1
Florida Heart CPR*
Childhood and Adolescent Obesity
3 hours
Objectives
Upon completion of this course, participants will be able to:
1. Describe the epidemiologic trends in overweight and obesity for children and adolescents.
2. Specify the prevalence of overweight and obesity in children and adolescents, in both the population as a whole and in specific ethnic/racial groups.
3. Describe the genetic, environmental, and developmental influences on the etiology of obesity.
4. Specify the appropriate anticipatory guidance for obesity prevention in infants, toddlers, school-age children, and adolescents.
5. Detail the metabolic, anatomic, psychological, and degenerative comorbidities associated with obesity in children and adolescents.
6. Discuss the available data on treatments for obesity in children and adolescents, including nutritional therapy, behavior therapy, weight-loss drugs, and weight-loss surgery.
Introduction
Obesity is perhaps the most pervasive medical problem faced by medical providers today. It is a common condition in any patient population in countries with a western diet and lifestyle, affects disease burden in virtually every medical specialty, has broad exposure in the media and popular press, and is the subject of intense research in biomedical, epidemiologic, sociologic, and psychological fields. Americans display a multitude of beliefs about the root causes of obesity, often drawn from personal experience, the popular press, marketing initiatives, or one portion of the medical research on the subject. Yet each such theory falls short of explaining the full spectrum of disease and its resistance to treatment. Although most physicians and their patients recognize that obesity is a major health problem, long-term treatment success is rare.
Against these odds, pediatric providers can still take action in several important ways:
· Equip yourself with an understanding of what is known in the field and -- equally important -- what is not known.
· Provide targeted anticipatory guidance for all patients to help them prevent obesity.
· Identify patients at particular risk for obesity, and provide additional guidance to help prevent or attenuate the problem in these individuals.
· Be alert for the medical and emotional consequences of obesity and treat these accordingly.
· Treat obesity and obesity-related disease with the best tools as they become available, if supported by sound research.
· Be a leader in promoting the cultural changes that can help prevent obesity and that will be required before the obesity epidemic can be reversed.
Definition and Epidemiology
Any definition of obesity is useful only if it predicts medical disability or complications. Because most medical complications of obesity are associated with body fat and not muscle mass, measures of obesity represent an attempt to estimate the adipose compartment. At present, there is no precise clinically practical method to measure body fat, so most methods rely on measurements of body weight as a surrogate for adiposity.
Body mass index (BMI), which is defined as weight in kilograms divided by height in meters squared (kg/m2), has been established as a useful standard measure of overweight and obesity. Although BMI does not directly measure body fat, it provides a reasonable estimate of adiposity which, in turn, also predicts risks for current or future medical complications of obesity.[1] BMI in children is correlated not only with other measures of body fat but also with blood pressure,[2,3] lipid levels,[4,5] and insulin levels.[6]
Because BMI naturally increases with increasing age, and also varies by pubertal stage[7] and gender, BMI percentiles are used to define degrees of overweight and obesity. The BMI-for-age growth charts, released by the Centers for Disease Control and Prevention (CDC) in 2000, show healthy reference standards for BMI during childhood and adolescence, and provide a practical way of tracking an individual's changes in BMI over time. The 85th percentile on the CDC standard charts, which defines children and adolescents "at risk for overweight," also corresponds approximately to a BMI of 25 kg/m2 by age 18, the adult definition of overweight. The 95th percentile on the standard chart, defining children and adolescents as "overweight," corresponds to about 30 kg/m2 by age 18 years, the standard adult definition of obesity.
Currently, 14% of children and adolescents in the United States are overweight and 20% are at risk for overweight (above the 95th and 85th percentiles for age and gender, respectively, based on the new CDC standards).[8] Since the 1960s, the prevalence of obesity in children and adolescents has tripled. Similar but more gradual trends are seen worldwide. African American and Mexican American children are disproportionately affected (See the sidebar, "Managing Overweight in Underserved Pediatric Populations.") Recent estimates suggest that obesity and physical inactivity are responsible for 400,000 deaths annually in the United States; thus, it is close to overtaking tobacco as the leading cause of preventable death.[9]
Etiology of Obesity
Determining the specific causes of this rapid increase in obesity rates is clearly important yet remarkably complex. Both genetic and environmental factors have been shown to contribute significantly to this problem. In general, genetic factors explain a large part of the variation of body weight within a given population in a common environment, whereas environmental factors tend to explain changes in obesity over time in that population. Importantly, there is also increasing evidence that obesity and metabolic diseases may be permanently influenced by environmental factors early in development. Adaptive responses to environmental conditions in gestation are proposed to produce a "thrifty phenotype" or metabolic program that affords an individual a better chance for survival. However, when that individual is then exposed to plentiful nutrition after birth, the metabolic program may be inappropriate for the new conditions and cause disease.
Genetic Influences on Obesity
Both animals and humans have a strong tendency to maintain a stable body weight over time owing to a close but sometimes imperfect matching of energy intake with energy expenditure. Animal studies in which energy intake is manipulated reveal powerful influences from homeostatic mechanisms defending body weight.[10] Similarly, the poor long-term results of weight reduction therapies in humans (about 95% of adults regain all weight after dieting) suggest that there are mechanisms that defend a highly individualized "set point" for body weight. When an individual has a heritable or acquired susceptibility to positive energy balance superimposed on these native homeostatic mechanisms, he or she has a tendency to become obese.
Studies of twins and adoptees provide useful estimates of the role of heritable factors in determining an individual's body weight (see Bouchard's 1997 summary of relevant articles on heritability[11]). Adoption studies tend to generate the lowest heritability estimates (30%), whereas twin studies provide the highest heritability estimates (70%). The variability in these estimates of heritability depends in part on definitions of obesity: more severe obesity tends to have a greater heritability factor than lesser variations in BMI.[12]
Any of the genes encoding a component of the mechanism for regulating body weight homeostasis could be considered a candidate gene for a predisposition or resistance to obesity. Specific mutations in a few of these genes have been shown to cause obesity in rare kindreds. Mutations with strong effects were found in the leptin gene,[13] the leptin receptor gene,[14] the propiomelanocortin (POMC) gene,[15] the prohormone convertase gene (PCSK1),[16] and the melanocortin 4 receptor gene (MC4R).[17] The latter is the most common gene in which specific mutations cause obesity, but it is still rare (42 mutations in 130 individuals published by 2003).[18]
Many other genes known to be involved in pathways regulating body weight, appetite, or energy expenditure have been analyzed for association with obesity within specific populations. By 2003, polymorphisms linked to 90 candidate genes had been shown to have some association with obesity phenotypes,[18] including ghrelin,[19] peroxisome proliferation-activated receptor gamma,[20] uncoupling proteins,[21] and the beta3-adrenoreceptor genes.[22]
Linkage studies in large populations have identified many chromosomal loci with associations to a variety of obesity-related phenotypes, including BMI, leptin levels, fat distribution, and hyperlipidemia.[23] One hundred thirty-nine such loci have been identified as of the 2003 gene map update,[18] some of which appear to represent the chromosomal regions of previously identified candidate genes such as the leptin or MC4 receptors. For many other regions or quantitative trait loci, the biologic mechanisms for the apparent linkage with obesity phenotypes remain unclear.
Syndromic obesity is rare but important to recognize because it may be associated with specific medical complications, possibly with predictable responses to treatment. For example, Prader-Willi syndrome has been associated with gastric rupture, and may respond in part to treatment with growth hormone.[24] Many of these syndromes, including Prader-Willi syndrome, are characterized by short stature, developmental delay, dysmorphic features, and hypogonadism. The coincidence of several of these features should prompt specific workup for syndromic obesity. Conversely, a child with normal cognitive function and good linear growth is very unlikely to have syndromic obesity.
Environmental Influences on Obesity
Epidemiologists have used cohort studies and case-control designs to determine which environmental factors may contribute to obesity. Such studies have pointed to dietary trends, sedentary lifestyle, decreases in structured physical activity, and psychosocial stressors as likely contributors to the obesity epidemic.[25] Several dietary factors have been proposed to play important roles. These include the easy availability and high caloric content of fast foods, general trends toward consumption of foods that are highly processed and contain high carbohydrates and/or total calories (including sugary beverages), decreased consumption of fiber and low-density foods, and the strong marketing techniques of the fast food industry. Other factors include decreases in structured physical activity, particularly for children, and decreasing lifestyle activity (occupations and transportation require less movement than in the past) and increasing sedentary activities (particularly television viewing and computer use). While each of these dietary or activity factors has been temporally related to trends of increasing obesity, causal relationships are difficult to prove. The most convincing studies are short-term intervention trials of decreasing television-viewing time,[26] decreasing caloric density (increasing water content) of food,[27] and decreasing glycemic index of foods.[28] It is important to note that, to date, no single factor among these has been shown to play a pivotal role in the increasing prevalence of obesity.
Developmental Influences on Obesity
The concept of metabolic programming first arose from epidemiologic studies in which it was observed that infants with low birthweight had a higher risk of developing diabetes and heart disease during adulthood,[29-31] suggesting that environmental factors early in development may have a permanent effect on the metabolic profile of an individual. Other epidemiologic studies support the idea that the combination of low birthweight and accelerated growth during childhood confers the greatest risk for diabetes.[32,33] Remarkably, observed associations between maternal hyperglycemia (and consequent unusually high birthweight)[34] and later development of metabolic syndrome suggest that a variety of abnormal conditions during gestation can have parallel effects on offspring.
Studies of the Dutch famine provide evidence that nutritional factors in utero have a causal relationship with subsequent metabolic phenotype. The Dutch population was abruptly subjected to famine conditions for 5 months in the winter of 1944-45. Children who were exposed to the famine in utero had higher risks of glucose intolerance and type 2 diabetes later in life, compared with infants who were in utero just before or after the famine.[35] Comparison with other famines suggests that abrupt restoration of adequate nutrition after birth further increases the risk for metabolic disease.[36]
Animal studies lend further support to the idea of metabolic programming. In rats, a variety of experimental conditions that restrict nutrition during gestation predispose the offspring to develop elements of the metabolic syndrome during maturity. In particular, the combination of maternal protein deprivation followed by plentiful nutrition during suckling causes increased appetite, insulin resistance, and shortened lifespan.[37,38] Similar effects are seen in animals exposed to cold ambient temperatures during gestation or early life. Offspring of low-protein-fed dams have proportionally smaller livers, and these livers have fewer but larger lobules than normal.[39] These animals also have increased hepatic gluconeogenesis and decreased ketogenesis, which are features of several experimental models of fatty liver.
Together, these studies in humans and animals present intriguing evidence that fetal malnutrition (either under-nutrition or some other perturbation of maternal-fetal metabolism) combined with over-nourishment during childhood may create a dangerous "metabolic program" predisposing to the metabolic syndrome. Which metabolic features of the intrauterine environment are most important and the timing of the critical period of over-nutrition during childhood are yet to be determined. However, it is reasonable to conclude that infants with low birthweight are at increased risk for developing the metabolic syndrome, particularly if obesity develops later in life, and that moderate rates of weight gain for these individuals during childhood may attenuate the effect of the gestational programming.
Obesity Prevention
Overview
Because environmental and developmental factors play important roles in the development of obesity in genetically susceptible individuals, the pediatric provider and parents can play critical roles in obesity prevention. Certainly, some parts of our culture and environment are beyond the individual's control. Computers and technology are prominent parts of the educational and work environment in many fields, reducing physical activity in daily life. The individual family has little control over the restaurants, services, and public facilities available in their neighborhood, or over the physical education available in their school, and much food-related advertising cannot be avoided.
Nonetheless, several specific areas of lifestyle can be useful for obesity prevention and can be controlled by the family. The pediatric provider can play an important role in identifying these lifestyle targets and supporting healthy lifestyle habits for all families in their practice, as recommended in a recent policy statement by the American Academy of Pediatrics.[40] These recommendations are appropriate whether or not a child or family is at risk for obesity. Table 1 outlines some important targets for anticipatory guidance to prevent obesity. The relevance of each of these targets is supported by multiple association studies (eg, breastfeeding, intake of sugared beverages, physical activity), and some are also supported by small intervention studies (eg, family-based behavioral modification techniques, television reduction). Large-scale intervention studies for the prevention of obesity in the family setting are currently lacking.