23 Childhood obesity: Prevalence and assessment

Ms. Shumayla and Meenal Dhall

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Contents:

    1.      Introduction 1.1 Obesity

a.  Childhood Obesity

2.      Causes of Childhood Obesity

2.1 Genetic Factors

2.2 Environmental factors

2.3 Sedentary Behavior and Physical Activity

2.4 Eating Habits

2.5 Socio-economic and Cultural factors

2.6 Obesity at Infancy

2.7 Screen Timing

2.8 Duration of Sleep

2.9 Genetic and Environmental Interaction

3.      Adiposity Rebound

4.      Comorbidities of Childhood Obesity

5.      Summary

 

Learning Objective:

  • To study childhood obesity, its causes and factors affecting.

    1. Introduction

 

1.1 Obesity

 

Globally, profile of diseases are transforming at a hasty pace catching the attention of various medical personnel and policy makers. This is true particularly in case of low and middle income countries that produce the major chunk of world population. Among these entities, obesity has reached global epidemic proportions with over 1 billion people classified as overweight and of those at least 30% as obese (WHO, 2003).

 

Overweight and obesity are considered a public health crisis that contributes substantially to a variety of chronic diseases, disability and premature mortality. During the past decade, both prevalence and degree of obesity have increased dramatically among children all over the world though their magnitude varies greatly between and within countries. Thus, the emerging epidemic of obesity and associated co-morbidities represents an enormous public health burden with economic and societal consequences of major significance.

 

1.2 Childhood Obesity

 

The global epidemic of obesity is involving all age groups. There are 22 million overweight or obese children under 5 years worldwide (WHO, 2003), which means that 10% of school-aged children in the world are affected (Lobstein et al., 2004). Overweight/Obesity among Children began in developed Countries in the late 1980’s (Reilly et al., 1999) and more recently the problem has extended into the developing World as well. There is a growing global childhood obesity epidemic, with a large variation in secular trends across countries (Wang and Lobstein, 2006). ).

 

IOTF has recently presented decadal increase in obesity prevalence among children across the globe. Figure 1 1 illustrates how the rates of childhood obesity have been increasing worldwide. Whilst the highest rates of childhood obesity are being observed in developed areas of the world such as North America and Western Europe, rates continue to increase at an alarming pace in many middle and low income countries (Lobstein et al., 2004). In 2011 globally more than 40 million children under the age of 5 years were overweight, of those around 35 million of these were living in developing countries (WHO, 2013).

 

Obesity is no more restricted to high income countries, but is also rising at a much faster rate in low and middle income countries. The constitution of the Developmental Origins of Health and Disease (DOHaD) society has drawn great interest to study the public health challenges faced by countries under rapid economic and nutrition transitions, particularly in those developing countries that have experienced economic development and improvement in people’s living standard, and as a result, a shift from under- to over-nutrition problems.

 

Until recently, there was little realization of severity of this problem in developing countries like India (Wang et al., 2009) . Recent trends in Indian populations indicated a rise in obesity both in adults and children. The paradox is that India like other developing countries suffer the dual health burden facing high rates of obesity coexisting with under-nutrition and other chronic deficiency diseases (Kapoor et al., 2009). In contrast to some western countries which have observed a complete shift in BMI distribution curve, most of the developing world is experiencing a dual nutritional burden with BM1 curve getting fatter towards both the ends.

 

Overweight for children and teenagers is usually calculated using the body mass index (BMI), a formula which combines values of height and weight. It is not a direct measure of body fat but correlates well among most people with direct measures of body fat such as underwater weighing. A child’s BMI is compared to a gender-specific BMI age-for-growth chart to obtain a percentile ranking, which shows the relative position of the child’s BMI among others of the same gender and age. A BMI percentile at the 95th or higher is classified as over-weight, and from 85th to 95th percentile as at risk for overweight.

 

Recently, an alternative classification system has been developed using growth curves created using data from several different countries, which identify BMI scores for children age 2-18 years which project to a BMI of 25 (overweight) or 30 (obese) at 18 years of age. Other Non-invasive measures to define the degree of obesity include waist circumference (WC), waist-to-hip ratio (WHR), to assess upper body fat predominance), and skin fold thickness (subscapular, triceps, suprailiac, abdominal and their sum or ratios).

 

Apart from these non-invasive methods, other validated parameters for measuring the degree of obesity also exist. These methods are used to define body composition, based on water, fat, protein, and mineral content of the human body. Such direct measurements of body fat content include dual energy X-ray absorptiometry (DEXA) hydro-densitometry or bioelectric impedance analysis (BIA). However, the use of such methods in childhood and adolescence is limited due to risk .The applicability of technical equipment which is validated mainly for adult use is another concern. These methods are currently used only for scientific reasons in the pediatric population (Korner et al., 2007).

Source Link: https://blogs.wsj.com/chinarealtime/2014/05/29/as-obesity-rises-chinese-kids-are-almost-as-fat-as-americans/

 

2. Causes of Childhood Obesity

 

Various factors are responsible for the development of overweight and obesity among Children. Body weight is shaped by a combination of genetic, behavioral, environmental, cultural and socio-economic influences. Additional factors that influence the degree of body fat mass are ethnic background, gender, developmental stage and age. Although the inter-individual variations of BMI are attributable to genetic factors, for the majority of individuals, overweight and obesity results from excess energy consumption and/or inadequate physical activity.

 

2.1 Genetic Factors

Several studies in the past have suggested genetic influence on adiposity resulting in chronic positive energy balance (Bouchard, 2008). More recently, studies have attempted a search for molecular basis of obesity. More than 430 genes, markers and chromosome regions have been associated with the obese Phenotype (Snyder et al., 2004 ).The genetic studies including twin studies suggest that, more than 50% of the inter-individual variations of BMI and the tendency to develop obesity is inherited (Snyder et al., 2004).

 

During the past years, very few single-gene obesity syndromes have been described. Monogenic causes of severe obesity that starts in early childhood include alterations of the ob-gene, leptin (Strobel et al., 1998), the leptin-receptor (Clement et al., 1998) and the melanocortin-4 receptor, MC4R (Farooqi et al., 2003). These syndromes account for up to 4- 7% cases of severe obesity (Vaisse et al., 2000).

 

In contrast to defined monogenic causes of severe obesity, the number of sequence variants and mutations as well as polygenic causes that have been shown to be functional is quite large. A total of 42 different mutations in 130 individuals have been identified for the MC4R, making MC4R mutations the most prevalent genetic cause of obesity identified to date. These mutations are typically associated with early onset and rather severe obesity. However, not surprisingly, the variation in phenotypic expression of obesity related to the MC4R gene points to variable penetrance and other genetic factors (Snyder et al., 2004).

 

One possible mechanism through which these mutations affect body weight is loss of normal regulation of food intake (Farooqi et al., 2003). As for the other genes, a missense R236G mutation in the POMC gene in unrelated children with severe obesity has been described (Challis et al., 2002). One report pertained to a family in which all affected members with overweight or obesity and insulin resistance were double heterozygotes for a premature stop mutation in PPARa (Savage et al., 2002).

 

Although several obesity cases identified so far could be ascribed to single gene defects, the polygenic approach towards many obesity cases is progressively revealed (Snyder et al., 2004). The load of information as for a polygenic predisposition towards obesity and related disorders in children is increasing steadily. Recent data suggests that genetic variants and haplotypes derived from ENPP1 (nucleotide pyrophosphatase/phosphodiesterase-1), which encodes a membrane-bound glycoprotein that inhibits the insulin-receptor tyrosine kinase activity resulting in reduced insulin sensitivity, increases the susceptibility to obesity and early impairment of glucose and insulin metabolism in children (Bottcher et al., 2006).

 

Apart from these genetic associations, Mendelian disorders exhibiting obesity as one of their clinical features have to be considered whenever a child has sever obesity. Such syndromes include the Prader-Willi-like syndrome linked to 6q16.2-q14 and the SIM1 gene, the Bardet-Bied1 syndrome, and the fragile X syndrome with Prader-Willi-like phenotype in which mutations in the FMR-1 gene are present (Snyder at al., 2004).

 

One of the classical forms of central obesity is Cushing’s syndrome, in which obesity, insulin resistance, glucose abnormalities, hypertension, and other features are invariably found, all of which are caused by pathologically elevated levels of cortisol. One of the genetic causes has been linked to mutations in the regulatory subunit R1A of the protein kinase A gene (PRKAR1A). This disease is part of the multiple neoplasia syndrome, the Carney complex (Stratakis, 2001). Silventoinen and colleagues (2010) opines that genetic factors probably have an important role in childhood obesity, but their role may be different or they may result from other genes than those that operate in adulthood.

 

2.2 Environmental factors

In the context of obesity, an environmental challenge is any behavior or lifestyle factor that has a bearing on energy intake or energy expenditure. Several lines of evidence support the premise that genetic factors alone cannot explain the demographic and ethnic variations in overweight and obesity prevalence. Although obesity has important genetic and familial components, the current epidemic has possibly resulted from technological advances (Kopelman, 2000; Silventoinen et al., 2010).

 

In a genetically stable population, the rapid increases in obesity must reflect environmental effects. In at least 50% of the cases, obesity is attributable to life style changes. A chronic positive energy balance then leads to an increase in fat mass and body weight. The development and severity of obesity is thus remarkably affected by lifestyle and environmental conditions in genetically predisposed individuals. Nowadays children are surrounded with Obesogenic Environments. The imbalance between calories consumed and expended through physical activity is caused by obesogenic environment which encourages the over-consumption of energy-dense foods, whilst reducing the opportunity for habitual physical activity.

 

Modern environments provide ample opportunities for sedentary pastimes and excessive food consumption in terms of high fat and sugar diet and increased portion size. A large number of obesity related risk factors are reported in literature. These operate during various stages of growth in children.

 

2.3 Sedentary Behavior and Physical Activity

There has been researches showing the evidences of reduction in habitual energy expenditure in children. A National survey using parent report found that approximately one-third of English children aged 5 years are not engaged in at least 60 minutes of physical activity daily (Stamataki et al., 2010). The physical activity level among children increased with age during the preschool period and gender differences in physical activity were present early in life. Physical activity in children can be measured either through a direct measurement of energy expenditure, observation or parent report. In school going children there is an inverse relationship between physical activity levels and body fatness.

 

In a longitudinal study by Moore et al. (1995) it was reported that physical activity levels at age 3 years were inversely related to body fatness at five years, also heavier children with low activity levels were found to gain more weight than lean children with low activity levels. The physical activity levels were positively related to BMI at age four years, but negatively associated with BMI at ages five and six years.

 

2.4  Eating Habits

Over the years Dietary habits and dietary patterns among young children have changed considerably. Children are eating more snacks than regular meals, and often the timings are unfettered. Studies have reported a direct association between snacking and obesity in children. Snacking is often associated with more energy dense foods and drink or more total food ingested, particularly outside the home where the types of foods commonly consumed as snacks are often high in fat or high in carbohydrates (sugar and/or starch).

 

Similarly, researchers at the Harvard School of Public Health examined 548 ethnically diverse Children, and found that those who had increased their intake of sugary and fuzzy beverages, had increased their body weight. The odds of this group of children becoming obese increased 1.6 times for each glass or can of a soft drink consumed each day (Ludwig et al., 2001). Children’s consumption of processed fruit juice, sweetened drinks, and snack foods has increased over the past 20 years.

 

The increase in prevalence of obesity is consistent with increase in energy intake of children. A UK-based cross-sectional survey showed high energy dense diets in young children to be higher in fat and lower in sugar content than lower energy dense diets (Gibson, 2000) The total dietary fat has been directly associated with adiposity. Portion sizes of foods/meals are also gaining prominence as a potential risk factor for obesity (Ebbeling et al., 2002). Epstein et al. (2001) reported that inadequate consumption of fruits has been identified as a detrimental risk factor for obesity.

 

2.5 Socio-economic and Cultural factors

Majority of the epidemiological findings about childhood obesity disclosed the fact that in highly developed countries, prevalence of obesity is inversely associated with education and socio-economic status (Prentice, 2006). In developed countries obesity may be a cause of economic disadvantage rather than a consequence as economic poverty or lack of education or both impair an individual’s ability to repel the current obesogenic environment. In industrialized countries, children from lower-income families are more prevalent to gain weight in excess as low income families may face barriers like food security, lack of healthy food choices like fruits and vegetables and lack of clean environment for physical activity.

 

In a household the sociocultural factors are the most investigated factors for assessing energy balance related behaviors. Every culture and community have their own set of preferences for food. Many communities have healthy choices including pulses, vegetable and fruits and some communities may have a tendency of eating fried and food with more fat. Also levels of physical activity is influenced by family members. It has been seen that father’s physical activity habits, time spent outdoors and school physical activity related policies do have an impact on children tendency to be physically active.

 

2.6 Obesity at Infancy

During Infancy there is rapid increase of body fat cells and changes in biological factors that influence the rate of growth of child. During infancy a number of growth and nutritional factors may influence the development of childhood obesity. In a systematic review Ong and Loos (2006) identified 21 studies and reported positive association between weight gain in first 2 years of life and subsequent obesity. Another study in the Wic (Women, Infants and Children Program) in New York state confirms the direct association of 0-6 months weight gain with BMI defined obesity at 4 years (as reviewed in Gillman, 2008).

 

An upward crossing of two major weight for length centiles in the first 6 months predicted high obesity risk at 5 years (Gillman, 2008). Association between rapid catch up growth and later obesity is also reported (Ong et al., 2000; Reilly et al., 2005). Over the past 10 years large numbers of epidemiological studies have focused on association between breastfeeding and childhood obesity. Positive association of breastfeeding and obesity was confirmed in childhood (Armstrong and Reilly, 2002), during adolescence and in adulthood. Many studies have investigated the relationship between breastfeeding and later overweight but some have found an inverse relationship as well (Arenz et al., 2004).

 

Two reviews found that an inverse relationship still remained after adjusting for confounding factors, such as parental obesity, maternal smoking or social class (Arenz et al., 2004). In one of the most comprehensive meta-analysis which included 33 studies (1981 to 2007), Published by the World Health Organization in 2007 (Horta and Victoria, 2013). The authors concluded that breastfed individuals were less likely to be overweight or obese.

 

2.7 Screen Timing

Media contribution in the development of child and adolescent obesity has been researched well.Television viewing and media has also been used as a proxy for measuring sedentary behavior among children. Among children aged 2-3 years from the USA, 41% watched 3 or more hours of television daily and 27% of children aged 4-6 years used computer (Certain and Kahn, 2002). Several research reports presented positive association between screen time and body fatness in school children. (Larowe et al., 2010.).

 

In another study by Gortmaker et al., (1996) found that spending more than three hours/day watching television was a risk factor for obesity in children after adjusting for potential confounders. Other studies also observed that more television exposure is a significant risk factor for the development of obesity among pre-school children(Gupta and Kapoor, 2010). Children who have a television in their room are also more likely to be overweight than those without one.

 

Galcheva (2008) carried out a research on content analysis of food advertisements that were screened on television during 12 hours period and found that 96.8% of advertisements were for unhealthy foods and 57% of them were aimed specifically at children.

 

2.8 Duration of Sleep

Duration of sleep also reported to be associated with children’s weight. In a nationally representative sample of children aged 3-12 years, associations between sleep and BMI and the overweight status of children were estimated using longitudinal data. An extra hour of sleep lowered young Children’s (3-7.9 years of age) risk for being overweight from 36% to 30%, and lessened older children’s risk (8-12.9 years of age) from 34.% to 30% (Snell et al., 2007). Sleep hours are important modulator of neuroendocrine function and glucose metabolism.

 

Sleep loss has been shown to result in endocrine and metabolic alterations, including decreased insulin sensitivity, decreased glucose tolerance, increased evening concentrations of cortisol, decreased levels of leptin, increased levels of ghrelin, increased appetite and hunger. Recent epidemiological and laboratory research confirm earlier findings of association between sleep loss and the increased risk of obesity (Beccuti and Pannain, 2011).

 

2.9 Genetic and environmental interaction

There are extensive evidences that parental obesity is strongly associated with childhood obesity/overweight conferring the risk through both shared genes and environmental factors. Researchers have opined that both genetic and environmental factors may contribute to obesity. Obesity is the quantitative extreme of the genetic and environmental influences that operated across the distribution of BMI. Genetic mutations alone cannot result in an obesity epidemic in all the populations of the world, over few decadesand despite of obesogenic environment, not everyone is obese. However, it is possible that genes and environment do not act independently, but rather interact with each other so that the genetic influence if stronger in higher-risk environment.

 

3. Adiposity Rebound

 

The period of intrauterine, infancy and preschool have all been considered as possible critical periods during which the long term regulation of energy balance may be programmed for the development of obesity that persists into adulthood. However little is known about the mechanisms that operate at each of these critical periods to entrain adult obesity. Adiposity Rebound literally means a ‘bounce back’ in adiposity. In early years of human growth, adiposity increases rapidly from the time of birth up to age of 1 year and thereafter decreases and gets stabilized over next few years, before rising again.

 

The phenomenon was first reported by Rolland-Caches et al. (1984). Since then, many researchers have reported age at adiposity rebound in different Populations. The range of the age of adiposity rebound is widely believed to be between 5-7 years of age. However, individual BMI curves drawn for children may differ regarding their percentile range level and age at adiposity rebound. Thus, some children may show an early or late dip in their respective BMI curves compared to others.

 

Research have confirmed that early AR is associated with an increased BMI in adolescence (Prokopec and Bellisle, 1993) and in early childhood (Williams, 2005). Children, who have an early adiposity rebound, are more likely to become obese in later life, hence identifying the age at which adiposity rebound occurs is a potential tool to identify critical period for childhood obesity. Adiposity rebound time may be a critical period in the development of childhood obesity.

 

4. Co-morbidities of Childhood Obesity

 

The increase in childhood obesity is leading to increase in the health consequences associated with excess body weight among children. Overweight and obesity in childhood and adolescence have adverse consequences on premature mortality and physical morbidity in adulthood. Obese children have higher risk of cardiovascular diseases, metabolic syndrome high blood pressure, increased serum triglyceride levels, insulin resistant type 2 diabetes and increased cholesterol levels. It has been suggested that increasing prevalence of childhood obesity could result in shorter lifespan of children than their parents.

 

Childhood obesity is a dynamic process in which cognition, behavior and emotional regulation interact with each other mutually. Apart from physical discomfort due to increased weight obese children may also be affected in their psychological and physical wellbeing. Depression has been found to be associated with obesity among adolescence in which females are more prone as compare d to their male counterparts. The children found to have fanatical concern due to social stigma regarding body image, poor self-perception of their physical appearance and low self-esteem. Expectation of rejection further leads in the progression of depression. Researchers have reported reduced health-related quality of life among obese and overweight children in physical, social and emotional aspects (Schwimmer et al., 2003)

 

Summary

 

The prevalence of obesity among youngsters presents epidemic proportions with significant implications for cardiovascular and metabolic health at a very early age in life. There are increasing rates of metabolic syndrome in children and adolescents, which points towards the premature development of cardiovascular disease (CVD) and Diabetes Mellitus Type 2 (DM2) in the next generation of adults. Insulin resistance, determined by abdominal obesity appears to represent the link between the components of metabolic syndrome in this age range, and functions as a predictor for CVD and disturbances in carbohydrate metabolism. Therefore, the obesity measurement should be considered a screening instrument for the identification of youngsters with a cardio-metabolic disease phenotype.

 

As a consequence of this abdominal obesity-insulin resistance binomial, a systemic inflammatory state is produced, which functions as a trigger for the athero-genic process. The earlier the onset of overweight, the more prematurely this will manifest clinically. Therefore, in order to implement primary prevention of this endemic, investigation/prevention/treatment of risk factors, such as obesity, dyslipidemia, and disturbances in carbohydrate metabolism and its consequences must begin in the initial stages of life.

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    Suggested Readings

  • Brownell, K. D., & Horgen, K. B. (2004). Food fight: The inside story of the food industry, America’s obesity crisis, and what we can do about it. Chicago, IL: Contemporary books.
  • Kiess, W., Marcus, C., & Wabitsch, M. (2004). Obesity in childhood and adolescence. Basel: Karger.
  • Hu, F. (2008). Obesity epidemiology. Oxford University Press.
  • Heinberg, L. J., & Thompson, J. (2009). Obesity in youth: Causes, consequences, and cures. American Psychological Association.