Attention Deficit Hyperactivity Disorder (ADHD) is a prevalent neurodevelopmental disorder in children. Abnormalities in sleep metrics among ADHD children gradually garnered attention. However, whether significant differences existed in sleep metrics between ADHD children and their typically developing (TD) counterparts remained controversial, with inconsistent conclusions across studies. Furthermore, the potential moderating effects of age and gender on these differential patterns remained insufficiently characterized.

The current study systematically analyzed multimodal sleep monitoring data (polysomnography, actigraphy, electroencephalography, and questionnaires) from 34 articles spanning three decades (44 independent studies: 2,239 ADHD children vs. 57,181 TD children), focusing on core sleep metrics (total sleep time, sleep efficiency, sleep latency, wake after sleep onset, awakening index, and stage shifts) and their complex moderating mechanisms.

The results demonstrated that ADHD children exhibited impaired sleep continuity (reduced total sleep time, increased stage shifts), severe sleep interruption (prolonged wake after sleep onset, elevated awakening index), and abnormal sleep process effectiveness (decreased sleep efficiency, extended sleep latency). Demographic analyses revealed that maturation exacerbated ADHD-related sleep deficits, and male ADHD children had more severe sleep problems than female ADHD children. Furthermore, the moderating effect of gender composition on the awakening index showed interaction effects with other sleep metrics. In addition, slow-wave sleep acted as both a moderator and mediator in group differences of the awakening index.

These findings provided novel neurodevelopmental explanations for sleep dysregulation in ADHD and proposed clinically translatable strategies involving gender-specific interventions and neuromodulation targeting slow-wave sleep.

Adolescence marks a critical period for the onset of anxiety disorders, yet they frequently remain undiagnosed due to barriers such as reluctance to self-disclose symptoms. Objective screening methods that bypass self-report may improve early detection. Speech-derived acoustic markers have emerged as a promising avenue for identifying anxiety disorders. This study investigates associations between acoustic properties of speech, anxiety severity, and anxiety diagnoses in adolescents, evaluated cross-sectionally and longitudinally.

Speech samples from 581 adolescents were collected during the Trier Social Stress Test. Acoustic features were extracted using OpenSMILE and analyzed for cross-sectional associations with anxiety severity (Spearman’s correlations) and longitudinal predictions of future anxiety (linear regressions). Random forest (RF) classifiers with 10-fold cross-validation were used to classify anxious and healthy individuals using acoustic features. Analyses were stratified by sex.

RFs achieved the highest performance for the longitudinal classification of social anxiety disorder (SAD), with an AUC-ROC of 85% (males) and 74% (females). Adding acoustic features to baseline measures increased the variance explained in anxiety by 5.4% (males) and 10.9% (females). In males, higher anxiety was cross-sectionally correlated with reduced pitch slope, narrower pitch range, lower F1 frequency, and greater MFCC1 variability. Females with higher anxiety showed reduced variability in pitch slope. Correlations did not survive multiple testing correction.

Acoustic speech markers elicited in socially evaluative contexts can accurately recognize SAD in male adolescents three years in advance. Performance is moderate for females and other anxiety disorders, underscoring the need for sex-specific approaches to diagnostic tool development.

Anorexia nervosa has potential to influence the development and function of the gastrointestinal system. We assessed the association between maternal anorexia nervosa and risk of gastrointestinal morbidity in offspring.

We analyzed a longitudinal cohort of 1,269,370 children born in Quebec, Canada, between 2006 and 2022. The exposure was maternal anorexia nervosa. The outcome was hospitalization for pediatric gastrointestinal disorders, including hypertrophic pyloric stenosis, inflammatory bowel disease, and other digestive morbidity. Follow-up ranged from 1 to 17 years. We used adjusted Cox regression models to obtain hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between maternal anorexia nervosa and pediatric gastrointestinal disorders.

A total of 2,447 children (0.2%) had a mother with anorexia nervosa. By age 17 years, the cumulative incidence of gastrointestinal disorders was higher among children whose mothers had anorexia nervosa than other children (165.7 vs. 129.4 per 1,000). Compared with no anorexia, maternal anorexia nervosa was associated with a greater risk of any childhood gastrointestinal disorder (HR: 1.42, 95% CI: 1.26–1.61), particularly hypertrophic pyloric stenosis (HR: 2.51, 95% CI: 1.35–4.66), inflammatory bowel disease (HR: 2.46, 95% CI: 1.67–3.64), and rectal hemorrhage (HR: 3.46, 95% CI: 1.97–6.09). Children whose mothers developed anorexia nervosa after age 20 years or were hospitalized more than once for anorexia had the greatest risk of gastrointestinal morbidity. The associations were not explained by digestive birth defects.

Maternal anorexia nervosa is associated with pediatric gastrointestinal disorders that could potentially be mitigated with psychosocial support, nutritional rehabilitation, and breastfeeding.

Evidence on psychological side effects (PSEs) of antipsychotic medication after remission from first-episode psychosis (FEP), and their momentary impact on daily life, is limited. This study examined how Dopamine-2 (D2) affinity and antipsychotic dosage relate to momentary PSEs.

This ecological momentary assessment (EMA) study included baseline data from 56 participants in the ongoing Handling Antipsychotic Medication: Long-term Evaluation of Targeted Treatment (HAMLETT) trial. Momentary mental states indicative of reduced affect intensity, stability, and variability, as well as avolition and mental fatigue, were assessed 10×/day for eight days (N = 3,005 data points). Since these PSEs may result from D2-receptor actions, antipsychotics were classified by receptor affinity and mechanism of action. Multilevel mixed-effects regression models examined serial cross-sectional associations between D2 affinity or dosage and concurrent PSEs, both overall and separately for mornings, daytimes, and evenings.

Higher antipsychotic dosages were associated with reduced affect variability (Beta [B] = −1.40 [95% confidence interval [CI]: −2.52; −0.29]) and decreased positive affect stability (B = 0.23 [95% CI: 0.04; 0.42]) and intensity (B = −1.11 [95% CI: −1.97; −0.24]). The latter was also associated with the use of high-affinity D2 antagonists versus partial D2 agonists (B = 12.98 [95% CI: 2.43; 23.53]) and versus low-affinity D2 antagonists (B = 10.04 [95% CI: 0.59; 19.49]). Other PSEs were not associated with D2 affinity/dosage. Results were relatively consistent across daytimes.

Higher antipsychotic dosage and high-affinity D2 antagonists were associated with decreased positive affect after remission from FEP, which may partly drive the frequently reported blunting of emotional experience.

Accumulating evidence suggests that stress, social relationships, and sex/gender differences in brain function, particularly of the orbitofrontal cortex (OFC), may drive problematic alcohol use. How these factors interact to effect alcohol use, and if they do so differently in men and women, has yet to be explored.

Using a subsample of the publicly available Human Connectome Project data consisting of young adults with problematic alcohol use (N = 491; 41.75% women, ≥1 symptom of alcohol abuse/dependence), we used a moderated moderation approach to test whether perceived stress and sex/gender moderated the effect of a multidimensional measure of social relationship quality on drinking levels. We subsequently tested whether OFC function moderated these effects.

We found that in women, higher friendship and companionship had a protective effect on drinking levels, particularly for women under high stress. In contrast, in men, higher friendship and companionship were linked to increased drinking levels under stress. Preliminary evidence suggested that this effect in men was driven by a subgroup of men with higher OFC reactivity to negative emotional faces.

Our findings suggest that women benefit from friendship and companionship as a form of stress-relief in the context of problematic drinking, whereas men do not, supporting the need of interventions that facilitate emotionally supportive, pro-recovery social environments particularly in men. Preliminary evidence further suggests a role of emotional dysregulation in men. Overall, our findings support the importance of developing sex/gender and neurobiologically informed interventions that target stress-related alcohol use.