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Background: Cross-sectional studies have shown that hyperactivity and impaired executive functioning are associated with symptoms of eating disorders in adolescence and adulthood. Whether hyperactivity and executive functions in early life can prospectively predict the emergence of eating disorder symptoms in adolescence remains unknown. The present study relies on a longitudinal design to investigate how hyperactivity at age 3, eating behaviours at age 3.5 and cognition at ages 3–6 were associated with the development of eating-disorder symptoms from 12 to 20 years old. Methods: Using archival data collected since 1997 from the Quebec Longitudinal Study of Child Development cohort (N = 2, 223), we used Latent Curve Models to analyse predictors of youth's trajectories of eating-disorder symptoms at four timepoints. Results: A quadratic (curvilinear) trajectory of eating-disorder symptoms was found to be most representative of the data. Higher hyperactivity at age 3 was associated with higher levels of eating-disorder symptoms at age 12, and this association was partially mediated by higher levels of overeating and cognitive inflexibility in childhood. Cognitive inflexibility in childhood also mediated the association between hyperactivity at age 3 and increases in eating-disorder symptoms during adolescence. Furthermore, working memory was indirectly related to eating-disorder symptoms via the mediational role of cognitive flexibility. Conclusions: Hyperactivity, overeating, cognitive inflexibility, and working memory early in life might precede the onset of eating-disorder symptoms in adolescence. Early behavioural and cognitive screening may help to identify children who are most at risk for eating disorders. This, in turn, could guide preventive interventions. Plain English summary: Eating-disorder symptoms, such as body image issues, maladaptive behaviors, and preoccupation with weight, tend to develop in adolescence. However, it is unclear whether early childhood characteristics or behaviours could be indicators of a risk of developing eating-disorder symptoms later. The current study examined the possible link between certain early behaviours (e.g., hyperactivity, childhood eating), early cognitive processes, and eating-disorder symptoms development in a community cohort followed from birth. Results showed that being hyperactive in early childhood predicts higher levels of eating-disorder symptoms at the beginning of adolescence (age 15), and that this is partially explained by a link between being hyperactive, being more rigid in our ways of thinking, and engaging in overeating behaviours. Additionally, more early rigid ways of thinking predicted the increase in symptoms over time. Our results demonstrate possible behaviours and characteristics that could be used to identify children at risk of eating disorders, which in future research could potentially help improve our preventive interventions. [ABSTRACT FROM AUTHOR]

Eating disorders have early origins, and there could be a continuum between childhood eating behaviors, such as overeating, and long-term disordered eating, but this remains to be shown. BMI, desire for thinness and peer victimization could influence this continuum, but their interactions are unknown. To fill this gap, the study used data from the Quebec Longitudinal Study of Child Development (N = 1511; 52% girls), in which 30.9% of youth presented a trajectory associated with high disordered eating from 12 to 20 years. The results support an indirect association between overeating at age 5 and disordered eating trajectories, with different mediation processes observed between boys and girls. The findings underscore the importance of promoting healthy body images and eating behaviors among youths. [ABSTRACT FROM AUTHOR]

Introduction: Eating disorders (EDs) have long been considered conditions exclusively affecting women, and studies in the ED field regularly exclude men. Research efforts are needed to better understand the role of gender and sex in EDs. This review describes the role of gender and sex in the development of EDs from a biopsychosocial perspective. Methods: The primary hypothesis of this narrative review is that gender and sex interact to influence ED risk. The literature review was conducted using the PubMed database. Results: This review first presents the general characteristics and prevalence of EDs according to gender and sex. Next, neurodevelopmental processes, neurobiology, gender roles, body image, and the minority stress model are addressed. Lastly, research perspectives to better include gender and sex in the field of EDs are discussed (e.g., representation of gender and sex diversities, development of appropriate assessment tools, and increasing awareness). Conclusion: Although substantial knowledge gaps remain, there is a growing recognition of the importance of integrating gender and sex in ED research that holds promise for further development in the field. [ABSTRACT FROM AUTHOR]

Background: Adolescence is a critical period for the development of eating disorders, but data is lacking on the heterogeneity of their evolution during that time-period. Group-based trajectories can be used to understand how eating disorders emerge and evolve over time. The aim of this study was to identify groups of individuals with distinct levels of eating disorder symptoms between 12 and 20 years and the onset of different types of symptoms. We also studied sex differences in the evolution and course of eating disorder symptoms from early adolescence to adulthood. Methods: Using archival data from the QLSCD cohort, trajectories of eating disorder symptomatology were estimated from ages 12 to 20 years using semiparametric models. These trajectories included overall eating disorder symptomatology as measured by the SCOFF (Sick, Control, One Stone, Fat, Food), sex, and symptom-specific trajectories. Results: Two groups of adolescents following distinct trajectories of eating disorder symptoms were identified. The first trajectory group included 30.9% of youth with sharply rising levels between 12 and 15 years, followed by high levels of symptoms between 15 and 20 years. The second trajectory group included 69.1% of youth with low and stable levels of symptoms between 12 and 20 years. Sex-specific models indicated that the proportion of girls in the high trajectory group was 1.3 times higher than the proportion of boys (42.8% girls vs. 32.3% boys). Trajectories of SCOFF items were similar for loss-of-control eating, feeling overweight, and attributing importance to food. The weight loss item had a different developmental pattern, increasing between 12 and 15 years and then decreasing between 17 and 20 years. Conclusions: The largest increase in eating disorder symptoms in adolescence is between the ages of 12 and 15. Yet, most prevention programs start after 15 years of age. Our findings suggest that, unlike common practices, eating disorder prevention programs should aim to start before puberty. Plain English summary: Eating disorders, typically involving preoccupation with eating, excessive exercise, and body image issues, are particularly common in adolescence. However, their evolution over time remains unclear as certain signs and symptoms may appear sooner than others. The current study studied the development of eating disorder symptoms in a community cohort followed from birth to adulthood. This study describes trajectories of eating disorder symptoms and risk from age 12 to 20 in both boys and girls. Results showed that the largest increase in eating disorder symptoms occurs between 12 and 15 years of age, both in overall symptomatology as well as in specific symptoms such as loss-of-control when eating, feeling overweight, and attributing importance to food. Additionally, more girls than boys appeared at risk for eating disorders, although the patterns represented by the trajectories were similar in both sexes. Our results highlight the importance of starting early prevention programs before the beginning of adolescence, when symptoms usually start to manifest. [ABSTRACT FROM AUTHOR]

Recent studies have reported altered methylation levels at disorder-relevant DNA sites in people who are ill with Anorexia Nervosa (AN) compared to findings in people with no eating disorder (ED) or in whom AN has remitted. The preceding implies state-related influences upon gene expression in people with AN. This study further examined this notion. We measured genome-wide DNA methylation in 145 women with active AN, 49 showing stable one-year remission of AN, and 64 with no ED. Comparisons revealed 205 differentially methylated sites between active and no ED groups, and 162 differentially methylated sites between active and remitted groups (Q < 0.01). Probes tended to map onto genes relevant to psychiatric, metabolic and immune functions. Notably, several of the genes identified here as being differentially methylated in people with AN (e.g. SYNJ2, PRKAG2, STAT3, CSGALNACT1, NEGR1, NR1H3) have figured in previous studies on AN. Effects also associated illness chronicity and lower BMI with more pronounced DNA methylation alterations, and remission of AN with normalisation of DNA methylation. Findings corroborate earlier results suggesting reversible DNA methylation alterations in AN, and point to particular genes at which epigenetic mechanisms may act to shape AN phenomenology. [ABSTRACT FROM AUTHOR]