Helga Ask

Depression and anxiety co-occur so frequently that comorbidity is more prevalent than the occurrence of either in isolation. The conventional latent-variable perspective offers limited insight into comorbidity because its inherent causal assumptions overlook causal relations among observable symptoms that are meaningful for explaining comorbidity. At the same time, comorbidity studies based on the network perspective have largely relied on cross-sectional data, which cannot capture the dynamic nature of mental disorders, or on two-wave panel data, which does not separate between- and within-variance and biases the estimation of dynamic processes. Therefore, we present a dynamic network analysis of depression-anxiety comorbidity with the panel graphical vector autoregressive model, using invariance partial pruning to consider possible network structural differences between biological sex. Results revealed the central role of fear in predicting depressive moods and anhedonia as a possible explanation of comorbidity. Anxiety symptoms temporally preceded depression symptoms. In the contemporaneous networks, nervousness and fear were connected to depressive mood. Furthermore, worry and rumination were more associated with depression, whereas beliefs about the uncontrollability of worry and threat monitoring were more associated with anxiety. No sex difference was discovered.

Background: Neurodivergent youth and youth with pre‐existing psychiatric disorders may have faced additional challenges in navigating the demands and restrictions of the COVID‐19 pandemic. However, less is known about how mental health outcomes and psychiatric healthcare utilization differed across diagnostic groups and other youth‐related factors. This systematic review synthesizes evidence on mental health symptoms and psychiatric healthcare use among youth with pre‐existing conditions during the pandemic. Methods: We searched PubMed, Web of Science and additional sources for cross‐sectional and longitudinal studies with data collected between March 2020 and May 2023. Eligible studies included neurodivergent youth and/or youth with psychiatric disorders confirmed through clinician diagnosis or medical records prior to the pandemic. Given the clinical and methodological diversity of studies, findings were synthesized narratively. Results: Forty‐eight studies met the inclusion criteria. Mental health outcomes showed mixed patterns both across and within diagnostic groups, with individual studies reporting symptom increase, stability and improvements. Evidence on psychiatric healthcare utilization was more limited and suggested different patterns between service use and psychotropic medication use. Compared to boys, girls were more likely to experience COVID‐related distress and increases in psychiatric service use during the pandemic. Age‐related findings varied across developmental stages and outcome domains. Most studies ( n = 40; 83.3%) had a moderate overall risk of bias (RoB), while seven (14.6%) had a high overall RoB. Conclusion: Mental health outcomes among youth with pre‐existing conditions during the COVID‐19 pandemic varied both within and across diagnostic groups. Outcomes were also associated with individual, developmental, contextual and service‐related factors. These findings suggest the importance of considering such factors alongside diagnosis when identifying clinical needs and planning support during large‐scale societal disruptions. Evidence on psychiatric healthcare utilization remains limited. More methodologically robust research is needed to clarify mental health and healthcare‐use patterns during major public health emergencies.

Background Adolescent mental health after the COVID-19 pandemic has been a major public health concern. Studies covering the post-pandemic period remain scarce and rarely include gender-diverse youth. We examined trends in mental health among cisgender, transgender, and nonbinary youth during the pandemic and through 2025. Methods Participants (N=636,201) were adolescents in grades 8-11 from the Finnish School Health Promotion study between 2019 and 2025, a repeated cross-sectional classroom survey. Validated questionnaires were used to assess clinical levels of depressive, generalized anxiety and social anxiety symptoms, as well as mental well-being. Results In 2025 there were 81,145 (48.6%) cisgender girls, 1137 (0.7%) transgender boys, 78,898 (47.2%) cisgender boys, 449 (0.3%) transgender girls, and 4658 (2.8%) nonbinary youth. Clinically significant depressive and generalized anxiety symptoms remained more prevalent in 2025 (reference) compared with pre-pandemic levels across all groups (ORs for 2019, 0.48-0.86; p<0.01). Compared with other groups, symptoms were most prevalent among transgender boys and nonbinary youth. Among cisgender youth, generalized anxiety symptoms increased across the post-pandemic period (ORs for 2021 and 2023, 0.81-0.95; p<0.0001). Nonbinary youth were the only group to show a recovery pattern in depressive, generalized anxiety, and social anxiety symptoms (ORs for 2021, 1.36-1.52; p<00001) and demonstrated improved mental well-being after the pandemic (beta for 2021, -0.68; p<0.0001). Conclusions The results indicate that the elevated levels of mental health problems among adolescents associated with the COVID-19 pandemic have not subsided. They also reveal persistent disparities by gender identity and call for targeted policy action.

Background/Objectives: Childhood appetitive traits are heritable behavioural phenotypes hypothesized to link genetic susceptibility to obesity risk. Yet their genetic architecture and role in mediating polygenic adiposity risk remain poorly understood. Methods: We conducted the largest survey of childhood eating behaviour to date, allowing us to perform genome-wide association studies of six appetitive domains derived from 18 items of the parent-reported Children’s Eating Behaviour Questionnaire in up to 31,018 eight-year-old children from the Norwegian Mother, Father and Child Cohort Study (MoBa). A trio-based design enabled decomposition of direct and indirect genetic effects on appetite and BMI. Results: We identified ten independent genome-wide significant loci for childhood eating behaviour, primarily across Food Responsiveness , Satiety Responsiveness , and Food Fussiness , eight of which lie at established childhood or adult BMI loci. Food Responsiveness and Satiety Responsiveness showed both phenotypic and genetic correlations with BMI trajectories from early childhood through adolescence. Statistical mediation analyses indicated that 22.1% and 10.4% of the aggregated genetic association with BMI at age 8 could be decomposed through these traits, respectively. Locus-specific patterns further suggested mechanistic pathways, with the FTO locus acting predominantly via Food Responsiveness , and the ADCY3 locus via Satiety Responsiveness . Trio analyses demonstrated that both BMI and eating behaviour associations were predominantly explained by children’s inherited alleles, with minimal contribution from indirect effect from parental adiposity, although parental genetic liability influenced reporting of Satiety Responsiveness . Conclusions: Childhood appetitive traits capture a substantial proportion of genetic susceptibility to adiposity through distinct eating behaviour pathways (under standard mediation assumptions). These effects are primarily driven by the child’s own genotype rather than indirect parental influences, positioning appetite as a plausible, biologically grounded target for early obesity prevention.

Eating disorders—including anorexia nervosa (AN), bulimia nervosa and binge-eating disorder—are clinically distinct but exhibit symptom overlap and diagnostic crossover. Genomic analyses have mostly examined AN. Here we conducted a genomic meta-analysis of case–control studies of binge-eating behavior (BE; 39,279 cases, 1,227,436 controls), alongside analyses of AN (24,223 cases, 1,243,971 controls) and its subtypes (all European ancestries). We identified six BE-associated loci, including loci associated with a higher body mass index and impulse-control behaviors. AN genome-wide association studies yielded eight loci, validating six loci. Subsequent polygenic risk score analysis demonstrated an association with AN in two East Asian ancestry studies. BE and AN exhibited similar positive genetic correlations with psychiatric disorders but opposing genetic correlations with anthropometric traits. Most of the genetic signal in BE and AN was not shared with body mass index. We have extended eating disorder genomics beyond AN; future work will incorporate multiple diagnoses and global ancestries.

Genome-wide association studies using large, population-based samples of unrelated individuals have discovered thousands of genetic associations with health and disease ¹ . These studies can help explain genetic and environmental risks. However, increasing evidence suggests that population-based estimates, while precise, can also reflect confounding that affects their use and interpretation. This confounding can be overcome using data from genotyped family members, such as nuclear mother–father–child trios ^2,3 . However, samples of genotyped families are rare ^4–11 . Here we illustrate some of the advantages of familial data using the Norwegian Mother, Father and Child Cohort Study (MoBa), a population-based cohort of parents and offspring with extensive genotype data ( n ≈ 230,000) (ref. ³ ), along with broad and longitudinal phenotyping of health and functioning. We provide an overview of MoBa and describe the quality control of genotype data tailored to this extensively related sample. We then use trio data to illustrate how family-based genomic designs can identify distinct direct and indirect sources of genetic influence and structural confounding. As examples, we analyse children’s height, educational achievement, depressive symptoms and sleep duration. These demonstrations highlight MoBa as a broadly valuable resource for advancing understanding of health and functioning across the lifecourse and generations.