Non-suicidal self-injury among individuals with an eating disorder: A systematic review and prevalence meta-analysis.

OBJECTIVE: This study aimed to quantify the prevalence of non-suicidal self-injury across eating disorders (EDs) and within diagnostic categories through systematic review and proportional, or so-called prevalence, meta-analysis. METHOD: Included studies had to contain individuals with a verified diagnosis of an ED. The last literature search was conducted on September 11, 2023, for studies published on or before September 2023 without a restriction on earliest publication year. Results were synthesized and analyzed using the "metaprop" package in R and presented using forest plots. Bias was assessed by a Peters' regression test and funnel plot. RESULTS: 79 studies published between 1985 and 2023 were included encompassing 32,334 individuals with an ED. Importantly, 42 studies were not included in any other meta-analyses on self-injury in EDs to date. Overall prevalence of non-suicidal self-injury was 34.59% (95%CI = 30.49-38.81). Prevalence in anorexia nervosa restrictive type, binge/purge type, bulimia nervosa, binge eating disorder and other specified feeding/eating disorder were 23.19% (95%CI = 16.96-30.03%), 41.98% (95%CI = 32.35-51.91%), 36.97% (95%CI = 30.69-43.46%), 21.21% (95%CI = 14.93-28.12%) and 37.65% (95%CI = 28.59-47.09%), respectively. Prevalence estimations could not be estimated for other ED categories due to lack of a sufficient number of studies. DISCUSSION: Non-suicidal self-injury is prevalent across both binge/purge and restrictive EDs. Considering the transdiagnostic nature of self-injurious behaviors in ED, the results highlight the importance of assessment and monitoring of self-injury in people with ED, irrespective of specific diagnoses. The method of determining self-injury varied across studies and may limit this study. PUBLIC SIGNIFICANCE: This study highlights the prevalence of self-injury across eating disorders irrespective of diagnosis and within specific EDs. While diagnoses known to exhibit self-injurious behaviors (e.g., bulimia nervosa, anorexia nervosa binge/purge subtype) demonstrated the highest prevalence of self-injury, all diagnoses were found to have a prevalence greater than 20%. These findings suggest the importance of assessing and monitoring all individuals with an eating disorder for the presence of self-injury.

OBJETIVO: Este estudio tuvo como objetivo cuantificar la prevalencia de la autolesión no suicida en los trastornos de la conducta alimentaria (TCA) y dentro de las categorías diagnósticas mediante una revisión sistemática y un metaanálisis proporcional, también llamado metaanálisis de prevalencia. MÉTODO: Los estudios incluidos debían contener individuos con un diagnóstico verificado de un TCA. La última búsqueda bibliográfica se realizó el 11 de septiembre de 2023, para estudios publicados en o antes de septiembre de 2023 sin restricción en el año de publicación más temprano. Los resultados fueron sintetizados y analizados utilizando el paquete "metaprop" en R y presentados mediante gráficos de bosque. El sesgo se evaluó mediante una prueba de regresión de Peters y un gráfico de embudo. RESULTADOS: Se incluyeron 79 estudios publicados entre 1985 y 2023 que abarcaron a 32,334 individuos que padecían un TCA. Es importante destacar que 42 estudios no se incluyeron en ningún otro metaanálisis sobre autolesión en TCA hasta la fecha. La prevalencia general de la autolesión no suicida fue del 34.59% (IC del 95% = 30.49-38.81). La prevalencia en la anorexia nerviosa subtipo restrictivo, subtipo atracones/purga, bulimia nerviosa, trastorno de atracones y otros trastornos especificados de la conducta alimentaria y de la alimentación fue del 23.19% (IC del 95% = 16.96-30.03%), 41.98% (IC del 95% = 32.35-51.91%), 36.97% (IC del 95% = 30.69-43.46%), 21.21% (IC del 95% = 14.93-28.12%) y 37.65% (IC del 95% = 28.59-47.09%), respectivamente. No se pudieron estimar las estimaciones de prevalencia para otras categorías de TCA debido a la falta de un número suficiente de estudios. DISCUSIÓN: La autolesión no suicida es prevalente tanto en los TCA subtipo de atracón/purgación como en los restrictivos. Dada la naturaleza transdiagnóstica de los comportamientos autolesivos en los TCA, los resultados resaltan la importancia de la evaluación y el monitoreo de la autolesión en personas que padecen TCA, independientemente de los diagnósticos específicos. El método para determinar la autolesión varió entre los estudios y puede limitar este estudio.

Childhood hyperactivity, eating behaviours, and executive functions: Their association with the development of eating-disorder symptoms in adolescence.

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.

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.

Childhood Overeating and Disordered Eating From Early Adolescence to Young Adulthood: A Longitudinal Study on the Mediating Role of BMI, Victimization and Desire for Thinness.

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.

Gender and sex in eating disorders: A narrative review of the current state of knowledge, research gaps, and recommendations.

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.

DNA methylation in people with anorexia nervosa: Epigenome-wide patterns in actively ill, long-term remitted, and healthy-eater women.

OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Pathways of association between disordered eating in adolescence and mental health outcomes in young adulthood during the COVID-19 pandemic.

OBJECTIVES: The COVID-19 pandemic has been associated with increased mental health problems. We investigated (1) associations between disordered eating in adolescence and mental health problems after one year of the pandemic and (2) the mechanisms explaining associations. METHOD: We analyzed data from a population-based birth cohort in Quebec, Canada (557 males and 759 females). High and low levels of disordered eating symptom trajectories were previously estimated (age 12, 15, 17, and 20 years). Anxiety, depression, non-suicidal self-injury, and suicidal ideation were assessed at 23 years (March-June 2021). Putative mediators included loneliness and social media use (age 22 years, July-August 2020). Analyses controlled for mental health and socio-economic status at age 10-12 years and were conducted for males and females separately. RESULTS: Females in the high-level disordered eating symptom trajectory were at increased risk for non-suicidal self-injury (OR 1.60; 95% CI 1.02-2.52) and suicidal ideation (2.16; 1.31-3.57), whereas males were at increased risk for severe anxiety (2.49; CI 1.11-5.58). Males and females in the high-level trajectory were more likely to report severe depression (2.26; 1.14-5.92 and 2.15, 1.36-3.38 respectively). Among females, associations were partially explained (17-35%) by loneliness during the first 4 months of the pandemic. CONCLUSION: Young adults who experienced disordered eating as adolescents were at increased risk of mental health problems during the pandemic. Loneliness partially mediated the effect, suggesting that pandemic mitigation resulting in increased social isolation may have exacerbated mental health problems among women with a history of disordered eating.

RéSUMé: OBJECTIFS: La pandémie de COVID-19 a été associée à une augmentation des problèmes de santé mentale. Nous avons investigué 1) les associations entre les problèmes de comportement alimentaire à l'adolescence et les problèmes de santé mentale après un an de pandémie et 2) les mécanismes expliquant les associations. MéTHODE: Nous avons analysé les données d'une cohorte de naissance basée sur la population au Québec, Canada (557 hommes et 759 femmes). Nous avons utilisé des trajectoires précédemment estimées indicatives d'un haut et bas niveau de problèmes alimentaires (à l'âge de 12, 15, 17 et 20 ans). L'anxiété, la dépression, l'automutilation et les idées suicidaires ont été évaluées à 23 ans (mars à juin 2021). Les médiateurs putatifs incluaient la solitude et l'utilisation des réseaux sociaux (à l'âge de 22 ans, juillet à août 2020). Les analyses contrôlaient la santé mentale et le statut socio-économique à l'âge de 10 à 12 ans et ont été menées séparément pour les hommes et les femmes. RéSULTATS: Les femmes dans la trajectoire des problèmes alimentaires élevés présentaient un risque accru d'automutilation non-suicidaire (OR 1,60; IC à 95 % 1,02-2,52) et d'idées suicidaires (2,16; 1,31-3,57), tandis que les hommes présentaient un risque accru d'anxiété sévère (2,49; IC 1,11-5,58). Les hommes et les femmes de la trajectoire élevée étaient plus susceptibles de déclarer une dépression grave (2,26; 1,14-5,92 et 2,15; 1,36-3,38, respectivement). Chez les femmes, les associations s'expliquaient en partie (17-35 %) par la solitude durant les 4 premiers mois de la pandémie. CONCLUSION: Les jeunes adultes ayant connu des problèmes de comportement alimentaire à l'adolescence couraient un risque accru de problèmes de santé mentale pendant la pandémie. La solitude a partiellement atténué l'effet, suggérant que l'isolation accrue entrainée par la pandémie peut avoir exacerbé les problèmes de santé mentale chez les femmes ayant des antécédents de problèmes de comportement alimentaire.

Developmental trajectories of eating disorder symptoms: A longitudinal study from early adolescence to young adulthood.

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.

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.

DNA methylation at the DMPK gene locus is associated with cognitive functions in myotonic dystrophy type 1.

Aim: Myotonic dystrophy type 1 (DM1) is caused by an unstable trinucleotide (CTG) expansion at the DMPK gene locus. Cognitive dysfunctions are often observed in the condition. We investigated the association between DMPK blood DNA methylation (DNAm) and cognitive functions in DM1, considering expansion length and variant repeats (VRs). Method: Data were obtained from 115 adult-onset DM1 patients. Molecular analyses consisted of pyrosequencing, small pool PCR and Southern blot hybridization. Cognitive functions were assessed by validated neuropsychological tests. Results: For patients without VRs (n = 103), blood DNAm at baseline independently contributed to predict cognitive functions 9 years later. Patients with VRs (n = 12) had different DNAm and cognitive profiles. Conclusion: DNAm allows to better understand DM1-related cognitive dysfunction etiology.

Placental Epigenome-Wide Association Study Identified Loci Associated with Childhood Adiposity at 3 Years of Age.

The aim of this study was to identify placental DNA methylation (DNAm) variations associated with adiposity at 3 years of age. We quantified placental DNAm using the Infinium MethylationEPIC BeadChips. We assessed associations between DNAm at single-CpGs and skinfold thickness using robust linear regression models adjusted for gestational age, child's sex, age at follow-up and cellular heterogeneity. We sought replication of DNAm association with child adiposity in an independent cohort. We quantified placental mRNA levels for annotated gene using qRT-PCR and tested for correlation with DNAm. Lower DNAm at cg22593959 and cg22436429 was associated with higher adiposity (ß = -1.18, q = 0.002 and ß = -0.82, q = 0.04). The cg22593959 is located in an intergenic region (chr7q31.3), whereas cg22436429 is within the TFAP2E gene (1p34.3). DNAm at cg22593959 and cg22436429 was correlated with mRNA levels at FAM3C (rs = -0.279, p = 0.005) and TFAP2E (rs = 0.216, p = 0.03). In an independent cohort, the association between placental DNAm at cg22593959 and childhood adiposity was of similar strength and direction (ß = -3.8 ± 4.1, p = 0.36), yet non-significant. Four genomic regions were also associated with skinfold thickness within FMN1, MAGI2, SKAP2 and BMPR1B genes. We identified placental epigenetic variations associated with adiposity at 3 years of age suggesting that childhood fat accretion patterns might be established during fetal life.

Mediation Analysis Supports a Causal Relationship between Maternal Hyperglycemia and Placental DNA Methylation Variations at the Leptin Gene Locus and Cord Blood Leptin Levels.

Changes in fetal DNA methylation (DNAm) of the leptin (LEP) gene have been associated with exposure to maternal hyperglycemia, but their links with childhood obesity risk are still unclear. We investigated the association between maternal hyperglycemia, placental LEP DNAm (25 5'-C-phosphate-G-3' (CpG) sites), neonatal leptinemia, and adiposity (i.e., BMI and skinfold thickness (ST) (subscapular (SS) + triceps (TR) skinfold measures, and the ratio of SS:TR) at 3-years-old, in 259 mother-child dyads, from Gen3G birth cohort. We conducted multivariate linear analyses adjusted for gestational age at birth, sex of the child, age at follow-up, and cellular heterogeneity. We assessed the causal role of DNAm in the association between maternal glycemia and childhood outcomes, using mediation analysis. We found three CpGs associated with neonatal leptinemia (p ≤ 0.002). Of these, cg05136031 and cg15758240 were also associated with BMI (ß = -2.69, p = 0.05) and fat distribution (ß = -0.581, p = 0.05) at 3-years-old, respectively. Maternal glycemia was associated with DNAm at cg15758240 (ß = -0.01, p = 0.04) and neonatal leptinemia (ß = 0.19, p = 0.004). DNAm levels at cg15758240 mediates 0.8% of the association between maternal glycemia and neonatal leptinemia (p < 0.001). Our results support that DNAm regulation of the leptin pathway in response to maternal glycemia might be involved in programming adiposity in childhood.

DNA methylation at LRP1 gene locus mediates the association between maternal total cholesterol changes in pregnancy and cord blood leptin levels.

Placental lipids transfer is essential for optimal fetal development, and alterations of these mechanisms could lead to a higher risk of adverse birth outcomes. Low-density lipoprotein receptor (LDLR), LDL receptor-related protein 1 (LRP1), and scavenger receptor class B type 1 (SCARB1) genes are encoding lipoprotein receptors expressed in the placenta where they participate in cholesterol exchange from maternal to fetal circulation. The aim of this study was thus to investigate the association between maternal lipid changes occurring in pregnancy, placental DNA methylation (DNAm) variations at LDLR, LRP1, and SCARB1 gene loci, and newborn's anthropometric profile at birth. Sixty-nine normoglycemic women were followed from the first trimester of pregnancy until delivery. Placental DNAm was quantified at 43 Cytosine-phosphate-Guanines (CpGs) at LDLR, LRP1, and SCARB1 gene loci using pyrosequencing: 4 CpGs were retained for further analysis. Maternal clinical data were collected at each trimester of pregnancy. Newborns' data were collected from medical records. Statistical models included minimally newborn sex and gestational and maternal age. Maternal total cholesterol changes during pregnancy (ΔT3-T1) were correlated with DNAm variations at LDLR (r = -0.32, p = 0.01) and LRP1 (r = 0.34, p = 0.007). DNAm at these loci was also correlated with newborns' cord blood triglyceride and leptin levels. Mediation analysis supports a causal relationship between maternal cholesterol changes, DNAm levels at LRP1 locus, and cord blood leptin concentration (pmediation = 0.02). These results suggest that LRP1 DNAm link maternal blood cholesterol changes in pregnancy and offspring adiposity at birth, which provide support for a better follow-up of blood lipids in pregnancy.