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Open access Aug 2026

Birth Weight and Neurodevelopmental Disorders Across Diagnostic Categories: A Registry-Based Case-Control Study in Clinically Ascertained Samples.

Increasing prevalence of neurodevelopmental disorders (NDDs) is a growing public health concern. Identifying early risk markers may facilitate earlier intervention and reduce long-term burden. Although birth weight has been widely studied in relation to NDDs, evidence from clinically ascertained samples with single and overlapping diagnoses remains limited. In this case-control study, we compared birth weight between clinically referred individuals with intellectual disability (ID), autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD) from the Norwegian BUPgen registry (n = 720) and a population-based sample from the Norwegian Mother, Father and Child Cohort Study (MoBa) (n = 98,716). Perinatal data were obtained through linkage to the Medical Birth Registry of Norway. Associations were examined using logistic regression adjusted for gestational age, sex, and parental age. Additional analyses assessed interactions by sex and parental age, and birth weight categories. For each 100 g decrease in birth weight, odds significantly increased for the groups any NDD (one or more NDD diagnoses; OR = 1.04) and multiple diagnoses (two or more co-occurring NDDs; OR = 1.07). In diagnosis specific analyses, odds significantly increased for ID (OR = 1.15) and ASD (OR = 1.03). No interactions were observed. In categorical analyses, low birth weight was associated with higher odds of ID (OR = 8.27, p < 0.001), multiple diagnoses (OR = 4.96, p < 0.001), and any NDD (OR = 2.11, p = 0.002). No associations were observed for high birth weight. These findings support low birth weight as an early marker of neurodevelopmental vulnerability across NDD outcomes.

Eden Nordvold Barak, Knut K. Kolskår, Christine Dahl et al. · 0 citations
Open access Jul 2026

Distinct Associations of Threat and Deprivation With Changes in Affective Control during Adolescence: A Longitudinal Population‐Based Study

ABSTRACT Childhood adversity has been linked to disruptions in the development of emotion regulation, yet few longitudinal studies have examined whether distinct dimensions of adversity are differentially associated with changes in affective inhibitory control across adolescence. This study examined whether threat and deprivation experiences differentially predicted changes in affective inhibitory control across early to middle adolescence. Participants were 902 adolescents (51.5% girls) from the UEVO study, assessed at ages 12–14 years at Time 1 (T1) and 15–16 years at Time 2 (T2). Affective inhibitory control was measured using an online emotional go/no‐go task. Adolescents showed fewer false alarms to angry no‐go stimuli at T2 than at T1, indicating improvement in affective inhibitory control over time. Latent change score modeling further supported this pattern, showing that adolescents with poorer baseline performance demonstrated greater improvement over time (β = −0.66, p < 0.001). In the primary model, higher levels of threat predicted less improvement in affective inhibitory control (β = 0.09, p = 0.013), whereas deprivation was not significantly associated with change (β = −0.05, p = 0.073). Neither threat nor deprivation predicted change in false alarms to neutral faces. In sensitivity analyses adjusting for gender, age, socioeconomic status (SES), and caregiver risk, threat remained a significant predictor of less improvement (β = 0.12, p = 0.004), whereas deprivation emerged as a small predictor of greater improvement (β = −0.06, p = 0.042). Post‐hoc multigroup analyses provided no evidence that the associations between adversity and change differed by gender. These findings suggest that threat and deprivation show partly distinct associations with affective inhibitory control, with threat‐related adversity emerging as the more consistent predictor of reduced improvement across early to middle adolescence.

Sjur S. Sætren, Tore Tjora, C. Tamnes et al. · 0 citations