplete, however, without consideration of the complex behavioral factors that influence obesity.Because of limited time and resources, clinicians need to have quick, evidence-based interventions that can help patients and their families recognize the importance of reducing overweight and obesity and take action. In an era of fast food, computers, and DVDs, it is not easy to persuade patients to modify their diets and to become more physically active. Because research concerning effective assessment of childhood obesity contains many gaps, this report is intended to provide a comprehensive approach to assessment and to present the evidence available to support key aspects of assessment. The discussion and recommendations are based on >300 studies published since 1995, which examined an array of assessment tools. With this information, clinicians should find themselves better equipped to face the challenges of assessing childhood overweight and obesity accurately.

Prevention and Treatment of Pediatric Obesity: An Endocrine Society Clinical Practice Guideline Based on Expert Opinion

Objective: Our objective was to formulate practice guidelines for the treatment and prevention of pediatric obesity. Conclusions: We recommend defining overweight as body mass index (BMI) in at least the 85th percentile but < the 95th percentile and obesity as BMI in at least the 95th percentile against routine endocrine studies unless the height velocity is attenuated or inappropriate for the family background or stage of puberty; referring patients to a geneticist if there is evidence of a genetic syndrome; evaluating for obesity-associated comorbidities in children with BMI in at least the 85th percentile; and prescribing and supporting intensive lifestyle (dietary, physical activity, and behavioral) modification as the prerequisite for any treatment. We suggest that pharmacotherapy (in combination with lifestyle modification) be considered in: 1) obese children only after failure of a formal program of intensive lifestyle modification; and 2) overweight children only if severe comorbidities persist despite intensive lifestyle modification, particularly in children with a strong family history of type 2 diabetes or premature cardiovascular disease. Pharmacotherapy should be provided only by clinicians who are experienced in the use of antiobesity agents and aware of the potential for adverse reactions. We suggest bariatric surgery for adolescents with BMI above 50 kg/m2, or BMI above 40 kg/m2 with severe comorbidities in whom lifestyle modifications and/or pharmacotherapy have failed. Candidates for surgery and their families must be psychologically stable and capable of adhering to lifestyle modifications. Access to experienced surgeons and sophisticated multidisciplinary teams who assess the benefits and risks of surgery is obligatory. We emphasize the prevention of obesity by recommending breast-feeding of infants for at least 6 months and advocating that schools provide for 60 min of moderate to vigorous daily exercise in all grades. We suggest that clinicians educate children and parents through anticipatory guidance about healthy dietary and activity habits, and we advocate for restricting the availability of unhealthy food choices in schools, policies to ban advertising unhealthy food choices to children, and community redesign to maximize opportunities for safe walking and bike riding to school, athletic activities, and neighborhood shopping.

Childhood and adolescent obesity. Prevalence and significance.

The prevalence of children and adolescents with body mass index (BMI) of greater than 95th percentile has doubled in the last 2 decades (present prevalence is 10.9%) and there is a 50% increase in the prevalence of those with a BMI greater than 85th percentile (present prevalence is 22.0%) in the US. There are substantial risks for morbidity in obese children even before they reach adulthood. Further, if obesity in childhood persists into the adult years, the morbidity and mortality is greater than if the obesity developed in the adult. Screening using appropriate historical and physical data will reveal those children most in need of modification of weight gain.

Growth Hormone Treatment for Short Stature

Fifteen short but otherwise normal children, 4.3 to 15.5 years old, with heights greater than 3 S.D. below the mean value for age, growth rates less than or equal to 5.0 cm per year, and normal serum levels of immunoreactive growth hormone in response to provocative stimuli (peak greater than or equal to 10 ng per milliliter) were treated with intramuscular injections of pituitary growth hormone (0.1 U per kilogram) three times weekly for six months, as were 14 children with documented growth hormone deficiency. In all the latter children growth rate increased by more tan 2.0 cm per year during treatment. In 6 of the 14 short normal children who remained prepubertal, growth rate also increased, by 2.2 to 4.2 cm per year during treatment; four of these children had normal base-line serum somatomedin C concentrations. In both short normal children and children with growth hormone deficiency, the increment in serum somatomedin C concentrations after 4 or 10 daily injections of growth hormone correlated with bone age but not with later growth or growth hormone levels. Among the short normal children, those who responded to growth hormone were younger and had a greater delay in bone age and a slower pretreatment growth rate than the nonresponders. These observations suggest that a dose of growth hormone comparable to that used for the treatment of hypopituitarism increases growth rate in some short normal children.

Effect of puberty on body composition.

Purpose of reviewHere we examine the effect of puberty on components of human body composition, including adiposity (total body fat, percentage body fat and fat distribution), lean body mass and bone mineral content and density. New methods and longitudinal studies have expended our knowledge of these remarkable changes. Recent findingsHuman differences in adiposity, fat free mass and bone mass reflect differences in endocrine status (particularly with respect to estrogens, androgens, growth hormone and IGF-1), genetic factors, ethnicity and the environment. During puberty, males gain greater amounts of fat free mass and skeletal mass, whereas females acquire significantly more fat mass. Both genders reach peak bone accretion during the pubertal years, though males develop a greater skeletal mass. Body proportions and fat distribution change during the pubertal years as well, with males assuming a more android body shape and females assuming a more gynecoid shape. Pubertal body composition may predict adult body composition and affects both pubertal timing and future health. SummarySexual dimorphism exists to a small degree at birth, but striking differences develop during the pubertal years. The development of this dimorphism in body composition is largely regulated by endocrine factors, with critical roles played by growth hormone and gonadal steroids. It is important for clinicians and researchers to know the normal changes in order to address pathologic findings in disease states.

Treatment of Cushing's Disease in Childhood and Adolescence by Transsphenoidal Microadenomectomy

Fifteen unselected children and adolescents with Cushings disease were treated by transsphenoidal exploration and microadenomectomy. In only three patients was radiographic examination of the sella turcica, including computed tomography, useful in indicating the presence and location of a pituitary microadenoma. Transsphenoidal microadenomectomy corrected hypercortisolism in 14 of the 15 patients; no adenoma was detected in one patient, and one required a second operation six months after the first because of incomplete removal of the adenoma. All 14 lost weight and cushingoid stigmata and had normal or catch-up growth (if epiphyses were not fused) and progression of puberty. In one patient, a recurrence was successfully treated by repeat microadenomectomy six years after the first procedure. The low morbidity and failure rate of the procedure, the low recurrence rate, the rapid amelioration of signs of hypercortisolism, and the preservation of pituitary function in the present study support transsphenoidal microadenomectomy as a low-risk approach to the initial treatment of Cushings disease in childhood and adolescence.

Adrenocortical function in the very low birth weight infant: Improved testing sensitivity and association with neonatal outcome

OBJECTIVE To evaluate adrenocortical function in ill preterm infants and investigate potential relationships between plasma cortisol concentrations and major neonatal outcomes. STUDY DESIGN Randomized trial of adrenocorticotropic hormone (1-24ACTH) stimulation testing, followed by a chart review. SETTING Two level III neonatal intensive care units, Sacramento, Calif. PARTICIPANTS Sixty-seven very low birth weight infants, born at 32 weeks of gestation or earlier weighing 1500 gm or less, who had endotracheal intubation and indwelling arterial access. RESULTS Most infants (76%) had baseline cortisol concentrations < 414 nmol/L (15.0 micrograms/dl), and of those, only 36% responded to stimulation with 1-24ACTH, 0.1 microgram/kg. Raising the 1-24ACTH dose to 0.2 microgram/kg resulted in a response rate of 67% (p = 0.09) but decreased the sensitivity of the test. An elevated mean 11-deoxycortisol/cortisol ratio indicated that decreased 11 beta-hydroxylase activity may limit cortisol production in some infants. Infants with baseline cortisol concentrations less than 414 nmol/L (15.0 micrograms/dl) were more likely to have chronic lung disease (p < 0.002) and less likely to have severe intraventricular hemorrhage (p < 0.02). Response to 1-24ACTH was not associated with a detectable difference in outcome. CONCLUSION Many very low birth weight infants have low cortisol and ACTH concentrations and are unable to mount a cortisol response to physiologic doses (0.1 microgram/kg) of 1-24ACTH. These findings suggest that delayed maturation of adrenal response may result in physiologically inadequate cortisol concentrations in stressed very low birth weight infants. This delayed maturation may contribute to the development of chronic lung disease.

Puberty, obesity and ethnicity

Lay and medical sources state that children enter puberty earlier now than in past decades. Although it is clear that puberty and menarche currently begin at younger ages than they did in past centuries, a comparison of the onset of puberty during the few past decades is more difficult to interpret. African-American girls do start puberty earlier and menarche is earlier than in White girls, and the gap between the two has widened during the past 20 years. This change between ethnic groups might be due to an increasing difference in body mass index (BMI) values. Greater BMI values are associated with pubertal onset or menarche; thus, if BMI continues to increase in childhood, earlier puberty might well be found in the general population in the future. In the absence of accurate data from the past or definitive studies at present, however, it cannot be stated with assurance that puberty today starts significantly earlier than it did in the past 4-5 decades across the whole population.

Metabolic syndrome in adolescents with spinal cord dysfunction.

Abstract Objective: The purpose of this study was to determine the prevalence of components of the metabolic syndrome in adolescents with spinal cord injury (SCI) and spina bifida (SB), and their associations with obesity in subjects with and without SCI and SB. Methods: Fifty-four subjects (20 SCI and 34 SB) age 11 to 20 years with mobility impairments from lower extremity paraparesis were recruited from a hospital-based clinic. Sixty able-bodied subjects who were oversampled for obesity served as controls (CTRL). Subjects were categorized as obese if their percent trunk fat measured by dual x-ray absorptiometry (DXA) was>30.0> for males and>35 .0> for females. Ten SCI, 24 SB, and 19 CTRL subjects were classified as obese. Fasting serum samples were collected to determine serum glucose, insulin, and lipid concentrations. Metabolic syndrome was defined as having #x003D;3 of the following components: (a) obesity; (b) high-density lipoprotein (HDL) <45 mg/dl for males;<50 mg/dl for females; (c) triglycerides #x003D;100 mg/dl; (d) systolic or diastolic blood pressure95th percentile for age/ height/gender, and (e) insulin resistance determined by either fasting serum glucose 100-125 mg/dl; fasting insulin #x003D;20 μU /ml; or homeostasis model assessment of insulin resistance #x003D;4.0 . Results: Metabolic syndrome was identified in 32.4>of the SB group and 55> of the SCI group. Metabolic syndrome occurred at a significantly higher frequency in obese subjects (SB = 45 .8>, SCI = 100>, CTRL = 63.2>) than nonobese subjects (SB = 0>, SCI = 10>, CTRL = 2.4>). Conclusions: The prevalence of metabolic syndrome in adolescents with SB/ SCI is quite high, particularly in obese individuals. These findings have important implications due to the known risks of cardiovascular diseases and diabetes mellitus associated with metabolic syndrome in adults, particularly those with spinal cord dysfunction.

The Regulation of Pubertal Growth

To understand the regulation of pubertal growth, it is important to understand the present concept of the control of the onset of puberty, the change in secretion of sex steroids during puberty, and the effects of these various factors upon the production and action of growth hormone (GH) and insulin-like growth factor (IGF). Nutrition plays a major role in this process because states of aberrant nutrition severely affect pubertal growth. In this article, all of these concepts will be discussed, including the effect of these factors upon bone growth during the increase in stature accomplished during puberty.