Melbourne School of Psychological Sciences - Theses

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    The role of biological stress and inflammation in sleep and mental health: a longitudinal perspective among at-risk adolescents
    Landau, Elizabeth Rebecca ( 2018)
    Objective: A healthy functioning body relies in part on a delicate balance between the immune and neuroendocrine (or immuno-endocrine) systems. Sleep disturbance, anxiety, and depression have each been associated with disruptions to the immuno-endocrine system. Recent literature also suggests that dysregulations of the immuno-endocrine system may precipitate sleep disturbance and mental health issues, suggesting a bi-directional role for immuno-endocrine functioning in sleep and mental health. Poor sleep, mental ill-health, and disturbed immuno-endocrine functioning have each been linked to a range of psychosocial, psychiatric, and medical comorbidities including risk for stroke, diabetes, and cardiovascular disease, greater medical expenses, increased substance use, disruptions to interpersonal relationships, poorer vocational outcomes, increased family violence, and more chronic mental and physical health conditions throughout the lifespan. While associations between sleep, mental health, and immuno-endocrine functioning are well- established in adults, less is known about immuno-endocrine functioning in the context of adolescent sleep and mental health, despite high prevalence rates of poor sleep, anxiety, and depression among youth. Further, targeted, preventative treatment interventions for adolescents at-risk of poor sleep, anxiety, and depression may buffer against the progression of mental health issues, as well as immuno-endocrine system dysregulation. However, no study to date has investigated the longitudinal impact of an early-intervention, psychological treatment intervention on biomarkers of immuno-endocrine health in a sample of at-risk-for- depression adolescents. Further, no study with youth has investigated the potential mechanistic role of immuno-endocrine dysregulation in common disease progressions from anxiety issues to depression onset, poor sleep issues to anxiety onset, or poor sleep issues to depression onset. Therefore, the aims of the current thesis were to investigate these gaps in the literature. Method: As part of a larger, multi-center and comprehensive ‘Sleep and Education: learning New Skills Early’ (SENSE) Study, the current thesis investigated the immuno-endocrine functioning of at-risk adolescent participants (n=122, 73 female) in the SENSE Study. The SENSE Study was a two-year, early intervention, randomized-control trial (RCT) researching the impact of a seven-week cognitive-behavioral and mindfulness-based intervention for adolescents who endorsed sleep disturbances and/or anxiety symptoms, known risk factors for the development of depression. The overarching aim of the SENSE Study was to investigate whether a multicomponent sleep intervention, which combined operant conditioning, stimulus control, sleep hygiene psychoeducation, cognitive therapy, and mindfulness-based techniques, would serve as a preventative measure for at-risk adolescents against the development of depression two years post-intervention. Participants were recruited from schools within the Melbourne metropolitan area and invited to participate if they endorsed elevated anxiety and/or poor sleep symptoms, and had no prior history of major depression. At baseline (Time 1; T1) participants (aged 12 to 16 years, mean aged 12.71 years) provided saliva samples across two consecutive days and completed a range of sleep and mood assessments including semi- structured mental health clinical diagnostic interviews, self-report questionnaires, and wrist- actigraphy (an objective measurement of sleep). Participants were randomized into either a seven-week sleep treatment intervention (n=63) or an active study skills control intervention (n=59). Participants completed the same assessments (excepting saliva sample collection) at post-intervention (Time 2; T2), and were assessed again (including saliva sample collection) at two-years post-intervention (Time 3; T3) when participants were aged between 14 and 18 years (mean aged 16.82 years). Thus, immuno-endocrine data was collected at T1 and T3. The current thesis investigated several cross-sectional and longitudinal associations among measures of sleep and mental health with diurnal levels of salivary C-reactive protein (CRP) and cortisol, biomarkers representative of overall systemic functioning of the immune system (CRP) and the neuroendocrine system (cortisol). This project was also the first to use the cortisol to CRP ratio as a measure of inter-system immuno-endocrine organization in the context of sleep and mental health among a sample of youth and in a longitudinal setting. First, for cross-sectional analyses, it was predicted that greater sleep disturbance and mental health issues would be associated with greater disruptions to the immuno-endocrine system (as indexed by higher morning and evening levels of CRP, lower morning and higher evening levels of cortisol, and less homeostatic cortisol to CRP ratio levels). Second, it was predicted that compared to participants in the control intervention, participants in the treatment intervention would display healthier immuno-endocrine functioning at two-year follow-up. Third, it was predicted that dysregulated immuno-endocrine functioning would aid in the progression of 1) anxiety issues to depression onset, 2) poor sleep issues to anxiety onset, and 3) poor sleep issues to depression onset. Finally, it was predicted that sex would be a moderator in all analyses. Results: First, cross-sectional multivariate regression analyses indicated that participants who self-reported longer sleep onset latency (the period of time attempting to fall asleep) at T1 had more blunted morning cortisol levels at T1, even when controlling for common covariates used in the literature. Sex did not moderate this relationship. Second, one-way analyses of covariance (ANCOVA) were conducted to investigate treatment effects on salivary levels of CRP and cortisol, which revealed no statistically significant effects of treatment conditions on biomarkers measured at T3. Two-way ANCOVAs investigating the effect of treatment and sex were also not significant. Third, longitudinal analyses revealed that participants with greater bedtime variability at T1 were less likely to experience depressive symptoms at T2, and more likely to experience a clinical anxiety episode by T3, although levels of CRP and cortisol did not mediate these paths. Finally, participants with an anxiety disorder at T1 were 4.58 times at risk of developing a depressive disorder by T3, although levels of CRP and cortisol did not mediate this path. Sex did not moderate any longitudinal analysis. However, a higher T1 cortisol to CRP ratio (indicative of elevated levels of cortisol relative to attenuated levels of CRP) significantly predicted the onset of a first-ever depressive disorder by T3, even when controlling for T1 depressive symptoms. Conclusion: The current study adds to the literature on links between sleep, mental health, and immuno-endocrine functioning in youth, a relatively new area of research. Results highlight important methodological considerations that future treatment studies should incorporate, considerations which may encourage benefits to the adolescent immuno-endocrine system. The continuation of immuno-endocrine biomarker assessment among youth populations will advance the knowledge of the potential biological underpinnings of sleep disturbance and poor mental health. Refinement of treatment interventions may pave the way for such underlying mechanisms to be harnessed and recruited along the path to treatment outcome goals. Moreover, that perceived sleep onset latency but not objective sleep onset latency was associated with more blunted cortisol levels suggests that interventions designed to target negative or inaccurate assessments of sleep may buffer against neuroendocrine health consequences. Lastly, the finding that adolescents with a more disorganized immuno- endocrine system (i.e., a higher cortisol to CRP ratio) were more at risk of developing depression is novel, and suggests that the cortisol to CRP ratio could serve as a disease risk biomarker for first-onset depression. Early identification of individuals at high risk of depression may prevent medical and psychiatric comorbidities throughout the lifespan.