ANXIETY IN ADOLESCENTS BORN 1999-2009: TEMPORAL TRENDS IN DIAGNOSIS, SYMPTOMS, AND EXPRESSION OF GENETIC LIABILITY

Background Anxiety disorders are among the most common mental health conditions in young people. Although anxiety shows moderate heritability, its expression is shaped by developmental, familial and cultural contexts. In many high income countries, rates of adolescent anxiety diagnoses have increased over recent decades, yet the mechanisms underlying these trends remain unclear. Rising diagnosis may reflect genuine increases in symptom burden, greater parental recognition of emotional difficulties, or shifts in diagnostic thresholds, help‑seeking or communication norms. Describing birth cohort differences in adolescent anxiety symptoms, maternal recognition, and diagnoses provide essential context for interpreting more mechanistic patterns. Advances in psychiatric genetics now allow detailed investigation of how genetic liability for anxiety is expressed within families. Polygenic scores (PGS) derived from recent GWAS index liability across the full anxiety spectrum. Applied in mother-father-child trios, PGS enable estimation of direct genetic effects (child PGS associated with own symptoms) and parent-to-child indirect genetic effects (parental PGS associated with adolescent outcomes via the family environment). Such within-family genetic associations estimated on outcomes such as anxiety symptoms and maternal recognition may also vary across historical time. Increasing openness about mental health and changes in parenting norms may alter how genetic liability is expressed or recognized in adolescents. Method Using preregistered analyses in the Norwegian Mother, Father and Child Cohort Study (MoBa), linked to diagnostic data from the Norwegian Patient Registry, we examine adolescents born between 1999 and 2009. We analyse temporal trends in self- and mother-reported anxiety symptoms (e.g., SCARED, miniSPIN), maternal recognition of emotional problems, and registry‑based diagnoses before age 15. Anxiety-related PGS, indexing both diagnostic and dimensional anxiety, are derived from recent large-scale genome-wide associations studies. Using trio based PGS models, we will first estimate associations between child, maternal, and paternal genetic liability and adolescent anxiety outcomes (e.g., symptoms, maternal recognition), distinguishing direct and indirect genetic pathways. We will then test whether these associations vary across birth cohorts. Finally, we will evaluate whether cohort based increases in anxiety diagnoses can be partly explained by historical changes in adolescent symptom and maternal recognition. Results Results will be presented at the conference. Discussion By integrating trio‑based genetic analyses with temporal and relational measures, this study provides new insight into how genetic liability for anxiety is expressed in adolescents and within families, and whether increasing diagnosis rates reflect changes in symptom burden, parental recognition, or shifts in the expression of genetic liability across birth cohorts.