Melbourne School of Psychological Sciences - Theses
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ItemThe acute and habitual effects of alcohol consumption on sleep in late adolescents( 2020)Adolescence is a critical time period for human development. It is associated with major interrelated changes to the brain and sleep regulatory systems. These changes continue into young adulthood, and often coincide with the onset and acceleration of alcohol use. This is concerning as research suggests alcohol consumption may harm the developing brain and sleep systems. Indeed, sleep is an essential neurophysiological process that is necessary for optimal health, functioning, and development. Disturbances to sleep are associated with adverse physiological and psychological consequences. Alcohol is well-known for its sleep disturbing properties. Research has reliably shown that pre-sleep alcohol ingestion in light-drinking late adolescents leads to characteristic objective sleep disruption. These effects are bi-phasic, manifesting as sedation in the first half of the sleep period, followed by major sleep disruption in the second half. However, there is growing evidence that young people may be less sensitive to the initial sedative effects of alcohol. Critically, the effects of acute alcohol consumption on sleep have not yet been investigated in young people who habitually engage in heavy alcohol use. It is well-established that chronic heavy alcohol use leads to enduring sleep disturbances, such as degradations in slow wave sleep (SWS), that persist into periods of long-term abstinence. This has been investigated exclusively in adults with long-term alcohol use disorders. It is currently unknown whether heavy-drinking young people also suffer disturbances to normal sleep. Due to their ongoing development, it is possible that young people experience unique alcohol-related sleep disturbances. These disturbances could negatively impact physical and mental health. The current study aimed to investigate the effects of acute and habitual alcohol use on sleep quality, architecture, and electroencephalography (EEG) spectral power, in male and female late adolescents, aged 18 to 21 years. Forty-six late adolescents were recruited (mean +/- standard deviation): 9 light-drinking males (20.0 +/- 0.9 years; 13.5 +/- 10.3 standard drinks [10g of ethanol] in the previous 30 days), 13 light-drinking females (19.4 +/- 1.2 years; 12.3 +/- 8.0 standard drinks), 11 heavy-drinking males (20.1 +/- 0.7 years; 133.4 +/- 78.8 standard drinks), and 13 heavy-drinking females (19.2 +/- 0.9 years; 81.9 +/- 25.6 standard drinks). Following an initial adaptation night, participants completed in-laboratory polysomnography under two conditions: pre-bedtime alcohol (peak breath alcohol concentration [BrAC] .10%) and placebo (BrAC .00%) consumption. Experimental nights were non-consecutive and counterbalanced over participants. Participants abstained from alcohol for 48 hours prior to testing. This single-blind, mixed-model study design included two repeated- (acute alcohol vs. placebo consumption, first vs. second half of the sleep period) and two between- (male vs. female, habitual heavy vs. light drinking) measures factors. Sleep quality (sleep onset latency, arousals, wake after sleep onset, sleep efficiency) and architecture (stage N1 sleep, stage N2 sleep, SWS, rapid eye movement [REM] sleep) variables were independently scored using standard American Academy of Sleep Medicine (2007) criteria by two experienced sleep researchers. Discrepancies between scorers were resolved by an independent adjudicator. All scorers were blinded to participant group and experimental condition. Power spectral analysis was conducted for five EEG frequency bands: beta (16 – 30 hertz; Hz), sigma (12 – <16 Hz), alpha (8 – <12 Hz), theta (4 – <8 Hz), and delta (0.5 – <4 Hz) for each sleep stage. Data were analysed using mixed-model analysis of variance and post-hoc t-tests. Correlations between habitual alcohol consumption, and sleep quality and architecture variables, were also performed. Mean BrAC at lights out was .08 +/- .01 percent following pre-sleep alcohol, and .00 +/- .00 percent following placebo consumption. Following acute alcohol consumption, in the first half of the sleep period, both heavy- and light-drinking late adolescents demonstrated fewer arousals (p< .001), less stage N1 sleep (p< .001), more SWS (p= .007), longer REM sleep onset latencies (p< .001), and less REM sleep (p< .001), compared to placebo. There were no differences observed in sleep onset latency (p= .720), wake after sleep onset (p= .850), or sleep efficiency (p= .811). In the first half of the sleep period, alpha EEG spectral power was higher following alcohol consumption in stage N2 sleep (p< .001), SWS (p< .001), and REM sleep (p= .005). Although delta spectral power was higher in SWS (p= .008) and REM sleep (p< .001) in the first half of the sleep period, delta power was lower in stage N2 sleep (p= .006). In the second half of the sleep period, there were more arousals (p< .001), more wake after sleep onset (p< .001), lower sleep efficiency (p< .001), more stage N1 sleep (p< .001), and less SWS (p= .004), following acute alcohol consumption compared to placebo, in both heavy- and light-drinking late adolescents. No differences in EEG spectral power were observed in the second half of the sleep period. By design, heavy-drinking participants had consumed more alcohol in the previous 30 days, and across their lifetimes, than light drinkers (p< .001). There were no differences in objective sleep quality between heavy- and light-drinking late adolescents. However, a correlational analysis showed that, in the placebo condition, higher alcohol consumption in the previous 30 days was associated with higher wake after sleep onset (Spearman's Rho= .312, p= .035), and lower sleep efficiency (Spearman's Rho= -.327, p= .027). Heavy drinkers had less all-night visually scored SWS (p= .026), and more stage N2 sleep (p= .008), than same-aged light drinkers, in the placebo condition. Furthermore, higher previous 30-day alcohol consumption was related to lower SWS (Spearman's Rho= -.261, p= .040) and higher stage N2 sleep (Spearman's Rho= .250, p= .027) percentage, in the placebo condition. Irrespective of experimental condition, heavy drinkers had shorter REM sleep onset latencies, compared to same-aged light drinkers (p= .038). Although there were no differences in all-night REM sleep percentage, heavy drinkers had less REM sleep in the second half of the sleep period compared to light drinkers, irrespective of condition (p= .016). There were no differences in delta spectral power between heavy- and light-drinking late adolescents in any sleep stage. However, heavy-drinking late adolescents had higher sigma spectral power in SWS (p= .029), and stage N2 sleep (p= .021), than same-aged light drinkers, regardless of experimental condition. There was an interaction between sex, acute alcohol use, and habitual alcohol use, for all-night SWS percentage (p= .003). This interaction suggested that heavy-drinking males had higher all-night SWS percentage following alcohol consumption compared to placebo, however, heavy-drinking females had lower all-night SWS. In light-drinking males and females, there were no differences in all-night SWS percentage following alcohol or placebo consumption. The current study demonstrated that both heavy- and light-drinking late adolescents experience substantial sleep disruption following a high dose of alcohol prior to sleep. In contrast to the adult literature, the current investigation reported no differences in sleep onset latency, wake after sleep onset, or sleep efficiency, in the first half of the sleep period. This supports growing evidence that young people may experience less initial physiological sedation following alcohol consumption. However, a direct adult comparison is needed to verify this. This unique physiological response could potentially contribute to higher levels of alcohol use in young people, as it permits them to consume higher doses of alcohol before experiencing sedation. The current study replicated previous findings of higher alpha and delta spectral power following pre-sleep alcohol in young people. This may represent alpha-delta sleep – a potential electrophysiological indicator of sleep disruption. It is possible that these objective sleep disturbances may compromise the restorative properties of sleep and contribute to the alcohol hangover. The current study reported more wake after sleep onset, and less sleep efficiency, following acute alcohol consumption, which may contribute to sleep restriction in young people. Critically, this investigation provided novel evidence that pre-sleep alcohol consumption disrupts sleep in heavy-drinking late adolescents. This indicates that this population may be repeatedly experiencing sleep disruption during the final stages of neural development. Furthermore, these effects may be amplified in heavy-drinking young women, however further research is needed to replicate these novel findings. Finally, the present study uniquely demonstrated that heavy habitual alcohol use in young people is associated with disturbances to normal sleep, irrespective of pre-sleep alcohol consumption. Despite their relatively short drinking histories, the pattern of deficits was similar to those reported in adults with long-term alcohol use disorders, including lower all-night SWS percentage. Furthermore, some sleep abnormalities may be unique to this developing age group, such as elevated sigma spectral power during SWS and stage N2 sleep. Evidence suggests SWS plays a functional role in neurophysiological growth and repair, and learning and memory. Enduring degradations in SWS may be particularly detrimental in young people, as neural development is still ongoing, and academic pressure is high, during this time period. Although longitudinal research is required, the sleep deficits observed in the current investigation may represent alcohol-related changes to the brain and sleep systems, and/or a predisposition to heavy alcohol use. In summary, the current study provided key objective evidence that both acute and habitual alcohol use in late adolescence disrupts sleep. This could have deleterious effects on the health, functioning, and development of young people. It is imperative that action is taken to prevent or reduce alcohol-related sleep disturbances during the final stages of human development. Interventions should aim to delay and reduce alcohol consumption, enhance cognitive function, and improve sleep quality to protect the health and wellbeing of young people.
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ItemThe role of biological stress and inflammation in sleep and mental health: a longitudinal perspective among at-risk adolescents( 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.
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ItemThe SENSE Study (Sleep and Education: learning New Skills Early): long-term outcomes of a randomised controlled trial of a cognitive-behavioural and mindfulness-based group sleep intervention to prevent depression and improve anxiety in at-risk adolescents( 2019)Objective: Depression is one of the most common and debilitating mental health problems and its incidence dramatically increases during adolescence. Accumulating evidence suggests that adolescent depression can be prevented with psychosocial interventions, but there is still insufficient evidence to support their widespread implementation. Notably, there is a need for randomised controlled trials of novel interventions that are delivered to community-based adolescents identified to be at-risk for developing depression (i.e., targeted prevention) rather than the general adolescent population (i.e., universal prevention). Improving sleep represents a promising and innovative therapeutic target for the prevention of adolescent depression. Not only are sleep problems, including insufficient and poor-quality sleep, common during adolescence, they also tend to precipitate the onset of depression. Further, sleep interventions may be especially effective if they are delivered to adolescents experiencing anxiety. Anxiety, particularly generalised anxiety, and sleep problems often co-occur, and anxiety is also a risk factor for the development of depression. Evidence from a small but growing number of studies indicates that multicomponent cognitive-behavioural and mindfulness-based sleep interventions can improve sleep in adolescent samples. However, few studies have investigated depression and anxiety outcomes, particularly using randomised controlled designs, active control comparison conditions, extended follow-up periods, a multi-method assessment of sleep (i.e., subjective and objective measures) and mental health (i.e., diagnosis and symptoms) outcomes, and in community-based samples. Notably, no randomised controlled trial has investigated whether a sleep intervention can prevent the first onset of major depressive disorder (MDD) in adolescents. The current study was designed to address these gaps in the literature. The primary aim of the study was to investigate the long-term efficacy of a seven-week cognitive-behavioural and mindfulness-based group sleep intervention for the targeted prevention of first onset MDD and improvement of depressive symptoms over a two-year follow-up period in community-based adolescents experiencing concurrent high levels of anxiety symptoms and sleep problems (i.e., ‘at-risk’ for depression). Given the association between sleep and anxiety, notably generalised anxiety disorder (GAD), and dearth of adolescent sleep intervention studies investigating anxiety outcomes, the secondary and exploratory aim of the study was to investigate the long-term efficacy of the sleep intervention for preventing the incidence of GAD and improving anxiety symptoms over a two-year follow-up period. Importantly, the study aimed to demonstrate that any beneficial effects to depression and/or anxiety outcomes occurred via the putative mechanism of improvements to subjective and objective indices of sleep. As best can be determined, the research reported in this thesis represents the only attempt to date to prevent first onset MDD by improving sleep in an adolescent sample, and the only randomised controlled trial of an adolescent sleep intervention to examine anxiety outcomes over a two-year follow-up period. It was predicted that, compared to adolescents allocated to the active control (study skills) intervention, adolescents allocated to the sleep treatment intervention would: show greater improvements in subjective and objective indices of sleep (i.e., reduced sleep onset latency, increased total sleep time, better overall sleep quality, and reduced weekday bedtime intra-individual variability and weekday-to-weekend bedtime shift) immediately following the intervention and over the two-year follow-up period; be less likely to develop first onset MDD during, and would report lower levels of depressive symptoms at, the two-year follow-up (primary outcomes); and would be less likely to develop new onset GAD during, and would report lower levels of anxiety symptoms at, the two-year follow-up (secondary outcomes). Further, it was predicted that any beneficial long-term effects for depression and anxiety outcomes (i.e., lower incidence of MDD or GAD and/or reduction in depressive and anxiety symptoms) would be significantly mediated by improvements in sleep associated with the sleep treatment intervention (i.e., sleep improvements immediately post-intervention and/or over the two-year follow-up period). Methods: Participant recruitment and eligibility assessments occurred from January 2013 to June 2014. A school-based screening (n = 1491) was conducted at 23 secondary schools (14 Government, 4 Catholic, 5 Independent) in metropolitan Melbourne, Australia, to identify community-based adolescents with high levels of self-reported sleeping problems (score > 4 on the Pittsburgh Sleep Quality Index; PSQI) and anxiety symptoms (score > 32 males/ > 38 female on the Spence Children’s Anxiety Scale; SCAS). Consenting participants who met screening criteria (n = 218) completed semi-structured diagnostic clinical interview (Kiddie-Schedule for Affective Disorders and Schizophrenia for school-age children-Present and Lifetime version; K-SADS-PL) at the University of Melbourne, primarily to exclude individuals (n = 30) with a lifetime history of MDD, consistent with the study’s aim to prevent first onset depression. Eligible participants (n = 144) were randomised (1:1 allocation on an individual basis, and conditions were balanced for age, gender and presence or absence of current anxiety disorder at baseline) to either a seven-week, face-to-face, multicomponent cognitive-behavioural and mindfulness-based group sleep improvement treatment intervention (Sleep SENSE; n = 71) or an attention-matched active control study skills intervention (Study SENSE; n = 73). The Sleep SENSE intervention aimed to address common sleep problems including insufficient sleep duration, prolonged sleep onset, and variability in sleep timing, and included anxiety management components to assist with managing anxiety during the pre-sleep period. Mental health and sleep were assessed using: the K-SADS-PL (for MDD and GAD diagnosis); the Center for Epidemiologic Studies-Depression scale (CES-D; depressive symptoms); the SCAS (anxiety symptoms); the PSQI (self-reported sleep onset latency, total sleep time, overall sleep quality); and week-long actigraphy with sleep diary (objective sleep onset latency, total sleep time, weekday bedtime intra-individual variability, and weekday-to-weekend bedtime shift). Assessments occurred on three occasions–pre-intervention, post-intervention, and two-years after the completion of the intervention. All outcome assessments were administered by researchers who were blind to participants’ intervention assignment. Statistical analyses: All analyses used a modified intention-to-treat approach. Specifically, the final analysed sample (n = 122, sleep treatment n = 62, control intervention n = 60; 60% female; M age = 14.5 years, SD = 0.95, range 12.04 to 16.31 years) included participants who were eligible for and started the interventions, including those who dropped out of the interventions or were lost to follow-up (n = 13) but excluded participants who were identified as ineligible after randomisation (n = 2) and those who were randomised but never started the interventions (sleep treatment n = 10, control intervention n = 10). Latent growth curve modelling with multiple mediation analysis was used to test the effect of condition (i.e., sleep treatment or control intervention) on the long-term depression (i.e., presence or absence of MDD diagnosis, and severity of depressive symptoms) and anxiety (i.e., presence or absence of GAD diagnosis, and severity of anxiety symptoms) outcomes via improvements in the seven sleep variables immediately post-intervention (i.e., ‘initial status’ which was centred at the post-intervention time point) and over the two-year follow-up period (i.e., average linear ‘rate of change’ scaled to represent change per year). That is, the latent growth process of a sleep variable (i.e., the latent variables of initial status and rate of change) was used the mediator in the tested models. In total, 28 separate models were estimated using Mplus (Version 7) software using maximum likelihood estimation with robust standard errors. Results: Regarding the primary outcomes, there was no statistical evidence that the sleep treatment intervention improved subjective or objective indices of sleep immediately post-intervention or over the two-year follow-up period, or significantly predicted the presence or absence of major depressive disorder during, or reductions in depressive symptoms at, the two-year follow-up, relative to the active control intervention. Regarding the secondary outcome, the sleep treatment intervention did not significantly predict reductions on anxiety symptoms at two-year follow-up. However, the sleep treatment intervention significantly reduced the conditional odds of having GAD during the two-year follow-up period by a factor of seven on average, relative to the active control intervention, although confidence intervals suggested a small effect. There were no statistically significant indirect effects in any of the model investigated. Regardless of condition, participants’ subjective (B = -1.77, 95% CI [-3.47, -0.07]) and objective (B = -4.53, 95% CI [-7.96, -1.10]) sleep onset latency and subjective total sleep time (B = -0.18, 95% CI [-0.31, -0.05]) decreased over time, and weekday bedtime intra-individual variability increased over time (B = 7.99, 95% CI [2.11, 13.86]). In addition, poorer subjective sleep quality (B = 1.46, 95% CI [0.38, 2.54]) and less objective total sleep time (B = -3.31, 95% CI [-6.33, -0.28]) immediately post-intervention predicted depressive symptoms at two-year follow-up, and reductions in weekday bedtime intra-individual variability over time were associated with a decreased likelihood of GAD during the two-year follow-up (B = -0.52, 95% CI [-0.86, -0.18]). Conclusions: Together, the findings do not support the long-term efficacy of a targeted multicomponent cognitive-behavioural and mindfulness-based group sleep intervention for the improvement of sleep problems and prevention of first onset major depressive disorder in a community-based sample of at-risk adolescents. However, they tentatively suggest that anxiety may be more responsive to the sleep intervention than depression. In the context of a robust study design, the findings are hypothesis-generating and raise important considerations for the design of future clinical trials investigating the role of adolescent sleep interventions on emerging psychopathology. Funding: Australian National Health and Medical Research Council Grant (APP1027076). Trial Registration: Australian New Zealand Clinical Trials Registry (ACTRN12612001177842; prospectively registered on 6th November 2012).
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ItemThe SENSE study (Sleep and Education: learning New Skills Early): postintervention effects of a randomised controlled trial of a cognitive-behavioural and mindfulness-based group sleep improvement intervention among at-risk adolescents( 2016)Objective: There is growing recognition that many adolescents obtain insufficient and/or poor quality sleep. Sleep problems are also a major risk factor for the emergence of mental health problems in adolescence. However, few studies have examined disturbed sleep as a potential mechanism in the treatment and prevention of mental health problems among adolescents. Adolescent sleep problems can be treated using a range of approaches. School-based sleep education programs, which are typically delivered to whole school classes, have been shown to have little impact on sleep behaviour or mental health. Cognitive-behavioural and mindfulness-based sleep programs, which are typically delivered to at-risk or already symptomatic adolescents, have been shown to be more effective in improving sleep and emotional distress, but studies evaluating their effectiveness have been limited in several ways, including small sample sizes and inadequate/lack of control groups. We conducted a systematic review and meta-analysis examining the efficacy of cognitive-behavioural sleep interventions among adolescents. Searches of PubMed, PsycINFO, CENTRAL, EMBASE, and MEDLINE were performed from inception to 1 May 2016. Eight trials were selected (n=234, mean age=15.24 years; female=63.18%). Main outcomes were subjective (sleep diary/questionnaire) and objective (actigraphy) total sleep time (TST), sleep onset latency (SOL), sleep efficiency (SE), and wake after sleep onset (WASO). There was a small number of randomised controlled trials (RCTs; n=3), and a high risk of bias across the RCTs; therefore within sleep condition meta-analyses were examined. At post-intervention, subjective TST improved by 29.47 minutes (95% CI = 17.18, 41.75), SOL by 21.44 minutes (95% CI = -30.78, -12.11), SE by 5.34% (95% CI = 2.64, 8.04), and WASO by a medium effect size (d = 0.59 [95% CI = 0.36, 0.82). Objective SOL improved by 16.15 minutes (95% CI = -26.13, -6.17), and SE by 2.82% (95% CI = 0.58, 5.07). Global sleep quality, daytime sleepiness, depression, and anxiety also improved. Gains were generally maintained over time. Our meta-analysis provides preliminary evidence that cognitive-behavioural sleep interventions are an effective treatment for adolescent sleep problems, producing clinically meaningful responses within active treatment conditions. Their efficacy is maintained over time, and results in significant alleviation of sleep problems and improvement in functional outcomes. However, further large-scale, high-quality RCTs are needed to confirm these findings. The aim of this thesis was to investigate the post-intervention effects of a cognitive-behavioural/mindfulness-based group sleep intervention on sleep, mental health, and cognitive style among at-risk adolescents. The study went beyond simply measuring treatment outcomes to also evaluate mechanisms of change. Based on the behavioural, cognitive, hyperarousal, and transdiagnostic models of insomnia, a number of specific mediators were hypothesised to account for therapeutic change in cognitive-behavioural and mindfulness-based sleep interventions for adolescents, including earlier bedtimes, more consistent bedtimes, increased sleep hygiene awareness, and decreased dysfunctional beliefs and attitudes about sleep, worry, rumination, pre-sleep arousal, anxiety, and depression. Method: A RCT was conducted across Victorian secondary schools in Melbourne, Australia. Adolescents (aged 12-17 years) were recruited using a two-stage procedure, consisting of an in-school screening (n=1491) followed by a diagnostic interview for those meeting screening criteria (n=218), to identify students with high levels of anxiety and sleeping difficulties, but without past or current major depressive disorder (n=144). Eligible participants were randomised into either a sleep improvement intervention (‘Sleep SENSE’) or an active control ‘study skills’ intervention (‘Study SENSE’). One hundred twenty three participants began the interventions (Female=60%; Mean Age=14.48, SD=0.95), with 60 in the sleep condition and 63 in the control condition. All participants were required to complete a battery of mood, sleep and cognitive style questionnaires, seven-days of wrist actigraphy (an objective measurement of sleep), and sleep diary entry at pre-and-post intervention. Results: The sleep intervention condition was associated with significantly greater improvements in subjective sleep (global sleep quality, sleep onset latency, daytime sleepiness), objective sleep onset latency, anxiety, pre-sleep arousal, and sleep knowledge compared with the control intervention condition, with small-medium effect sizes. Parallel multiple mediation models showed that there were bidirectional relationships between improvements in subjective sleep quality and pre-sleep arousal/global anxiety. Conclusion: The SENSE study is an efficacy trial of a selective group-based sleep intervention for the treatment and prevention of sleep and mental health problems among at-risk adolescents experiencing both sleep and anxiety disturbance. The study provides evidence, using a methodologically rigorous design, including an active control comparison condition, that a multi-component group sleep intervention that includes cognitive-behavioural and mindfulness-based therapies, can improve wakefulness in bed variables, daytime dysfunction, anxiety, pre-sleep arousal, and sleep knowledge among at-risk adolescents. The results also provide evidence that pre-sleep arousal and anxiety are particularly important for adolescents’ perceived sleep quality, and should be key targets for new treatments of adolescent sleep problems. Public Health Significance: Given the high prevalence of adolescent sleep and internalising problems, the implications of an effective adolescent sleep intervention for clinical practice and public policy are potentially significant. However, changing sleep behaviour, especially objective measures of sleep, in this age group, has been challenging. This thesis shows that the Sleep-SENSE program can improve objective and subjective indices of sleep, as well as anxiety symptoms, when compared to an active control intervention. The results also showed that reductions in pre-sleep hyperarousal represent a key psychophysiological mechanism for therapeutic improvements in subjective sleep problems among anxious adolescents, and that cognitive behavioural and mindfulness-based sleep interventions should be directed towards adolescents with vulnerability for hyperarousal. Sleep SENSE is one of the only interventions demonstrated to be efficacious in improving sleep and mental health amongst vulnerable adolescents. Furthermore, the program is likely to be cost-effective - it involves a simple screening process and a group intervention format - and could be disseminated to a wide range of clinical and non-clinical settings in primary care, mental health, adolescent health and sleep medicine, and may assist in the treatment and prevention of adolescent sleep and mental health problems. The intervention also lends itself to flexible modes of delivery (e.g., non-specialist practitioners, group settings, individual settings, school-based, internet and other e-health modes of delivery), further enhancing its translational potential.
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ItemThe effect of arousal induced hypocapnia on upper airway dilator muscle activity following the return to sleep( 2016)Obstructive sleep apnea (OSA) is characterised by repetitive collapse of the upper airway during sleep. These episodes of collapse generally terminate with an arousal from sleep. The large ventilatory response associated with arousal is thought to predispose to further obstruction following the return to sleep by inducing hypocapnia and a subsequent reduction in upper airway dilator muscle activity. However, studies of healthy individuals and OSA patients on CPAP, have found no evidence for reduced dilator muscle activity post-arousal, rather dilator muscle activity tends to be increased. These discrepancies may be due to study limitations or alternatively, the theorised effects of arousal may be incorrect. It is possible that arousal does not induce hypocapnia, or hypocapnia is induced, but post-arousal dilator muscle activity is driven by a stimulus other than CO2. For instance, after-discharge may drive dilator muscle activity post-arousal. To assess these possibilities we conducted two studies. Study 1 determined whether untreated OSA patients experience hypocapnia following arousals that terminate obstruction. Hypocapnia was assessed by creating an end-arousal CO2 change value (end-arousal ∆CO2) which was the PETCO2 on the last breath of arousal minus the individual’s wakefulness PETCO2. The mean end-arousal ∆CO2 was -0.6±1.8mmHg below wakefulness CO2, suggesting that the OSA patients were hypocapnic on the last breath of arousal. However, despite hypocapnia, both peak and tonic genioglossus activity were elevated above pre-arousal levels for the first two breaths following the return to sleep. In no instance did peak or tonic genioglossus activity fall below pre-arousal levels. Further, it was demonstrated that the more negative the end-arousal ∆CO2 (more reduced below wakefulness), the greater the genioglossus muscle activity was on the first five breaths following the return to sleep. Study 2 determined whether dilator muscle after-discharge occurs following arousal and whether it is inhibited by hypocapnia. Healthy individuals were mechanically hyperventilated to (1) induce hypocapnia and (2) remove the effects of negative pressure upon dilator muscle activity. To assess normocapnia, mechanical ventilation was maintained, but additional CO2 was bled into the circuit. Study 2 demonstrated that arousal induced by auditory stimuli increased peak and tonic genioglossus activity above pre-arousal levels following the return to sleep. For the tonic component of genioglossus activity, the duration of after-discharge was no different between CO2 conditions, however for peak genioglossus activity, after-discharge was shorter following the return to sleep during hypocapnia (2 breaths) compared to normocapnia (6 breaths). These findings suggest that arousal is not detrimental to dilator muscle activity following the return to sleep. Consistent with prior literature, dilator muscle activity was improved post-arousal for both the untreated OSA patients and the healthy participants. It is likely that this elevation in genioglossus activity was driven by an after-discharge mechanism that becomes active at arousal and then persists following the return to sleep. These findings suggest that arousal does not predispose to further obstruction on return to sleep via reduced upper airway dilator muscle activity. Such findings have implications for current studies attempting to treat OSA by administering sedatives to reduce the incidence of arousal.
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ItemSleep, mood, and cognitive vulnerability in adolescents: a naturalistic study over restricted and extended sleep opportunities( 2013)Introduction: It is well established that for adolescents, school days are associated with sleep restriction, and that insufficient sleep has been linked to mood disturbances. This longitudinal study assessed sleep, mood, and life stress over the school term and vacation periods with restricted and extended sleep opportunities. The relationships between objective and subjective sleep, as well as between sleep and mood were examined. A cognitive model was proposed and tested to assess whether sleep-specific (i.e., dysfunctional beliefs and attitudes about sleep) and global (i.e., dysfunctional attitudes) cognitive vulnerabilities played a role in these relationships. Methods: One-hundred and forty-six adolescents (47.3% male) aged 16.2+/-1.0 years (M+/-SD) from the general community wore an actigraph continuously for four weeks: the last week of a school term (Time-E), the following two-week vacation (Time-V), and the first week of the next term (Time-S). Social demographic information, chronotype, and cognitive vulnerabilities were assessed at Time-E. Subjective sleep, symptoms of depression, anxiety, and life stress were repeatedly measured at Time-E, Time-V, Time-S, and the middle of the subsequent school term. Regression analyses were used to explore the relationship between sleep and mood, and structural equation modelling was used to examine changes of variables over time, as well as the moderating roles of cognitive vulnerabilities. Results: Compared with school days, sleep during the vacation was characterized by later timing, longer duration, lower quality and greater variability. Daily changes in actigraphy- measured sleep over the vacation period showed linear delays in sleep timing throughout the vacation, while changes in time-in-bed were non-significant. The first vacation week was characterized by a linear decrease in total sleep time and sleep quality, and these changes stabilized during the second vacation week. Compared to vacations, school terms were associated with higher symptoms of depression, anxiety, and life stress. Poorer sleep quality, particularly poorer subjective perception of sleep quality, was significantly associated with higher symptoms of depression and anxiety. Sleep- specific cognitive vulnerability moderated the relationship between objective and subjective sleep onset latency during extended but not restricted sleep opportunity. After controlling for life stress, global cognitive vulnerability played different moderating roles in the relationship between subjective sleep and mood over school term and vacation periods. Higher global cognitive vulnerability was associated with a stronger relationship between subjective sleep and symptoms of anxiety (but not depression) during the school term, as well as with a stronger relationship between subjective sleep and symptoms of depression (but not anxiety) during the vacation period. Conclusion: Sleep, mood, and life stress changed markedly over the school term and vacation periods. Changes in sleep over the vacation suggested that the recovery from school- related sleep restriction was completed within two weeks’ extended sleep opportunity, and the average sleep duration over this period suggested that sleep requirements in adolescence may be less than conventionally described in the media and in the scientific literature. Cognitive vulnerabilities played important roles in the relationship between sleep and mood. Adolescents with higher cognitive vulnerability might be more emotionally vulnerable towards school-related sleep restriction. These findings have important implications for future studies, as well as practical implications for policies and interventions designed to improve adolescents’ wellbeing.
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ItemGetting to the heart of teen depression: the relationship between depression and cardiovascular risk in adolescents during wakefulness and sleep( 2013)Depression has been identified as an independent cardiovascular risk factor in adults, where its presence results in higher rates of mortality and adverse cardiac events in patients with and without known cardiovascular disease (CVD). Recent literature suggests preclinical signs of cardiovascular risk are also present in adolescents experiencing depressive symptoms, however little is known about the effects of adolescent clinical depression on cardiovascular health. Moreover, no study has investigated the cardiovascular functioning of clinically depressed individuals during sleep, a state which involves cardiovascular changes including the characteristic decrease or ‘dip’ in blood pressure (BP). The aim of this study was to determine whether clinical depression is associated with an increased risk of cardiovascular disease in otherwise healthy adolescents. Experiment One sought to examine cardiovascular functioning during quiet wakefulness. Participants (n = 889, 352 male) aged 12-18 years were recruited from Victorian secondary schools in the general community. Subsequent to completing mood questionnaires and clinical interviews, 50 eligible participants (25 [6 male] clinically depressed, 25 [6 male] control) took part in a morning cardiovascular assessment at the University of Melbourne. Variables assessed included automatic clinical and continuous beat-to-beat finger arterial BP, heart rate (HR), endothelial functioning, pulse transit time (PTT), as well as cholesterol, glucose and glycohaemoglobin levels. In addition, the cumulative risk of present modifiable risk factors such as smoking was calculated according to the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) risk score, which has been shown to predict coronary calcification in young populations. It was predicted that, compared to controls, depressed adolescents would show evidence of a number of early pathophysiological processes. As hypothesised, between-group analyses revealed depressed adolescents had significantly poorer endothelial functioning, which resulted in decreased vasodilation, and shorter PTT suggesting deterioration in vascular integrity and structure. Depressed adolescents also presented with higher fasting glucose and higher triglyceride levels compared with controls. Furthermore, risk score calculations revealed significantly higher PDAY risk scores in the depressed group indicative of increased engagement in unhealthy behaviours and a higher probability of having advanced atherosclerotic lesions. Contrary to predictions however, no significant differences were found in BP or HR measurements. In order to have a more complete understanding of the cardiovascular health of depressed adolescents, Experiment Two was designed to asses BP and HR during sleep. The BP profile at sleep onset was of particular interest as a blunted decline in BP is associated with target organ damage and increased cardiovascular risk. A subgroup of female participants (8 clinically depressed, 10 control) who completed Experiment One also participated in an overnight cardiovascular assessment. Whole-night polysomnography was conducted with continuous beat-to-beat finger arterial BP and HR monitored via Portapres and ECG, respectively. Data were analysed as an average of the first 6 hours of sleep as well as 2-minute epochs of stable sleep averaged within sleep stages. Further analyses of 30-second epochs were averaged across the pre-sleep wakefulness and the first ≥5 minutes of continuous stable Stage 2 in the sleep onset period. Analyses revealed that although no significant group differences in BP or HR were found during morning wakefulness, depressed adolescents presented with higher systolic, diastolic and mean arterial BP across the whole night and across sleep stages. The difference between groups (~11 mmHg) was found to not only be statistically but also clinically significant. Depressed adolescents also displayed a blunted systolic BP decline at sleep onset compared with controls. This heightened nocturnal BP and blunted decline represent early changes in BP regulation and could be a preclinical marker for depressed adolescents at high risk of cardiovascular disease. A number of plausible mechanisms may explain the heightened BP including a failure to shift to parasympathetic dominance during sleep, increased cortisol levels as a result of a dysregulated hypothalamic-pituitary-adrenocortical axis, and limited vasodilation at night due to endothelial dysfunction as found in Experiment One. Although the mechanisms are still unclear, the results suggest that depression has a significant adverse effect on the cardiovascular system in the early stages of life. Given that risk factors are known to continue to adulthood, the heightened nocturnal BP, increased triglyceride and vascular changes may increase risk for future cardiovascular problems such as hypertension. Identification of those at high-risk and intervention should therefore be actioned as early as adolescence as a way to decrease the prevalence and global burden of CVD.
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ItemThe effects of acute alcohol consumption on sleep and memory in young adults( 2013)Sleep is a basic physiologic drive fundamental to human survival. Adequate sleep is particularly important for maturation of biological and neuronal processes. Adolescence and young adulthood are unique developmental periods characterised by numerous changes to neural physiology, as reflected in dramatically altered sleep behaviour. These biological changes are accompanied by a tendency for increased alcohol consumption due to social and environmental changes occurring during this time. These neuronal changes may result in the brains of adolescents and young adults being at a heightened vulnerability for alcohol related disruption. Thus, the consequences of acute alcohol consumption may be particularly relevant to these developmentally unique age groups. Patterns of alcohol consumption during adolescence and young adulthood are often characterised by repeated acute exposure to high concentrations of alcohol. Acute consumption of alcohol has been linked to numerous cognitive deficits including disruptions to memory. Alcohol consumption has also been linked to disruptions in the continuity and architecture of sleep in adults. Specifically, alcohol is known to act initially as a sedative, reducing sleep onset latency. It also increases slow wave sleep (SWS) and decreases rapid eye movement (REM) sleep early in the sleep period. However, subsequently it decreases SWS, increases REM sleep and also increases sleep disruptions in the second half of the sleep period. Sleep disruptions have been linked to memory deficits and it is thought that sleep processes may play an important role in memory consolidation. In particular, SWS and REM sleep have been highlighted as being particularly important for sleep related memory consolidation. Although the independent relationships between alcohol and memory deficits, alcohol and sleep disruption, and sleep and improved memory are well researched in adults, less is known about adolescents and young adults. Additionally, no studies to date have assessed the effects of alcohol on sleep related memory consolidation in any age group. Adolescents and young adults are increasingly reliant on memory processes as they transition from high school, and are exposed to challenging tertiary education and workplace environments. Given that they are also in the midst of rapid physiological development, alcohol related disruptions to sleep and memory may be particularly detrimental to this age group. In light of the limited knowledge about the impact of acute alcohol use on young adult sleep and memory, the present investigation had two aims. The first experiment aimed to characterise the effects of acute alcohol consumption on sleep quality and architecture in young adults, and secondarily, to assess whether the half night sleep architecture effects seen in previous literature may be as a result of changes to sleep cycle length, rather than changes to sleep architecture. In accordance with the adult literature, it was hypothesised that alcohol would act initially as a sedative, being associated with shorter sleep onset latencies, but subsequently disrupt sleep, with more sleep disturbances in the second half of the sleep period. It was also hypothesised that alcohol would alter sleep architecture, being associated with more SWS and less REM sleep in the first half, but less SWS and more REM sleep in the second half of the sleep period. The second experiment aimed to elucidate whether any sleep disruptions found would disrupt sleep related memory processes in this age group. It was hypothesised that alcohol would disrupt memory directly, being associated with decreased performance on a procedural memory task in a daytime waking condition. It was also expected that alcohol would disrupt sleep related memory consolidation by disrupting sleep, resulting in an absence of improvement in the performance of a procedural memory task following a night of sleep when compared to a night of sleep deprivation. Placebo administration, however, was expected to be associated with enhanced performance on the procedural memory task following a night of sleep when compared with sleep deprivation. Participants for the first experiment were 24 (12 female) 18-21 year old light drinking volunteers. All underwent three nights of polysomnography (PSG) in a sleep laboratory- an adaptation night followed by alcohol and placebo nights counterbalanced over participants. All participants received a standardised meal 5 hours before lights out and were allowed to sleep from their normal bedtime until natural awakening from sleep. On alcohol nights, in the half hour starting one hour before lights out, participants were dosed with vodka mixed with orange juice in order to achieve a breath alcohol concentration (BrAC) of .1% on the basis of weight, height and total body water. On placebo nights, participants received an equivalent volume of orange juice with a straw dipped in vodka. Results indicated that young adult sleep was altered by alcohol, in a pattern broadly consistent with the adult literature. Slow wave sleep was increased and REM sleep was decreased in the first half of the sleep period, and particularly in the first sleep cycle, while SWS was decreased and sleep disturbances were increased in the second half of the sleep period, and particularly very late in the night. Unexpectedly, however, there was no effect of alcohol on sleep onset latency and no rebound of REM sleep late in the sleep period- findings that are discrepant with the adult literature on alcohol and sleep, and may reflect developmental differences in sleep systems. Sleep cycle analysis also showed that the half night sleep architecture changes observed were not due to changes in sleep cycle length. Further, spectral analyses indicated that alcohol simultaneously promoted delta and alpha activity in the electroencephalogram (EEG) at frontal sites in the first sleep cycles. This finding is suggestive either of an arousal influence which may compete with the sleep maintenance influence of delta sleep, or of a phenomenon similar to, or the same as, alpha-delta sleep- an EEG pattern that indicates the presence of an extremely disruptive stimulus during sleep. Given the disruptive influence of alcohol observed in this experiment, the second experiment examined the possible cognitive consequences of this sleep disturbance. Participants for the second experiment were 36 (18 female) 18-21 year old right handed young adults selected using the same criteria as experiment one, and randomly assigned to one of three groups- normal sleep, sleep deprivation or daytime waking groups. They participated in two experimental nights- one alcohol and one placebo- each preceded by an adaptation night of PSG. Alcohol dosing procedures were identical to experiment one. Normal sleep and sleep deprivation participants learned a procedural memory task 3 hours prior to their normal bedtimes before 8 hours of sleep (with PSG) or sleep deprivation and were retested on the memory task the morning after the condition. Daytime waking participants learned the memory task one hour after awakening but underwent the same sequence of events in the same length of time as the other participants, being tested on the task after 8 hours of daytime wakefulness. Contrary to predictions, results indicated that there were significant improvements in performance on the memory task from the test to the subsequent retest in all three groups with no differences between groups or alcohol condition. This indicated that memory was consolidated over time, regardless of whether that time was spent asleep or awake, and irrespective of alcohol consumption. In other words, results showed no evidence of sleep related memory consolidation and so the effect of alcohol on this process could not be assessed. In summary, findings confirmed that similar to adults, alcohol consumption in young adulthood drastically disrupts the continuity and architecture of subsequent sleep. Additionally, they highlighted the rationale of examining sleep in this age group, as the absence of a shortened sleep onset latency and a REM sleep rebound after alcohol is uncharacteristic of findings in adults. We speculate that these findings may indicate that alcohol may have some unique effects on young adult sleep due to maturational differences in the sleep system. Results further extend previous findings indicating the presence of increased alpha and delta activity at frontal EEG sites, which may suggest an impairment of sleep’s restorative qualities after alcohol use. Regardless of these impacts, results also indicate no evidence of a sleep related memory enhancement effect and no direct effect of alcohol on memory. Therefore, there was no opportunity to assess the effects of alcohol on sleep related memory consolidation. These findings are discrepant with the adult literature, and suggest that procedural memory consolidation may be robust to alcohol related interference in young adults, and be time dependent rather than state dependent, happening independently of sleep-wake states. These findings make important contributions to the field’s understanding of the independent relationships between alcohol and sleep, sleep and memory and alcohol use and memory. They highlight the disruptive influence of pre sleep alcohol use on young adult sleep, particularly very late in the sleep period, and extend previous literature, pointing to more subtle alcohol-related disruptions in the sleep EEG. They also highlight the importance of distinguishing between memory consolidation and sustained performance enhancements when assessing the sleep related memory consolidation effect. Future investigations into these effects should include an older comparison group and utilise alternative types of memory tasks (e.g. declarative or episodic tasks), allowing for a more direct assessment of age related differences and of the possible existence of the sleep related memory enhancement for different types of memory. This would assist educational opportunities for young adults- a developmentally unique age group known to engage in risky drinking.