A Clinical Guide to Pediatric Weight Management and Obesity, 1st Edition


Obesity in the Context of Child and Adolescent Development

Obesity results from energy imbalance and is the final common pathway of deviations from the individual's optimal energy intake and expenditure. Children, in contrast to adults, have a requirement for growth that operates in addition to all the other modifiers of energy balance (Table 4.1). There may be critical periods of development in childhood that are especially sensitive to obesity-promoting factors and increase the likelihood of later obesity. The intrauterine environment has been found to have a much greater impact on later obesity and obesity-related comorbidities than previously thought. Feeding patterns and breastfeeding or formula feeding have a lasting influence on obesity risk and susceptibility. Rapid weight gain in early childhood, causing a crossing of growth percentiles (adiposity rebound), may predict obesity later in life. Emotional and psychological factors in the child or adolescent and parenting style and interaction can have an impact beyond childhood. Shared family environment and learned behavior can magnify a child's predisposition for obesity. Awareness of this complex interplay of influences affecting an obese child or adolescent can help in developing a strategy for regaining energy balance (Fig 4.1). Individual child, family, and community factors can affect energy intake and expenditure (Fig 4.2).

Intrauterine Influences and Obesity

Influences on energy regulation begin during intrauterine life, and the intrauterine environment is thought to have a significant effect on later obesity. Infants born to diabetic mothers tend to have a greater amount of adipose tissue and an increased


likelihood of developing obesity, impaired glucose tolerance, and type 2 diabetes during childhood (1). The effects of the intrauterine environment may persist over time. Children whose mothers were diabetic during pregnancy had greater rates of obesity at the ages of 5 to 9 years than expected in a normal population (2). Nine- to 14-year-old children of mothers with gestational diabetes had greater rates of obesity independent of physical activity, television watching, energy intake, breastfeeding duration, mother's body mass index (BMI), and other maternal and family variables than children born to mothers without diabetes during pregnancy (3).

TABLE 4.1. Factors affecting energy balance in children and adolescents

·   Genetic predisposition

·   Requirements for growth

·   Interactions with the nutritional environment

·   Family influences

·   Activity opportunities

·   Motor development

·   Emotional/psychological states


FIG. 4.1. Factors influencing energy balance in the child.


FIG. 4.2. Energy balance in the context of the child.

Exposure to excess of glucose and resulting hyperinsulinemia in utero may alter insulin receptor expression and insulin sensitivity to the extrauterine environment (4).


As the obesity epidemic worsens and the prevalence of diabetes in adult and young adult women increases, the risk of pregnancy complicated by diabetes will increase as well. This will mean that infants from these pregnancies will have greater risk for future obesity and diabetes, and a vicious cycle of increasing obesity and obesity-related comorbidity will be created. Unexpectedly, infants born small for gestational age have also been found to have an increased incidence of obesity in childhood (5), particularly if they are introduced into an energy-rich environment, which causes rapid growth. Intrauterine growth in a restrictive nutritional environment due to maternal undernutrition may lead to exposure to increased amounts of fatty acids, which can stimulate adipose tissue hyperplasia (6). External factors such as maternal hypertension and smoking can increase the risk for reduced intrauterine growth and become additive risk factors for obesity.

Infants born of a diabetic pregnancy, small for gestational age infants who have experienced rapid catch-up growth, and infants in families in which a parent or parents are obese are all at risk for childhood obesity.


In addition to optimizing nutrition and activity habits for all children and families, these at-risk infants and their families may need additional attention focused on energy balance in order to maintain a normal growth trajectory.

Early Influences on Obesity

The first year of life is a period of rapid growth and development. And early nutrition can influence later obesity. Breastfeeding has been shown to have a role in reducing later obesity.

Proposed mechanisms include effects on total caloric intake, insulin secretion, and modulation of fat deposition (7). Rate of weight gain between birth and 4 months of age as well as birth weight has been associated with an increased risk of obesity at age 7 years (8) and at age 20 years (9). Rates of weight gain vary greatly in the first 1 to 2 years of life, with growth in infants accelerating or decelerating across percentiles (10). Infants who showed growth accelerations in weight between birth and age 2 years have been found to be heavier and taller, with a greater percentage of body fat, at age 5 years. Children who were lighter, shorter, and thinner at birth (signs of intrauterine growth restraint) were more likely to experience “catch-up” weight gain (10). The mechanism for this catch-up growth is not known, although greater food intake has been observed (10). Leptin has been proposed as a possible mediator of this effect. Concentrations of cord blood leptin are positively correlated with birth weight but inversely related to weight gain in infancy; low concentrations at birth may induce catch-up growth by reducing inhibition of satiety (11). There is evidence that early adiposity rebound is a predictor of childhood, adolescent, and adult obesity. Adiposity rebound is the rise in BMI after reaching a


nadir in the child at 4 to 6 years of age (12). Another way of viewing adiposity rebound is as a descriptor of the phenomenon of “crossing growth percentiles.”

Parent factors and parent-child interactions can affect weight gain in a child. In a prospective study of children from birth to 9.5 years of age, five independent risk factors for childhood overweight were found. Parental overweight was the strongest factor, which was mediated by the child's temperament. The remaining risk factors were low parental concerns about the child's thinness, the child's persistent tantrums over food, and less sleep time in childhood (13).

Attention to detail is important because small energy imbalances in feeding and eating patterns, activity patterns, and parent-child interactions around food can result, over time, in significant weight gain. For example, if a child either consumes 150 kcal/day or reduces activity expenditure by 150 kcal/day, he or she will gain 15 lb over the course of 1 year (Fig. 4.3).

Emotional and Psychological Stress

Psychological and emotional states have often been linked to changes in weight. In one study, oppositional defiant disorder was found more commonly in children who were chronically obese during childhood and adolescence than in normal weight children or children who either developed obesity in childhood and then normalized their weight or developed obesity in adolescence. Among this same group of chronically obese children, boys had higher rates of depression than did children in other weight categories (14).

Depression has been found to predict obesity. In a study of adolescents in 7th to 12th grade, those who had a depressed mood were more likely to have follow-up obesity. In contrast, obesity at the start of the study did not predict follow-up depression (15).

Family Influence on Energy Balance

Nutritional Influences

Parents and families clearly influence the nutritional environment of their children. These influences can be subtle. In a study of 3- to 5-year-olds over a 6-year period, children's body fat increased linearly with parent disinhibition. Parental dietary restraint was also associated with the child's increase in body fat when coupled with disinhibition. The authors speculated that this association could be “mediated by direct parental role modeling of unhealthy eating behaviors, or through other indirect, and probably subconscious, behavioral consequences such as the suppression of the child's innate regulation of dietary intake” (16). In addition to directly affecting eating behavior and modeling, and healthy eating habits, parents play a major role in determining the child's and family's nutritional environment and negotiating lifestyle change.

Parental involvement is essential in obesity intervention.





FIG. 4.3. In this example, curve B represents an excess weight gain of 7.5 lb/year between the ages of 6 and 12 years. This represents a daily calorie excess of 75 kcal. Curve C illustrates the impact of early weight gain. Patient C weighed 55 lb at age 2 years. From age 2 to 6 years she gained 18 lb/year, representing an excess calorie imbalance of 16 lb/year, or 160 kcal/day. Curve A represents an excess weight gain over the 6 years between the ages of 6 and 12 years of 19 lb/year, or 190 kcal/day.



Children of parents who took charge of the lifestyle changes in the family lost more weight than did children in families in which the child was the person responsible for the change (17). This study also supported an authoritative parenting style, which is defined as firm and supportive parenting. Parents were encouraged to assume a leadership role in the environmental change, allowing for appropriate granting of a child's autonomy in modifying family and child nutrition and activity (18). Parenting skills that target gradual increases in activity and reduction in high-fat, high-calorie foods are considered essential in obesity treatment (19).

Activity Opportunities

Energy expenditure is the other modifiable component of the energy equation. Energy expenditure in childhood and adolescence varies with developmental stage; opportunities in the community for physical activity; and family, school, and peer influences.

Obesity itself can impact the ability to exercise.

On exercise testing, morbidly obese adolescents were found to have severe deconditioning (20) with exercise capability far below that of normal weight peers. In another study, obese adolescents performed significantly more poorly on walk-run and unloaded cycling testing, which was thought to be due to increased energy demands required to move excess body weight (21).

In a group of prepubertal children, similar findings showed that walking and running were energetically more costly for obese children, based on their excess weight. Calorie expenditure was comparable in the obese and normal weight groups when calculated by energy expenditure per body weight or fat-free mass (22). In a study of prepubertal children, total energy expenditure was correlated with body weight, fat-free mass, resting energy expenditure, and peak VO2 max during exercise. Reduced energy expenditure has been found in a group of infants prior to the development of obesity (23). However, other studies have not identified a link between total energy expenditure and subsequent obesity (24). Although there is no clear evidence that explains the link between total energy expenditure and the etiology of obesity, there is evidence that the quality and duration of physical activity can be a factor in maintaining energy balance (25).

Obese children and adolescents may face barriers to increasing activity.


Overweight girls report more body-related resource and social barriers to physical activity than normal weight girls, with overweight boys reporting higher body-related barriers than normal weight boys. Body-related barriers are related to self-consciousness about looks when engaging in physical activity. Resource issues


include lack of skills, equipment, knowledge, and interest as well as a place to do physical activity. Lack of partners for physical activities and teasing constitute social barriers to physical activity (26). Families need to be aware of these factors in order to facilitate an increase in their obese child's or adolescent's activity.


FIG. 4.4. Energy imbalance in the community.

Television, video games, and computers all contribute to increased sedentary activity.

A study showed that children who watched television at least 4 hours per day were less likely to engage in vigorous physical activity and had greater BMIs and skin fold measurements than those who watched television less than 2 hours per day (27). A randomized controlled study, which resulted in reduced television viewing in first-grade children, led to significant relative decreases in BMI (28). Maternal depression has been linked to increased television watching in children and was found to be additive to maternal obesity as a risk factor for this behavior (29). Parents clearly have a role in limiting television viewing and screen time and need to be aware that in so doing they are making a major contribution to their child's health.

Influence of the Community

Community factors can also affect energy balance in terms of available activity environments, maximizing physical activity and nutrition in schools, and attention to healthy eating environments and marketing strategies (Fig. 4.4).




  1. Dabelea D, Pettitt DJ. Intrauterine diabetic environment confers risks for type 2 diabetes mellitus and obesity in the offspring in addition to genetic susceptibility. J Pediatr Endocrinol Metab.2001;14: 1085–1091.
  2. Plagemann A, Harder T, Kohlhoff R, Rohde W, Dorner G. Overweight and obesity in infants of mothers with long-term insulin dependent diabetes or gestational diabetes. Int J Obes Relat Metab Disord.1997;21:451–456.
  3. Gillman MW, Rifas-Shiman S, Berkey CS, Field AE, Colditz GA. Maternal gestational diabetes, birth weight and adolescent obesity.Pediatrics.2003;111(3):e221–e226.
  4. Freinkel N. Of pregnancy and progeny (Banting lecture 1980). Diabetes.1980;29:1023–1035.
  5. Veening M, Van Weissenbruch M, Delemarre-Van de Wall H. Glucose tolerance, insulin sensitivity and insulin secretion in children born small for gestational age. J Clin Endocrinol Metab.2001; 879:4657–4661.
  6. Martin RJ, Hausman GJ, Hausman DB. Regulation of adipose cell development in utero. Proc Soc Exp Biol Med.1998;219:200–210.
  7. Owen CG, Martin RM, Whinecup PH Smith GD, Cook DG. Effect of infant feeding on the risk of obesity across the life course: a quantitative review of published evidence. Pediatrics.2005;115: 1367–1377.
  8. Stettler N, Zernel BS, Kumanyika S, Stallings VA. Infant weight gain and childhood overweight status in a multicenter cohort study.Pediatrics.2002;109:192–199.
  9. Stettler N, Kumanyika SK, Katz SH, Zernel BS, Stallings VA. Rapid weight gain during infancy and obesity in young adulthood in a cohort of African Americans. Am J Clin Nutr.2003;77:1374–1378.
  10. Ong KK, Ahmed ML, Emmett PM, Preece MA, Dunger DB. Association between postnatal catch-up growth and obesity in childhood: prospective cohort study. BMJ.2000;320:967–971.
  11. Ong KK, Ahmed ML, Sherriff A, Woods KA, Watts A, Golding J, Dunger DB. Cord blood leptin is associated with size at birth and predicts infancy weight gain in humans ALSPAC Study Team. Avon Longitudinal Study of Pregnancy and Childhood. J Clin Endocrinol Metab.1999;84:1145–1148.
  12. Whitaker RC, Pepe MS, Wright JA, Seidel KD, Dietz WH. Early adiposity rebound and the risk of adult obesity. Pediatrics.1998;101:E5.
  13. Agras WS, Hammer LD, McNicholas F, Kraemer HC. Risk factors for childhood overweight: a prospective study from birth to 9.5 years.J Pediatr.2004;15:20–25.
  14. Mustillo S, Worthman C, Erkanli A, Keeler G, Angold A, Costello EJ. Obesity and psychiatric disorder: developmental trajectories.Pediatrics.2003;111(4 Pt 1):851–859.
  15. Goodman E, Whitaker RC. A prospective study of the role of depression in the development and persistence of adolescent obesity.Pediatrics.2002;110:497–504.
  16. Hood MY, Moore LL, Sundarajan-Ramamurti A, Singer M, Cupplies LA, Ellison RC. Parental eating attitudes and the development of obesity in children. The Framingham Children's Study. Int J Obes Relat Metab Disord.2000;24:1319–1325.
  17. Golan M, Weizman A, Apter A, Fainaru M. Parents as exclusive agents of change in the treatment of childhood obesity. Am J Clin Nutr.1998;67:1130–1135.
  18. Golan M, Crow S. Targeting parents exclusively in the treatment of childhood obesity: long term results. Obes Res.2004;12:357–361.
  19. Barlow SE, Dietz WH. Obesity evaluation and treatment: Expert Committee recommendations. The Maternal and Child Health Bureau, Health Resources and Services Administration and the Department of Health and Human Services. Pediatrics.1998;102:E29.
  20. Gidding SS, Nehgme R, Heise C, Hassink S. Severe obesity associated with cardiovascular deconditioning, high prevalence of cardiovascular risk factors, diabetes mellitus/hyperinsulinemia, and respiratory compromise. J Pediatr.2004;144:766–769.
  21. Norman AC, Drinkard B, McDuffie JR, Ghorbani S, Yanoff LB, Yanovski, JA. Influence of excess adiposity on exercise fitness and performance in overweight children and adolescents. Pediatrics.2005;115:e690–e696.
  22. Maffeis C, Schutz Y, Schena F, Zaffanello M, Pinelli L. Energy expenditure during walking and running in obese and nonobese prepubertal children. J Pediatr.1993;123:193–199.
  23. Roberts SB, Savage J, Coward WA, Chew B, Lucas A. Energy expenditure and intake in infants born to lean and overweight mothers.N Engl J Med.1988;318:461–466.
  24. Stunkard AJ, Berkowitz RI, Stalling VA, Scholeller DA. Energy intake, not energy output, is a determinant of body size in infants. Am J Clin Nutr.1999;69:524–530.



  1. Goran ML, Sun M. Total energy expenditure and physical activity in prepubertal children; recent advances based on doubly labeled water method. Am J Clin Nutr.1998;68:944S–999S.
  2. Zabinkski M, Saelens BE, Stein RI, Hayden-Wade HA, Wilfley DE. Overweight children's barriers to and support for physical activity.Obes Res.2003;11:238–246.
  3. Anderson RE, Crespo CJ, Bartlett SJ, Cheskin LJ, Pratt M. Relationship of physical activity and television watching with body weight and level of fatness among children: results from the Third National Health and Nutrition Examination Survey. JAMA.1998;279:938–942.
  4. Robinson TN. Reducing children's television viewing to prevent obesity. A randomized controlled trial. JAMA.1999;282:1561–1567.
  5. Burdette HL, Whitaker RC, Kahn RS, Harvey-Berino J. Association of maternal obesity and depressive symptoms with television-viewing time in low-income preschool children. Arch Pediatr Adolesc Med.2003;157:894–899.