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University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Address reprint requests to: Rita P. Raman, MD, MS, CNS, FACN, JD, Professor of Pediatrics, University of Oklahoma Health Sciences Center, P.O. Box 26901, Oklahoma City, OK 73190. E-mail: rita-raman{at}ouhsc.edu
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONREFERENCES |
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Key words: childhood obesity, obesity etiology, diabetes, cardiovascular risk, growth
Key teaching points:
• Childhood obesity is a risk factor for adult obesity.
• Prenatal influences impact the onset of obesity, diabetes and hypertension in later life.
• Being overweight in childhood is associated with medical and social consequences.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONREFERENCES |
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However, despite the high prevalence of obesity and the associated health risks, the etiology of obesity remains complex. Multiple factors, including prenatal and perinatal nutrition, energy utilization, genetic and environmental factors are all considered factors that contribute to the etiology of obesity. Epidemiological studies and animal experiments suggest that perinatal nutrition influences predisposition to adult obesity, cardiovascular disease, hypertension and type 2 diabetes [7,8]. Low birth weight has been associated with several chronic diseases in adults, including diabetes [9], hypertension [10] and obesity [11].
Definition of Obesity in Children
Efforts to understand the etiology and impact of obesity in childhood requires that we understand normal body weight and body composition in children and define obesity in an age and developmentally appropriate manner. The appropriate cut-off points for designation of obesity in childhood are critical. In adults the upper limit of body mass index (BMI) of 25 kg/m2 and a desired range of 20 to 23 kg/m2 appears to be supported by data [12]. The use of the body mass index provides a relatively height-independent measure of weight, which has been used to assess morbidity and mortality in population studies. Although the references for BMI in children have been established [13,14], these remain problematic especially in adolescence where substantial differences in onset of puberty and variations in body fat accumulations occur. The WHO growth evaluations and Tanner growth curves provide an alternate means for assessing individual growth in children in percentile or Z-scores [15]. The 85th and 90th percentiles, a Z score of 2.0 and a weight for height of 120% above median for age have all been used in defining obesity, as have measurements of skin-fold thickness [16].
Health Risks Related to Obesity
Overweight children are at risk for various chronic conditions in later life [17], and this risk may exist even independently of obesity in adult life. Obese children have adverse serum lipid levels, insulin resistance, elevated blood pressure [18], and calcifications in the aorta and coronary arteries [19]. In a recent report, evaluation of 813 overweight schoolchildren revealed that 58% of the overweight children already had at least one risk factor for cardiovascular disease and, using overweight as a screening tool, could identify at least 50% who had two or more risk factors [20]. Central fat distribution appears to influence lipid levels [21] and may be related to insulin resistance [22]. Weight reduction has a beneficial effect on cardiovascular risk factors, with possibly a greater effect in girls with abdominal adiposity [23].
Obesity is also associated with increased risk of non-insulin dependent diabetes mellitus in adults [24] and in obese children and adolescents [25]. Visceral fat appears to influence insulin secretion and insulin resistance [26]. Childhood obesity is also a significant predictor of adult blood pressure [27]. Hypertension may be associated with hyperinsulinemia [28]. There are significant long-term morbidities such as cerebral hemorrhage and heart disease associated with hypertension [29]. It is reassuring that intervention with diet and exercise has been shown to lower blood pressure [30].
Overweight children tend to be taller than non-overweight children and have enhanced bone age and earlier maturation [31]. Early maturation is associated with increased fatness in adulthood and with truncal obesity [32], with the children who demonstrated early maturation being already fatter at the onset of the early maturation.
Being overweight is associated with social and economic consequences. The number of years of education, family income and rates of marriage were all lower and the poverty rates higher in women, but not in men, who had been obese in late adolescence and early adulthood [33]. Eating disorders and weight preoccupation occurs more frequently in overweight women [34]. Obesity has also been associated with sleep apnea [35], pseudotumor cerebri [36] and polycystic ovary disease [37].
Excess body weight causes orthopedic disorders such as bowing of the tibia and femur. Also noted is the resulting overgrowth of the proximal tibial epiphysis or Blount’s disease [38]. Slipped femoral epiphysis also occurs more frequently with overweight [39].
Obesity is associated with significant morbidity and mortality, and often with multisystem involvement. With the increasing prevalence of obesity, it is reasonable to anticipate that these associated conditions will pose an even greater public health challenge.
Genetics Influences and Obesity
There is much evidence supporting the role of genetic influences on body morphology and the interplay of genetic and environmental influences in determining adiposity [40]. Quantitative genetic theory is used to estimate the heritability of obesity and, in twin studies, to estimate the variation in adiposity that is due to within-population genetic variation [41]. Obese parents have been reported to frequently have obese children, although normal weight parents may also sometimes have obese children. Body Mass Index values are more similar among family members than among unrelated persons. Studies conducted with comparisons of identical twins and fraternal twins, and in comparisons of identical twins reared apart, have led to the suggestion that 70% of the variation in BMI may be genetically based in etiology [42]. In adoption studies the heritability estimates are about 30%, and in family studies the estimates of heritability of BMI have been intermediate. In twin pairs, a substantial genetic contribution to fat mass was detected, with genes estimated to account for 75% to 80% of the phenotypic variation and for 62.5% of the total variation in percentage body fat [43].
Interaction of genotype with environmental influences has been studied under conditions of excess caloric consumption and of calorie deprivation. In these studies, in response to excess calorie consumption there was about threefold more variance in the response observed between the twin pairs than within the twin pairs for gain in body weight and fat, supporting the thesis that when excess energy is available, some individuals are more prone to gain weight and accumulate fat [44], and the differences appear to be influenced by the genetics of the individual. Similarly, in response to negative energy balance, induced by increasing energy expenditure through exercise while maintaining a constant daily energy and nutrient intake, the intra-pair similarity in response was greater than the inter-pair responses [45].
Some individuals are relatively insensitive to dietary intervention [46], whereas others are sensitive. The heterogeneity in response to dietary intervention is reported in children also [47]. Genetic epidemiology and molecular epidemiology studies suggest that genetic factors are involved in determining the susceptibility to gaining or losing fat in response to diet and in the development of comorbidities associated with obesity [48].
Perinatal and Developmental Influences and Obesity
There are three distinct growth phases recognized in childhood that are critical in development of obesity. The three growth phases are the fetal/infant phase which is primarily limited by nutrient availability to the mother, placenta or the infant, the childhood growth phase which is regulated by growth hormone and insulin-like growth factors and may also be limited by nutrient availability, and the pubertal or adolescent growth phase which is regulated primarily by the sex steroids [49]. Low birth weight may be associated with increased risk of obesity in later life [50]. Disproportionate fetal growth is also an important marker for future risk and may be a reflection of early programming [51].
The concept of sensitive periods in development at which factors may induce long lasting influences was initially considered an entraining process [52]. More recently the term programming has been used to characterize this process [53]. At critical stages during early life a limit is set for the upper limits of metabolic competence and provides a possible explanation for the obesity noted in young men after famine exposure in utero [54], an interaction of the impaired competence with an environment that challenges the upper limits of the metabolic capacity and increases the risk of disease development.
In humans, data from the Dutch famine studies has been used to understand the effects of nutritional deficiency in fetal life to subsequent development of obesity. In military inductees at age 19 years, the young men born to mothers who were exposed to the famine during pregnancy had a higher frequency of obesity as compared to controls [55]. Exposure to famine during early pregnancy results in a twofold increase in frequency of obesity in adulthood as compared with control group. The Dutch famine experience suggests that the first trimester of pregnancy represents a critical period of vulnerability to the subsequent development of obesity. Nutrient limitation during development is considered to modify the hypothalamus and the set point for regulation of energy.
Growth in fetal life and growth in infancy influence the subsequent fat accumulation in the abdomen [56]. Higher waist-hip ratio in later life is associated with decreased growth during fetal life and early infancy, and at any level of obesity there is higher waist-hip ratio in men who weighed less at birth. Thus, impaired growth in early life may predispose to increased accumulation of abdominal fatness.
The third trimester of pregnancy also presents a critical period. Infants born to diabetic mothers demonstrate both increase in body weight and body fat [57], and subsequently the prevalence of obesity in these children is increased at 15 to 19 years of age [58]. Higher incidence of insulin resistance syndrome is noted in Mexican-Americans as compared with non-Hispanic white Americans, and the birth weight and current BMI are related to the prevalence of insulin-resistance syndrome. There was noted a 25% incidence of insulin-resistance in those in the lowest third birth weight category and in the highest tertile for BMI as adults [59].
Significant anthropometric differences are noted in the newborn among the races (Table 1) and with gender. In black neonates, not only is body weight lower, but total fat mass is lower in black vs. white infants (Fig. 1), and fat, as a percent of body weight, was also significantly lower in black vs. white neonates (Fig. 2). Lean mass was not significantly different between the races [60]. Whether the lower birth weight may be related to the high incidence of obesity and hypertension noted in African-American adults has not been evaluated. At present the factors contributing to the differences and the relevance of the lower birth weight and lower fat mass in black neonates as compared to white infants is unclear.
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Childhood Influences and Obesity
In childhood, there is a phase of increased adiposity that occurs up to one year of age, followed by lesser adiposity until four to eight years of age, and then a subsequent phase of increase in adiposity lasting through childhood [64,65]. The body mass index declines until four to five years of age [66], and subsequently rebounds. This rebound phase may represent a time of vulnerability to development of obesity [67]. A critical period for development of obesity is in adolescence. A third of adult obesity in women has its onset in adolescence [68], and the central fat accumulation in adolescent males poses increased morbidity and mortality risks.
In a study examining preventive measures in non-obese children, the prevalence of obesity was shown to be lower when the parents were educated on diet [69]. In the treatment of obese children, inclusion of the parents in the program results in better weight change patterns in the children at five and ten years of age [70].
In the United States obesity is more prevalent in urban and densely populated areas and is more prevalent in winter and spring as compared to summer and fall seasons [71]. Parental obesity is also correlated with obesity in childhood [72]. The exact mechanisms by which these environmental factors effect prevalence of obesity have not been elucidated, although influences on levels of physical activity and on patterns of dietary intakes are possible mechanisms. Fewer than 40% of high school students are engaged in vigorous physical activities, with decline in participation through the high school years, and greater decline in activity noted for females than for adolescent males [73]. Increased television viewing and diminished physical activity may contribute to the increase in obesity noted in adolescence [74].
Conclusion
Childhood obesity presents a major health problem in the United States, and with it there is a significant risk for the persistence of obesity into adulthood and the occurrence of related morbidities. Knowledge of factors that predispose to the development of obesity and the factors that facilitate treatment is critical to mitigating the adverse outcomes associated with obesity.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONREFERENCES |
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