treatment of pediatric obesity

18. Pate RR, Dowda M, Ross JG. Associations between physical activity and physical fitness in American children. Am J Dis Child. 1990;144:1123–1129
19. Ross JG, Dotson CO, Gilbert GG, Katz SJ. What are kids doing in school physical education? J Phys Educ Recr Dance. 1985;56:31–34
20. Luepker RV, Perry CL, McKinlay SM, et al. Outcomes of a field trial to improve children’s dietary patterns and physical activity. The child and adolescent trial for cardiovascular health. JAMA. 1996;275:768–776
21. Ross JG, Dotson CO, Gilbert GG, Katz SJ. After physical education— physical activity outside of school physical education programs. J Phys Educ Recr Dance. 1985;56:35–39
22. Taras HF, Sallis JF, Patterson TL, Nader PR, Nelson JA. Television’s influence on children’s diet and physical activity. Dev Behav Pediatr. 1989;10:176–180
23. Sallis JF, Nader PR, Broyles SL, et al. Correlates of physical activity at home in Mexican-American and Anglo-American preschool children. Health Psychol. 1993;12:390–398
24. Desmond SM, Price JH, Lock RS, Smith D, Stewart PW. Urban black and white adolescents’ physical fitness status and perceptions of exercise. J School Health. 1990;60:220–226
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26. Dietz WH, Gortmaker SL. Do we fatten our children at the television set? Obesity and television viewing in children and adolescents. Pedi- atrics. 1985;75:807–812
27. Klesges RC, Shelton ML, Klesges LM. Effects of television on metabolic rate: potential implications for childhood obesity. Pediatrics. 1993;91: 281–286
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29. Klesges RC, Eck LH, Hanson CL, Haddock CK, Klesges LM. Effects of obesity, social interactions, and physical environment on physical activity in preschoolers. Health Psychol. 1990;9:435–449
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Theory. Englewood Cliffs, NJ: Prentice-Hall; 1986 35. Janz NK, Becker MH. The health belief model: a decade later. Health
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ior. Englewood Cliffs, NJ: Prentice-Hall; 1980 37. Reynolds KD, Killen JD, Bryson SW, et al. Psychosocial predictors of
physical activity in adolescents. Prev Med. 1990;19:541–551 38. Tappe MK, Duda JL, Ehrnwald PM. Perceived barriers to exercise
among adolescents. J School Health. 1989;59:153–155 39. Theodorakis Y, Doganis G, Bagiatis K, Gouthas M. Preliminary study of
the ability of reasoned action model in predicting exercise behavior of young children. Percept Motor Skills. 1991;72:51–58
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Treatment of Pediatric Obesity
Leonard H. Epstein, PhD; Michelle D. Myers, MA; Hollie A. Raynor, MS, RD; and Brian E. Saelens, MA
ABSTRACT. The primary goal of childhood obesity interventions is regulation of body weight and fat with adequate nutrition for growth and development. Ideally, these interventions are associated with positive changes in the physiologic and psychological sequelae of obesity. To contribute to long-term weight maintenance, interventions should modify eating and exercise behaviors such that new, healthier behaviors develop and replace unhealthy behaviors, thereby allowing healthier behaviors to persist throughout development and into adult- hood. This overview of pediatric obesity treatment, using predominantly randomized, controlled studies, high- lights important contributions and developments in pri- marily dietary, activity, and behavior change interventions, and identifies characteristics of successful treatment and maintenance interventions. Potential pos-
itive (eg, reduction in blood pressure, serum lipids, and insulin resistance) and negative (eg, development of disordered eating patterns) side effects of treatment also are described. Recommendations for improving implementation of childhood obesity treatments, including application of behavioral choice theory, improving knowledge of response extinction and recovery in regards to behavior relapse, individualization of treatment, and integration of basic science with clinical outcome research, are discussed. Pediatrics 1998;101:554–570; pediatric obesity, treatment, weight maintenance.
ABBREVIATIONS. BMI, body mass index; PSMF, protein-sparing modified fast; HDL, high-density lipoprotein.
There has been a lot of interest in developing effective treatments for obesity, with the over- whelming majority of this research focused on
treating adults. A salient characteristic of the adult obesity treatment is that although obese adults can
From the Department of Psychology, State University of New York at Buffalo, Buffalo, New York. Received for publication Oct 24, 1997; accepted Nov 6, 1997. PEDIATRICS (ISSN 0031 4005). Copyright © 1998 by the American Acad- emy of Pediatrics.
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lose significant amounts of weight, maintenance of weight loss has proven to be a persistent problem.1–3
There are several more hopeful signs in the treatment of pediatric obesity by using dietary and activity changes. For example, two research groups have shown successful maintenance of treatment effects 5 years4 and 10 years5,6 after initiation of treatment. In direct comparisons of children and adults in families provided similar family-based interventions, preadolescent children responded with greater relative weight loss and better maintenance of weight loss, although there was still considerable relapse.7 Al- most one third of the children treated were nonobese after 10 years.7 This is encouraging, but it indicates that a significant amount of work is required to improve long-term maintenance of pediatric obesity treatment.
There are behavioral and biological reasons to be optimistic about treating pediatric obesity. For example, it may be easier to mobilize support through families for obese children than for obese adults; obese children also generally have not had the unhealthy eating or activity patterns as long as obese adults. In addition, treatment of pediatric obesity can take advantage of growth and increases in lean body mass as well as weight change.5,8 Furthermore, instead of shrinking adipose cells, treatment at an early age prevents the development of excess adipose cells.
Despite these potential advantages, many pediatric studies show a decrement in treatment effects over time. The goal of this report is to provide an overview of the treatment and prevention of pediatric obesity, to highlight important contributions and developments in treatment, and to identify characteristics of successful treatment. First, treatment of pediatric obesity is reviewed. Next, the positive and negative side effects of treatment are presented. Third, ideas for improving implementation of pediatric obesity treatment, including new directions and areas for future research, are discussed. This report concludes with a brief summary.
METHODS The goals for treating childhood obesity are regulating body
weight through adequate nutrition for growth and development, thereby preventing interruption of linear growth, minimizing loss of lean body mass, and preventing endocrine disturbances.9 In addition, ideal treatments should be associated with positive changes in physiologic and psychological sequelae of obesity. Treatments should modify eating and exercise behaviors along with the factors that regulate these behaviors, so that the new, healthier behaviors persist throughout development.
This review is organized according to major components of treating pediatric obesity, including dietary, activity, and behavior change components. In addition, more aggressive approaches, including pharmacologic and surgical interventions, are reviewed. The quality of the study design was considered, with the focus on randomized, controlled studies. In some areas, such as surgery and drug studies, there are limited randomized controlled studies, and we present uncontrolled research in these areas. When studies did not provide sufficient detail to know how the groups were developed (ie, whether subjects were allowed to self-select them- selves to groups or whether they could have been placed in groups on the basis of factors that could bias interpretation of treatment and control differences), we erred on the conservative side and considered them not to be randomized studies. (To give
sufficient attention to the discussion of new ideas, many details of intervention and supporting studies are not discussed.)
The details of the randomized studies that were reviewed are presented in Tables 1 and 2 for clinical studies and in Tables 3 and 4 for school-based studies. These tables include subject age, group assignment, sample size, sex distribution, dietary components, exercise component, and results. There were several dependent measures used across studies; the most common were changes in percent of overweight, body mass index (BMI), body weight, and percent of body fat. Where available, we have provided the baseline values, end of treatment changes, and end of follow-up changes. To provide a common definition of when treatment ends and follow-up begins, we considered treatment to be continuing as long as subjects were seen at least once per month. The most relevant information is significance in the rate of change among groups over time, but if this information was not available, within- group differences are presented.
Although this review is divided into contributions of diet, activity, and behavior change components, treatment efficacy is derived from integration of the components of treatment. For example, although most treatments include a dietary component, it is generally recognized that nutrition intervention is ineffective as a solitary treatment for pediatric obesity.10 Extracting the contribution of treatment components is complicated further by vari- ations in multiple components of treatment across studies. Differ- ent caloric ranges for the diet are in the context of different types of exercise programs and different methods to enhance behavior change.
RESULTS
Dietary Components Diet therapy for obesity is founded on the hypoth-
esis that obese individuals consume too much energy relative to energy expenditure or they consume an imbalance of macronutrients. Therefore, the general goals of most dietary interventions involve reducing and stabilizing caloric intake, reducing fat intake, and restructuring eating habits to follow more closely current dietary recommendations, resulting in increased nutrient density.
If positive energy balance is attributable to excess intake, then the degree of reduction in caloric intake should relate to treatment success. Amador et al11
demonstrated this by randomizing children to a restricted diet (0.17 MJ/kg of expected body weight for height) versus a less restricted diet (0.25 MJ/kg of expected body weight for height) and found significantly better results after 1 year for the diet with the lower caloric intake. There is very little work on diet composition beyond calories. When obese children of elementary-school age were given 15 g of fiber supplementation combined with a reduced-energy diet for 4 weeks, they demonstrated no significant increases in weight loss or significant decreases in energy intake compared with the results from 4 weeks of the reduced-energy diet alone.12 The caloric level of the diet influences weight loss. There has been no research on the contribution of fat content to treatment success.
There are a number of general approaches studied to reduce caloric intake and teach better eating habits. One approach is to provide individualized dietary interventions. In a controlled study on exercise, no weight loss was observed for preadolescents who were provided with individualized dietary recommendations for 16 weeks without exercise.13 Another approach is the diabetic exchange system, with a caloric level calculated to produce 1 lb of weight loss
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TABLE 1. Characteristics of Child and Adolescent Obesity Treatment Studies on Clinical Samples
Source Age (y)
Between-group Variable N % Girls Diet Exercise
Amador et al11 10–13 R 1. Restrictive diet 47 47.9 Restricted to 30% of Exercise information (1,2) 2. Nonrestrictive diet 47 energy requirement
(1), nutrition information (1,2)
Aragona et al50 5–11 R 1. Response cost 1 reinforcement
5 100 Nutrition information (1,2)
Daily exercise instructions and program for parents
2. Response cost 3 (1,2) 3. Control 5
Bacon and 5–17 R 1. Fenfluramine 20 ;71.4 1000–1200 kcal (1,2) None Lowrey41 2. Placebo
Within-subject design, order randomized
Becque et al14 12–13 R 1. Exercise 11 58.3 ADA exchange for 50 min, 33/wk supervised 2. No exercise 11 21–2 lb/wk (1,2) aerobic activity @ 60%– 3. Control 14 80% maximal heart rate
(1) Brownell et al56 12–16 RS 1. Mother and child seen
separately 14 78.6 Nutrition information
(1,2,3) Exercise information (1,2,3)
15
3. Child seen alone 13 Coates et al51 13–17 RS 1. Daily contact, reinforced for
weight 8 68.4 Caloric goals estimated
for 21–2 lb/wk Minimal exercise
information (1,2,3,4) 2. Weekly contact, reinforced
for weight 8 (1,2,3,4)
11
11
Coates et al55 13–17 RS 1. Mother and child seen separately
31 Total
Exercise information (1,2)
2. Child seen alone Duffy and 7–13 R 1. Cognitive treatment 14 ;78.6 Traffic-light diet (1,2) Lifestyle, aerobic, and
Spence30 2. Progressive relaxation 13 calisthenic activity (1,2) Epstein et al20 6–12 RS 1. Behavior modification 14 ;38.5 Traffic-light diet 900– Exercise information (1,2)
2. Nutrition education Total 1200 or 1500 kcal (1,2) Epstein et al6,29 6–12 RS 1. Mother and child targeted 76 69.6 Traffic-light diet limit Exercise information (1,2,3)
2. Child targeted Total 1200–1500 kcal (1,2,3) 3. Nonspecific target
Epstein et al19 8–12 R 1. Aerobic activity 1 diet 51 ;78.4 Traffic-light diet 900– Aerobic (1,3) or lifestyle 2. Lifestyle activity 1 diet Total 1200 or 1500 kcal (1,2) (2,4) activity; isocaloric 3. Aerobic activity alone across groups 4. Lifestyle activity alone
Epstein et al6,28 8–12 R 1. Exercise 18 NR Traffic-light diet (1,2) Lifestyle activity (200–400 2. No exercise 18 kcal/day) (1) 3. Control 17
Epstein et al6,26 8–12 R 1. Programmed aerobic activity
41 Total
Aerobic (1), lifestyle (2), or calisthenic (3) activity;
2. Lifestyle activity isocaloric across groups 3. Calisthenics
Epstein et al25 8–12 RS 1. Exercise 23 100 Traffic-light diet 900– Supervised exercise, 3-mile 2. No exercise Total 1200 kcal (1,2) walk 33/wk (1)
Epstein et al27 5–8 R 1. Behavior modification 8 100 Traffic-light diet 900– Lifestyle activity (1,2) 2. Education 11 1000 or 1200 kcal (1,2)
Epstein et al6,52 8–12 R, IV 1. Parent overweight 41 NR 1200 kcal (1,2) Lifestyle activity (1,2) 2. Parent normal weight Total
Epstein et al49 8–12 R 1. Mastery criteria 44 ;74.4 Traffic-light diet from Lifestyle activity (1,2) 2. No mastery criteria (yoked) Total 900–1800 to 900–1200
kcal (1,2) Epstein et al21 8–12 R 1. Reinforced for 1activity 61 73.0 Traffic-light diet 1000– 1Activity (1), 2sedentary
2. Reinforced for 2sedentary behavior
Total 1200 kcal (1,2,3) (2), or both 1activity and 2sedentary (3)
3. Reinforced for both 1activity 1 2sedentary
Figueroa-Colon 7–17 RS? 1. PSMF fast diet 10 57.9 10 Wk of 50% protein, 20 Min supervised aerobic et al33 2. Hypocaloric balanced diet 9 600–800 kcal (1); 10
wk of hypocaloric balanced diet (800– 1000 kcal) (2)
activity (10 min @ 70% maximal heart rate); lifestyle activity (Cooper’s aerobic point system) (1,2)
Flodmark et al24 10–11 R 1. Family therapy 44 52.3 Nutrition information Exercise information (1,2) 2. No family therapy Total 1500–1700 kcal, ,30%
fat kcal (1,2)
per week.14–16 In these studies, diet plus exercise programs were associated with better physiologic outcomes than were the no-treatment control groups.
A third dietary approach is the traffic-light diet, which is used for preschool17 and preadolescent13,18–30
children. The traffic-light diet is a structured eating plan (900 to 1300 kcal) used to guide participants’ eating patterns to meet age recommendations of the basic four food groups, and now the food pyramid, thereby increasing the nutrient density of the diet. The traffic-light diet groups foods into categories: green foods (go) may be consumed in unlimited quantities; yellow foods (caution) have average nutritional value for the foods within their food group; and red foods (stop) provide less nutrient density per calorie because of high fat or simple carbohydrate content.
Most interventions using the traffic-light diet as part of a comprehensive treatment have produced a significant decrease in obesity18–21,23,25–30 in preadolescent children. The traffic-light diet is associated with an im-
provement in nutrient density for protein, calcium, iron, vitamin A, thiamine, and riboflavin and a decrease in nutrient density for fat in preadolescents.18
Significant changes in eating patterns have been reported when comprehensive obesity treatment has been combined with the traffic-light diet.29,30 Reduc- tions in “red foods” have been observed after treatment,23,29,30 with significant associations between changes in intake of “red food” and weight loss29 or decrease in percent of overweight.30 Finally, obese children of elementary-school age who were treated with the traffic-light diet also showed a greater decrease in rated palatability for high-fat/low-sugar, low-fat/high- sugar, and high-fat/high-sugar foods and a greater increase in rated palatability for low-fat/low-sugar foods than did comparable lean children who were not treated.31 In addition to short-term effects, long-term obesity changes extending from 5 to 10 years after initiation of treatment have been observed with the traffic-light diet in combination with behavioral, exercise, and familial components.5–7,32
TABLE 1. Continued
Source Age (y)
Between-group Variable N % Girls Diet Exercise
Graves et al23 6–12 RS 1. Parent problem-solving 40 NR Traffic-light diet (1,2,3) Physical activity (1,2,3) 2. No parent problem-solving Total 3. Education only
Gropper and 6–12 R 1. Fiber supplements (15 g) 8 62.5 ADA exchange, 500 kcal None Acosta12 2. Placebo less than baseline
Within-subject design, order randomized
intake (1,2)
Hills and Parker13 Prpb R 1. Exercise 10 NR Nutrition information 60 Min, 13/wk supervised 2. No exercise 10 (1,2) aerobics; 20 min, 3–43/
wk home aerobics (1) Israel et al48 8–12 R 1. Parent training 12 69.7 Nutrition information Exercise information (1,2)
2. No parent training 12 (1,2) 3. Control 9
Israel et al53 8–13 RB 1. Enhanced child self- regulation
16 NR Nutrition information (1,2)
18
16 ;77.3 Nutrition information (1,2)
2. Child seen alone 15 Mellin et al79 12–18 R 1. Treatment 37 78.8 Nutrition information (1) Supervised exercise (1)
2. Control 29 Mendonca and
Brehm58 8–15 R 1. Perception of treatment
choice 18
2. No perception of treatment choice
Rocchini et al15 10–17 R 1. Exercise 25 ;52.8 Calorie exchange 40 Min, 33/wk supervised 2. No exercise 26 program for 21 lb/ aerobic activity @ 70–75% 3. Control 22 wk (1,2) maximal heart rate (1)
Senediak and Spence22
12 ;33.3 Traffic-light diet, food exchange (1,2)
30 Min, 33/wk aerobic activity, lifestyle activity
2. Gradual schedule behavior modification
12 (1,2)
3. Attention control 11 4. Control 10
Wadden et al57 12–16 RS 1. Mother and child seen separately
14 100 1000–1500 kcal, low-fat foods (1,2,3)
Lifestyle activity (1,2,3)
14
3. Child seen alone 19 Wheeler and 2–10 R 1. Behavior modification 14 52.5 Not described (1) Not described (1)
Hess43 2. Control 14
N indicates number of subjects entering treatment (per group if available); R, subjects were randomly assigned; RS, subjects were stratified on key variables and then randomly assigned; NR, not reported, IV, individual variable as between-group variable; ?, unsure of degree of randomization; Prpb, prepubertal; RB, subjects were randomized to groups balanced on key variables.
TABLE 2. Outcomes of Child Obesity Treatment Studies on Clinical Samples
Source OW, %*
BF, %†
Results
Amador et al11 .97 0–6 0–12 BW,Rx,FU:1.2 %ile 1 218.8a 1 214.9a (analyzed by gender)
2 29.6b 2 24.8b
Aragona et al50 0–3 0–11 OW,BMI,Rx:1,2.3 (29.6) (21.7) 105.6 1 (215.7) (22.4) 211.3a 1 (211.8) (21.2) 20.7 OW,BMI,FU:15253 (34.1) (22.8) 104.6 2 (214.2) (22.2) 29.6a 2 (27.1) (20.3) 17.3 (41.7) (23.1) 99.3 3 (21.8) (20.2) 10.9b 3 (22.5) (10.6) 15.5
Bacon and .97 0–2 lb/mo None BW,Rx:152 Lowrey41 %ile 1 24.3
2 21.9 Becque et al14 0–5 None BW,BF,Rx:15253
149.4 38.3 1 23.5 23.0 169.8 44.0 2 20.9 23.5 151.1 39.8 3 17.0 10.7
Brownell et al56 0–4 0–12 OW,Rx,FU:1.2,3 59.9 45.5 183.9 1 217.1a 24.7a 218.5a 1 220.5a 24.6a 216.9a BMI,BW,Rx:1.3 50.4 42.4 177.1 2 27.0b 23.0 211.7 2 25.5b 20.1b 16.4b BMI,BW,FU:1.2,3 57.4 42.0 178.4 3 26.8b 22.0b 27.3b 3 26.0b 20.1b 17.0b
Coates et al51 0–4 0–10 OW,Rx,FU:1.2,3,4 37.3 1 212.0‡ 1 28.0‡ 39.4 2 25.2 2 110.4 37.3 3 26.2 3 22.4 46.1 4 25.0 4 15.8
Coates et al55 0–5 0–18 OW,Rx,FU:152 32.5 1 28.6 1 28.4‡ 30.9 2 25.1 2 28.2‡
Duffy and 0–2 0–8 OW,Rx,FU:152 Spence30 45.5 125.7 1 27.8‡ 23.1 1 28.9‡ 17.1
51.5 122.2 2 29.1‡ 23.1 2 29.2‡ 13.6 Epstein et al20 0–5 None OW,Rx:1.2
68.4 129.1 1 217.5a 28.6 60.9 135.4 2 26.4b 23.4
Epstein et al6,29 0–8 0–120 OW,Rx:15253 39.0 24.1 106.4 1 216.0‡ 1 215.3a OW,FU:1.3 41.2 25.0 117.9 2 217.0‡ 2 23.0 45.4 25.1 119.8 3 219.0‡ 3 17.6b
Epstein et al19 0–6 0–17 OW,BMI,Rx:1525354 37.2 24.1 110.1 1 210.3‡ 21.3‡ 1 10.1a 11.2a OW,BMI,FU:2,4.1,3 40.5 24.9 116.6 2 219.0‡ 23.0‡ 2 213.8b 21.5b
38.7 25.3 126.4 3 213.9‡ 22.1‡ 3 29.7a 20.7a
34.0 24.0 115.1 4 213.2‡ 22.0‡ 4 211.2b 21.0b
Epstein et al6,28 0–6 0–120 OW,Rx:1,2.3 44.0 1 216.0a 1 28.4 OW,FU:152 44.0 2 221.0a 2 210.0 44.0 3 13.0b
Epstein et al6,26 0–12 0–120 OW,BW,Rx:15253 47.8 123.9 1 216.3‡ 12.4 1 210.9a OW,FU:1,2.3 48.3 124.0 2 216.1‡ 22.3 2 219.7a
48.0 123.9 3 217.5‡ 22.3 3 112.2b
Epstein et al25 0–12 None OW,Rx:152 48.0 118.3 1 225.4‡ 28.5‡ BW,Rx:1.2 48.1 118.7 2 218.7‡ 23.0
Epstein et al27 41.9 22.8 0–12 None OW,BMI,Rx:1.2 39.2 22.7 1 226.3a 23.7a
2 211.2b 21.3b
Epstein et al6,52 20–80 0–12 0–120 OW,Rx:2.1 1 27.7a 1 13.1 OW,FU:152 2 216.3b 2 211.1
Epstein et al49 0–12 0–24 OW,Rx:1.2 60.6 127.4 1 226.5a 1 215.4 OW,FU:152 58.8 121.5 2 216.7b 2 210.6
Epstein et al21 51.8 33.2 0–4 0–12 OW,Rx:2.1 Total Total 1 213.0a 23.5 1 29.0a 21.2a OW,FU:2.1,3
2 220.0b 25.0 2 218.0b 24.8b BF,Rx:15253 3 217.0 24.5 3 210.0a 22.2 BF,FU:2.1
Figueroa-Colon 0–15 None OW,Rx:1.2 et al33 82.2 33.1 166.1 1 223.3‡ 22.5 12.9 BMI,BW,RX:152
78.3 31.2 148.3 2 220.3 22.7 22.0 Flodmark 0–14 0–26 BMI,Rx:1.2
et al24 24.7 1 10.3a 1 11.1 BMI,FU:152 25.5 2 10.6b 2 11.6
The protein-sparing modified fast (PSMF),33 a more restrictive diet, has been used to treat severe pediatric obesity. The PSMF usually consists of 600 to 900 kcal and 1.5 to 2.5 g of high-biological-quality protein per kilogram of ideal body weight per day, usually provided as lean meat; vitamin and mineral supplementation and consumption of at least 1.5 L of water per day is encouraged. The PSMF is designed to maximize weight loss, preserve mineral balance, and achieve positive nitrogen balance, thereby con- serving lean muscle mass in growing individuals. PSMF diets are usually of short duration (4 to 12 weeks), conducted under close medical supervision, and not commonly used with prepubertal children. Figueroa-Colon and coworkers33 reported an 11.2-kg weight loss in 10 weeks, but at 15 months the decrease in percent of overweight was similar to the
decrease in percent of overweight achieved by a less restrictive dietary prescription.33
These studies show that there are several different approaches to improving food choice and reducing caloric intake in obese children. There are no com- parative studies in which other aspects of treatment are held constant as the type of dietary recommendations are varied. The effect of diet depends on the context in which it is presented in treatment; dietary recommendations are complemented by strong components of behavior change to enhance weight control.20 Very little is known about specific components of dietary recommendations, such as macronutrient content of the diet. Likewise, no studies have con- centrated on the pattern of eating in obese children or on the distribution of food in meals and snacks. The degree to which the diet is rigid or flexible
TABLE 2. Continued
BF, %†
Results
Graves et al23 0–5 0–8 OW,BW, Rx,FU:1.2,3 53.0 128.9 1 224.3a 211.2a 1 224.5a 29.1a
56.3 128.9 2 213.1b 23.9b 2 210.2b 20.5b
51.8 115.8 3 210.3b 20.5b 3 29.5b 12.5b
Gropper and $20 0–2 lb/mo None BW,Rx:152 Acosta12 1
2 20.7 20.1
Hills and Parker13
113.5 1 212.1 110.4 2 15.7
Israel et al48 0–2 0–12 OW,Rx:2.1.3 45.9 114.1 1 27.2a 24.8a 1 210.2a 111.5 OW,FU:1.2 53.1 126.1 2 211.6b 25.4a 2 21.3b 111.6 BW,Rx:1,2.3 56.0 128.0 3 20.9c 12.6b BW,FU:152
Israel et al53 0–7 0–36 OW,Rx,FU:152 (time 48.1 1 215.6 1 24.8 effect significant, 45.9 2 212.5 2 16.4 contrasts not reported)
Kirschenbaum 0–2 0–14 OW,Rx,FU:152 et al54 58.1 122.8 1 26.3‡ 1 27.6‡
39.0 115.1 2 27.1‡ 2 26.2‡ Mellin et al79 0–3 0–15 OW,Rx,FU:1.2
36.5 174.2 1 25.9‡ 26.8 1 29.9‡ 28.5 29.5 169.3 2 20.3 10.3 2 20.1 12.8
Mendonca and 0–3 0–9 BW,Rx:1.2 Brehm58 47.4 127.7 1 27.6a 1 21.0 BW,FU:152
49.1 135.7 2 24.3b 2 15.8 Rocchini et al15 0–5 None BW,BF,Rx:1,2.3
158.4 41.0 1 25.3a 26.0a
160.6 43.0 2 25.5a 24.0a
160.6 41.0 3 18.8b 11.0b
Senediak and Varied 0–7 OW,BW,Rx:2.1.3,4 Spence22 34.6 114.2 1 0–1 25.3a 23.7a 1 213.0a 22.4a OW,BW,FU:1,2.3
34.9 110.1 2 0–4 213.6b 27.9b 2 219.2a 26.1a
41.7 105.2 3 0–1 21.4c 20.7c 3 25.9b 10.6b
37.6 103.6 4 0–1 12.3c 11.7c
Wadden et al57 0–10 None BMI,BW,Rx:15253 36.7 223.1 40.4 1 17.7 32.8 191.6 39.5 2 13.7 35.1 211.0 41.6 3 16.6
Wheeler and 0–7 None OW,Rx:1.2 Hess43 40.4 1 24.1a
38.9 2 16.3b
* Baseline. † Change. ‡ Value significantly different from baseline value (not reported when between-group differences are reported). OW indicates overweight; BW, body weight; BF, body fat; Rx, treatment period; FU, follow-up period; values with different superscript letters differ significantly from each other. Treatment period was designated as the period when meetings occurred at least monthly (except for the study by Flodmark, when meetings were more sporadic). Values in parentheses were derived for this table from data provided by the authors.
should be studied. If the goal is for children to develop a taste for fruit, should candy be removed from their diet, eaten occasionally, or eaten whenever re- quested? There is very little research studying the effects of dietary change on food preference,34 which may be very important if long-term compliance is desired. Finally, research on food choice and preference has not kept up with the rapid changes in the foods available to children, and the influence of sugar and fat replacements should be studied with regard to the health of the children as well as their use in facilitating long-term dietary change.
Exercise Exercise treatments are designed to increase en-
ergy expenditure to produce or increase negative energy balance. In most obesity treatments, the major impact on energy balance occurs through decreasing
caloric intake,35 but increasing the caloric expenditure of obese children may accelerate weight loss and potentiate maintenance of weight changes.36 How- ever, exercise should be combined with dietary intervention. For example, extra physical activity had no significant effects on weight in the absence of dietary intervention.37
Several studies have included diet and aerobic exercise. Hills and Parker13 found differences in skin- fold changes but not in weight in preadolescent children provided weekly supervised exercise sessions plus a three- or four-time per week home aerobic activity program versus diet alone. Rocchini and col- leagues14,15 explored the benefits of aerobic activity designed to maintain heart rate between 60% and 80% of maximal exercise heart rate for 40 to 60 min- utes in 20-week interventions. In both studies, both diet and diet plus exercise were equal for weight and
TABLE 3. Characteristics of Child Obesity Treatment Studies on School Samples
Source Age (y) Group Assignment
Between- group variable
N % Girls Diet Exercise
Blomquist 8–9 EO 1. Exercise 22 0.0 None reported Supervised intense et al37 2. Control 21 physical activity, 45
min, 23/wk (1) Botvin et al44 7th, 8th Rsch 1. Treatment 119 NR Nutrition information Supervised aerobic
grades 2. Control Total (1) activity (1) Christakis 13–14 RSclass 1. Treatment 55 0.0 Nutrition information Extra exercises 1
et al46 2. Control 35 (1) basketball league (1) Figueroa-Colon 9–13 Rsch 1. Treatment 12 42.1 10 Wk of 50% protein 45 Min, 53/wk (25 min
et al85 2. Control 7 600–800 kcal then 16 wk of hypocaloric balanced diet (1)
@ 75% maximal heart rate) (1)
Lansky and 12–15 Rclass 1. Behavior 36 54.9 Food exchange, 1200 Supervised aerobic Brownell47 modification kcal (1), nutrition activity (1,2)
2. Education 35 information (2) Lansky and ;13.1 RS 1. Treatment 30 54.5 Food exchange (1) Supervised aerobic
Vance45 (mean) 2. Control 25 activity (1)
N indicates number of subjects entering treatment (per group if available); EO, subjects ranked according to overweight, even/odd assignment to group; Rsch, schools were randomly assigned; NR, not reported; RSclass, classes were stratified on key variables and then randomly assigned; Rclass, classes within schools were randomly assigned; RS, subjects were stratified on key variables and then randomly assigned.
TABLE 4. Outcomes of Child Obesity Treatment Studies on School Samples
Source OW, %* BMI* BW, lb* Rx, mo OW, %† BMI† BW, lb† Results
Blomquist et al37 0–4 BW,Rx:152 91.1 1 11.8 93.9 2 11.8
Botvin et al44 $20 0–3 1
NR NR NR OW,BW:1.2 (x2 analyses)
2 Christakis et al46 0–18 BW,Rx:1.2
41.1 160.9 1 210.9 15.8a OW,Rx:NR 39.6 158.4 2 22.3 113.5b
Figueroa-Colon et al85 0–6 OW,BMI,BW,Rx:1.2 71.8 30.9 153.1 1 224.3‡ 23.8‡ 212.3‡ 64.0 28.8 136.8 2 20.3 10.2 16.2‡
Lansky and Brownell47 57.4 0–4 OW,BW,Rx:152 Total 1 23.0 14.6
2 22.1 14.2 Lansky and Vance45 0–3 OW,BW,Rx:1.2
43.9 152.1 1 25.7a 11.3a
47.5 157.8 2 12.4b 17.3b
* Baseline. † Change. ‡ Value significantly different from baseline value (not reported when between-group differences are reported). OW indicates overweight; BW, body weight; Rx, treatment period; NR, not reported; values with different superscript letters differ significantly from each other.
body fat changes, although the diet plus exercise groups showed better improvements in other physiologic parameters. Epstein and colleagues demonstrated a significant effect of exercise implemented initially in a structured camp setting beyond that of diet from baseline to 6 months, with a significant difference between the groups maintained at 12 months.25
Another type of exercise program that has been studied is lifestyle exercise, which attempts to increase energy expenditure in regular daily activity as well as during periods of exercise. Lifestyle exercise was shown to be superior to isocaloric programmed aerobic exercise after 17 months of observation, with the addition of the traffic-light diet showing no additional effect on percent of overweight.19 In a follow-up study, diet plus lifestyle exercise were significantly more effective than diet plus aerobic exercise at 2 years,26 but both exercise programs were superior to diet plus calisthenic control at 10 years of observation (219.7% and 210.9% vs 112.2%).6 How- ever, in one study, lifestyle exercise was not found to have additional effects beyond diet over 1-year28 and 10-year6 intervals.
The effects of exercise can add to dietary interventions to enhance weight loss and improve long-term maintenance. Preliminary data suggest that less structured, more flexible lifestyle exercise may be superior to more structured and higher intensity aerobic exercise for weight control.6 As with diet, the effect of an exercise program varies as a function of the other components of treatment. There are many unanswered questions about the best exercise approach. Are reliable differences observed as a function of exercise intensity, or is the volume of expenditure most important? Do specific types of exercise have reliable effects on appetite or dietary compliance? Can the new American College of Sports Med- icine/Centers for Disease Control and Prevention guidelines for moderate activity change38 be used in childhood obesity treatment? Should exercise be presented in structured ways, as in team sports or group activities, or should children be taught more general principles for increasing activity? Are there important age and developmental differences in coordina- tion or motor learning that would provide recommendations for different exercise interventions?
Surgical Treatments In an uncontrolled study, jejunoileal bypass sur-
gery was used to treat 11 adolescents who were at least 100% over their ideal body weight. At 10-year follow-up, they had maintained a weight loss rang- ing from 45 to 90 kg.39 However, a significant number of complications were encountered by all participants, including encephalopathy, nephrolithiasis, cholelithiasis, renal cortical nephropathy, hypopro- teinemia, systemic fatty acid deficiency, and many other nutritional deficiencies. Three of the 11 adolescents had complications from the bypass that were severe enough that surgery to reverse the operation was necessary. Thus, although this surgery did produce a large amount of weight loss that was maintained over 10 years, the side effects of the procedure
were extremely costly, and the investigators did not recommend additional use of this operation for adolescents.39
Drug Treatments With the surge of interest in the use of pharmaco-
therapy to treat adult obesity, the suggestion has been made that the use of anorectic pharmacologic agents, specifically protocols that include fenfluramine, should be evaluated for treatment of pediatric obesity.40 One controlled study did not find significant decreases in weight or body fat when fenfluramine was combined with diet intervention.41 A more recent study found that treating adolescent obesity with an energy-restricted diet and d-fenfluramine produced significant decreases in BMI from baseline, but these differences were not significantly different than the control treatment of diet and placebo.42
These studies do not provide confidence in the efficacy of current pharmacologic interventions for pediatric obesity.
Behavior Change in Pediatric Obesity Treatment Given the complexity of behavior change and the
difficulty in adherence to treatment protocols, an understanding of factors that influence behavior change is needed. The importance of including behavior therapy in the treatment of childhood obesity was demonstrated by Epstein and colleagues.20 They reported that the addition of the behavioral techniques of contingency contracting, self-monitoring of caloric intake and weight, praise, and stimulus control to nutrition education significantly improved reduction in percent of overweight compared with nutrition education alone over a 5-month period (217.5% vs 26.4%). Other investigators have reported the superiority of behavioral treatment versus no-treatment controls.43–45 However, in some school- based programs that have targeted the child alone, behavior modification has neither been necessary for treatment gains46 nor provided treatment gains beyond that of education.47
In an additional test of the role of behavior therapy in obesity treatment, families who have received intense behavioral intervention might be expected to do better than families who receive less behavioral treatment. Israel and colleagues48 found that at 1-year follow-up, children whose parents had partic- ipated in a short course in general behavior management had significantly better weight control than children in an intervention that focused only on weight reduction. Families that master behavior change also might be expected to do better in treatment than families provided the same intervention without mastery. Epstein and colleagues49 found that children in the mastery group had significantly better treatment outcome than did children in the nonmastery group at 12 months. At 24 months, children in the mastery condition had larger changes in percent of overweight than did nonmastery control children (215.4% vs 210.6%), but the results were no longer significantly different.
Behavior therapy is designed to teach new behaviors, and thus research showing differences in learn-
ing as a function of the interval between teaching periods may be relevant to scheduling treatment sessions. Senediak and Spence22 assessed the effects of rapid (eight sessions in 4 weeks) or gradual (eight sessions over 15 weeks) behavioral treatment versus a nonspecific control condition and a wait-list control group. At 26-week follow-up, the gradual behavioral group had more significant weight change than did the rapid group, who had more weight change than did the nonspecific control group.
Aragona et al50 compared the effects of response cost (loss of monetary deposit contingent on meeting attendance, self-monitoring, and child weight-loss criteria) with or without reinforcement versus a no- treatment control group in a small sample of 5- to 11-year-old children. At follow-up, no treatment effect was found, although reinforcement appeared to add a slight benefit for the group in terms of less weight regain. The goals targeted for reinforcement also can influence outcome. Coates and coworkers51
contrasted groups in which changes in caloric intake or weight were targeted and reinforced according to meeting daily or weekly goals. At 10 months, the best results were obtained for adolescents reinforced for weight change on a daily basis.
Obesity has been considered a disorder of self- control, and two studies evaluated whether self- management treatment would enhance child weight control. In both studies, children were provided comprehensive behavioral family-based programs; neither the study by Epstein and colleagues6,52 nor the study of Israel and colleagues53 observed significant effects of child self-control training.
Research on obesity treatment in children and adolescents has tested the influence of including multiple family members. In a long-term study, Epstein and colleagues29 explored the influence of selection of targeting parents and children by randomizing families to one of three groups for behavior change: 1) nonspecific target, 2) child target, and 3) child and parent target. At posttreatment and 2-year follow- up, children in all groups demonstrated similar changes in percent of overweight; however, at 10- year follow-up, the parent–child group had significantly better changes in weight status than did the nonspecific control, with the child-only group in between. Despite the intuitive nature of the conclusion that including parents in treatment improves treatment outcome, a number of studies have not found that targeting parents adds to treatment effects in preadolescent54 and adolescent55 samples.
If both parent and child are treated, the structure of the treatment sessions may be important. Two studies explored the effect of parent participation in adolescent weight change by randomizing families into one of three groups: 1) child-alone group, 2) child and mother treated together, and 3) child and mother treated in separate groups. At 1-year follow-up of a white sample,56 children in the child– mother separate group decreased their percent of overweight significantly more than did children in either the child–mother together or the child-alone groups, which did not differ (220.5% vs 25.5% and 26.0%, respectively). However, no differences were
observed in black children by similar methods after 10 months.57
Mendonca and Brehm58 evaluated the role of perception of choice in therapeutic outcome of behavioral obesity treatment. Children who perceived that they chose the type of treatment reduced in percent of overweight more than did children in the no- choice control at 12 weeks. No treatment effect was found at 9 months, but the small sample size and attrition precluded meaningful interpretation at this time point.
On the basis of behavioral choice theory,59 Epstein and colleagues21 evaluated the influence of treatments in which children are targeted and reinforced for greater activity, less sedentary behavior, or a combined group. The children reinforced for reducing sedentary behavior showed a significantly greater decrease in percent of overweight compared with the children reinforced for increased activity, with the combined group in between; at 1-year follow-up, the group reinforced for less sedentary behavior maintained their weight loss, whereas the combined group had gained weight and become equivalent to the group reinforced for activity.
Graves and colleagues23 found that problem-solving, a component of many behavioral treatments, is necessary for successful treatment, because families provided behavioral treatments with parental problem-solving had significantly better outcomes at 8-month follow-up than families not provided training in problem-solving. However, Duffy and Spence30 found no additional benefit of cognitive therapy techniques such as targeting monitoring of negative thoughts, restructuring of maladaptive thoughts, problem-solving, and self-reinforcement in addition to behavioral techniques for 7- to 10-year- old and 10- to 13-year-old children at 8-month follow-up.
Finally, one study assessed the effects of family therapy on treatment of obesity in 10- and 11-year- old children.24 At the end of 14 months, neither group showed decreases in obesity, but children in the family therapy group had significantly smaller increases in BMI than did children in the conven- tional dietary counseling group. This difference dis- appeared 1 year later.
The use of behavior change methods in treatment is critical to long-term success of obesity treatment, and interventions for behavior change act in concert with the diet and exercise components to determine outcome. Some preliminary observations on behavior change can be made. The research suggests that effects are enhanced for programs that include behavior therapy,20 with outcome related to intensity of treatment.48 Furthermore, parental involvement can be an important part of child obesity treatment.29,56
However, there are many unanswered questions about how treatment should be implemented. How important is general parent training, or should the parent training be specific to eating and activity change? How are different parent training programs adapted to the age of the child, because different programs are needed for preschoolers, preadolescents, and adolescents?60 What do we know about
parent motivation to help children change their dietary or physical activity practices? What is the role of specific components of parent training, including parent use of goal-setting, parent problem-solving, and parent application of rewards for attained changes? How many sessions are optimal, and how should the meetings be scheduled? Because parent- ing approaches need to change as the child grows older, should regular booster sessions be scheduled to train parents in developmentally appropriate methods? What is the best combination of parent modeling and parent support of desired behavior to produce long-term stable improvement in food choice and activity choice? Can school-based education teach skills needed for obesity treatment and prevention, and can school and community programs be linked to clinical activities to reinforce treatment efforts?
Side Effects of Treatment
Positive Physiologic Side Effects of Treatment Besides the overtly obvious goal of a decrease in
percent of overweight or overfat, treatment goals for pediatric obesity should include improvement in other physiologic parameters such as blood pressure, serum lipids, and insulin resistance. Research has found that after treatments that produce significant decreases in body fat, percent of overweight, or weight, adolescents demonstrated significant decreases in systolic and diastolic blood pres- sures.15,16,33,51,56 A change in serum lipids also has been documented as a positive outcome in the comprehensive treatment of pediatric obesity.4,42,51,57,61,62
For children, significant reductions in fasting serum cholesterol and triglycerides and significant increases in high-density lipoprotein (HDL) serum cholesterol have been found after comprehensive treatment, with serum HDL levels remaining significantly higher than baseline levels at 5-year follow- up.4,61,62 Epstein et al62 reported that at 5-year follow- up, changes in relative weight and fitness were significantly associated with change in HDL levels. Sasaki and colleagues63 found that a long-term aerobic exercise program, which resulted in significant decreases in body fat in children, resulted in significant increases in HDL concentrations. In addition, dietary treatments have been associated with significant reductions in fasting serum cholesterol,64,65 triglycerides,64 and low-density lipoproteins.64
Other improvements in the metabolic profile of obese children and adolescents have been documented after treatment. Investigators have reported decreases in fasting serum insulin levels after comprehensive treatment for obese children4 and adolescents.16 At 5-year follow-up, insulin levels were not significantly different from levels at baseline,4 but occurrence of hyperinsulinemia had decreased, and a significant negative correlation was found between serum insulin levels at the end of treatment and a decrease in relative weight over the follow-up.4 Hoff- man and coworkers66 reported significant increases in mean insulin sensitivity when obese children treated with an energy-reduced diet showed signifi-
cant reductions in body weight, but Gutin and col- leagues67 found no significant changes in fasting insulin after weight change.
Psychological Benefits of Weight Reduction Obese children seeking treatment often experience
psychological comorbidity,68–72 and obesity treatment may improve their psychological status. There has been considerable research on self-esteem73,74 and psychopathology73 in obese children. There has been some debate about whether psychological problems cause obesity or are caused by obesity and whether the prevalence of psychological problems is greater in obese than in nonobese children and adolescents.73,74
Most of the research in this area has targeted self- esteem. Although self-esteem may change during some interventions, this change is not consistently associated with decreases in percent of overweight. For example, in school-based interventions designed for prepubertal children, increases in self-esteem occurred in the absence of weight change,75 and equivalent improvements in self-esteem were demonstrated for both experimental and control groups.76
Wadden and colleagues57 found significant increases in self-esteem and decreases in depression in black girls; however, consistent with other studies, no re- lationship was found between self-esteem or depression and changes in weight.77,78 Furthermore, studies of adolescents have demonstrated equivalent increases in self-esteem for both treatment and control groups79 as well as no increase in self-esteem during treatment.80 Research to date suggests that improvement in self-esteem in obese children in treatment may be better accounted for by nonspecific treatment effects than by improvement in weight status.
Parent and child psychological problems may influence treatment outcome.81 Epstein and col- leagues72 demonstrated that parental distress had negative effects on child weight loss during the treatment phase, which were mediated by their child’s level of anxiety and depression. At 2-year follow-up, parental distress affected child weight change through effects on the child’s social problems; children who had greater social problems had less successful treatment. Obesity treatment also may influence child psychological changes. We are in the process of collecting follow-up psychosocial data on obese children treated in a 16-week, family-based behavioral treatment program. Preliminary analyses show an improvement in child behavior checklist82
values at 1 year, with the greatest decrease shown for social problems. Significant reductions also have been observed for anxiety and depression, with- drawn behavior, attention problems, and somatic complaints. The broad-band internalizing and total- problems scales also have shown significant improvements. More importantly, the improvement in weight status from baseline to 1-year assessment is associated with improvement in psychosocial func- tioning, with significant positive correlations between weight loss and social problems, somatic complaints, and total problems.
Negative Physiologic Effects of Treatment With any dietary intervention that reduces energy
and consequential macro- and micronutrient intake during a period of growth, there is the potential of impairing linear growth. Growth failure has been reported in the overzealous treatment of hypercho- lesterolemia in children because of inadequate energy, fat, and micronutrient intake,83 and investiga- tors33,84 have reported significant reductions in height velocity during interventions with obese children. Amador et al11 found that more restrictive energy intakes (0.17 instead of 0.25 MJ/kg) prescribed to children in the early stages of puberty produced significantly less height gain in the children during a 6-month treatment; there was no significant difference in height gain between the two groups from baseline to 12-month measures. Also, increases in lean body mass were lower in the more restricted energy group than in the less restricted energy intake group, both after treatment and from baseline to 12-month measures.11 Positive growth velocity z scores in children also have been documented after the children were treated for obesity.85
However, these changes in growth velocity must be interpreted within the context that obese children experience an earlier growth spurt than their nonobese counterparts;86 thus, obese children may natu- rally undergo a deceleration in height velocity later in development.8 This hypothesis reconciles the data that children with earlier growth spurts are not taller as adults than children who mature later.87,88 In our long-term, 10-year follow-up studies, we have not found that the more successful children show less growth,5 and height percentiles showed the expected decrease over 10 years, so that children came to resemble their same-sex parent in height. Multiple- regression analysis found that child percent of overweight change made no contribution to predicting height change, and that child sex, age, baseline height, percent of overweight, midparent height, and height change from baseline to 5 years accounted for 95% of the variance in growth that occurred from baseline to 5-year follow-up.8
Eating Disorders Dietary restriction that can be part of weight-con-
trol programs is a defining characteristic of both anorexia and bulimia nervosa.89 A number of studies have found caloric restriction to precede binge-eating. For example, in one study, 75% of bulimic patients interviewed reported that the inability to maintain a low-carbohydrate diet immediately preceded bulimic symptoms.90 More importantly, prospective studies of adolescent girls suggest that dietary restriction predates bulimic symptoms,91 with one study reporting that adolescent girls who were diet- ing had an eightfold increased risk for being diagnosed with an eating disorder compared with non- dieters.92
However, few of the obesity treatments described above assessed the prevalence of disordered eating after obesity intervention, which would require significant long-term follow-up. Only Epstein and col-
leagues6 report the prevalence of eating disorders in 158 individuals who had been treated for obesity. At the 10-year follow-up, 4% of the subjects (all female) reported having been treated for eating disorders, which compares favorably with population prevalence rates #9% in studies that used self-reported diagnoses and prevalence rates #5% in studies that diagnosed eating disorders by means of structured interviews.93 Given that obese adults presenting for obesity treatment have higher rates of eating disorders than do community samples of obese adults,94 it would not have been surprising to have found even higher rates of eating disorders than those in community samples of children. Thus, moderate caloric restriction in a structured behavioral intervention may not carry the increased risk for development of disordered eating found by more drastic caloric restriction.89 Clearly, more work is needed in this area; however, it would be worthwhile to determine whether appropriate education and skills training during development in obese pediatric patients might prevent eating disorders as well as to understand what characteristics of treatment, if any, are associated with developing eating disorders.
DISCUSSION
Improving Implementation of Pediatric Obesity Treatment
Substantial progress has been made in the development of treatments for childhood and adolescent obesity. However, most pediatric obesity interventions are marked by small changes in relative weight or adiposity and substantial relapse, although there is some evidence for long-term efficacy.5,6 It is pre- mature to assume that there are standardized treatments that are efficacious, and research is needed to improve treatment outcome and maintenance of treatment effects. There are many new developments in diet, exercise, and behavior change that should be incorporated into treating childhood obesity; however, for brevity, we focus here on behavior change. Additional new findings in eating and exercise behaviors that can inform treatment development are described by both Birch and Fisher95 and Kohl and Hobbs.96
First, given the central role of behavior therapy in the treatment of child and adolescent obesity, a thor- ough understanding of behavioral principles and their use is a necessary component of successful weight control programs.97–99 It is possible that interventions that claim to have a behavioral component may be misusing behavioral techniques or misapply- ing behavioral principles. Stunkard99 notes that behavior therapy for obesity was and sometime still is seen as a set of tools to micromanage within-meal eating behaviors such as the rate of eating and bite size. However, there is little empirical evidence that these behaviors are associated with weight status or that changes in these behaviors correlate with weight loss.100 Behavior therapy for obesity has expanded considerably from these roots and demands a current knowledge of the factors that influence energy balance behaviors as well as an awareness of behavioral
principles and their application to changing activity and eating habits if long-term maintenance is to be achieved.
More comprehensive assessments of the process of behavior change are needed. There are few studies that provide measures of compliance to treatment outcome, and these studies may be compromised by the well-documented problems that have been noted in self-reporting of dietary and activity changes.101,102
If behavior change strategies are to be effective, it is critical to ensure that people are in fact implementing these programs as planned and are demonstrating mastery of new skills.49 The mediators of behavior change are assumed to be changes in eating and activity. However, as Baranowski and colleagues103
have pointed out for community health interventions, the link between the hypothesized mediators and health outcomes is weak. The same could be said for obesity treatment, and one solution may be studies that focus on modifying the proposed mediators instead of assuming that changes in the mediators will influence outcome. Until eating and activity patterns can be modified reliably, investigators must rely on weak treatments to attempt modification of behaviors that are quite resistant to change. Research also is needed to assess the short- and long-term effects of exercise and diet interventions on regulation of food intake, body composition, fat distribution, energy metabolism, and substrate use. In the long term, it is more cost-effective to focus on development of methods that modify the proposed mediators of change reliably and test for changes in proposed mediators rigorously than to ignore mediators and focus only on weight loss.
Behavioral Economic Research An example of using advances in behavior theory
to inform treatment development is application of behavioral choice theory.59,97 Behavioral choice theory provides a conceptual and methodologic frame- work for understanding behavioral choice. One important choice for obese children is whether to be active or sedentary. In general, obese children choose to be sedentary when they are given the option of engaging in physical or sedentary activity, because they have a more negative perception of physical activity104 and find physical activity less reinforcing than sedentary activity relative to their nonobese peers.105 Highly reinforcing sedentary activities compete with physical activity and decrease children’s levels of physical activity. Behavioral choice theory suggests that one way to increase physical activity is to increase the relative reinforcing value of physical activity relative to sedentary activity, either by increasing the reinforcing value of physical activity or by decreasing the reinforcing value of sedentary activity. This reframing of physical activity as a choice between physical and sedentary activity requires consideration of sedentary activity when interventions to increase physical activity are being designed. This is particularly important in obese populations, because participation in sedentary activity has been found to be cross-sectionally and longitudinally related to childhood and adult obesity.106,107
Both laboratory research and clinical outcome research show that positively reinforcing reductions in high-preference sedentary activities increases the physical activity of obese children to a magnitude similar to that obtained by positively reinforcing increases in physical activity.21,108,109 In clinical research, no benefits have been observed for targeting the combination of reduced sedentary behavior and increased activity.21 Children who are reinforced for decreasing time spent in some of their high-preference sedentary activities reallocate time from these behaviors to engage in both lower preference sedentary activities and physical activity.108,109
One advantage of reinforcing reductions in sedentary activity to increase physical activity is the greater choice and control afforded by this contingency compared with contingencies that reinforce increases directly in physical activity. Maintaining choice and control is important in establishing reinforcing value,110 and enhancing these variables may minimize the sense of deprivation associated with reducing common sedentary behaviors. Deprivation is a powerful way to increase the reinforcing value of an activity or other commodity,111 and interventions that minimize the sense of deprivation are likely to have more long-term behavior change and decreased likelihood of relapse.
Children reinforced for decreasing sedentary activities choose to replace these activities with physical activity or nontargeted sedentary activities, thus maintaining their control over the choice between physical and sedentary activity. Additional support for the need to maintain children’s choice and control about activity choice comes from examination of var- ious techniques to decrease sedentary behavior. There is some evidence that different strategies for reducing sedentary activity have different effects on physical activity. In a laboratory study that compared the effects of positive reinforcement, punish- ment, and restriction to reduce sedentary activity, each strategy was found to be equally effective in reducing time spent in the targeted sedentary activities. However, children reinforced for decreasing sedentary activity were more physically active than a noncontingent control group, whereas children who had their targeted sedentary activities removed from their environment (restriction) did not engage in significantly more physical activity than the noncontingent control group. Children in the restriction group increased their liking for the targeted sedentary activities, whereas children reinforced for decreases in the targeted sedentary activities decreased their liking for these activities over time.109
Reinforcing a reduction in access to sedentary behaviors that compete with being active represents one method for modifying the environment that may lead to obesity. When obesity is being treated, the role of environmental and stimulus control of active behavior should be considered at multiple levels. At the individual level, families may want to increase the cues and opportunities to be active and reduce cues to be sedentary. It is obvious that the larger environment also influences eating and activity. Weather may influence activity, as may having safe
places to play. Children who live in an environment where they can walk or bicycle to school may expend many more calories than children who are driven or bused to school. Access to after-school and weekend active play or sports teams also can enhance activity levels.
Memory Research Another research area that has considerable rele-
vance for obesity treatment is learning and memory research designed to understand response extinction and recovery. One of the most common and least understood aspects of obesity treatment is relapse, a ubiquitous occurrence in obesity treatment. Most therapists assume that extinction of a behavior or replacement of an unwanted behavior with a new behavior removes a response from the subject’s repertoire. The appearance of relapse therefore implies that the treatment was ineffective.
Bouton and colleagues have begun to understand processes that account for recovery of response after extinction. In a series of animal studies, Bouton has explored the influence of stimulus cues presented when a response is learned (context of the learning) on extinction of that response. Bouton and col- leagues112 have demonstrated that context influences recovery of a response that is not reinforced and that has been reduced in frequency. Many treatment approaches attempt to replace a response with a new response pattern by counterconditioning. If the same context is present when both behaviors are learned, spontaneous recovery of the initial response is expected, which demonstrates that learning the new response pattern does not destroy the initial learning.113 If the new behavior is learned in a different context from the initial behavior, presenting the context for the more adaptive behavior will retard relapse to the initial set of behaviors.114 Furthermore, the context during extinction appears to be more important than the context for initial learning. What is learned during response extinction includes memories of being reinforced for a response during learning as well as memories of not being reinforced for the response when treatment occurs. The response observed depends on which memory is retrieved.115
This model has many clinical implications for treatments that attempt to influence weight status by development of positive behaviors (eg, exercise) and extinction of problematic behaviors (eg, overcon- sumption of high-fat foods). Ignoring problematic behaviors or reinforcing competing behaviors does not destroy the original reinforcement associations that maintained the problematic behavior.116 Chang- ing contingencies for the child’s behavior has added an association to the child’s memory and behavioral repertoire (ie, candy request–no candy) rather than replaced the original association (ie, candy request– candy).
Context and memory may be very important processes for long-term behavioral regulation. Treat- ments designed to make permanent changes in behavior must take into account that acquired associations may not disappear completely from the repertoire of associations that produce behavior. Re-
lapse prevention, such as expanding the contexts in which extinction conditioning takes place or training children to become aware of extinction cues, may help increase the maintenance of treatment gains for overweight children.
Individualization of Treatment Treating obesity as a homogeneous condition, with
all participants receiving a common intervention, might contribute to the mixed treatment outcomes that are reported. Research has identified many etiologic factors of obesity, including genetic, metabolic, biochemical, environmental, psychological, and physiologic variables.117,118 However, at the individual level, it is probably rare for all of these factors to be involved in development and maintenance of obesity; consequently, the etiology and maintenance of obesity can be very different from one individual to another. Conceptualization of obesity in this way suggests that interventions need to be heterogeneous and individualized; treatments included in interventions should depend on factors that are believed to be involved with development and maintenance of obesity for that individual.117–120 Research is needed to identify which treatment components are successful with different etiologic and maintenance factors of obesity.
Excess intake could be attributable to individual differences in food craving or satiety. The most commonly craved foods in obese individuals are choco- late, cakes, cookies, ice cream, and other desserts,121
which are composed predominantly of simple carbo- hydrates and fat. Drewnowski121 suggests that food cravings for fat and sugar may involve endogenous opioid peptides; animal research has linked fat and sucrose intake to the endogenous opioid system, in- dicating a potential mechanism for food cravings. If the mechanism for food cravings can be identified, treatment would involve identifying the critical dimension of the food (eg, nutrient, sensory cue, etc) that is the source of the craving and substituting more appropriate foods that also contain the critical dimension necessary to evoke the neurochemical system linked with the food craving.
Barkeling and colleagues122 observed that obese children ate lunch significantly faster and did not decelerate their eating toward the end of the meal as much as do children of normal weight. Because deceleration of food intake toward the end of a meal is considered to be a sign of satiation, this lack of deceleration might indicate a deficient satiation sig- nal or an impaired behavioral response to satiation signals.122 For obese children who show impaired satiation responses, interventions that focus on strengthening satiation signals through conditioning satiation to orosensory cues or strengthening behavioral responses to satiation signals by training individuals to focus on internal cues (learning to identify when hungry or full and to show appropriate behavioral responses such as beginning or terminating eating) might be appropriate.123,124
Interventions designed to promote attending to internal cues are consistent with a nondieting approach that has been proposed as an alternative to
current treatment paradigms, which usually empha- size some amount of energy restriction combined with increased activity.125,126 If subjects could reliably attend to internal cues that would help them match energy intake to energy requirements for a healthy body weight, there might be a reduction in restrained eating and preoccupation with food as a result of perceived food deprivation.124 Training in food regulation would reduce the parent’s perceived need to control the child’s intake, which Johnson and Birch127
have found to interfere with a child’s ability to self- regulate energy intake. In this paradigm, parental responsibilities might be different than in a usual weight-control program. Parents would be responsi- ble for providing nutritious and pleasing foods at predictable and comfortable times during the day. Children would be allowed to choose from the available foods; they also would choose how much to eat, so that they can respond to their internal signals of hunger, appetite, and satiety.125
Another important factor that may introduce heterogeneity to treatment effects are racial and ethnic factors. Although we are not aware of any research that has contrasted treatment response of different ethnic groups in the same study, investigators from one research group have shown a different pattern of response to a common treatment in white56 and black57 teenagers. Obese black and white girls differ in body composition,128 and resting energy expenditure is different in obese black and white women.129
These physiologic differences, in addition to the increased prevalence of obesity in the black community,130 suggest that additional information is needed to understand etiologic differences as well as differences in the response to treatment in different racial and ethnic populations.
If there is heterogeneity in causes for obesity and factors that maintain the obese state, providing a standard group intervention, as is currently usually done, would be sufficient only for those individuals who receive the appropriate intervention by chance. With better assessment techniques, more homogeneous groupings of obese children and adolescents can be achieved, with interventions targeted appro- priately to these groups.
Obesity and Comorbid Conditions As reviewed by Dietz,131 obesity is associated with
a variety of comorbid medical conditions, including some that are critical in disease development, such as hypertension, hyperlipidemia, and insulin resistance. Treatment of obesity in these cases should be useful in preventing morbidity and mortality associated with obesity and comorbid diseases. However, there is a series of less prevalent conditions that are associated with morbidity and mortality during childhood and adolescence that may require more aggressive treatment, such as pseudotumor cerebri and sleep apnea.
There is no research designed specifically to study obesity in association with comorbid conditions. Re- search in these areas is needed to evaluate whether these children are responsive to the same interventions as children without these often medically seri-
ous conditions. If these children do not respond to the common dietary, activity, and behavior change components of treatment, more aggressive treatments may be justified.
If individual difference variables such as the degree of obesity or comorbid medical or psychiatric conditions influence treatment outcome, it may be worthwhile to consider a graded approach to treatment. Children or adolescents who are more obese or have comorbid conditions that require immediate treatment may require more aggressive treatment, such as pharmacotherapy or PSMF. In these cases, it is important to monitor the comorbid condition care- fully and evaluate whether changes in obesity in fact do result in changes in comorbid status. If weight control does not reduce comorbid problems, then other interventions in addition to weight control must be considered.
One unique aspect of treating children with comorbid medical problems may be motivation for treatment. Most treatment outcome research that was reviewed used subjects who were motivated to participate in an obesity treatment study. However, many obese youth in treatment because of a comorbid condition may not be motivated to participate, or if they are motivated, their parents may not be motivated to take part in treatment. It may be important to be able to assess motivation for change, taking advantage of concepts in the stages of change model.132 If it is determined that there is not sufficient motivation for behavior change, motivational inter- viewing133 may be a useful technique for enhancing motivation to lose weight.
Integrate Basic and Clinical Research Advances in basic science should be integrated
into treatment development. Rapid increases in our knowledge of the genetic and molecular basis for obesity provide a stimulus for development of new pharmacologic approaches to obesity treatment. Un- derstanding the influence of genes on eating behavior and obesity also is important for understanding the complementary role of the environment in obesity as well as for identifying specific etiologic factors that may lead to some individuals being at high risk. For example, identifying the genetic basis for behavioral phenotypes, such as impairments in satiety, may be important in developing more focused treatments that target specific behaviors instead of the usual broad-based group methods for treatment.
As reviewed by Birch and Fisher95and Kohl and Hobbs,96 basic behavioral sciences also are providing new insights into processes that may influence eating and exercise behavior. It is important for childhood obesity researchers to be familiar with new developments in child development, learning, and psycho- biology, to name just a few areas that can make important contributions to treatment development. The basic behavioral sciences often are ignored by clinical researchers;97 consequently, new developments that can inform better behavior change strategies are not incorporated into treatment programs. The pharmaceutics industry takes rapid advantage of new genetic and metabolic findings for drug de-
velopment and testing, but there is no industry that uses behavioral scientists to read basic behavioral science and neuroscience for treatment development. This responsibility falls to the individual investigator or investigative team to translate basic science into clinical interventions.
Investigators focusing on pharmacologic interventions generally do not reduce attempts to find new pharmacologic treatments when current treatments are not effective. Rather, the search for new drugs goes on, and often the next generation of drug treatment provides better results. Hopefully, we will see the same type of progress made with behavioral and psychosocial interventions for obesity, and investigators will persist in developing more powerful treatments.
CONCLUSIONS
Future Directions This review provides an overview of contempo-
rary research in treating childhood obesity. The focus is on clinical interventions, although some school- based treatments are discussed. There are many opportunities for treatment development outside the clinic setting—in school-based and community- based programs—although initial research on school-based programs has not been particularly promising.134 In addition, prevention of obesity, instead of treatment of the problem after it has developed, may be important to public health. There is very little research available on prevention,135 and prevention approaches are needed at the population level as well as in targeted high-risk populations. Although progress has been made in treating obese children, research is needed that makes contact with developments in nutrition, exercise, and behavioral science to improve long-term weight regulation, maximizing the positive benefits of weight regulation and minimizing the negative side effects of treating obese children.
ACKNOWLEDGMENTS This work was supported in part by National Institutes of
Health Grants HD 25997, HD 20289, and HD 34284.
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