What are the epidemiologic trends in childhood obesity?
What demographic factors are associated with childhood obesity? Which children are in the high-risk groups?
How can I help families understand the steps they can take to reduce pregnancy-related risk factors for childhood obesity?
What are effective ways to screen for obesity and to communicate about the screening?
This chapter will address the following American College of Graduate Medical Education competencies: patient care, medical knowledge, and interpersonal and communication skills.
Patient Care: This chapter will enable pediatric health care providers to help families understand the risk of obesity in their child and work to optimize healthy family lifestyle behaviors and environments, allowing mothers to modify the risk of obesity in their subsequent pregnancies as well.
Medical Knowledge: This chapter will help pediatric health care providers improve their assessment of individual risk in light of the population risk factors and population risk of their practice.
Interpersonal and Communication Skills: Understanding the value of communicating body mass index (BMI) screening results, framing recommendations in a health context, and relaying ways to reduce barriers to screening and communication are core skills that this chapter will review so that pediatric health care providers can help families achieve effective strategies for obesity prevention and treatment.
Since large, national cross-sectional data of height and weight became available in the 1960s through the National Health Examination Survey (NHES) and in the 1970s through the National Health and Nutrition Examination Survey (NHANES), it has become clear that obesity prevalence has increased dramatically across all ages, races, and ethnic groups. First estimations of prevalence of children with obesity were around 5% in the 1960s.1 Recent estimates of prevalence suggest that roughly 17% of children and adolescents have obesity, while nearly a third have either overweight or obesity. Strikingly, 12% are above the 97th percentile for BMI.2 While obesity in children and adolescents has tripled in the period since data became available, certain populations that are followed longitudinally have demonstrated a 5-fold increase in the rates of obesity.3 Understanding which groups may be at higher risk allows tailoring of population and individualized prevention measures.
The United States leads developed nations in the number of children and adolescents with overweight and obesity. Our federal government aimed to reduce the proportion of children and adolescents who have obesity to 5% in its Healthy People 2010, a goal that was far from attained. In Healthy People 2020, reducing the proportion of children with obesity and overweight by 10% (from 16.1%-14.5%) is 1 of the 26 highest priority health issues (http://www.healthypeople.gov/).
Compared with increases in obesity prevalence in the latter part of the 20th century, prevalence in the last decade shows some stability, especially in females and non-Hispanic white children and adolescents. Overall trends over the last decade suggest that there are statistically significant increases in obesity among men and boys, but not among women and girls4; in non-Hispanic black males, annual increases in prevalence continue, and this trend appears to be driven by the 12- to 19-year age group.2 Nonetheless, considering rates of increase in obesity since the 1970s, some have suggested that obesity prevalence will continue to increase by 2030, with Mexican American boys and non-Hispanic black girls and adolescents being most affected, demonstrating rates well above 40%.5
Recent stabilization in levels of obesity appears to have included younger children as well. When examining state-level data of preschool-aged children enrolled in assistance programs, trends over the last decade suggest a slight decrease in obesity prevalence and an increase in overweight prevalence.6 Although the percentage of Hispanic children may have increased over the last decade, and obesity prevalence in this group tends to be higher, the overall trend of obesity in preschool-aged children enrolled in a state Women, Infants, and Children (WIC) program decreased. This suggests that even some young, poor children, who are commonly believed to be at higher risk for obesity, have experienced a plateau in prevalence.7
Although the slope of increase in prevalence shows signs of plateauing, the numbers of those affected and the environment of risk for obesity still merit substantial work. On a global scale, the epidemic spreads unimpeded. Around the world, 43 million children are estimated to have overweight or obesity, defined as more than 2 or 3 standard deviations (SDs) above the mean of World Health Organization (WHO) growth standards. In 2010, this was equivalent to a prevalence of 6.7%. Some projections suggest that by the end of this decade, 10% of children worldwide will have overweight or obesity.8
When large cohorts of adolescents are followed over time, nearly all who have a BMI greater than the 95th percentile in adolescence will have obesity as adults,9 and adults with a BMI over 30 have higher all-cause mortality in addition to many well-described morbidities.10 As pediatric health care providers, we can link childhood obesity to adult obesity with a growing body of literature on BMI tracking, and, therefore, to adult morbidity and mortality.
Although obesity has increased among all categories, there are distinct differences by age, sex, race or ethnicity, family income, and education. In 2009 to 2010, obesity prevalence in 2 to 5 year olds was 12.1%, among children aged 6 to 11 years was 18%, and among adolescents aged 12 to 19 years was 18.4%.2 Among non-Hispanic white children and adolescents, 16.1% of males were found to have obesity compared to 11.7% of females; differences in obesity prevalence between boys and girls who were non-Hispanic black or Hispanic were not significant. Non-Hispanic black children had the highest rates of obesity in the NHANES data from 2009 to 2010 with rates of 24.3%, Hispanic children followed with rates of 21.2%, and non-Hispanic white children had rates of 14%.2
Obesity affects children from all income groups but is more likely to occur in families with low incomes. Of the approximately 12 million children who have obesity, 3 million (24%) live in families above the 350% poverty level, 4.5 million (38%) have incomes between 130% and 350% of the poverty level, and another 4.5 million (38%) live below 130% of the poverty level. Using data from 2008, children and adolescents in households below 130% of the federal poverty level had higher rates of obesity (21.1% boys, 19.3% girls) than households with more than 350% of the federal poverty (11.9% boys, 12% girls). The relationship between low income and obesity varies with race or ethnicity. Non-Hispanic white boys in households above 350% of poverty level have rates of obesity of 10.2%, versus 20.7% for these boys living in households under 130% of the poverty level. Non-Hispanic white girls have rates of 10.6% and 18.3%, respectively. There is no significant difference among non-Hispanic black and Mexican American children.11
When the head of household is a college graduate, obesity prevalence is nearly half in boys and a third in girls when compared to households where the head of household has less than a high school degree. This trend remains significant in non-Hispanic white and non-Hispanic black girls, and is most striking in non-Hispanic white girls, where only 7% have obesity in homes with a college graduate versus 22% where the head of household has less than a high school education. However, obesity prevalence has increased in all categories of income level and education as it has in all age, sex, and race or ethnicity categories since the last century, requiring pediatricians to screen every patient regardless of their demographic group.12
Over 20 years ago Dr. David Barker documented the relationship between birth weight and coronary artery disease, giving rise to the Barker hypothesis, which connected fetal nutrition to later adult chronic disease.13 Both animal and human studies are uncovering risk factors for child obesity that are present even before conception and continue in the in utero environment, affecting fetal development. Many of these risk factors are potentially modifiable. This offers the pediatrician an opportunity to provide counseling to families that may reduce the likelihood that future offspring will develop obesity or cardiovascular and metabolic diseases.
A substantial literature now relates maternal BMI to childhood weight status.14,15 Emerging evidence suggests that preconception maternal obesity may be a stronger predictor of child obesity than gestational weight gain (GWG).15,16 Paternal prenatal obesity has also been found to be a strong predictor of child obesity.15
Recommendations for appropriate GWG established by the Institute of Medicine and the American College of Obstetricians and Gynecologists have changed significantly in recent years.17 The guidelines are stratified based on prepregnancy maternal BMI and recommend significantly less overall weight gain during pregnancy. Controversy remains over what constitutes the GWG that most likely yields a healthy offspring. However, it is clear that excess GWG is associated with infants who are large for gestational age (LGA). In addition, independent of birth weight, excess GWG is associated with overweight and obesity in early childhood.14,18,19 Although there are published guidelines for recommended activity and nutrition during pregnancy, there is little evidence regarding what specific dietary factors may lead to childhood obesity. Maternal sugar consumption, particularly from beverages sweetened with high-fructose corn syrup, has been associated with offspring obesity in early childhood20; high levels of omega-3 fatty acids, found in fish and plant-based oils, in mid-pregnancy cord-blood samples have been found to be protective of obesity at age 3 years.21
The association between maternal gestational diabetes mellitus (GDM) and offspring obesity in childhood and adulthood is well described. A 2012 meta-analysis found that GDM is associated with a 61% increased risk of child obesity at age 7 years independent of birth weight.22 In addition, a 2013 study of Mexican American women found that even for women of normal weight and who do not meet criteria for GDM, incremental elevations in blood glucose during pregnancy were associated with elevations in offspring BMI z-score at age 7 years.23
In the past several years, a number of studies have demonstrated a clear link between tobacco exposure and subsequent child obesity. A 2010 meta-analysis confirmed this association and demonstrated a new finding that maternal smoking is also associated with early adult metabolic syndrome.24 Maternal smoking during pregnancy is associated with offspring obesity at age 5 to 10 years, and 18 years, as well as in adulthood with a dose-dependent effect. The associations become stronger the more cigarettes the mother smokes per day. For example, a child whose mother smoked 25 cigarettes or more during pregnancy is nearly 3 times as likely to develop obesity as an adult than a matched peer whose mother did not smoke at all.25 Several studies that have developed risk models for childhood obesity based on prenatal and early childhood factors have included maternal smoking as 1 of the 4 strongest risk factors (the others being GWG, birth weight, and early childhood rate of growth).18,26,27 The association may be related to the finding that infants born to mothers who smoked during pregnancy have, on average, shorter birth lengths than their nonexposed peers.28 Encouragingly, this risk was reversed if the mother stopped smoking during the first trimester. Interestingly, paternal smoking is also linked to offspring obesity, although less strongly and only in adulthood.25
Maternal stress has been suggested as a cause for excess offspring adiposity, as suggested by animal models that demonstrate that glucocorticoid exposure in utero causes metabolic dysregulation and obesity in the offspring. The human model is more complex because maternal stress is often confounded by a multitude of risk factors for obesity (smoking, poor nutrition, race or ethnicity, socioeconomic status, etc). However, 2 studies have demonstrated an independent association between maternal stress and offspring obesity at school entry in low-income women20 and in a group of women who were victims of a natural disaster.29
Many other behaviors and exposures have been proposed as contributing agents; yet at this time, the science to explain these relationships is in its infancy. Maternal preeclampsia resulting in preterm delivery30 and exposure to environmental endocrine disrupting agents31 are currently under investigation. Many of these factors may continue to act in an epigenetic fashion even after delivery.
It has been suggested that both LGA and small for gestational age (SGA) births are related to childhood obesity. A 2011 meta-analysis found a clear relationship between LGA infants (> 4000 g) and later obesity, both in early childhood as well as young adulthood. The relationship between SGA is not as direct20 and later obesity may be mediated by rapid infant growth. So striking is this finding that one can predict future obesity by the rate of growth in the first 6 months of life, irrespective of birth weight.32 One might hypothesize that infants born SGA are “encouraged” to eat to “catch up” with the growth curve, and thus are more likely to demonstrate early rapid weight gain than their normal birth-weight peers.
Case
You are completing the kindergarten well-child check for a patient whom you have followed since birth. The child’s BMI is at the 95th percentile, up from the 93rd last year. Both parents have obesity and smoke cigarettes. The parents tell you they are planning for their second child, and the mother hopes to become pregnant within the next year. The child’s mother recalls that she gained 70 lb during her pregnancy with your patient and was diagnosed as having gestational diabetes which resolved postpartum. The mother was able to quit smoking during her first pregnancy and intends to quit with the next pregnancy as well. The parents are both concerned about their 5-year-old’s weight status, because there is a strong family history of heart disease and they know that weight problems are related to health issues. They want to know if there is anything they can do now to prevent their next child from becoming overweight.
You contemplate the clinical scenario and how best to lower the risk of obesity in the child who will be your patient but who has not yet even been conceived. You counsel the anxious parents that taking steps toward a lifestyle of good nutrition by reducing sugar (especially sugary beverages) and a well-balanced diet with appropriate portions, and becoming more active as a family will not only help the parents’ and the 5-year-old’s health, but will set the stage for good health for their next child. You strongly encourage both parents to stop smoking and explain the risks; you provide them information to contact a free quit line. Last, you emphasize that good prenatal care including follow-up with mother’s obstetrician is essential and should stress optimal weight gain and blood sugar control.
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