Childhood obesity is a profoundly complex problem and serves as an example of a biospsychosocial issue. Scientific inquiry has provided incredible insight into the complex etiology of weight gain but must be viewed as an interaction between a human’s propensity to conserve calories for survival in a world with an abundance of it. This article provides a brief overview divided between biological (nature) and psychosocial and behavioral (nurture) factors.
Scientific inquiry has provided incredible insight into the causes of and contributors to childhood obesity, a profoundly complex biopsychosocial issue. An ecological approach to understanding obesity best captures the overlapping factors involved ( Fig. 1 ). In this article, the authors provide a brief overview divided between biological (nature) and psychosocial and behavioral (nurture) factors. However, as with any complex condition, the line between the two can often be blurred.
Nature
The genetic and biological determinants of weight and obesity are intertwined. With the discovery of leptin in 1994, the understanding of energy regulation, appetite, and adiposity has exploded, and the field has become increasingly complex as a result. Continued discoveries implicate other contributors, from intestinal microbes to stress.
Neuroendocrine Control of Body Weight
In simplest terms, neuroendocrine control of weight is a balance between short- and long-term control of weight, overall energy intake, and energy expenditure. This balance can also be better understood when divided between the central nervous system (primarily the brain) and the body (primarily the gastrointestinal [GI] tract and adipose tissue).
Short-term control
Short-term control of body weight largely concerns control of energy intake. Meal initiation is primarily influenced by environmental stimuli such as food, emotions, time of the day, and peers. However, once the meal begins, neuroendocrine factors exert significant influence, thereby affecting the size of the meal, the amount of energy ingested, and when the meal is terminated ( Table 1 ). Some signals released in response to ingested or circulating nutrients coordinate the digestion and absorption of nutrients and feelings of satiety. Opposing signals, such as those initiated by ghrelin, act to stimulate appetite by increasing before a meal and decreasing after a meal is finished. In obese individuals, serum ghrelin levels are decreased and, alone, are unlikely to be a significant contributor to individual obesity status. However, ghrelin tends to increase during diet-induced weight loss and may explain increased levels of hunger with dieting. Most of the short-term GI signals have local effects, such as slowing gastric emptying and overall proximal GI motility, and also act centrally, either directly or via vagal actions.
| Name | Origin | Action and Effect |
|---|---|---|
| Amylin | Pancreas (β-cells); cosecreted with insulin | Reduces meal size via brainstem mechanisms |
| Cholecystokinin | Intestine (I-cells) | Controls meal size by slowing gastric emptying, stimulates gallbladder contractions, likely activates vagal receptors to terminate meal |
| Ghrelin | Stomach | Potent appetite stimulation, likely via central nervous system mechanism |
| Glucagonlike peptide 1 | Intestines (L-cells) | Stimulates insulin release, reduces appetite |
| Oxyntomodulin | Colon | Reduces appetite |
| Pancreatic polypeptide | Pancreas | Reduces appetite, likely by inhibiting pancreatic, gallbladder, and GI tract activity |
| Peptide YY (PYY 3–36 ) | Intestines (ileum/colon), cosecreted with glucagonlike peptide 1 | Reduces appetite, slows gastric emptying |
Long-term control
Long-term control is divided between the brain and body through levels of adiposity. These adiposity signals from the body act to communicate energy storage levels centrally, which then act to adjust energy intake and expenditure ( Table 2 ).
| Name | Origin | Action and Effect |
|---|---|---|
| Adiponectin | Adipose tissue | Enhances insulin sensitivity, decreases inflammation |
| Agouti-related peptide | Arcuate nucleus (hypothalamus) | Increases appetite, decreases metabolism |
| Arcuate nucleus | Hypothalamus | Area of energy regulation; location of CART, POMC, AgRP, NPY |
| Cocaine-amphetamine–regulated transcript neurons | Arcuate nucleus (hypothalamus) | Reduces energy intake |
| Insulin | Pancreas | Reduces energy intake |
| Leptin | Adipose tissue | Reduces energy intake |
| α-Melanocyte–stimulating hormone | POMC (ARC, hypothalamus) | Reduces energy intake |
| Neuropeptide Y | Arcuate nucleus | Increases appetite; decreases metabolism |
| Orexin | Hypothalamus | Increases appetite |
| Oxyntomodulin | Colon | Reduces appetite |
| Pro-opiomelanocortin | Arcuate nucleus (hypothalamus) | Releases α-melanocyte–stimulating hormone, reduces energy intake |
| Periventricular nucleus | Hypothalamus | Appetite and autonomic regulation |
The primary signals from the body are leptin and insulin, both of which exhibit long-term control of food intake and metabolism. Leptin is secreted in proportion to fat content of adipocytes and downregulates neurons that control food intake in the arcuate nucleus. Obese individuals may have relative leptin resistance, similar to insulin resistance, contributing to obesity. As with leptin, serum insulin levels increase in proportion to body fat and act centrally to relay energy stores.
An important discovery in the understanding of weight control is the endocrine function of adipose tissue. Leptin has an important role in the long-term control of body weight, whereas other hormones and cytokines released from adipose tissue affect overall health. Adiponectin has an important antiinflammatory function in the body and is generally viewed as a protective countermechanism to inflammatory processes originating in adipose tissues. Visceral adiposity, long known to be linked to the metabolic syndrome and cardiovascular disease, is detrimental to health through inflammatory mechanisms, primarily through adipokines. Interleukin 6, tumor necrosis factor α, plasminogen activator inhibitor 1, and visfatin are adipose-derived signals involved in atherosclerosis, insulin resistance, and inflammation.
The brain’s principal region for energy balance is the arcuate nucleus, located in the hypothalamus, which controls energy intake (eating) and expenditure (metabolism). In addition to direct influence by circulating nutrients indicating satiation (eg, glucose, fatty acids, and some amino acids), the arcuate nucleus receives signals from leptin and insulin, expressing receptors for most adiposity signals regulating long-term control of weight. Neurons controlling these processes are agouti-related peptide/neuropeptide Y (AgRP/NPY) and pro-opiomelanocortin/cocaine-regulated and amphetamine-regulated transcript (POMC/CART). AgRP/NPY neurons are anabolic in nature, stimulating appetite and reducing metabolism, whereas POMC/CART neurons are catabolic, inhibiting food intake via release of α-melanocyte–stimulating hormone. Neurons of the arcuate nucleus project to many other areas of the brain, particularly the hypothalamic paraventricular nucleus and the lateral hypothalamus. The paraventricular nucleus is a major determinant of energy expenditure, synthesizing anorexigenic factors corticotropin-releasing hormone and oxytocin, thereby regulating the body’s response to stress. The lateral hypothalamus is responsible for orexigenic peptides, melanin-concentrating hormone, and orexin. Other areas of the brain key to control of body weight are also influenced by hypothalamic projections. The mesolimbic-dopamine system influences the body’s hedonic and reward responses to food. The autonomic centers of the brainstem exert influence on the GI tract. Fig. 2 illustrates how short- and long-term control of weight across the body and brain are integrated.
The endocannabinoid system, involved in the control of appetite, is found in the central and peripheral nervous system, liver, muscle, GI tract, and adipose tissue. On exposure to palatable food, the system releases endocannabinoids that act on the cannabinoid-1 receptor, which affects satiety. This action overrides satiation, resulting in continued eating. There is some evidence that endocannabinoids play a role in peripheral tissues, linked to ghrelin release and adipose tissue regulation.
Genes and Other Contributors to Obesity
Although many genetic contributors to obesity have been identified in the past few decades, only 176 known cases of obesity have been linked to single-gene mutations in humans. However, an increasing number of mutated genes can be traced to obesity phenotypes. The 2005 Human Obesity Gene Map indicates that 253 quantitative trait loci are related to obesity phenotypes, with 127 candidate genes. Possible candidate genes have been identified on every chromosome except Y. A few genetic abnormalities have been identified, with only 1 having a treatment avenue presently (see Fig. 2 ).
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Leptin deficiency has been described in a few small series of families of Pakistani origin, characterized by severe obesity, hyperphagia, and other abnormalities. These rare cases are responsive to leptin therapy. Mutations in the leptin pathway, particularly the receptor gene, may account for up to 3% to 4% of cases of severe early-onset obesity. However, these genetic abnormalities are unlikely to respond to leptin therapy.
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Mutations in POMC have been described, resulting in a lack of central appetite signaling and therefore hyperphagia. Affected patients have red hair and adrenal insufficiency as well. Mutations in an enzyme that cleaves POMC have also been identified; these individuals are characterized by hypoglycemia, hypogonadotropic hypogonadism, and intestinal malabsorption.
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The melanocortin 3 (MC3R) and melanocortin 4 (MC4R) receptors are key in feeding behaviors. MC3R abnormalities may have a role in body weight regulation in African American children. MC4R mutations are found in more than 3% of early-onset severe obesity in children. Heterozygous and homozygous mutations seem to cause obesity, hyperphagia, and hyperinsulinism, as well as tall stature.
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Brain-derived neurotrophic factor is thought to play a role downstream in the leptin pathway and may be linked to early onset-obesity in patients with WAGR syndrome.
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Albright hereditary osteodystrophy (AHO) is associated with pseudohypoparathyroidism, and also involves the leptin pathway. Individuals with AHO also have short stature, developmental delays and mental retardation, brachydactyly, and ectopic ossifications.
Although the connection between a particular single nucleotide polymorphism and obesity is not always clear, large genome-wide association studies hint at possible links, such as the fat mass– and obesity-associated gene and reduced satiety or perilipin A gene and resistance to weight loss. Advances in genomics are rapidly identifying important areas of exploration.
There are numerous genetic syndromes associated with obesity, and, for many, the link is not clear. Syndromes may result in behavioral and health issues that lead to increased energy intake or decreased activity or may have disruptions in the central control of appetite that result in hyperphagia. Typically, obesity is not the presenting sign of the syndrome but is important in the clinical care of the child. For instance, Prader-Willi syndrome (short stature, hypotonia, developmental delay) involves significant hyperphagia, as do Bardet-Biedl (short stature, developmental delay, retinitis pigmentosum, polydactyly) and Alström (blindness or vision loss, hearing loss, hyperinsulinemia) syndromes. Many other syndromes are associated with obesity, including Cohen syndrome, fragile X, Sotos syndrome, Turner syndrome, and Beckwith-Wiedemann syndrome.
Infectious etiologies
Infectious causes include a form of adenovirus (AD36) that results in increased adipose tissue in animal models. Laboratory studies using human adipose tissue demonstrates increased adipocyte formation, and individuals with higher obesity levels are more likely to have antibodies to AD36. Although it is unlikely the obesity epidemic is a result of widespread adenovirus infection, there seems to be some link between the two.
Gut microbiota
Similar to adenovirus, the predominance of particular strains of colonic bacteria have been associated with higher levels of obesity in animal models, with increasing evidence of an association in humans. Theories linking obesity and gut microbes revolve around the bowel flora’s use of energy from ingested food, bacterial fermentation of food into readily absorbable fatty acids, and influences on metabolism in peripheral organs.
Stress
Chronic stress affects weight status through dysregulation of the hypothalamic-pituitary-adrenal axis, resulting in altered cortisol metabolism. Stress can result from multiple causes, for example, sleep deprivation, malnutrition, depression, and environmental stressors such as poverty. These factors may be related to obesity risk, even in the prenatal period.
Medications
Many medications, particularly antipsychotics, cause weight gain. High-dose inhaled glucocorticoids, oral glucocorticoids, antipsychotics (risperidone, olanzapine, clozapine), mood stabilizers (lithium), antidepressants (tricyclics), anticonvulsants (valproate, carbamazepine), oral contraceptives, and insulin and insulin secretagogues are the more commonly reported ones, but there is a lack of studies in children. Some antihypertensives, such as propranolol, nifedipine, and clonidine, can also lead to weight gain, as do many chemotherapy agents. It is unclear what mechanisms are involved. With antipsychotics, for example, a complex interplay of hunger disruption, metabolic effects, and unknown mechanisms have been reported.
Endocrinologic Conditions
Of children referred for evaluation of obesity, endocrinologic causes are only found in 2% to 3% of cases. Table 3 lists the most common disorders seen. Cushing syndrome has a prevalence of approximately 1 in a million, whereas insulinomas are even more rare. Hypothalamic obesity usually results from damage to the hypothalamus; these cases tend to occur in pediatric patients associated with surgery or radiation therapy. An example is children treated for craniopharyngiomas, which has high rates of obesity development posttreatment.
| Condition | Significant Signs and Symptoms |
|---|---|
| Hypothyroidism | Short stature and obesity but weight below 95th percentile for age |
| Growth hormone deficiency | Decreased linear growth velocity with increasing weight gain, increased central adiposity |
| Cushing syndrome | Decreased linear growth velocity, increased central adiposity, abdominal striae, insulin resistance |
| Insulinoma | Increased food intake to counteract low blood sugars |
| Hypothalamic obesity | Hyperphagia, other endocrine disorders; |
| Pseudohypoparathyroidism type 1A | Multiple other endocrine deficiencies |
Although pure genetic contributors to obesity, such as the mythical fat gene, are quite rare, there are many genetically linked causes that can increase a child’s risk of obesity. There is evidence for the existence of a thrifty genotype and phenotype. The protection of energy stores through famine and hunting/gathering societies has produced a human with a fine-tuned system of weight control described earlier. However, these factors are largely absent for most humans in industrialized nations today.
Nurture
Although there have been great discoveries in the biological determinants of obesity in children, the rapid increase in obesity prevalence almost certainly points to environmental changes having the greater impact. External influences on obesity vary by life stage, circumstance, and genetic predisposition. Changes in the nutritional and activity environments of children and families over the past several decades have likely had the greatest impact on the present epidemic.
Obesity and the Life Cycle
Prenatal
Antenatal and in utero environment
The antenatal environment influences fetal development. Fetal growth may be determined by cell counts, maternal brain centers that control satiety and appetite, and endocrine function even before conception. Antenatal stress or placental insufficiency may also influence altered pancreatic function and insulin sensitivity. These effects can persist into adulthood, increasing the risk for obesity-related conditions, such as metabolic syndrome.
Maternal malnutrition and famine
Nutrient restriction from maternal malnutrition in the first 2 trimesters of pregnancy is strongly linked to birth weight and an increased risk of obesity in young children. In a historical cohort study of boys with intrauterine exposure to famine within the first 2 trimesters of development (the “Dutch Hunger Winter” during World War II), an increase of 94% in the risk of developing childhood obesity was found. This may be attributable to structural and functional abnormalities of the endocrine system caused by nutrient restriction and disturbance in insulin and glucose homeostasis.
Maternal diabetes
Many studies have investigated prenatal exposure to diabetes in utero, indicating an increased prevalence of childhood overweight or obesity if the mother was diabetic during pregnancy. Mechanisms potentially responsible for this increased prevalence include fetal hyperglycemia and hyperinsulinemia caused by the diabetic mother’s poor glycemic control. Insulin levels in the third-trimester amniotic fluid have also been linked to childhood obesity and the development of insulin resistance and systolic hypertension.
Maternal smoking during pregnancy
Children exposed to prenatal cigarette smoke are more likely to exceed the 90th percentile for body mass index (BMI, calculated as weight in kilograms divided by height in meters squared) during adolescence. In one longitudinal study, 14% of 6-year-old children exposed to maternal smoking in the womb were obese, compared with 8% of those who were unexposed. Additional studies confirm these findings, even after adjusting for multiple maternal confounders. Proposed mechanisms for this association include nicotinic effects on leptin and maternal appetite and impaired fetal oxidative metabolism due to carbon monoxide and cyanide compounds found in cigarette smoke.
Maternal weight and pregnancy
Maternal weight both before and during pregnancy, and the magnitude of weight gain during pregnancy, are linked to increased risk of overweight or obesity in the offspring. Maternal obesity, especially in the first trimester, markedly increases the risk that a child will be obese by age 4 years. Maternal weight gain during pregnancy is also associated with a higher likelihood of childhood obesity, and the odds of having a child with a BMI above the 95th percentile at age 7 years increases by 3% for every kilogram of weight gained during pregnancy.
Postnatal
Breastfeeding
Breastfeeding versus formula feeding is an important nutritional decision that may affect childhood obesity risk. In some studies, breastfeeding was protective against child and adolescent obesity, whereas others have found little effect. The evidence suggests that breastfeeding reduces risk for pediatric weight gain; formula-fed children have an obesity prevalence of 4.5% compared with 2.8% in breast-fed children. More recent investigations indicate that breastfeeding for 6 months or more has a modest protective effect against adolescent obesity but not overweight. In one report, breastfeeding more than 6 months was associated with the lowest risk of overweight and obesity in 5-year-old children.
Early postnatal years
As with breastfeeding, overnutrition and early childhood feeding practices are major contributors to childhood obesity, influencing leptin concentrations and adiposity later in life. The rate at which infants gain weight during their first few months, and the type of infant feeding (formula or breast milk), is linked to weight status in later childhood as well as adult cardiovascular disease risk. Independent of birth weight and weight at age 1 year, rapid weight gain even within the first 4 months of life is associated with an increased risk of overweight at age 7 years.
Early childhood feeding and parenting
Home and social environments, parenting styles, and family feeding practices are the primary influences on early childhood nutrition behaviors. Nearly two-thirds of all meals consumed by children come from home, despite the prevalence of fast-food restaurants and convenient dining establishments. Thus, the home environment and family feeding behaviors are crucial components in the development of childhood nutritional habits and have an undeniable influence on childhood weight status.
Authoritarian parenting styles, characterized by restriction, pressures to eat certain food items, and overmonitoring, are most consistently linked to pediatric weight gain. However, children raised by authoritative parents who promote responsibility, monitoring, and modeling are more likely to have healthier nutrition and lower BMIs. Child-centered feeding practices, positive nutrition encouragement, and parents’ intake of fruits and vegetables are also positively associated with fruit and vegetable consumption in their children. These data support the notion that family factors are crucial components in the prevention and treatment of pediatric obesity.
Early introduction of solid food may have a contribution to the development of obesity. There is some evidence that rapid weight gain in infancy can predict later obesity, with infants already being exposed to unhealthy dietary patterns. Most studies tracking obesity development to infancy have not accounted for age of first solid food introduction. An Australian study found that delayed introduction of solids did significantly reduce the odds of overweight and obesity at age 10 years, and a prevention study seemed to lower risk of obesity development by delaying introduction of solids as part of a multicomponent intervention. One review of the literature did not find an association between age of solid food introduction and obesity development, but available evidence has not answered this question sufficiently.
Adiposity rebound
Adiposity rebound, when a child reaches a BMI nadir before body fat increases, typically occurs between ages 5 and 6 years. Normal-weight children with at least 1 overweight parent at the time of adiposity rebound are nearly 5 times as likely to be obese as an adult. If both parents are obese, children before the adiposity rebound have a 13-fold risk of being obese adults. Risk for adult obesity increases with earlier onset of childhood obesity. Children who reach adiposity rebound earlier are 5 times more likely to develop adult obesity, and those who are already overweight at the time of adiposity rebound have 6 times the risk for adult obesity.
Changes in the Family
It is intuitive that changes in family structure affect nutrition and physical activity habits of families. Family meals, fast food, early childhood feeding practices, sleep routines, parenting style, media use, family-based physical activity, adult obesity levels, socioeconomic status, and interaction with health services are key factors associated with childhood obesity and are most likely moderated by changes in the family. Families in the United States have experienced substantial changes as the child obesity epidemic has developed. In 1970, approximately 85% of children lived with 2 married parents; by 2010 this estimate decreased to 66%, and most of the change occurred between 1970 and 1990 ( Table 4 ). During the same period, children living in a mother-only household increased from 11% to 23%, with significant differences across racial groups. This is important because children from mother-only households are at substantially increased risk for living in poverty, a major risk factor for childhood obesity and poor health outcomes. During this same period, there was a substantial growth in women’s labor force participation, increasing from 43% in 1970 to 66% by 2009. However, there is little direct evidence linking these changes in the family to obesity risk in children.
| Living with 2 Married Parents | Living with Mother Only | Living with Father Only | Living with No Parent | |
|---|---|---|---|---|
| 1970 | 85.0 | 10.9 | 1.1 | 3.0 |
| 1980 | 76.6 | 18.0 | 1.7 | 3.7 |
| 1990 | 72.5 | 21.6 | 3.1 | 2.8 |
| 2000 | 69.1 | 22.4 | 4.2 | 4.1 |
| 2010 | 65.7 | 23.1 | 3.4 | 4.1 |
| Decade change | ||||
| 1970–1980 | −10.4 | +65.1 | +54.5 | +23.3 |
| 1980–1990 | −5.4 | +20.0 | +82.4 | −24.3 |
| 1990–2000 | −4.7 | +3.7 | +35.5 | +46.4 |
| 2000–2010 | −4.9 | +3.1 | +19.0 | 0.0 |
Lifestyle and Environment
Diet
Among dietary factors linked to obesity, high-fat and sugar-containing food have been the most studied. Although overconsumption of some food items leads to excessive weight gain and obesity, other patterns (eg, consuming a diet high in fruits and vegetables) are thought to protect against obesity. Fruits and vegetables have high water and dietary fiber contents, making them low in energy density. Although the mechanisms for their action remain unclear, eating a diet high in fruits and vegetables may help reduce body weight and fat by displacing energy-dense food from the diet. Fiber in fruits and vegetables helps reduce total energy intake by initiating satiety and altering postprandial hormones through a reduction in glycemic load. Yet in a recent review of studies about fruit and vegetable intake and adiposity levels in children, only 1 of 5 observed the expected inverse relationship between fruit and vegetable intake and adiposity. In a cross-sectional analysis, the lifestyle behavioral pattern of eating dinner, cooked meals, and vegetables was inversely related with obesity in children. There are limitations to these studies, with others drawing different conclusions on the link between fruits, vegetables, and obesity. However, no studies show a worsening of weight status with increased vegetable and fruit consumption.
American eating patterns have changed drastically in the past 3 decades. In children aged 2 to 18 years, energy density and portion sizes of key food items, including salty snacks, fruit drinks, french fries, hamburgers, cheeseburgers, pizzas, and Mexican fast food, increased from 1977 to 2006. McConahy and colleagues showed that nearly 20% of variance in daily energy intake can be attributed to portion size. Similarly, portion size, but not energy density, of snacks was the primary determinant of energy intake. At the same time, portion sizes of food items in the American diet have increased in the last several decades.
In one study, doubling the portion size of food items offered to preschool-aged children during a 24-hour period increased energy intake by 12% but only in certain food items. However, there was no compensatory reduction in other food items, leading to a higher daily energy intake. In contrast, an earlier study suggested young children can self-regulate energy intake up to 30 hours after a meal. In general, increasing portion sizes and energy density of food items and meals raises meal consumption from approximately 10% to 40% and daily energy intake by 12%. However, there is a dearth of well-designed studies on how portion size and energy density affect energy intake in children.
Rising rates of obesity coincide with the increased consumption of added sugars. For children and adolescents aged 2 to 18 years, nearly 20% of total energy intake is from added sugars in food items and beverages. Recent systematic reviews ranged from finding no evidence to strong evidence that sugar-sweetened beverages make a significant contribution to BMI in children. Cross-sectional studies in children showed positive associations (at least in subgroup analyses) between the use of sugar-sweetened beverages and measures of obesity (weight, BMI, body fat), although others showed either weak or no association between these variables. In a study of more than 10,000 children and adolescents, overweight people consumed a higher proportion of their total intake from soft drinks than did normal-weight individuals. Observational follow-up studies reported positive associations between intake of sugar-sweetened beverages and overweight/obesity.
Activity
Arguments that the obesity epidemic is caused largely by reduced physical activity and not energy intake are based on national survey data indicating that daily energy intake is unchanged or reduced in the last several decades. Not only is daily energy expenditure decreasing but also sedentary activities are increasing. In one report, children who watched more than 4 hours of television daily had the highest BMIs, and those who watched less than 1 hour daily had the lowest BMIs. In a separate study in Mexico City, the odds ratio of obesity was 1.12 for each hour of television watched per day and 0.90 for each hour of moderate to vigorous physical activity per day. The investigators found no such effect for time playing videogames.
In an early meta-analysis looking at the relationships between sedentary behaviors and obesity in children and youth, a statistically significant association was observed between television viewing and body fatness in children. However, in one study, television viewing only explained approximately 1% of the variance in body fatness, whereas video and computer game use showed no effect with body fatness. Studies have also failed to find correlations between television viewing and BMI. Although there is biological plausibility linking television viewing to body fatness, most of the evidence is from cross-sectional studies, which many demonstrate fairly small responses. In a randomized controlled trial, an intervention specifically geared to reduce television viewing and video game use in children aged 8 to 9 years produced an improvement in body fatness over a 6-month follow-up. Other intervention studies that did not specifically intervene on these sedentary behaviors reported decreases in television viewing and body fatness but were not necessarily causal. Currently there is a lack of empirical data to support claims that television viewing, playing video games, or using computers leads to obesity or interferes with physical activity. A possible confounder to these analyses is consumption of energy-dense snacks while participating in sedentary behaviors. As Proctor and colleagues found, children who watched the most television and had a fat intake of more than 34% of their daily kilocalorie consumption gained the most body fat from ages 4 to 11 years.
Overall, low levels of physical activity, defined by not meeting recommended levels, are problematic and mirror increased sedentary activity. This disruption in energy balance can explain much of the increase in pediatric obesity.
Sleep
The link between pediatric obesity, higher body fat, and sleep duration has been widely demonstrated in the literature and was recently reviewed in this journal. Although trials are ongoing, no interventions have reported on the manipulation of sleep patterns and the influence on weight gain in children. In adults, however, studies have shown that chronic sleep deprivation may lead to weight gain, which can be attributed to the influence of sleep on hormonal secretions. Restricted sleep is associated with increased food intake, including both meals and snacks, thereby increasing obesity risk. Lack of sleep can also lead to reduced physical activity and increased sedentary behaviors.
Although causation cannot be established, epidemiologic studies in children have indicated a definitive association between reduced sleep duration at night and increased weight status. Several reviews and meta-analyses agree that children who sleep less have an increased risk for obesity between 56% and 89%. Increased BMI in children is associated with reduced sleep duration, which is most likely because of an increase in adipose tissue deposits.
Industrialization and Obesity
Obesity and associated health issues are a worldwide health concern. Increased consumption of a more Western diet means that eating sugar and fat-laden, highly processed, energy-dense food items occurs globally. Popkin describes nutrition transition as existing in several stages, with urbanization, economic growth, and technological changes for work, leisure, and food processing leading the changes in stages. Obesity is evident in stage 4, or the degenerative disease period, characterized by increased intake of fat, sugar, and processed food items and a more prominent presence of technology in work and leisure.
Although urbanization, a demographic factor, improves growth patterns in children, it also increases the proportion of children above the 95th percentile for weight-for-age. Major social and economic changes in communities, such as transitioning from physical to mechanized transportation, introduction of processed food items and supermarkets, and television access, also change obesity and overweight prevalence in children. For example, the proportion of children (5–12 year age group) above the 85th percentile for BMI increased from less than 15% to nearly 50% in less over 20 years in the White Mountain Apache reservation.
The Built Environment
he built environment is a likely explanation for disparities in several health indicators, including the prevalence of obesity. There is substantial evidence showing that alterations in built environments regarding physical activity and eating are a factor in childhood obesity. For example, neighborhood differences in food access influence levels of obesity. In adolescents and adults, better availability to healthful food products leads to healthier food intake, including more fruits and vegetables, less dietary fat, and improved diet quality. Consequently, lower risks for obesity in children and adolescents are associated with better access to a supermarket.
Schools play a prominent role in a child’s nutrition because most children eat at least 1 meal per day at school and spend approximately 6 hours per day in this setting. The presence of fast-food establishments within 0.1 mile from a school was associated with a 5% increase in obesity rates, whereas further distances had no effect on obesity rates in the school.
Urban sprawl is also associated with adult obesity, whereas walkable neighborhoods and communities with sidewalks, safe intersections, accessible destinations, appealing green spaces, and public transit have improved activity levels and health. For each additional hour spent in a car per day, there is a 6% increase in the likelihood of obesity; for each additional kilometer walked, a nearly 5% decrease in obesity is present. A policy statement from the American Academy of Pediatrics has called for a multidisciplinary approach to building communities that promote active lifestyles in children.
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