We examined the role of psychosocial factors in overweight and obesity development.

UK Millennium Cohort Study data of children with normal weight at baseline were analysed. Weight changes were determined from baselines at ages 11 (n = 7979) and 14 (n = 6906) to follow-up at age 17. Baseline individual psychosocial factors were combined into two distinct indexes (caregiver-reported child mental health, child-reported psychosocial well-being). Regression models examined the associations between baseline indexes and individual psychosocial factors and overweight and obesity development (vs. no development) and body mass index (BMI) z-score changes.

Worse child mental health, but not psychosocial well-being, at age 11 was associated with overweight and obesity development (OR = 1.14; 95% CI = 1.02, 1.27) and increased BMI z-scores (β = 0.08; 95% CI = 0.04, 0.12) to age 17. No psychosocial indexes at age 14 predicted the outcomes. Further analyses showed that child mental health at ages 11 vs. 14 was more likely to predict the outcomes. Based on individual factors, externalising symptoms and experiencing peer bullying at age 11 may be important contributors to overweight and obesity development.

Poor child mental health at age 11 is associated with overweight and obesity development by age 17. Late childhood/early adolescence may be a sensitive period in which psychosocial factors predict body weight trajectories.

Worse psychosocial factors, particularly poor mental health, at ages 11, but not 14, were associated with overweight and obesity development and increased BMI z-scores by age 17. Late childhood/early adolescence may be a sensitive period for mental health in predicting future weight change. Future research will benefit from exploring this potential sensitive period and understanding potential mechanisms.

Eating disorders (EDs) are known as chronic mental disorders that can cause adverse physical and mental effects and affect different age groups, including children, and disrupt their growth and development. Based on this, the aim of this research is to determine the global prevalence of EDs in children.

To conduct this research, each of the databases PubMed, Scopus, Web of science, Embase, ScienceDirect and Google Scholar search engine were systematically searched using relevant keywords ("prevalence,""outbreak,""eating disorder,""feeding disorder,""eating problem,""appetite disorder,"to find all the studies that refer to the prevalence of EDs in children until July 23, 2024 to obtain and perform further evaluations. After data extraction, their analysis was done by Comprehensive Meta-Analysis software (Version 2); Random effects model was used for analysis and I2 index was also used to check the heterogeneity of studies.

Based on the global prevalence of EDs in children based on meta-analysis was 1% (95% CI: 0.6-1.6); Subgroup analysis based on the study of eating disorders in children showed that the prevalence of pica among children is 2.1% (95% CI: 1-4.6), the prevalence of binge eating disorder is 1% (95% CI: 0.6-1.8), and the prevalence of anorexia nervosa and Bulimia nervosa among children is 0.6% (95% CI: 0.01-34.4) and 0.1% (95% CI: 0-0.4), respectively.

Considering the importance of nutrition in children and the report of EDs among them, healthcare workers and medical personnel must pay attention to this category of disorders by timely informing parents to reduce the complications caused by it.

This observational study compared children with and without binge eating (BE) on biobehavioral measures of reward responsiveness, inhibitory control, and emotion processes, while accounting for the impact of weight.

Children aged 9 to 10 years completed the baseline wave of the Adolescent Brain Cognitive Development Study (316 with BE; 7,681 without BE [no-BE]). The prevalence of binge-eating disorder in the BE group was 17.0%; clinically significant internalizing and externalizing symptoms were endorsed by 8.5% and 4.5% of the sample, respectively. The monetary incentive delay (MID) task, stop signal task (SST), and emotional N-Back (EN-Back) task were administered during neuroimaging. Analyses assessed effects of group (BE vs no-BE) on task performance and corresponding neural signal in regions of interest (ROIs). Weight status was evaluated as a covariate and as a moderator of effects.

Adjusting for weight status, the BE group (vs no-BE) group showed lower activation during anticipation of reward, specifically large reward (vs no reward), in the composite ROI consisting of the dorsal striatum, nucleus accumbens, orbital frontal gyrus, amygdala, and insula. Groups did not differ significantly in other behavioral or neural outcomes. No interactions between group and weight status were observed.

Blunted anticipatory responses to monetary reward were associated with binge eating during peri-adolescence and may play a role in binge eating pathophysiology. Results challenge prior findings in BE that may be confounded by weight, and highlight the importance of future prospective research across binge-eating disorder stage of illness.

Binge eating disorder, the most common eating disorder, is associated with several negative psychosocial consequences. This study used data from the Adolescent Brain Cognitive Development (ABCD) Study and compared children (ages 9-10) with and without binge eating on neurobiological and behavioral measures of reward responsiveness, inhibitory control, and emotion processes. Children with binge eating showed lower neural activation during anticipation of reward, specifically large reward, compared to youth without binge eating. These findings suggest that blunted anticipatory response during peri-adolescence may play a role in binge eating pathophysiology.

There is limited evidence on how changes in obesity from childhood to adolescence are associated with adolescent mental health. We examined the associations between childhood obesity trajectories, obesity episodes, and mental health at age 17.

Data were from the UK Millennium Cohort Study. Obesity trajectory groups at ages 7 and 17 (n = 8306) and previous obesity episodes (number of sweeps with obesity) at ages 7, 11 and 14 (n = 7246) were examined. Caregiver and self-reported internalising and externalising symptoms at age 17 were used to measure mental health. Linear regression models were used.

Relative to never developing obesity, obesity development (β = 1.01; 95% CI = 0.71, 1.32) and persistence (β = 1.18; 95% CI = 0.74, 1.61) were associated with higher internalising symptoms at age 17 and worsening (increase in scores) of these symptoms between ages 7 and 17 (β = 0.87; 95% CI = 0.57, 1.17 and β = 0.86; 95% CI = 0.56, 1.26 for development and persistence, respectively). Obesity development was associated with higher externalising symptoms at age 17 (β = 0.52; 95% CI = 0.25, 0.80) and worsening of these symptoms over time (β = 0.30; 95% CI = 0.07, 0.53). Having multiple past obesity episodes was not associated with worsening mental health independent of follow-up weight status. There were no differences in mental health outcomes between children who reversed versus never developed obesity.

Obesity development or persistence from ages 7 to 17 are associated with worsening mental health. If childhood obesity is reversed, there appears to be no evidence of a negative association between previous obesity and mental health at age 17.

The present study was developed to investigate how litter reduction-induced obesity promotes early depressive-related behaviors in rodent offspring.

We employed a standardized litter size reduction protocol, dividing litters into groups: normal litters (NL), consisting of six males and six females pups and small litters (SL), comprising two males and two females pups. Maternal behavior was monitored during the initial week of lactation. Subsequently, we assessed the pups for weight gain, locomotor activity, social play behavior, and performance in forced swimming test. We further evaluated the weights of retroperitoneal and perigonadal fat tissues, along with the expression of glial fibrillary acidic pprotein (GFAP) in the hippocampus and prefrontal cortex of the offspring.

Our results indicated that litter size reduction led to an increased the maternal behavior. In contrast, offspring from the SL group displayed greater weight gain and increased, retroperitoneal and perigonadal fat. Both male and female rodents in the SL group exhibited decreased social play behavior, and male offspring spent more time immobile during the forced swimming test, suggesting a depressive-like phenotype. Notably, we observed an increase in the GFAP expression in the prefrontal cortex of male rodents, with a trend toward increased expression in the hippocampus.

Obesity may facilitate the development of early depressive-like behaviors, potentially associated with elevated GFAP expression in the prefrontal cortex.

While recent works suggested that overweight/obesity may impair executive function (EF), the overweight/obesity-EF relationship has not been well studied in adolescents. Furthermore, no research has investigated adolescent EF impairments across the weight spectrum (e.g., underweight or thinness, normal, overweight/obesity), especially those with underweight condition, with the moderating effect of negative emotions in the weight-EF association being limitedly investigated. We aimed to determine whether overall and abdominal weight spectrum associated with EF impairments and to identity whether negative emotions moderate the weight-EF link in adolescents.

We applied a subsample of the SCHEDULE-A project. Adolescents (11-18 years) were recruited using a multi-stage cluster random sampling approach. We measured the overall and abdominal weight spectrum by body mass index z-score and waist-to-height ratio, respectively. We used the Behavior Rating Inventory of Executive Function (BRIEF) to evaluate adolescent EF in nature setting, and utilized the Depression Anxiety and Stress Scales (DASS-21) to assess three types of negative emotional status (i.e., depression, anxiety, and stress).

Of the 1935 adolescents, 963 (49.8%) were male. We observed that abdominal, not overall, overweight was associated with the Global Executive Composite (GEC) impairment (OR = 1.59, 95% CI 1.07-2.35), particularly for inhibit, emotion control, shift, working memory, and monitor domains. Furthermore, depression moderated the abdominal overweight-GEC association (P = 0.032 for interaction term), especially for emotional control, working memory, and initiate dimensions. Moreover, we also found abdominal thinness was associated with the Metacognition Index problem (OR = 1.33, 95% CI 1.04-1.72), particularly for plan and monitor areas.

Both abdominal overweight and thinness were associated with adolescent EF, and depression would be a modifiable target to improve EF in adolescents with abdominal overweight. Future longitudinal studies are needed to investigate the causal relationship between abdominal weight spectrum and EF, as well as the underlying mechanisms among adolescents suffering from depression.