Relationship of pressure to be thin with gains in body weight and fat mass in adolescents.

BACKGROUND: Sociocultural pressure to be thin is commonly reported by adolescents; yet, to what extent such pressure is associated with weight gain has not been evaluated longitudinally. OBJECTIVE: Examine whether pressure to be thin was positively associated with weight and fat gain in adolescents. METHODS: Participants were 196 healthy adolescent (age 15 ± 1 years old) girls (65%) and boys of varying weights (BMI 25 ± 7 kg/m2 ) studied at baseline and 1-year follow-up. At baseline, adolescents and their mothers reported pressure to be thin by questionnaire. At baseline and follow-up, BMI was calculated, and fat mass was assessed with air displacement plethysmography. Multiple regression was used to examine associations between baseline pressure to be thin and 1-year changes in BMI and fat mass. RESULTS: Accounting for multiple covariates, including baseline BMI or fat, adolescent-reported pressure from parents and peers and mother-reported pressure toward their teen were associated with greater gains in either adolescent BMI or fat (ps < .05). Adolescent weight status was a moderator of multiple effects (ps < .05). CONCLUSIONS: Parental and peer pressure to be thin were associated with increases in BMI and fat mass during adolescence, particularly in heavier adolescents. Further research is necessary to clarify how this association operates reciprocally and to identify underlying explanatory mechanisms.

Serum leptin and loss of control eating in children and adolescents.

BACKGROUND: Both insufficiency and resistance to the actions of the adipocyte-derived hormone leptin promote hunger, increased food intake and greater body weight. Some studies suggest that adults reporting binge eating have increased serum leptin compared with those without binge eating, even after adjusting for the greater adiposity that characterizes binge eaters. Pediatric binge or loss of control (LOC) eating are prospective risk factors for excessive weight gain and may predict development of metabolic abnormalities, but whether LOC eating is associated with higher leptin among children is unknown. We therefore examined leptin and LOC eating in a pediatric cohort. METHODS: A convenience sample of 506 lean and obese youth (7-18 years) was recruited from Washington, DC and its suburbs. Serum leptin was collected after an overnight fast. Adiposity was measured by dual-energy X-ray absorptiometry or air displacement plethysmography. LOC eating was assessed by interview methodology. RESULTS: Leptin was strongly associated with fat mass (r=0.79, P<0.001). However, even after adjusting for adiposity and other relevant covariates, youth with LOC eating had higher serum leptin compared with those without LOC episodes (15.42±1.05 vs 12.36±1.04 ng ml(-1), P<0.001). Neither reported amount of food consumed during a recent LOC episode nor number of LOC episodes in the previous month accounted for differences in leptin (P>0.05). The relationship between LOC eating and leptin appeared to be significant for females only (P=0.002). CONCLUSIONS: Reports of LOC eating were associated with higher fasting leptin in youth, beyond the contributions of body weight. Prospective studies are required to elucidate whether LOC eating promotes greater leptin or whether greater leptin resistance may promote LOC eating.

Hyperphagia among patients with Bardet-Biedl syndrome.

BACKGROUND: The importance of hyperphagia as a cause for energy imbalance in humans with Bardet-Biedl syndrome (BBS) has not been established. We therefore compared hyperphagic symptoms in patients with BBS vs. controls. METHODS: We studied 13 patients with BBS and 23 non-syndromic controls with similar age, sex and body mass index (BMI) z-score. A 13-item hyperphagia questionnaire was completed by patients' parents/guardians. RESULTS: Total hyperphagia questionnaire score was higher in BBS than controls (27.6 ± 9.0 vs. 19.1 ± 7.9, P = 0.005). Behaviour and drive subscales were higher for BBS than controls (12.5 ± 4.1 vs. 7.8 ± 3.2, P = 0.001, and 11.2 ± 4.1 vs. 8.3 ± 3.8, P = 0.04, respectively); severity was not significantly different between groups (3.8 ± 1.5 vs. 3.0 ± 1.3, P = 0.072). After adjustment for demographic variables and BMI z-score, total and behaviour subscale scores remained significantly different between groups, suggesting food-seeking activity, rather than preoccupation with food may be the main hyperphagic feature among patients with BBS. CONCLUSION: Appetite dysregulation may contribute to obesity in BBS.

Children's binge eating and development of metabolic syndrome.

BACKGROUND: Binge eating predisposes children to excessive weight gain. However, it is unknown if pediatric binge eating predicts other obesity-associated adverse health outcomes. OBJECTIVE: The objective of this study was to investigate the relationship between binge eating and metabolic syndrome (MetS) in children. METHOD: Children aged 5-12 years at high risk for adult obesity, either because they were overweight/obese when first examined or because their parents were overweight/obese, were recruited from Washington, DC and its suburbs. Children completed a questionnaire assessment of binge eating at baseline and underwent measurements of MetS components at baseline and at a follow-up visit approximately 5 years later. Magnetic resonance imaging was used to measure the visceral adipose tissue (VAT) in a subset. RESULTS: In all, 180 children were studied between July 1996 and August 2010. Baseline self-reported binge eating presence was associated with a 5.33 greater odds of having MetS at follow-up (95% confidence interval (CI): 1.47, 19.27, P=0.01). The association between binge eating and body mass index (BMI) only partially explained changes in MetS components: baseline binge eating predicted higher follow-up triglycerides, even after accounting for baseline triglycerides, baseline BMI, BMI change, sex, race, baseline age and time in study (P = 0.05). Also, adjusting for baseline VAT and demographics, baseline binge eating predicted greater follow-up L(2-3) VAT (P = 0.01). DISCUSSION: Children's reports of binge eating predicted development of MetS, worsening triglycerides and increased VAT. The excessive weight gain associated with children's binge eating partly explained its adverse metabolic health outcomes. Reported binge eating may represent an early behavioral marker upon which to focus interventions for obesity and MetS.

Construct validity of the emotional eating scale adapted for children and adolescents.

BACKGROUND: Emotional eating, defined as eating in response to a range of negative emotions, is common in youths. Yet, there are few easily administered and well-validated methods to assess emotional eating in pediatric populations. OBJECTIVE: The current study tested the construct validity of the Emotional Eating Scale (EES) Adapted for Children and Adolescents (EES-C) by examining its relationship to observed emotional eating at laboratory test meals. METHOD: A total of 151 youths (8-18 years) participated in two multi-item lunch buffet meals on separate days. They ate ad libitum after being instructed to 'eat as much as you would at a normal meal' or to 'let yourself go and eat as much as you want'. State negative affect was assessed immediately before each meal. The EES-C was completed 3 months, on average, before the first test meal. RESULTS: Among youths with high EES-C total scores, but not low EES-C scores, higher pre-meal state negative affect was related to greater total energy intake at both meals, with and without the inclusion of age, race, sex and body mass index (BMI) standard deviation as covariates (ps<0.03). DISCUSSION: The EES-C demonstrates good construct validity for children and adolescents' observed energy intake across laboratory test meals designed to capture both normal and disinhibited eating. Future research is required to evaluate the construct validity of the EES-C in the natural environment and the predictive validity of the EES-C longitudinally.