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J Sleep Res ; : e13709, 2022 Aug 29.
Article in English | MEDLINE | ID: covidwho-2234797

ABSTRACT

The COVID-19 pandemic is a rare stressor that has precipitated an accompanying mental health crisis. Prospective studies traversing the pandemic's onset can elucidate how pre-existing disease vulnerabilities augured risk for later stress-related morbidity. We examined how pre-pandemic sleep reactivity predicted maladaptive stress reactions and depressive symptoms in response to, and during, the pandemic. This study is a secondary analysis of a randomised controlled trial from 2016 to 2017 comparing digital cognitive behavioural therapy for insomnia (dCBT-I) against sleep education (N = 208). Thus, we also assessed whether dCBT-I moderated the association between pre-pandemic sleep reactivity and pandemic-related distress. Pre-pandemic sleep reactivity was measured at baseline using the Ford Insomnia Response to Stress Test. In April 2020, participants were recontacted to report pandemic-related distress (stress reactions and depression). Controlling for the treatment condition and the degree of COVID-19 impact, higher pre-pandemic sleep reactivity predicted more stress reactions (ß = 0.13, ± 0.07 SE, p = 0.045) and depression (ß = 0.22, ± 0.07 SE, p = 0.001) during the pandemic. Further, the odds of reporting clinically significant stress reactions and depression during the pandemic were over twice as high in those with high pre-pandemic sleep reactivity. Notably, receiving dCBT-I in 2016-2017 mitigated the relationship between pre-pandemic sleep reactivity and later stress reactions (but not depression). Pre-pandemic sleep reactivity predicted psychological distress 3-4 years later during the COVID-19 pandemic, and dCBT-I attenuated its association with stress reactions, specifically. Sleep reactivity may inform prevention and treatment efforts by identifying individuals at risk of impairment following stressful events.

2.
Sleep Med ; 94: 70-75, 2022 06.
Article in English | MEDLINE | ID: covidwho-1768546

ABSTRACT

BACKGROUND: Survivors of childhood abuse are prone to adult insomnia, but the mechanisms for this development are poorly understood. Abuse that occurs during sensitive developmental periods might affect risk for insomnia by impacting emerging stress regulatory processes. Sleep reactivity refers to the sensitivity of the sleep system to stress and is a robust risk factor for insomnia. Recent evidence shows stress exposure itself worsens sleep reactivity, thereby increasing insomnia vulnerability. In this preliminary study, we hypothesized the association between childhood abuse experiences and adult insomnia would be mediated through greater sleep reactivity. METHODS: Community adults were recruited from the United States during the COVID-19 pandemic between June 2020 and June 2021 (N = 241, 88% female, Mage = 39, SD = 13.40). Participants completed a cross-sectional survey that included the Childhood Trauma Questionnaire, Ford Insomnia Response to Stress Test, Insomnia Severity Index, and a measure of general COVID-19 stress. RESULTS: Reporting more frequent childhood emotional, physical, or sexual abuse was associated with more severe insomnia during the COVID-19 pandemic. Only childhood emotional and physical (but not sexual) abuse histories were associated with greater sleep reactivity, which exerted an indirect effect on the relationships between these two abuse types and insomnia symptoms. These findings were robust to the effects of gender, age, and stress about the COVID-19 pandemic. CONCLUSIONS: This preliminary study suggests recurrent emotional and physical abuse in childhood might promote later insomnia through heightened sleep reactivity. Stress management interventions could be important to prevent insomnia for abuse survivors by bolstering resilience of the sleep system.


Subject(s)
COVID-19 , Child Abuse , Sleep Initiation and Maintenance Disorders , Adult , Child , Cross-Sectional Studies , Female , Humans , Male , Pandemics , Sleep/physiology , Sleep Initiation and Maintenance Disorders/epidemiology
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