Nonlinear associations between insomnia symptoms and circadian preferences in the general population: Symptom-specific and lifespan differences in men and women.

OBJECTIVES: This study investigated (non)linear associations between different eveningness characteristics (bedtime, wake time, morning affect, and peak performance time) and insomnia symptoms (difficulties initiating sleep, difficulties maintaining sleep, and nonrestorative sleep) in a large general population sample. METHODS: The data came from digital surveys about insomnia (Minimal Insomnia Scale) and circadian preferences (Children's Chronotype Questionnaire/Composite Scale of Morningness) completed by the Dutch general population (37,389 participants aged 4-91years, 42.4% men) in the Lifelines cohort substudy Comorbid Conditions of ADHD. RESULTS: Using generalized additive modeling, we found that different characteristics of eveningness related to insomnia either exponentially (later wake time/peak performance time, worse morning affect) or quadratically (early and late bedtime/midpoint of sleep). While difficulties initiating sleep and nonrestorative sleep were strongly associated with all eveningness characteristics, difficulties maintaining sleep related only to earlier bedtimes. These relationships were similar for men and women but varied partly in shapes and strengths across the lifespan. Additional analyses showed that bedtime and wake time were associated with insomnia symptoms only when their combination would result in an unusually long or short preferred time in bed. CONCLUSION: The association between eveningness and insomnia symptoms highly depends on whether eveningness is reflected by daytime performance or sleep-wake time. The pattern and strength of these associations also vary depending on age and insomnia symptom, but less so on sex. Future sleep-related research and policies relying on circadian preferences should account for the nonlinearity, dimension/symptom-related specificity and age-related differences in the association between eveningness and insomnia symptoms.

Longitudinal effects of environmental noise and air pollution exposure on autism spectrum disorder and attention-deficit/hyperactivity disorder during adolescence and early adulthood: The TRAILS study.

BACKGROUND: Exposure to ambient noise and air pollution may affect the manifestation and severity of Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD). However, evidence is limited, and most studies solely assessed environmental exposures during pregnancy and early childhood. OBJECTIVE: To examine the longitudinal effects of ambient noise and air pollutants on ASD and ADHD symptom severity during adolescence and early adulthood. METHODS: Using a longitudinal design, we included 2750 children between 10 and 12 years old from the TRacking Adolescents' Individual Lives Survey (TRAILS) in the Netherlands, who were assessed in 6 waves from 2001 to 2017. ASD was measured by the Children's Social Behavior Questionnaire and the Adult Social Behavior Questionnaire. ADHD was measured by Child Behavior Checklist and the Adult Behavior Checklist. Ambient noise and air pollution exposures, including Ozone (O3), soot, sulfur dioxide (SO2), nitrogen dioxide (NO2), particulate matter 2.5 (PM2.5), and PM10 were modeled at the residential level according to standardized protocols. The longitudinal associations between exposures and symptom outcomes were examined using linear mixed models. RESULTS: We found evidence that higher levels of exposure to PM were associated with more severe ASD and ADHD symptoms. This association decreased over time. We did not observe any other consistent associations of noise or other air pollutants with ASD and ADHD severity. CONCLUSION: The current study provides evidence for the negative impact of PM on ASD and ADHD symptoms. We did not find evidence of the negative health impact of other air pollutants and noise exposures on ASD or ADHD symptoms. Our study adds more evidence on the presence of associations between PM air pollution and neurodevelopmental diseases among adolescents and young adults.

Reward Sensitivity at Age 13 Predicts the Future Course of Psychopathology Symptoms.

Background: There are numerous observations of reward sensitivity being associated with different psychiatric disorders. Nonetheless, most studies investigating this relationship have been cross-sectional. Additionally, current knowledge is fragmentary as studies often investigate only one disorder at a time. The present study addresses these gaps by investigating whether reward sensitivity at age 13 predicts the course of nine psychopathology domains (attention and hyperactivity, autism spectrum, reactive aggression, proactive aggression, mood, anxiety, smoking, alcohol use, and cannabis use) over a 14-year follow-up period. Methods: We used dimensional outcomes on 2,523 individuals over five measurement waves between ages 13 and 26 of the Dutch Tracking Adolescents' Individual Lives Survey (TRAILS). Reward sensitivity was measured with the Behavioral Activation System (BAS) scale. The longitudinal associations between reward sensitivity and psychopathology were examined using growth curve analysis within a multilevel framework. Results: Reward sensitivity at age 13 was associated with changes in psychopathology over time. Reward sensitivity had a stable main effect on the future course of reactive and proactive aggression problems and anxiety problems. The effect of reward sensitivity increased over time for alcohol and cannabis use. Post-hoc analyses showed that reward sensitivity also had a stable effect on attention problems and hyperactivity and smoking when based on the fun-seeking subscale for both domains and when changing the informant who reported on attention problems and hyperactivity. No evidence was found for a longitudinal association between reward sensitivity and autism spectrum problems and mood problems. Conclusion: The current study provides evidence for the long-lasting effects of reward sensitivity on the course of different domains of psychopathology.