A Clinical Guide to Pediatric Weight Management and Obesity, 1st Edition
Epidemiology of Childhood Obesity
The Epidemic of Obesity
The rapid rise in obesity among children and adults has been declared a worldwide epidemic (1). Obesity is increasing at an alarming rate in both developed and developing countries. Similar factors are operating across the globe to raise obesity rates in children (2):
- Increases in economic welfare
- Stability of the food supply
- Rising standards of living
- Increases in energy-dense diets
- Television ownership
- Increase in sedentary leisure time
Alterations in global, national, community, family, and childhood nutrition and activity patterns have been rapid and pervasive.
Transitions in patterns of physical activity and nutrition have caused rates of obesity to approach those of malnutrition for the first time (3). Unfortunately, changes in systems of nutritional support, the activity environment, and leisure activities have yet to stop the increase in children's weight.
Shifts in the Population
The percentage of adults who are at a healthy weight has declined progressively over the past two decades (Fig. 2.1) (4), with a corresponding increase in overweight and obesity. Since 1980, adult overweight has risen by 17.8% and obesity by 16% (4).
Children and adolescents have paralleled this trend (Fig. 2.2) (4). Obesity has risen by 10.2% from 1980 to 2000 in 12- to 19-year-olds and by 9.3% in 6- to 11-year-olds (4).
FIG. 2.1. Percent healthy weight, overweight, and obesity in adults.
FIG. 2.2. Percent obesity in children and adolescents.
In the past 25 years, major shifts toward obesity have occurred in all populations. Genetic predisposition to obesity clearly exists; for example, children of obese parents (one or both) have a much greater incidence of obesity (5). In fact, a child whose parent or parents are obese has only a 10% chance of having a normal weight by the end of adolescence (Fig. 2.3) (5).
Genetics alone, however, cannot explain the epidemic proportions of the obesity problem. A gene-environment interaction is clearly at work. One explanation is called the “thrifty genotype hypothesis” (6). For most of human history, populations
were dependent on a problematic food supply—times of plenty alternating with scarcity. Survival was predicated on the ability of an individual to conserve energy stores and minimize energy expenditure. In this situation, the theory states, a population would eventually develop in which individuals “programmed” for cycles of “feast or famine” with energy-efficient metabolisms would predominate. In recent history, food has become plentiful and energy expenditure has decreased.
FIG. 2.3. Prevalence of obesity in young adults with at least one obese parent. (Data from
Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med. 1997;337:869–873, with permission.
Populations and individuals who are energy efficient now have excess calories to store as adipose tissue, and obesity is the result.
This theory may also explain why the susceptibility to obesity seems to differ between ethnic populations who developed under different conditions of energy availability. Developing nations are also experiencing this phenomenon as improved health status, food availability, and decreased energy expenditure are accelerating the societal transition from high rates of malnutrition to obesity.
Predisposition to obesity may also be increasing on an individual level. It is true that obesity “runs in families,” indicating traditional inheritance patterns for energy regulation. However, the concept of programming an individual's response to the environment has recently emerged in the “thrifty phenotype” hypothesis. Hales and Barker (7) noted that older individuals with increased rates of diabetes had smaller than average birth weights. Reduced birth weight has also been associated with increased insulin resistance (8), cardiovascular disease, and increased central adiposity (9). In this theory, infants who had a relatively energy-restricted intrauterine environment altered their genetic programming accordingly. In other words, these infants were responding to an environment of scarcity by becoming more energy efficient. However, when these infants are born into an energy-rich environment,
their intrauterine adaptations work against them; they develop central obesity and susceptiblity to later obesity-related comorbidities (10).
The intrauterine environment also plays a critical role at the other end of the birth weight spectrum. Infants born to diabetic or obese mothers tend to be larger than normal. These infants are exposed to higher levels of glucose in utero and mount a greater insulin response, and this may alter insulin receptor expression and change insulin sensitivity to the extrauterine environment (11). This programming increases their risk for later obesity and diabetes, thereby perpetuating this cycle of altered response to the energy environment (12).
Susceptible Populations—Adverse Environments
Obesity affects minority populations disproportionately. Rates of obesity among African American and Hispanic populations are greater than those for Caucasian children and have escalated more rapidly (Fig. 2.4) (4). The reasons for this disparity are not entirely clear.
Obesity-promoting influences may be more intense in disadvantaged and ethnic minorities. For example, African American and Hispanic children watch more television, movies, and videos than Caucasian children, as do children from low-income families of all ethnic groups. (13). The complexity of the interaction between ethnicity and obesity is illustrated in the different explanatory models (14) for fruit and vegetable consumption among white, African American, and Hispanic adults of similar low to moderate economic status. Among white adults, having a garden, being single with no child, or being married with a young child was positively associated with fruit and vegetable consumption. Among African Americans, fruit and vegetable consumption was associated with a higher educational level. Hispanic adults reported that liking fruits and vegetables as a child, changing their diet for health reasons, and having food skills were positively associated with fruit and vegetable consumption (14).
Sometimes, even well-intentioned services may inadvertently encourage obesity. The National School Lunch and National School Breakfast Program, for example, is used more by low-income and minority children (13). Tables 2.1 and 2.2 list the food composition of school-provided breakfast and lunch (15).
FIG. 2.4. Childhood obesity and ethnicity.
TABLE 2.1. Minimum nutrient and calorie levels for school lunches—nutrient standard menu planning approaches (school week averages)
TABLE 2.2. Minimum nutrient and calorie levels for school breakfasts—nutrient standard menu planning approaches (school week averages)
Although caloric intake represents a gross estimation of energy need (depending on activity and growth requirements), it is easy to see that a 5-year-old child eating breakfast and lunch at school would have already consumed 900 kcal before arriving home, not counting a midmorning snack, which might be 100 to 200 kcal. An average kilocalorie intake, assuming more than 60 minutes of activity per day, is 1,600 kcal/day (16); dinner, snacks, and beverage intake would need to be limited to 500 to 700 kcal to meet this goal. It is easy to see how energy imbalance can occur. In addition, the minimum energy content of school meals is not varied across the age range from elementary school to high school, despite changes in energy needs.
Conditions that limit activity may be more common in minority populations and among low socioeconomic groups. For example, in 2003, 15.3% of African American adults had chronic conditions that limited activity compared with 10.2% of Hispanic individuals and 11.8% of white adults (4). The impact of poverty is significant and additive: The percentage of persons in poverty with chronic, activity-limiting conditions rose to 26.1% for African Americans, to 15.5% for Hispanic adults, and to 26.2% for white individuals (4). The effect on children is not known; however, the impressive limitation of activity among family members in minority and disadvantaged populations may play a role in activity availability in the family setting for these children.
Shifts in the Environment
The more “obesity promoting” the environment becomes, the higher the rate of obesity in the population.
Obesity-promoting trends include:
- Increased portion sizes
- Higher rates of sweetened beverage consumption
- Increased television and screen time
- Increased snacking
- Decreased physical activity in schools, neighborhoods, and communities
Portion sizes have increased dramatically from 1977 to 1996; soft drinks, salty snacks, french fries, and desserts are just some examples of food that are offered in larger amounts both inside and outside the home (17). Table 2.3 and Figure 2.5 illustrate the increases in snack food, fast food, and soft drink kilocalories over a 20-year period in the United States (17).
Increasing portion size has several implications. More food is offered at each meal and snack, irrespective of energy expenditure, increased portions are often seen as “value added” in terms of food dollars spent, and expectations may be raised
for larger servings at home. In terms of children, extra-sized portions offered in restaurants and fast food establishments are uniform and not tailored to the individual age or activity level of the child.
TABLE 2.3. Increases in snack and fast food kilocalories over a 20-year period in the United States
The excess calories represented by snack food, french fries, and soft drinks can add up to marked increases in weight over time. For example, one extra serving of chips (salty snack food) per day in excess of the calories needed would have resulted in a weight gain of 13 lb/year in 1977 and 23 lb/year in 1994. Figure 2.6 illustrates the pounds per year of weight gain resulting from one extra serving of salty snack food, french fries, or a soft drink in excess of energy expenditure (17).
Television viewing has also increased over time and has been associated with higher rates of obesity. In a survey of children from 1988 to 1994, it was found that more than one half of 8- to 16-years-old watched more than 2 hours of television per day. Many children were watching more than 5 hours per day, and the same study found that “on the average, 17% of non-Hispanic black children watched 5 hours or more a day, whereas only 9% of Latino American and 6% of non-Hispanic white children watched television for 5 or more hours a day” (18).
FIG. 2.5. Increase in snack and soft drink kilocalories per portion.
FIG. 2.6. Pounds of weight gain per year for one extra serving per day. (Data from
Nielsen SJ, Popkin BM. Patterns and trends in food portion sizes, 1977–1998. JAMA. 2003;289(4): 450–453.
Children are a vulnerable population in the current nutrition and activity environment.
They encounter high-calorie foods at home, schools, daycare, and community centers and in restaurants and fast food establishments. They are a target group for marketing and advertising aimed at snack foods and sugared beverages. Families are busy and under stress, and are often making nutrition and activity choices “on the run.” Moreover, children are being afforded little opportunity for activity in school, with declining physical education and recess periods and after school programs aimed at homework completion instead of outdoor time. Parents and families are the interface between the child and environment but may often not have the knowledge or necessary parenting skills to combat the influences acting on their children. Figure 2.7 shows the complexity of the interactions facing parents, families, and pediatricians in combating the obesity epidemic.
The rising rates of obesity are the harbinger of increased morbidity and mortality for a generation of children who, for the first time in a century, may have a shorter life expectancy than their parents.
This book will address, in depth, obesity-related comorbidities. Some examples of obesity-related comorbidities—diabetes, nonalcoholic steatohepatitis, slipped capital femoral epiphysis, and pseudotumor cerebri—are highlighted in the following discussion.
FIG. 2.7. The complexity of the interactions facing parents, families, and pediatricians in combating the obesity epidemic.
The lifetime risk of diabetes is now estimated to be 1 in 3 for boys and 2 in 5 for girls born in the year 2000 (19). Along with the increased lifetime risk for diabetes, the prevalence of type 2 diabetes in children has been reported to range from 4.1 per 1,000 in 12- to 19-year-old children in the United States (20) up to 50.9 per 1,000 in 15- to 19-year-olds in the high-risk Pima Indian population (21). Worldwide, the number of individuals with diabetes has tripled since 1985 (22).
Impaired glucose tolerance is a precursor to type 2 diabetes and is increased in obesity. In a study of obese children referred to a hospital clinic, Sinha et al. (23) found impaired glucose tolerance in 25% of the 55 children aged 4 to 10 years and 21% of 112 obese adolescents 11 to 18 years old, along with 4 adolescents who had previously undiagnosed diabetes.
Nonalcoholic steatohepatitis (NASH) is another significant comorbidity of obesity, previously seen in adults, which has appeared in children and adolescents.
NASH has a prevalence of 3% in the general population and increases to 20% to 40% in obese individuals. Cirrhosis occurs in 25% of adults with NASH, and these patients account for up to 10% of liver-related deaths (24). The prevalence of NASH in childhood is not yet known. Nonalcoholic fatty liver disease, a precursor to NASH, has a prevalence of 2.6% in Japanese children (25). In a study from Italy, nonalcoholic fatty liver disease was found in 52.8% of obese children (26).
Slipped Capital Femoral Epiphysis
Slipped capital femoral epiphysis, a comorbidity of obesity unique to the pediatric population, has been reported to have an annual incidence of 2.22 per 100,000 for boys and 0.76 per 100,000 for girls in a study from Japan. This incidence is five times higher than that in 1976 (27).
Pseudotumor cerebri is more common in obese than in normal weight children. In a study from Nova Scotia, the annual incidence in children was found to be 0.9 per 100,000. Cases were 2.7 times more likely in girls and twice as likely in adolescents (28). In another study, obesity was found in 29% of children and adolescents with pseudotumor cerebri (29).
Health care providers are at the epicenter of the obesity epidemic.
Prevention is critical, and every practitioner should have a strategy for encouraging healthy eating and activity habits in families and children at every health encounter. However, many children are already overweight or obese. These are the children and families who need our urgent attention. Intervention to prevent the development of comorbidities, treatment of existing comorbidity, and reversal of obesity whenever possible are critical tasks that cannot wait.
- Lobstein T, Baur L, Uauy R; IASO International Obesity TaskForce. Obesity in children and young people: a crisis in public health. Obes Rev.2004;(suppl 1):4–104.
- Wang Y, Monteiro C, Popkin BM. Trends of obesity and underweight in older children and adolescents in the United States, Brazil, China, and Russia. Am J Clin Nutr.2002;75(6):971–977.
- Rodgers A, Ezzati M, Vander Hoorn S, Lopez AD, Lin RB, Murray CJ; Comparative Risk Assessment Collaborating Group. Distribution of major health risks: findings from the Global Burden of Disease Study. PLoS Med2004;1(1):e27.
- Centers for Disease Control and Prevention. National Center for Health Statistics, National Health Examination and Nutrition Survey, Hispanic Health and Nutrition Survey (1982–1984) and National Health Examination Survey (1963–1965 and 1966–1970) with chart book on trends in the health of Americans. Hyattsville, MD: National Center for Health Statistics; 2004.
- Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med.1997;337(13):869–873.
- Neel JV. Diabetes mellitus: a “thrifty” genotype rendered detrimental by “progress”? Am J Hum Genet.1962;14:353–362.
- Hales CN, Barker DJ. The thrifty phenotype hypothesis. Br Med Bull.2001;60:5–20.
- Veening MA, Van Weissenbruch MM, Delemarre-Van De Wall HA. Glucose tolerance, insulin sensitivity and insulin secretion in children born small for gestational age. J Clin Endocrinol Metab.2002;87(10):4657–4661.
- Oken E, Gillman MW. Fetal origins of obesity. Obes Res.2003;11:496–506.
- Valdez R, Athens MA, Thompson GH, Bradshaw BH, Stern MP. Birthweight and adult health outcomes in a biethnic population in the U.S. Diabetologia.1994 Jun;37(6):624–631.
- Freinkel N. Of pregnancy and progeny (Banting lecture 1980). Diabetes.1980;29:1023–1035.
- Dabelea D, Petitt DJ. Intrauterine diabetic environment confers risks for type 2 diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. J Pediatr Endocrinol Metab.2001;14(8):1085–1091.
- Kumanyika S, Grier S. Targeting interventions for ethnic minority and low-income populations. Future Child.2006;16(1):187–207.
- Devine CM, Wolfe WS, Frongillo EA, Bisogni CA. Life-course events and experiences; association with fruit and vegetable consumption in 3 ethnic groups. J Am Diet Assoc.1999; 99(3):309–314.
- http://teamnutrition.usda.gov/Resources/menuplanner_chapter2.pdf (accessed July 14, 2006).
- http://www.mypyramid.gov/mypyramid/results.html?age=5&gender=male&activity=active (accessed July 14, 2006).
- Nielsen SJ, Popkin BM. Patterns and trends in food portion sizes, 1977–1998. JAMA.2003;289(4): 450–453.
- Crespo CJ, Smit E, Troiano RP, Bartlett SJ, Macera C, Andersen RE. Television watching, energy intake and obesity in US children: results from the Third National Health and Nutrition Examination Survey, 1988–1994. Arch Pediatr Adolesc Med.2001;155(3):360–365.
- Narayan KM, Boyle JP, Thompson TJ, Sorensen SW, Williamson DF. Lifetime risk for diabetes mellitus in the United States. JAMA.2003;290:1884–1890.
- American Diabetes Association. Type 2 diabetes in children and adolescents. Diabetes Care.2000;23(3):381–389.
- Fagot-Campagna A, Pettitt DJ, Engelgau MM, Ríos Burrows N, Geiss LS, Valdez R, Beckles GL, Saaddine J, Gregg EW, Williamson DF, Narayan KM. Type 2 diabetes among North American children and adolescents: an epidemiological review and a public health perspective.J Pediatr.2000;136(5): 664–672.
- Bloomgarden ZT. Type 2 diabetes in the young: the evolving epidemic. Diabetes Care.2004; 27(4): 998–1010.
- Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K, Savoye M, Rieger V, Taksali S, Barbetta G, Sherwin RS, Caprio S. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med.2002;346:802–810.
- Youssef WI, McCullough AJ. Steatohepatitis in obese individuals. Best Pract Res Clin Gastroenterol.2002;16(5):733–747.
- Tominaga K, Kurata JH, Chen YK, Fujimoto E, Miyagawa S, Abe I, Kusano Y. Prevalence of fatty liver in Japanese children and relationship to obesity: an epidemiological ultrasonographic survey. Dig Dis Sci.1995;40(9):2002–2009.
- Franzese A, Vajro P, Argenziano A, Puzziello A, Iannucci MP, Saviano MC, Brunetti M, Rubino A. Liver involvement in obese children. Ultrasonography and liver enzyme levels at diagnosing and during follow-up in an Italian population. Dig Dis Sci.1997;42(7):1438–1442.
- Noguchi Y, Sakamaki T. Multicenter Study Committee of the Japanese Pediatric Orthopaedic Association Epidemiology and demographics of slipped capital femoral epiphysis in Japan: a multicenter study by the Japanese Paediatric Orthopaedic Association. J Orthop Sci.2002;7(6):610–617.
- Gordon K. Pediatric pseudotumor cerebri: descriptive epidemiology. Can J Neurol Sci.1997;24(3): 219–221.
- Scott IU, Siatkowski RM, Eneyni M, Brodsky MC, Lam BL. Idiopathic intracranial hypertension in children and adolescents. Am J Ophthalmol.1997;124(2):253–255.