Depressive symptoms and cardiorespiratory fitness in obese adolescents.

PURPOSE: Depressive symptoms in adolescents have been associated with reduced physical activity. However, existing studies have relied on questionnaire measures of physical activity, which may not necessarily reflect actual energy expenditures. We sought to evaluate the relationship between depressive symptoms and objectively measured cardiorespiratory fitness among severely obese adolescents. METHODS: One hundred thirty-four obese (body mass index [kg/m(2)]: ≥95th percentile) adolescent girls and boys (ages: 12-17 years) reported their depressive symptoms on the Children's Depression Inventory. Adolescents also participated in a maximal cycle ergometry exercise test to measure cardiorespiratory fitness. Body composition was assessed with dual-energy X-ray absorptiometry scanning. RESULTS: Among the 103 adolescents who reached maximal exertion, those with elevated depressive symptoms (16%) displayed poorer cardiorespiratory fitness than those without elevated depressive symptoms (maximal oxygen uptake: 1,873.2 ± 63.6 vs. 2,012.9 ± 28.6 mL/min, p < .05). Symptoms of anhedonia also were related to lower fitness levels (p < .05). These effects were observed after accounting for age, sex, race, and lean mass. CONCLUSIONS: Among obese adolescents, elevated depressive symptoms are associated with poorer objectively measured cardiorespiratory fitness. Future experimental tests should investigate whether cardiorespiratory fitness acts as a mediator of adolescent depressive symptoms' effect on obesity or obesity-related health comorbidities.

Longitudinal study of depressive symptoms and progression of insulin resistance in youth at risk for adult obesity.

OBJECTIVE The purpose of this study was to determine whether having childhood depressive symptoms is a risk factor that prospectively predicts impairment in glucose homeostasis. RESEARCH DESIGN AND METHODS A non-treatment-seeking sample of 115 children (aged 5-13 years), oversampled for being at risk for adult obesity, was assessed at baseline and again ~6 years later. Children self-reported depressive symptoms using the Children's Depression Inventory at baseline. Insulin resistance was assessed at baseline and follow-up with the homeostasis model assessment of insulin resistance index (HOMA-IR). RESULTS Children's depressive symptoms were a significant predictor of follow-up HOMA-IR, fasting insulin, and fasting glucose in models accounting for baseline HOMA-IR, insulin, or glucose values; sex; race; baseline age; baseline BMI; change in BMI at follow-up; family history of type 2 diabetes; and time in the study (P < 0.01). CONCLUSIONS In this study, depressive symptomatology at baseline predicted the progression of insulin resistance during child and adolescent development independent of changes in BMI. Research is needed to determine whether early intervention to decrease elevated depressive symptoms in youth ameliorates later development of insulin resistance and lessens the risk of type 2 diabetes.

Links between mothers' and children's disinhibited eating and children's adiposity.

Few studies have examined relationships between parents' and children's specific disinhibited eating behaviors. We investigated links among mothers' and children's binge/loss of control eating, eating in the absence of hunger, and children's adiposity in 305 non-treatment-seeking youth, aged 8-17 years (13.62±2.65 years; 49.8% female) and their mothers. Youths' loss of control eating and eating in the absence of hunger were assessed by interview and self-report questionnaire. Children's adiposity was assessed with BMI-z and air displacement plethysmography. Maternal binge eating, eating in the absence of hunger and highest, non-pregnant BMI were self-reported. In structural equation models controlling for mothers' BMI, mothers' binge eating related to children's loss of control eating, and mothers' eating in the absence of hunger related to children's eating in the absence of hunger. Mothers' binge eating and children's eating in the absence of hunger were unrelated, as were mothers' eating in the absence of hunger and children's loss of control. Further, mothers' binge eating was indirectly related to children's adiposity through children's loss of control eating. Likewise, mothers' eating in the absence of hunger indirectly related to children's adiposity through children's eating in the absence of hunger. Mothers and children share similar, specific disinhibited eating styles.

A prospective study of pediatric loss of control eating and psychological outcomes.

Loss of control (LOC) eating in youth is associated cross-sectionally with eating-related and psychosocial distress and is predictive of excessive weight gain. However, few longitudinal studies have examined the psychological impact and persistence of pediatric LOC eating. We administered the Eating Disorder Examination and self-reported measures of depressive and anxiety symptoms to 195 boys and girls (mean age = 10.4 years, SD = 1.5) at baseline and again 4.7 years (SD = 1.2) later to 118 of these youth. Missing data were imputed. Baseline report of LOC was associated with the development of partial- or full-syndrome binge eating disorder (p = .03), even after accounting for the contribution of sex, race, baseline characteristics (age, disordered eating attitudes, and mood symptoms), body mass index growth between baseline and follow-up, and years in study. Half (52.2%; 95% CI [1.15, 6.22]) of children who endorsed experiencing LOC at baseline reported persistence of LOC at follow-up (p = .02). Compared with children who never reported LOC eating or reported LOC only at baseline, those with persistent LOC experienced significantly greater increases in disordered eating attitudes (ps < .001) and depressive symptoms (p = .027) over time. These data suggest that LOC eating in children is a problematic behavior that frequently persists into adolescence and that persistent LOC eating is associated with worsening of emotional distress.

Eating in the absence of hunger in adolescents: intake after a large-array meal compared with that after a standardized meal.

BACKGROUND: Eating in the absence of hunger (EAH) is typically assessed by measuring youths' intake of palatable snack foods after a standard meal designed to reduce hunger. Because energy intake required to reach satiety varies among individuals, a standard meal may not ensure the absence of hunger among participants of all weight strata. OBJECTIVE: The objective of this study was to compare adolescents' EAH observed after access to a very large food array with EAH observed after a standardized meal. DESIGN: Seventy-eight adolescents participated in a randomized crossover study during which EAH was measured as intake of palatable snacks after ad libitum access to a very large array of lunch-type foods (>10,000 kcal) and after a lunch meal standardized to provide 50% of the daily estimated energy requirements. RESULTS: The adolescents consumed more energy and reported less hunger after the large-array meal than after the standardized meal (P values < 0.001). They consumed ≈70 kcal less EAH after the large-array meal than after the standardized meal (295 ± 18 compared with 365 ± 20 kcal; P < 0.001), but EAH intakes after the large-array meal and after the standardized meal were positively correlated (P values < 0.001). The body mass index z score and overweight were positively associated with EAH in both paradigms after age, sex, race, pubertal stage, and meal intake were controlled for (P values ≤ 0.05). CONCLUSION: EAH is observable and positively related to body weight regardless of whether youth eat in the absence of hunger from a very large-array meal or from a standardized meal. This trial was registered at clinicaltrials.gov as NCT00631644.

Puberty and observed energy intake: boy, can they eat!

BACKGROUND: Anecdotal reports suggest that adolescent males consume large quantities of food to meet the growth demands of pubertal development. However, limited experimental data exist to support this impression. OBJECTIVE: The objective was to measure energy intakes of youth at different pubertal stages. DESIGN: Participants were 204 volunteers (50.5% male) aged 8-17 y. Pubertal development was categorized by physical examination into prepuberty (males: testes < 4 mL; females: Tanner breast stage 1), early-mid puberty (males: testes = 4-12 mL; females: Tanner breast stages 2-3), or late puberty (males: testes >12 mL; females: Tanner breast stages 4-5). Energy intake was measured as consumption from a 9835-kcal food array during 2 lunch time meals. RESULTS: Males consumed more energy than did females across all pubertal stages (P < 0.001). Intake increased with pubertal development (P < 0.001), but the timing and magnitude of change varied by sex (P = 0.02). Males' unadjusted energy intake was greater in late puberty (mean +/- SE: 1955 +/- 70 kcal) than in prepuberty (1287 +/- 90 kcal) or early-mid puberty (1413 +/- 92 kcal) (P < 0.001). Females' unadjusted energy intake tended to be lower among prepubertal girls (905 +/- 140 kcal) than among females in early-mid puberty (1278 +/- 82 kcal, P = 0.07) or late puberty (1388 +/- 68 kcal, P = 0.01). After adjustment for fat-free mass, fat mass, height, overweight status, race, and meal instruction, the main effect of sex (P < 0.001) remained significant, but the effect of puberty was not significant (P = 0.66). CONCLUSIONS: The observed intake patterns are congruent with known sexual dimorphisms for body composition, peak growth velocity, and pubertal development. Consistent with their higher energy requirements, males can consume significantly larger amounts of food than females, especially during later puberty. This trial was registered at clinicaltrials.gov as NCT00320177.