James N. Roemmich

A Randomized Trial of the Effects of Reducing Television Viewing and Computer Use on Body Mass Index in Young Children

OBJECTIVE To assess the effects of reducing television viewing and computer use on childrens body mass index (BMI) as a risk factor for the development of overweight in young children. DESIGN Randomized controlled clinical trial. SETTING University childrens hospital. PARTICIPANTS Seventy children aged 4 to 7 years whose BMI was at or above the 75th BMI percentile for age and sex. INTERVENTIONS Children were randomized to an intervention to reduce their television viewing and computer use by 50% vs a monitoring control group that did not reduce television viewing or computer use. MAIN OUTCOME MEASURES Age- and sex-standardized BMI (zBMI), television viewing, energy intake, and physical activity were monitored every 6 months during 2 years. RESULTS Children randomized to the intervention group showed greater reductions in targeted sedentary behavior (P < .001), zBMI (P < .05), and energy intake (P < .05) compared with the monitoring control group. Socioeconomic status moderated zBMI change (P = .01), with the experimental intervention working better among families of low socioeconomic status. Changes in targeted sedentary behavior mediated changes in zBMI (P < .05). The change in television viewing was related to the change in energy intake (P < .001) but not to the change in physical activity (P =.37). CONCLUSIONS Reducing television viewing and computer use may have an important role in preventing obesity and in lowering BMI in young children, and these changes may be related more to changes in energy intake than to changes in physical activity.

Growth at Puberty

Somatic growth and maturation are influenced by a number of factors that act independently or in concert to modify an individuals genetic potential. The secular trend in height and adolescent development is further evidence for the significant influence of environmental factors on an individuals genetic potential for linear growth. Nutrition, including energy and specific nutrient intake, is a major determinant of growth. Paramount to normal growth is the general health and well-being of an individual; in fact, normal growth is a strong testament to the overall good health of a child. More recently the effect of physical activity and fitness on linear growth, especially among teenage athletes, has become a topic of interest. Puberty is a dynamic period of development marked by rapid changes in body size, shape, and composition, all of which are sexually dimorphic. One of the hallmarks of puberty is the adolescent growth spurt. Body compositional changes, including the regional distribution of body fat, are especially large during the pubertal transition and markedly sexually dimorphic. The hormonal regulation of the growth spurt and the alterations in body composition depend on the release of the gonadotropins, leptin, the sex-steroids, and growth hormone. It is very likely that interactions among these hormonal axes are more important than their main effects, and that alterations in body composition and the regional distribution of body fat actually are signals to alter the neuroendocrine and peripheral hormone axes. These processes are merely magnified during pubertal development but likely are pivotal all along the way from fetal growth to the aging process.

Family-Based Obesity Treatment, Then and Now: Twenty-Five Years of Pediatric Obesity Treatment

OBJECTIVE Family-based treatments for pediatric obesity were developed over 25 years ago. Over that time, youth have become more obese and the environment more obesiogenic, which may influence efficacy of pediatric weight control. Mixed-effects regression models were used to compare the efficacy of programs initiated 20 to 25 years ago to current programs through 24-month follow-up, as well as to reanalyze 10-year outcomes of previous research using contemporary measures and analytic strategies. MAIN OUTCOME MEASURES z-BMI and percent overweight. RESULTS Results showed significant reductions over time, with no differences in z-BMI change for older versus contemporary studies. Age was a predictor of z-BMI up to 24 months, with younger children showing larger change. Mixed-effects regression models replicated previous long-term effects of family-based interventions. Gender was a predictor of long-term z-BMI change, with girls benefiting more over time than did boys. CONCLUSION The efficacy of the family-based behavioral approach to treating pediatric obesity replicates over a 25-year period. Challenges in evaluating treatment effects over time are discussed. Ideas for studying choice of treatments that vary in effect size and for strengthening family-based behavioral treatments are noted.

Reducing Sedentary Behavior: Role in Modifying Physical Activity

EPSTEIN, L.H., and J.N. ROEMMICH. Reducing sedentary behavior: role in modifying physical activity. Exerc. Sport Sci. Rev., Vol. 29, No. 3, pp 103–108, 2001. Decreased physical activity is associated with the increased incidence of obesity. Behavioral economic research demonstrates that reducing sedentary behaviors in children increases physical activity. Understanding how people choose physical or sedentary activities can aid in developing public health initiatives that increase access to physical activity, while reducing access to sedentary behaviors.

BEHAVIORAL THERAPY IN THE TREATMENT OF PEDIATRIC OBESITY

This article was designed to make a strong case for the importance of studying behavior and using behavioral therapy in the treatment of pediatric obesity. Behavioral treatments have been the most studied approaches to pediatric obesity, with great success. Six studies that provided long-term results are presented, and ideas for translating behavioral therapy into common pediatric practice are presented. Additional progress is needed to incorporate new findings in learning and behavioral neuroscience into clinical interventions and to integrate behavioral therapy with pharmacologic interventions and genetic predispositions and new advances in nutrition and exercise science.

Increasing Healthy Eating vs. Reducing High Energy-dense Foods to Treat Pediatric Obesity

Objective: The objective was to compare targeting increased eating of healthy foods vs. reducing intake of high energy‐dense foods within the context of a family‐based behavioral weight control program.

Habituation as a determinant of human food intake.

Research has shown that animals and humans habituate on a variety of behavioral and physiological responses to repeated presentations of food cues, and habituation is related to amount of food consumed and cessation of eating. The purpose of this article is to provide an overview of experimental paradigms used to study habituation, integrate a theoretical approach to habituation to food based on memory and associative conditioning models, and review research on factors that influence habituation. Individual differences in habituation as they relate to obesity and eating disorders are reviewed, along with research on how individual differences in memory can influence habituation. Other associative conditioning approaches to ingestive behavior are reviewed, as well as how habituation provides novel approaches to preventing or treating obesity. Finally, new directions for habituation research are presented. Habituation provides a novel theoretical framework from which to understand factors that regulate ingestive behavior.

Effect of Peers and Friends on Youth Physical Activity and Motivation to be Physically Active

OBJECTIVE To test whether the presence of a peer or a friend increases the motivation to be physically active in overweight and non-overweight youth in a laboratory setting. METHODS Youth motivation to be physically active as a function of the social context was measured using a computerized relative reinforcing value task to earn points exchangeable for physical and/or sedentary activities. RESULTS The presence of a friend (p<.001) increased youths; motivation to be physically active. The presence of a peer increased overweight youths; motivation to be physically active, whereas this was not the case for lean youth (p=.47). Participants biked a greater distance in the presence of a friend than when alone (p<.001). Overweight youth biked a greater distance in the presence of a peer than when alone, while this was not the case for lean youth (p=.23). CONCLUSIONS Friendships may increase youths motivation to engage in physical activity and promote greater physical activity in non-overweight and overweight youth.

Pubertal alterations in growth and body composition. VI. Pubertal insulin resistance: Relation to adiposity, body fat distribution and hormone release

Objective: To investigate the independent influence of alterations in fat mass, body fat distribution and hormone release on pubertal increases in fasting serum insulin concentrations and on insulin resistance assessed by the homeostasis model (HOMA).Design and Subjects: Cross-sectional investigation of pre- (n=11, n=8), mid- (n=10, n=11), and late-pubertal (n=10, n=11) boys and girls with normal body weight and growth velocity.Measurements: Body composition (by a four-compartment model), abdominal fat distribution and mid-thigh interfascicular plus intermuscle (extramyocellular) fat (by magnetic resonance imaging), total body subcutaneous fat (by skinfolds), mean nocturnal growth hormone (GH) release and 06:00 h samples of serum insulin, sex steroids, leptin and insulin-like growth factor-I (IGF-I).Results: Pubertal insulin resistance was suggested by greater (P<0.001) fasting serum insulin concentrations in the late-pubertal than pre- and mid-pubertal groups while serum glucose concentrations were unchanged and greater (P<0.001) HOMA values in late-pubertal than pre- and mid-pubertal youth. From univariate correlation fat mass was most related to HOMA (r=0.59, P<0.001). Two hierarchical regression models were developed to predict HOMA. In one approach, subject differences in sex, pubertal maturation, height and weight were held constant by adding these variables as a block in the first step of the model (r2=0.36). Sequential addition of fat mass (FM) increased r2 (r2(inc)remental=0.08, r2=0.44, P<0.05) as did the subsequent addition of a block of fat distribution variables (extramyocellular fat, abdominal visceral fat, and sum of skinfolds; r2inc=0.11, r2=0.55, P<0.05). Sequential addition of a block of hormone variables (serum IGF-I and log(10) leptin concentrations; r2inc=0.04, P>0.05) did not reliably improve r2 beyond the physical characteristic and adiposity variables. In a second model, differences in sex and pubertal maturation were again held constant (r2=0.25), but body size differences were accounted for using percentage fat data. Sequential addition of percentage body fat (r2(inc)remental=0.11, r2=0.36, P<0.05), then a block of fat distribution variables (percentage extramyocellular fat, percentage abdominal visceral fat, and percentage abdominal subcutaneous fat; r2inc=0.08, r2=0.44, P=0.058), and then a block of serum IGF-I and log(10) leptin concentrations (r2inc=0.07, r2=0.51, P<0.05) increased r2. Mean nocturnal GH release was not related to HOMA (r=−0.04, P=0.75) and therefore was not included in the hierarchical regression models.Conclusion: Increases in insulin resistance at puberty were most related to FM. Accumulation of fat in the abdominal visceral, subcutaneous and muscular compartments may increase insulin resistance at puberty beyond that due to total body fat. Serum concentrations of leptin and IGF-I may further modulate HOMA beyond the effects of adiposity and fat distribution. However, the results are limited by the cross-sectional design and the use of HOMA rather than a criterion measure of insulin resistance.

Gender differences in leptin levels during puberty are related to the subcutaneous fat depot and sex steroids

Little is known about the influence of adiposity and hormone release on leptin levels in children and adolescents. We utilized criterion methods to examine the relationships among sex steroids, body composition (4 compartment), abdominal visceral and subcutaneous fat (magnetic resonance imagery), total subcutaneous fat (sum of 9 skinfolds), energy expenditure (doubly labeled water), aerobic fitness, and serum leptin levels in prepubertal and pubertal boys ( n = 16; n = 13) and girls ( n = 12; n = 15). The sum of skinfolds accounted for more variance in leptin levels of all girls [coefficient of determination ( R 2) = 0.70, P < 0.001] and all boys ( R 2 = 0.60, P < 0.001) than the total fat mass (girls, R 2 = 0.52, P < 0.001; boys, R 2 = 0.23, P < 0.001). Total energy expenditure, corrected for the influence of fat-free mass, correlated inversely with leptin ( R 2 = 0.18, P = 0.02). Gender differences in leptin disappeared when corrected for sex steroid levels or the combination of adiposity and energy expenditure. In multiple regression, the sum of skinfolds and free testosterone and estrogen levels accounted for 74% of the variance in leptin levels. We conclude that serum leptin levels are positively related to subcutaneous adiposity but negatively related to androgen levels. Energy expenditure may be negatively related to leptin levels by reduction of the adiposity, or a common genetic factor may influence both the activity and serum leptin levels.Little is known about the influence of adiposity and hormone release on leptin levels in children and adolescents. We utilized criterion methods to examine the relationships among sex steroids, body composition (4 compartment), abdominal visceral and subcutaneous fat (magnetic resonance imagery), total subcutaneous fat (sum of 9 skinfolds), energy expenditure (doubly labeled water), aerobic fitness, and serum leptin levels in prepubertal and pubertal boys (n = 16; n = 13) and girls (n = 12; n = 15). The sum of skinfolds accounted for more variance in leptin levels of all girls [coefficient of determination (R2) = 0.70, P < 0.001] and all boys (R2 = 0.60, P < 0.001) than the total fat mass (girls, R2 = 0.52, P < 0.001; boys, R2 = 0.23, P < 0.001). Total energy expenditure, corrected for the influence of fat-free mass, correlated inversely with leptin (R2 = 0.18, P = 0.02). Gender differences in leptin disappeared when corrected for sex steroid levels or the combination of adiposity and energy expenditure. In multiple regression, the sum of skinfolds and free testosterone and estrogen levels accounted for 74% of the variance in leptin levels. We conclude that serum leptin levels are positively related to subcutaneous adiposity but negatively related to androgen levels. Energy expenditure may be negatively related to leptin levels by reduction of the adiposity, or a common genetic factor may influence both the activity and serum leptin levels.