Youth's energy intake during a laboratory-based loss-of-control eating paradigm: Associations with reported current dieting.

Dieting is theorized as a risk factor for loss-of-control (LOC)-eating (i.e., feeling a sense of lack of control while eating). Support for this association has largely relied on retrospective self-report data, which does not always correlate with objectively assessed eating behavior in youth. We hypothesized that during a laboratory-based LOC-eating paradigm, children and adolescents who reported current (at the time of the visit) dieting would consume meals consistent with LOC-eating (greater caloric intake, and intake of carbohydrates and fats, but less intake of protein). Participants were presented with a buffet-style meal and instructed to "Let yourself go and eat as much as you want." Current dieting (i.e., any deliberate change to the amount or type of food eaten to influence shape or weight, regardless of how effective the changes are) was assessed via interview. General linear models were adjusted for fat mass (%), lean mass (kg), height, sex, protocol, race and ethnicity, pre-meal hunger and minutes since consumption of a breakfast shake. Of 337 participants (Mage 12.8 ± 2.7y; 62.3 % female; 45.7 % non- Hispanic White and 26.1 % non-Hispanic Black; MBMIz 0.78 ± 1.11), only 33 (9.8 %) reported current dieting. Current dieting was not significantly associated with total energy intake (F = 1.63, p = .20, ηp2 = 0.005), or intake from carbohydrates (F = 2.45, p = .12, ηp2 = 0.007), fat (F = 2.65, p = .10, ηp2 = 0.008), or protein (F = 0.39, p = .53, ηp2 = 0.001). Contrary to theories that dieting promotes LOC-eating, current dieting was not associated with youth's eating behavior in a laboratory setting. Experimental approaches for investigating dieting are needed to test theories that implicate dieting in pediatric LOC-eating.

Associated features of pediatric loss-of-control eating severity during a laboratory-based feeding paradigm.

Laboratory-based loss-of-control eating (LOC-eating; i.e., feeling like one cannot stop eating) paradigms have provided inconsistent evidence that the features of pediatric LOC-eating are consistent with those of DSM-5-TR binge-eating episodes. Thus, this study investigated whether recent LOC-eating (in the prior month) and/or greater LOC-eating severity during a meal are positively associated with faster eating rate, energy intake when adjusting for hunger, post-meal stomachache and sickness (a proxy for eating until uncomfortably full), depression, and guilt. Recent LOC-eating was assessed via interview. Participants were presented with a buffet-type meal and instructed to "Let yourself go and eat as much as you want." Immediately following, youth reported on their experience of LOC-eating during the meal (LOC-eating severity). Eating rate (kcal/min) was computed by dividing total energy intake by the duration of the meal. Prior to and following the meal, youth reported hunger, sickness, and stomachache via sliding Visual Analog Scales, depression via the Brunel Mood Scale and guilt via the PANAS-X. Three-hundred-ten youth participated (61.2 % Female; 46.3 % non-Hispanic White, 12.96 ± 2.72 y). Recent LOC-eating was not significantly associated with any DSM-5-TR binge-eating feature during the laboratory meal (ps = 0.07-0.85). However, LOC-eating severity during the meal was positively associated with eating rate, eating adjusted for hunger, post-meal sickness and stomachache, and guilt (ps < 0.045). LOC-eating severity during a laboratory-based feeding paradigm meal, but not recent LOC-eating, was associated with several features of DSM-5-TR binge-eating episodes. Future studies should assess multiple components of LOC-eating to further characterize the phenomenology of pediatric LOC-eating.

Associations of food reinforcement and food- related inhibitory control with adiposity and weight gain in children and adolescents.

Some, but not all studies have reported that, among youth with disordered eating and high weight, the relative reinforcing value of food (RRV-F, i.e., how hard a person will work for a high-energy-dense food when another reward is available) is greater, and food-related inhibitory control (i.e., ability to withhold a response to food-related stimuli) is lower, compared to peers without disordered eating or overweight. In most studies, high RRV-F and low food-related inhibitory control have been studied separately, as independent factors, with each suggested to predict excess weight and adiposity (fat mass) gain. We hypothesized that the interaction of these factors would prospectively exacerbate risk for weight and adiposity (fat mass) gain three years later in a sample of healthy youth. At baseline, RRV-F was measured using a Behavior Choice Task with the rewards being standardized servings of chocolate candies, cheese crackers, or fruit snacks. Food-related inhibitory control was determined by performance in response to food and non-food stimuli during a Food Go/No-Go task. At baseline and 3-year visits, total body adiposity was measured by dual-energy X-ray absorptiometry (DXA) and body mass index (BMI) was obtained using measured weight and height. A linear regression was conducted with 3-year adiposity as the dependent variable. RRV-F, food-related inhibitory control, and the RRV-F x food-related inhibitory control interaction as independent variables. Baseline adiposity, age, height, sex, race/ethnicity, and days between visits were included as covariates for model predicting 3-year adiposity. Baseline BMI, age, sex, race/ethnicity, and days between visits were included as covariates for model predicting 3-year BMI. One-hundred and nine youth (mean 12.4±2.7y, mean 0.50±1.02 BMIz, 30.3% with overweight/obesity, 45.9% female, 51.4% non-Hispanic White), 8-17 years at baseline, were studied. Baseline food-related inhibitory control (ßunstandardized = 0.33, p = .037, 95% CI [.02, 0.64]), but not baseline RRV-F (ßunstandardized = -0.003, p = .914), 95% CI [-0.05, 0.05]) was significantly associated with 3-year adiposity such that those with the poorest food-related inhibitory control (great number of commision errors) had the greatest adiposity gain. The interaction between RRV-F and food-related inhibitory control did not predict 3-year adiposity (ßunstandardized = -0.07, p = .648, 95% CI [-0.39, 0.25]). The pattern of findings was the same for models examining non-food related inhibitory control. Neither baseline food-related inhibitory control (ßunstandardized = 2.16, p = .256, 95% CI [-1.59, 5.92]), baseline RRV-F (ßunstandardized = 0.14, p = .660, 95% CI [-0.48, 0.75]), nor their interaction (ßunstandardized = -1.18, p = .547, 95% CI [-5.04, 2.69]) were significantly associated with 3-year BMI. However, non-food related inhibitory control (ßunstandardized = 0.54, p = .038, 95% CI [.22, 7.15]) was significantly associated with 3-year BMI. In summary, food-related inhibitory control but not RRV-F, was associated with changes in adiposity in a sample of children and adolescents. Among generally healthy youth, food-related inhibitory control may be a more relevant risk factor than food reinforcement for adiposity gain. Additional data are needed to determine how inhibitory control and reward systems, as well as other disinhibited eating behaviors/traits, may interact to promote excess weight gain over time in youth.

Negative affect and loss-of-control eating in relation to adiposity among non-Hispanic youth identifying as black or white.

Negative affect and loss-of-control (LOC)-eating are consistently linked and prevalent among youth identifying as non-Hispanic Black (NHB) and non-Hispanic White (NHW), particularly those with high weight. Given health disparities in high weight and associated cardiometabolic health concerns among NHB youth, elucidating how the association of negative affect with adiposity may vary by racial/ethnic group, and whether that relationship is impacted by LOC-eating, is warranted. Social inequities and related stressors are associated with negative affect among NHB youth, which may place this group at increased risk for excess weight gain. Across multiple aggregated protocols, 651 youth (13.0 ± 2.7 y; 65.9 % girls, 40.7 % NHB; 1.0 ± 1.1 BMIz; 37.6 % LOC-eating) self-reported trait anxiety and depressive symptoms as facets of negative affect. LOC-eating was assessed by interview and adiposity was measured objectively. Cross-sectional moderated mediation models predicted adiposity from ethno-racial identification (NHB, NHW) through the pathway of anxiety or depressive symptoms and examined whether LOC-eating influenced the strength of the pathway, adjusting for SES, age, height, and sex. The association between ethno-racial identity and adiposity was partially mediated by both anxiety (95 % CI = [0.01, 0.05]) and depressive symptoms (95 % CI = [0.02, 0.08]), but the mediation was not moderated by LOC-eating for either anxiety (95 % CI = [-0.04, 0.003]) or depressive symptoms (95 % CI = [-0.07, 0.03]). Mechanisms underlying the link between negative affect and adiposity among NHB youth, such as stress from discrimination and stress-related inflammation, should be explored. These data highlight the need to study impacts of social inequities on psychosocial and health outcomes.