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Both sleep problems and unemployment are common in adults with autism spectrum disorder; however, little research has explored this relationship in this population. This study aimed to explore factors that may be associated with the presence of an International Classification of Sleep Disorders-Third Edition defined sleep disorder in adults with autism spectrum disorder (IQ > 80). A total of 36 adults with autism spectrum disorder and 36 controls were included in the study. Participants completed a 14-day actigraphy assessment and questionnaire battery. Overall, 20 adults with autism spectrum disorder met the International Classification of Sleep Disorders-Third Edition criteria for insomnia and/or a circadian rhythm sleep-wake disorder, while only 4 controls met criteria for these disorders. Adults with autism spectrum disorder and an International Classification of Sleep Disorders-Third Edition sleep disorder had higher scores on the Pittsburgh Sleep Quality Index and were more likely to be unemployed compared to adults with autism spectrum disorder and no sleep disorder. The findings demonstrate, for the first time, that sleep problems are associated with unemployment in adults with autism spectrum disorder. Further research exploring the direction of this effect is required; sleep problems that have developed during adolescence make attainment of employment for those with autism spectrum disorder difficult, or unemployment results in less restrictions required for optimal and appropriate sleep timing.

Further examination of the molecular regulators of long-term calorie restriction (CR), reported to have an anxiolytic effect, may highlight novel therapeutic targets for anxiety disorders. Here, adult male Hooded Wistar rats were exposed to a 25% CR whilst anxiety-like behaviour was assessed at 6-, 12-, and 18-months of age via the elevated plus maze, open field, and acoustic startle tests. Next-generation sequencing was then used to measure transcriptome-wide gene expression in the hypothalamus, amygdala, pituitary, and adrenal glands. Results showed an anxiolytic behavioural profile across early, middle, and late adulthood by CR, with the strongest effects noted at 6-months. Transcriptomic analysis by seven attribute weighting algorithms, including Info Gain Ratio, Rule, Chi Squared, Gini Index, Uncertainty, Relief, and Info Gain, led to the development of a signature of long-term CR, independent of region. Complement C1q A chain (C1qa), an extracellular protein, expression was significantly decreased by CR in most regions examined. Furthermore, text mining highlighted the positive involvement of C1qa in anxiety, depression, neurodegeneration, stress, and ageing, collectively identifying a suitable biomarker candidate for CR. Overall, the current study identified anxiety-related phenotypic changes and a novel transcriptome signature of long-term CR, indicating potential therapeutic targets for anxiety, depression, and neurodegeneration.

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This study aimed to investigate the relationship between sleep, psychopathology (anxiety, depression and presleep arousal) symptoms, and cortisol in adults with autism spectrum disorder (ASD). The sample composed of 29 adults with ASD (51.7% males) and 29 control adults (51.7% males) aged 21-44 years. Thirteen adults with ASD were medicated for a comorbid diagnosis of anxiety and/or depression (ASD-Med), while the remaining 16 adults with ASD were not medicated for such diagnoses (ASD-Only). Participants completed a questionnaire battery, 14-day sleep/wake diary and 14-day actigraphy assessment. On one day during the data collection period, participants collected five saliva samples, hourly, prior to sleep and two morning samples; immediately upon waking and 30 min thereafter for the analysis of cortisol. Cortisol 1 hr prior to habitual sleep onset time was associated with poorer sleep efficiency in both ASD groups and increased wake after sleep onset duration (ASD-Only). Higher subjective somatic arousal was also associated with increased sleep onset latency, regardless of group, and poorer sleep efficiency in the ASD-Only group. ASD-Only participants had significantly greater reductions in evening cortisol concentrations compared to both ASD-Med and control participants. No significant group differences were found for the cortisol awakening response. Findings suggest a hyperarousal hypothesis of insomnia in adults with ASD. Moreover, the low cortisol levels observed in ASD-Only adults suggest dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Longitudinal studies exploring the interplay between insomnia, anxiety and HPA axis regulation across the lifespan in those with ASD are warranted. Autism Res 2019, 12: 897-910.Lay Summary: Both objective (cortisol) and subjective (somatic) physiological arousal were associated with poor sleep quality in adults on the autism spectrum. Adults with autism spectrum disorder (ASD) who were not medicated for a comorbid diagnosis of anxiety and/or depression also had dampened cortisol secretion, suggesting a dysregulation of the hypothalamic pituitary axis. Longitudinal studies investigating the relationship between sleep, psychopathology symptoms and physiological arousal in autistic individuals are warranted.

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