International epidemic of childhood obesity and television viewing

Childhood obesity is one of the most serious global public health challenges of the 21st century. The prevalence of this problem has increased at an alarming rate in many countries. The main causes of childhood obesity are; sedentary lifestyle, unhealthy eating patterns, genetic factors, socio-economic status, race/ethnicity, media and marketing, and the physical environment. Children are clearly being targeted as a receptive market by the manufacturing industry. Undoubtedly, television provides one of the most powerful media through which products can be advertised. Furthermore, food advertising accounted for the largest percentage of these advertisements in virtually all countries. Detailed nutritional analysis of food advertisements identified that up to 90% of food products have a high fat, sugar or salt content. Therefore TV viewing is recently identified as one of the risk factors contributing to development of childhood obesity by several mechanisms. This review provides some facts and figures about the global trend of rising obesity among children, amount and content of television and especially food advertisements being watched by children and its possible mechanisms how to cause adverse effects on children's health and contribute to childhood obesity.     

Prevention of childhood obesity

The increasing prevalence of childhood obesity, its attendant morbidity, and the limited success of therapy mandate increased attention to preventive approaches. Environmental and family variables serve to identify families with children at risk for the development of obesity. Although the behavioral correlates that link these risk factors to childhood obesity remain unclear, inactivity and increased dietary intake of fat appear at this time to be the most logical foci for preventive interventions. Television viewing, which promotes both increased food consumption and reduced activity, represents a major concern at which counseling should be directed.     

Aetiology of overweight and obesity in children and adolescents

The epidemic diffusion of obesity in industrialised countries has promoted research on the aetiopathogenesis of this disorder. The purpose of this review is to focus mainly on the contribution that European research has made to this field. Available evidence suggests that obesity results from multiple interactions between genes and environment. Parents obesity is the most important risk factor for childhood obesity. Twin, adoption, and family studies indicated that inheritance is able to account for 25% to 40% of inter-individual difference in adiposity. Single gene defects leading to obesity have been discovered in animals and, in some cases, confirmed in humans as congenital leptin deficiency or congenital leptin receptor deficiency. However, in most cases, genes involved in weight gain do not directly cause obesity but they increase the susceptibility to fat gain in subjects exposed to a specific environment. Both genetic and environmental factors promote a positive energy balance which cause obesity. The relative inefficiency of self-adapting energy intake to energy requirements is responsible for fat gain in predisposed individuals. The role of the environment in the development of obesity is suggested by the rapid increase of the prevalence of obesity accompanying the rapid changes in the lifestyle of the population in the second half of this century. Early experiences with food, feeding practices and family food choices affect children's nutritional habits. In particular, the parents are responsible for food availability and accessibility in the home and they affect food preferences of their children. Diet composition, in particular fat intake, influences the development of obesity. The high energy density and palatability of fatty foods as well as their less satiating properties promotes food consumption. TV viewing, an inactivity and food intake promoter, was identified as a relevant risk factor for obesity in children. Sedentarity, i.e. a low physical activity level, is accompanied by a low fat oxidation rate in muscle and a low fat oxidation rate is a risk factor of fat gain or fat re-gain after weight loss. Conclusion Further research is needed to identify new risk factors of childhood obesity, both in the genetic and environmental areas, which may help to develop more effective strategies for the prevention and treatment of obesity.     

Epidemiology of childhood obesity in Europe

At present, estimation of the prevalence and secular trends in paediatric obesity in Europe is severely hampered by methodological problems in the definition of obesity and the paucity of data sets that mirror the demographic, cultural and socioeconomic composition of the European population. The available cross-sectional data, however imperfect, suggest that there are complex patterns in prevalence which vary with time, age, sex and geographical region. Overall, the prevalence of obesity in young children is relatively low compared to adolescents. Gender differences in prevalence are inconsistent. The highest rates of obesity are observed in eastern and southern European countries and even within countries there may be marked variability in the rates of obesity. It is not clear whether the trends in paediatric obesity are a simple consequence of an overall increase in fatness in Europe or whether there may be sub-groups of children who, at certain ages, are either particularly susceptible to environmental challenges or are selectively exposed to such challenges. The respective contributions of dietary energy intake and patterns of physical activity to the aetiology of childhood obesity present a confused and confusing picture. Changing demographic and social circumstances throughout Europe are linked to childhood obesity but it is highly unlikely that these interact in similar ways in the genesis of obesity in different individuals and population groups. Conclusion At present, our limited understanding of the variability in susceptibility to obesity in European children and adolescents provides powerful justification for the development of preventive strategies which are population based rather than selectively targeted at high-risk children.     

Childhood obesity

Several conclusions can be drawn on the basis of the research reviewed: Obese children are more likely to become obese adults than are their thinner peers. Parent weight may interact with child weight status in the etiology of adult obesity. Obese children with obese parents are more likely to become obese adults than are obese children with thin parents. The prediction of adult obesity from childhood obesity improves with the age of the child. As the obese child gets older, he or she is more likely to become an obese adult. The inclusion of parents in the treatment process is important for the success of childhood weight control. It may be best to see the parent and child separately in treatment meetings rather than together. Children with thin parents may do better in weight control than children of obese parents. Adherence to exercise is likely to be a problem with obese children, and the choice or design of an exercise program should take these adherence problems into account. Nutritional adequacy of the child's diet should be evaluated both in terms of what the child is eating as well as in terms of the prescribed diet. Likewise, growth of the obese child during dieting should be monitored and should be related to expected height, which can be based on parent height. In summary, childhood obesity is a problem that places a child at great risk for becoming an obese adult. However, a growing body of research has emerged that has identified important risk factors for the development of obesity in children. Likewise, treatment methods have been developed that produce significant and long-lasting effects on childhood weight status. Continued development of treatment methods would be of great potential importance in the prevention and treatment of this prevalent problem.     

News media framing of childhood obesity in the United States from 2000 to 2009

The American public holds mixed views about the desirability of government action to combat childhood obesity. The framing of coverage by news media may affect citizens' views about the causes of childhood obesity and the most appropriate strategies for addressing the problem. We analyzed the content of a 20% random sample of news stories on childhood obesity published in 18 national and regional news sources in the United States over a 10-year period (2000-2009). News media coverage patterns indicated that by 2003, childhood obesity was firmly on the news media's agenda and remained so until 2007, after which coverage decreased. We identified changes in news media framing over time and significant differences according to news source. News coverage of causes of childhood obesity that were linked to the food and beverage industry increased in the early years of the study but then decreased markedly in later years. Similarly, mention of solutions to the problem of childhood obesity that involved restrictions on the food and beverage industry followed a reverse U-shaped pattern over the 10-year study period. News stories consistently mentioned individual behavioral changes most often as a solution to the problem of childhood obesity. Television news was more likely than other news sources to focus on behavior change as a solution, whereas newspapers were more likely to identify system-level solutions such as changes that would affect neighborhoods, schools, and the food and beverage industry.     

The development of obesity in childhood

Multiple factors appear to influence and promote the development of obesity: The importance of genetic factors has been demonstrated in some studies, however, it is very difficult to distinguish between environmental and genetic influences. Independently, increased birthweight, massive weight gain in the first months after birth and overweight of the mother or of both parents seem to be risk factors, which are able to promote the development of childhood obesity. In the past few years more attention has been paid to psychological factors and their influence on appetite, physical activity and energy balance. Whether metabolic changes on cellular and microcellular basis can cause obesity is not sufficiently known until now. Nutrition in early childhood and fat cell hyperplasia and hypertrophia induced by nutritional factors probably do not imply persistence of obesity but may promote obesity and worsen the prognosis of therapy. Due to the fact that a high percentage of obese adolescents remain obese in adulthood, and due to the poor results in the treatment of obesity as well as the association of overweight with an increased risk for morbidity and mortality an effective therapy and prevention of obesity even during childhood seem to be of great importance.     

Variation analysis of β3-adrenergic receptor and melanocortin-4 receptor genes in childhood obesity

BACKGROUND: Decreased energy expenditure and increased food intake are principal causes for obesity. In the present study, genotypes of beta(3)-adrenergic receptor (beta(3)AR) and of melanocortin-4 receptor (MC4R), both of which are believed to have a close link to the cause of obesity, were analyzed and compared with phenotypes of childhood obesity. METHODS: Thirty-five obese children with moderate to severe obesity were enrolled. Direct sequencing of the MC4R coding region and pinpoint-polymerase chain reaction were used to detect genomic variation in the beta(3)AR gene using peripheral blood-derived DNA. RESULTS: Allele frequency of Trp64Arg variation in the beta(3)AR gene in the obese subjects was 0.16, which is comparable with that in the healthy general population in eastern Asia. Comparison of phenotypical characteristics did not show a significant difference between Trp/Trp and Trp/Arg subjects. It was notable that body height SD was significantly higher in the Trp/Trp than the Trp/Arg subjects (0.93 +/- 1.0 SD vs 0.07 +/- 1.3 SD, P= 0.03). Annual weight gains were far beyond a hypothetical fat gain in an Arg64 heterozygote with decreased energy consumption, suggesting increased food intake in childhood obesity. There was, however, no variation in the MC4R gene despite thorough sequencing of the entire coding region. CONCLUSIONS: The Trp64Arg variation in the beta(3)AR gene has no relationship to the degree or the incidence of childhood obesity. The majority of childhood obesity can be characterized as tall stature, more rapid weight gain than that expected by decreased energy expenditure. Further investigation is necessary in regard to the increased food intake as a major cause of childhood obesity.     

Sleep and obesity in children and adolescents

The purpose of this review is to provide a comprehensive update of epidemiologic studies that have assessed the association between sleep and obesity risk. Data suggest that short sleep is associated with an increased risk for being or becoming overweight/obese or having increased body fat. Late bedtimes are also a risk factor for overweight/obesity. Findings also suggest that changes in eating pathways may lead to increased body fat. Future experimental studies are needed to enhance our understanding of the underlying mechanisms through which sleep may play a role in the development and maintenance of childhood obesity.     

Myths about childhood obesity.

Childhood obesity is a multifactorial and complex disease. Myths such as those that we have described may distract our patients from the underlying behaviors that contribute to the disease or may deflect the blame perceived by obese patients and their parents. Myths that suggest that the obese are inactive, eat differently, or eat more junk food suggest that obese individuals are socially deviant and justifies the intense discrimination directed against them. The myth that obesity represents an untreatable disease helps free health-care professionals from the responsibility to understand and care for obese children. Dispelling the myths about childhood obesity represents a critical step in prevention and treatment.     

Pediatric obesity prevention and management

Obesity has reached epidemic proportions worldwide in turn redirecting the goals of the Pediatric well care visit. There is no effective pharmacological or surgical treatment available for this entity but if left unaddressed it can lead to detrimental medical complications. Several known contributors to obesity exist which allow the development of successful prevention programs. Prior to initiating such a program, a pediatric practitioner should be equipped with the skills of identification of overweight and its risk factors as well as strong knowledge of treatment options. We attempt to provide the appropriate guidelines for childhood obesity prevention in this review.     

Role of dietary factors and food habits in the development of childhood obesity: a commentary by the ESPGHAN Committee on Nutrition

This Comment by the Committee on Nutrition of the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition aims to provide a summary of the role of nutrition-related factors on obesity prevention in children ages 2 to 18 years. This Comment emphasizes that dietary interventions should be incorporated into a multidisciplinary strategy for obesity prevention. No single nutrient has been unequivocally associated with the development of obesity. Methodological limitations in study design and the complex nature of obesity must be taken into account when interpreting the association with reported dietary factors. Energy intake should be individually determined, taking into account energy expenditure and growth. Preferential intake of slowly absorbed carbohydrates and limiting the ingestion of rapidly absorbed carbohydrates and simple sugars should be promoted. No specific recommendations for macronutrient intakes to prevent obesity can be made. Plant foods can be used as the main food contributors to a well-balanced diet with adequate monitoring of nutrient intake. Plain water should be promoted as the main source of fluids for children instead of sugar-sweetened beverages. Children should eat at least 4 meals, including breakfast, every day. Regular family meals should be encouraged. Regular consumption of fast food with large portion sizes and high energy density should be avoided. Healthy food options should be promoted for snacking. Food portion sizes should be appropriate for age and body size. Nutrition and lifestyle education aimed at the prevention of obesity should be included in the routine care of children by health care professionals.     

Reframing the early childhood obesity prevention narrative through an equitable nurturing approach

High‐quality mother–child interactions during the first 2,000 days, from conception to age 5 years, are considered crucial for preventing obesity development during early life stages. However, mother–child dyads interact within and are influenced by broader socio‐ecological contexts involved in shaping child development outcomes, including nutrition. Hence, the coexistence of both undernutrition and obesity has been noted in inequitable social conditions, with drivers of undernutrition and overnutrition in children sharing common elements, such as poverty and food insecurity. To date, a holistic life‐course approach to childhood obesity prevention that includes an equitable developmental perspective has not emerged. The World Health Organization (WHO) Nurturing Care Framework provides the foundation for reframing the narrative to understand childhood obesity through the lens of an equitable nurturing care approach to child development from a life‐course perspective. In this perspective, we outline our rationale for reframing the childhood narrative by integrating an equitable nurturing care approach to childhood obesity prevention. Four key elements of reframing the narrative include: (a) extending the focus from the current 1,000 to 2,000 days (conception to 5 years); (b) highlighting the importance of nurturing mutually responsive child‐caregiver connections to age 5; (c) recognition of racism and related stressors, not solely race/ethnicity, as part of adverse child experiences and social determinants of obesity; and (d) addressing equity by codesigning interventions with socially marginalized families and communities. An equitable, asset‐based engagement of families and communities could drive the transformation of policies, systems and social conditions to prevent childhood obesity.     

Non-alcoholic fatty liver disease and childhood obesity

Obesity has emerged as a significant global health problem in the pediatric population. Pediatric liver disease is a serious complication of childhood obesity. Non-alcoholic steatohepatitis (NASH) is an entity in the spectrum of non-alcoholic fatty liver disease (NAFLD) ranges from fat in the liver — simple steatosis, NASH/ steatohepatitis — fat with in ammation and/or fibrosis to advanced fibrosis and cirrhosis when fat may no longer be present. NASH is associated with obesity, diabetes, insulin resistance (IR), and hypertriglyceridemia. Children get NAFLD, and the incidence of this pediatric liver disease is rising as childhood obesity becomes increasingly prevalent. Although much remains to be learned about pediatric NAFLD, it is already evident that children with NASH risk progressive liver damage, including cirrhosis. Liver biopsy is required for definitive diagnosis, and other causes of fatty liver in childhood must be excluded. Gradual weight loss through increased regular exercise and a low-fat, low-refined carbohydrate diet appears to be effective. Drug treatments are being developed. The important message is that childhood obesity poses important health problems, including but not limited to potentially severe chronic liver disease. Early diagnosis of children who are only overweight is a worthy goal so that strategies to limit obesity can be instituted as early as possible. Identification of genetic risks is important, but management will invariably require changes in environmental factors. In addition to individual treatment, a multifaceted, societal initiative is required for solving the childhood obesity epidemic.     

Ethnic issues in the epidemiology of childhood obesity

Childhood obesity may be seen as a marker for high-risk dietary and physical inactivity practices. Recent increases in the prevalence of overweight and obesity among American children are not limited to one age, gender, or ethnic group, which suggests that unique behaviors of the members of various racial or ethnic subgroups of the population are unlikely to be the major contributing factors. Rather, it seems that environmental changes promoting increased energy intake and decreased energy output are occurring and have widespread impact on children from various backgrounds. Although no ethnic group is immune from the current shift in energy balance, differential rates of overweight seem to exist among ethnic groups. National probability samples of African-American, Hispanic, and white children in the United States provide clear evidence that white children are at lower risk for childhood overweight than are African-American or Hispanic children. Of concern is the lack of national data on the prevalence of overweight and obesity for Native-American and Asian-American groups. Also of concern is the aggregation of racial and ethnic subgroups, which may render prevalence rates meaningless. This possibility is clearly true with some surveys of weight status that combine diverse populations, such as Asians and Pacific Islanders, into one group. The high rates of obesity in African-American, Hispanic, and Native-American children are of concern. Although parental SES is associated inversely with childhood obesity among whites, higher SES does not seem to protect African-American and Hispanic children against obesity. In these groups, childhood obesity does not seem to be associated significantly with parental income and education. Health consequences of childhood obesity include a higher prevalence of type 2 diabetes and an increased risk for adverse levels of lipids, lipoproteins, and blood pressure. The effects of recently reported unprecedented levels of childhood overweight on subsequent risk for obesity in middle age are not known until future longitudinal data can be collected. It seems likely, however, that future health consequences of current early and severe childhood obesity will be staggering. Funding for adult follow-up of longitudinal studies of high-risk African American, Hispanic, and Native-American children is needed urgently to provide information on the long-term effects of childhood obesity. Halting the obesity epidemic is a formidable task, but the success in recent decades of drastically reducing childhood undernutrition offers hope and should spur similar action and leadership efforts. Promotion of efforts to reduce excess caloric intake with efforts to increase energy expenditure should receive paramount attention in the design of health programs. Given the relatively few published obesity-prevention and treatment studies that are designed to address specific cultural issues, it is important to promote the development of culturally appropriate intervention strategies that are shown to be effective among youth of diverse backgrounds. Although the dietary and activity goals will be similar, parental, family, and community messages and techniques grounded in cultural traditions and norms will be different for each ethnic group. This approach is crucial in the United States, a country with an increasingly diverse population.     

Genetics and the pathophysiology of obesity

Obesity is a complex disease that involves interactions between environmental and genetic factors. Obesity results from an imbalance between food intake and energy expenditure over several years. The genetic approach both in animal models and in humans has allowed immense progress in the understanding of body weight regulation. Monogenic forms of obesity in humans have been characterized and result from mutations in genes involved in the central pathways of food intake regulation. However, these cases are extremely rare and generally obesity must be considered as a complex polygenic disease involving interactions between multiple genes and the environment. Numerous studies, including studies in children, have tried to identify "susceptibility" genes. At present, the results are not conclusive inasmuch as they are highly variable between studies and because the relative risk associating a specific gene allele and obesity remains low. Thus, it seems highly premature to genotype obese patients on a large scale for predictive testing. When specific pharmacological treatments based on recent discoveries become available, however, genetic testing could help discriminate between the subtypes of obesity that may respond differentially to treatment.     

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.     

Children, adolescents, obesity, and the media

Obesity has become a worldwide public health problem. Considerable research has shown that the media contribute to the development of child and adolescent obesity, although the exact mechanism remains unclear. Screen time may displace more active pursuits, advertising of junk food and fast food increases children's requests for those particular foods and products, snacking increases while watching TV or movies, and late-night screen time may interfere with getting adequate amounts of sleep, which is a known risk factor for obesity. Sufficient evidence exists to warrant a ban on junk-food or fast-food advertising in children's TV programming. Pediatricians need to ask 2 questions about media use at every well-child or well-adolescent visit: (1) How much screen time is being spent per day? and (2) Is there a TV set or Internet connection in the child's bedroom?     

Markets and childhood obesity policy

In examining the childhood obesity epidemic from the perspective of economics, John Cawley looks at both possible causes and possible policy solutions that work through markets. The operation of markets, says Cawley, has contributed to the recent increase in childhood overweight in three main ways. First, the real price of food fell. In particular, energy-dense foods, such as those containing fats and sugars, became relatively cheaper than less energy-dense foods, such as fresh fruits and vegetables. Second, rising wages increased the "opportunity costs" of food preparation for college graduates, encouraging them to spend less time preparing meals. Third, technological changes created incentives to use prepackaged food rather than to prepare foods. Several economic rationales justify government intervention in markets to address these problems. First, because free markets generally under-provide information, the government may intervene to provide consumers with nutrition information they need. Second, because society bears the soaring costs of obesity, the government may intervene to lower the costs to taxpayers. Third, because children are not what economists call "rational consumers"--they cannot evaluate information critically and weigh the future consequences of their actions-the government may step in to help them make better choices. The government can easily disseminate information to consumers directly, but formulating policies to address the other two rationales is more difficult. In the absence of ideal policies to combat obesity, the government must turn to "second-best" policies. For example, it could protect children from advertisements for "junk food." It could implement taxes and subsidies that discourage the consumption of unhealthful foods or encourage physical activity. It could require schools to remove vending machines for soda and candy. From the economic perspective, policymakers should evaluate these options on the basis of cost-effectiveness studies. Researchers, however, have as yet undertaken few such studies of obesity-related policy options. Such analyses, once available, will help policymakers achieve the greatest benefit from a fixed budget.     

Risk factors for obesity in 7-year-old European children: the Auckland Birthweight Collaborative Study.

OBJECTIVE: To identify risk factors associated with obesity in primary school children, with a particular focus on those which can be modified. To identify critical periods and growth patterns in the development of childhood obesity. METHODS: 871 New Zealand European children were enrolled in a longitudinal study at birth and data were collected at birth, 1, 3.5 and 7 years of age. Data collected at 7 years included weight, height, bioelectrical impedance analysis (BIA), television viewing time and a 24 h body movement record (actigraphy). The outcome measure was percentage body fat (PBF), which was calculated at 3.5 and 7 years using BIA. Univariate and multiple regression analyses were carried out using PBF as a continuous variable. RESULTS: Multivariable analysis found maternal overweight/obesity, maternal age, female gender, sedentary activity time and hours of television viewing to be independently associated with PBF at 7 years. Growth variables (birth weight, rapid weight gain in infancy, early (1-3.5 years) and middle childhood (3.5-7 years)) were also independently associated with adiposity at 7 years. There was a strong correlation between PBF at 3.5 years and PBF at 7 years. CONCLUSIONS: Many primary school aged children start on the trajectory of obesity in the preschool years, which suggests interventions need to start early. Maternal overweight/obesity, television watching, sedentary activity time and rapid weight gain in infancy, early and middle childhood are risk factors for childhood obesity, and are all potentially modifiable.