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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ItemWellbeing and functioning in emerging adulthood: A longitudinal study of determinants and mechanisms( 2018)During the key periods of adolescence and emerging adulthood, individuals can be particularly vulnerable to experiencing suboptimal wellbeing and functioning. With potential long-term impacts on adult trajectories, early wellbeing promotion is critical. This study aimed to further understand wellbeing development across adolescence and into emerging adulthood, by examining the role of a range of individual and environmental characteristics. The individual characteristics examined included temperament, anxiety symptoms, and depression symptoms. Environmental characteristics included parental responses to emotion expression, parental mental health, stressful life events, and maltreatment. The role of emotion regulation strategies were also explored in relation to the characteristics and wellbeing. The study utilised a longitudinal community cohort from the Adolescent Development Study, recruited from schools across Melbourne, Australia. The sample included 245 families who completed questionnaires across three time points. At time 1 (mean age = 12.45), measures of temperament, depression symptoms, anxiety symptoms, parental depression symptoms, parental anxiety symptoms, and parental responses to offspring emotion expression were completed. At time 2 (mean age = 15.01), adolescents completed measures of stressful life events and maltreatment. They completed emotion regulation and wellbeing measures at the final time point (mean age = 18.83). Predictor variables were factor analysed within each domain in order to provide sufficient representation of the structure of the data. A series of path analyses, controlling for gender and SES revealed that temperament traits, neglect, and abuse predicted wellbeing and functioning outcomes. Bootstrap path analyses (using 95% confidence intervals for the indirect effect) revealed significant associations between the emotion regulation strategies of rumination, distraction, mindfulness, cognitive reappraisal, and expressive suppression with the individual and environmental characteristics, and wellbeing and functioning outcomes. Findings suggest that wellbeing development across adolescence and emerging adulthood is associated with individual characteristics (e.g., temperament), as well as environmental experiences that deviate from adaptive ranges (e.g., neglect). The various patterns found in the study reinforce the salience of examining wellbeing as a multifaceted construct, with aspects of wellbeing potentially having different developmental pathways. Furthermore, emotion regulation strategies may be important for wellbeing pathways, with maladaptive strategies (e.g., rumination) being associated with lower wellbeing and adaptive strategies (e.g. mindfulness) associated with higher wellbeing. Therefore, emotion regulation may be a suitable target for optimising youth wellbeing.
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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 psychological significance of different adolescent perfectionist profiles( 2018)Perfectionism has historically been regarded as a significant risk factor in the development and maintenance of psychological disorders. However, perfectionism is not always associated with poor psychological outcomes. Indeed, contemporary multidimensional perfectionism questionnaires include both adaptive and maladaptive dimensions, and recent research suggests a better understanding of perfectionism is achieved by focusing on combinations of these dimensions (rather than individual dimensions) to identify adaptive and maladaptive perfectionist subgroups/profiles. The purpose of the research reported herein was to investigate the nature of these subgroups in adolescents. Study 1 (n = 105, 17-year-olds) (Sironic & Reeve, 2012) examined perfectionist subgroups based on the Almost Perfect Scale-Revised (APS-R: Slaney, Rice, Mobley, Trippi, & Ashby, 2001), as well as the Depression Anxiety Stress Scales (DASS: Lovibond & Lovibond, 1995) and Motivated Strategies for Learning Questionnaire (Pintrich, Smith, Garcia, & McKeachie, 1991). It was hypothesised that four meaningful perfectionist subgroups could be derived from the APS-R’s High Standards and Discrepancy dimensions, and that each subgroup would rate their anxiety, depression, stress, and learning metacognitive beliefs differently. As predicted, cluster analysis of High Standards and Discrepancy dimension responses yielded four subgroup profiles: (1) high High Standards/low Discrepancy; (2) high High Standards/high Discrepancy; (3) low High Standards/high Discrepancy, and; (4) low High Standards/low Discrepancy). Subgroups were related to psychopathological symptoms and learning metacognitions in predictable ways. The low High Standards/high Discrepancy subgroup claimed to use metacognitive self-regulation significantly less often than the high High Standards/low Discrepancy and high High Standards/High Discrepancy subgroups; and the two high Discrepancy subgroups exhibited significantly higher depression ratings than the high High Standards/low Discrepancy subgroup. These findings support a four-subgroup account of perfectionism. The findings were interpreted as suggesting that the low High Standards/high Discrepancy subgroup might lack insight into (or deny) their perfectionistic tendencies—a tendency often associated with psychological disorders. Some suggest that perfectionism may be either externally and/or internally motivated. Insofar as this is correct, it is possible that students in this fourth subgroup are not seeking their own high standards but adopting the standards of significant others. Study 2 was designed to investigate this possibility. In Study 2 (n = 938, 14- to 17-year-olds) (Sironic & Reeve, 2015), high school students completed three commonly used perfectionism questionnaires (i.e., the Frost Multidimensional Perfectionism Scale, FMPS: Frost, Marten, Lahart, & Rosenblate, 1990; Child and Adolescent Perfectionism Scale, CAPS: Flett, Hewitt, Boucher, Davidson Munro, 2000; and APS-R), as well as the DASS. Preliminary analyses revealed commonly observed factor structures for each perfectionism questionnaire. Exploratory factor analysis of item responses from the three questionnaires (combined) yielded a four-factor solution (factors were labelled High Personal Standards, Concerns, Doubts and Discrepancy, Externally Motivated Perfectionism, and Organisation and Order). A latent class analysis of individuals’ mean ratings on each of the four factors yielded a six-class solution. Three of the six classes represented perfectionist subgroups (labelled adaptive perfectionist, externally motivated maladaptive perfectionist, and mixed maladaptive perfectionist) and three non-perfectionist subgroups (labelled non-perfectionist A, non-perfectionist B, and order and organisation non-perfectionist). Each subgroup was meaningfully associated with depression, anxiety, and stress symptoms. The mixed maladaptive perfectionist and externally motivated maladaptive perfectionist subgroups reported significantly higher levels of self-reported depression, anxiety, and stress compared with the adaptive perfectionist and non-perfectionist subgroups. The mixed maladaptive perfectionist and externally motivated maladaptive perfectionist subgroups did not differ in their depression and anxiety ratings, but the mixed maladaptive perfectionist subgroup reported significantly greater levels of stress than the externally motivated maladaptive perfectionist subgroup. The same three perfectionism questionnaires used in Study 2 were used in Study 3 (n = 299, 19-year-olds) (Sironic, Paul, & Reeve, under review at the time of thesis submission). Study 3 sought to establish whether externally motivated perfectionism was also an important aspect in a university undergraduate sample, and whether perfectionists’ beliefs about thinking (their clinical metacognitive beliefs, as measured by the Meta-Cognitions Questionniare-30 Shortened Version (MCQ-30: Wells & Cartwright-Hatton, 2004)) may differentiate perfectionist subgroups and help better explain their DASS depression, anxiety, and stress symptoms. Study 2’s four-factor solution was confirmed by factor analysis of items from the three perfectionism questionnaires, and the same three perfectionist subgroups were identified using latent class analysis of individuals’ average ratings on each factor. Clinical metacognitive beliefs and depression, anxiety, and stress ratings varied in expected ways in the different subgroups, with the externally motivated maladaptive perfectionists at greatest risk of poor psychological outcomes. Overall, the findings of the three studies offer new insights into the conceptualisation of adolescent perfectionism. Support was found for the existence of three perfectionist subgroups (one adaptive, two maladaptive) in adolescence. Findings showed that three out of 10 students were classified as maladaptive perfectionists, and that maladaptive perfectionists were more prevalent than adaptive perfectionists. Notably, the externally motivated maladaptive perfectionist subgroup seemed to possess the poorest metacognitive skills and be most at risk of experiencing psychopathology symptoms. These findings have implications for the treatment of perfectionists. They suggest that intervention strategies are needed to address issues associated with externally motivated perfectionism (i.e., the impact of parents, teachers or significant others); and that enhancing metacognitive skills could be included as part of an intervention strategy.
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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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ItemTemperament change during adolescence: Normative growth trajectories and the association of temperament change and pubertal development factors with adolescent psychopathology( 2016)Purpose of the study: This study examined the nature of temperament change during adolescence, using a longitudinal design to describe normative changes and individual heterogeneity in the developmental trajectories of traits. The study design allowed for further investigation of whether individual changes in temperament are associated with specific risk for depressive disorders. Pubertal timing and tempo were examined as developmentally salient factors that may potentially contribute to individual level changes in traits, including changes associated with depressive disorders. Method: A community sample of 245 adolescents participated in the longitudinal assessment of four temperament traits (Affiliation, Effortful Control, Negative Emotionality, Surgency), using the Early Adolescent Temperament Questionnaire, across five time points from early adolescence (mean age 11.62 years) to late adolescence (mean age 18.88 years). Univariate and multivariate latent growth modelling approaches, including latent growth models, latent class growth models and growth mixture models, were used to analyse normative and individual trajectories of temperament change. Adolescent depression was assessed via a questionnaire measure of symptoms and clinical interviewing to determine case level depressive disorders. To examine the specificity of associations between temperament and depression, questionnaire and interview measures were also used to assess adolescents’ broader risk for psychopathology, including anxiety and externalising symptoms and case level disorders. Pubertal timing and tempo were assessed during early adolescence using measures based on the Pubertal Development Scale. Results: Analyses of normative temperament trajectories revealed non-linear changes for Affiliation, Negative Emotionality and Surgency, reflecting both increases and decreases in temperament maturity during adolescence. The normative trajectory for Effortful Control showed linear decreases across adolescence. There was evidence of significant heterogeneity of temperament development, including individual differences in baseline levels of traits and in the degree and direction of change. The extent of heterogeneity was more sufficiently represented by significant individual level variance around univariate trajectories of normative change, rather than by sub-groups of individuals in multivariate models. Increased risk for depression was associated with lower baseline Surgency and Effortful Control, higher baseline Negative Emotionality and overall decreases in Affiliation, as well as relatively greater decreases in Effortful Control and slower decreases in Negative Emotionality compared with same age and gender peers. However, while specific risk for depressive disorders was associated with decreases in Affiliation during adolescence, further associations were observed between baseline levels and changes in traits with other categories of psychopathology. There was no evidence that pubertal timing and tempo are sources of temperament change during adolescence, however pubertal timing showed significant associations with adolescent psychopathology. Conclusions: This study contributes to existing literature on temperament that describes adolescence as a developmental period when normative temperament changes do not show overall increases in maturity. This study also highlights the need for further research to identify sources of temperament change during adolescence, as pubertal timing and temperament may be independent risk factors for psychopathology during adolescence. The findings add to accumulating evidence suggesting that changes in temperament influence an individual’s level of risk for adolescent psychopathology, over and above risk from baseline levels of traits. This includes evidence of temperament changes that confer specific risk for depression, including decreases in Affiliation, rather than general risk for psychopathology. Such findings may assist with targeting prevention or early intervention efforts against adolescent depression.
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ItemTuning in to teens: examining the efficacy of an emotion-focused parenting intervention in reducing pre-adolescents’ internalising difficulties( 2014)The transition from childhood to adolescence coincides with an increase in anxiety, a peak in somatic complaints, and a post-pubertal rise in depression by mid-adolescence, particularly for girls. For those affected, internalising difficulties result in considerable stress and impairment for the young person even if symptoms do not reach criteria for clinical diagnosis. Up to 50% of all adult psychological disorders have their onset during adolescence, highlighting the importance of identifying methods of prevention that are evidence-based. Emotional competence has been found to be an important protective factor for healthy social, emotional, and behavioural functioning. Both adolescents and adults with internalising difficulties show deficits in aspects of emotional competence. Research in child development suggests that parents’ emotional competence and emotion socialisation practices are related to children’s emotional functioning, including child internalising difficulties. This research has not yet been translated into intervention or prevention programs targeting parents of adolescents. The current study examined the efficacy of the Tuning in to Teens parenting program in improving emotion socialisation practices in parents of pre-adolescents and in measuring the impact on youth internalising difficulties. Grounded in emotion socialisation theory, this program teaches parents skills in responding to emotions in ways that enhance emotional competence in the young person, while also improving parent-youth communication and connectedness. A group-randomised control design was used where participants were recruited from schools and randomised into intervention and control conditions. Data were collected from 225 parents and 224 youth during the young person’s final year of elementary school (6th grade) and again, 10 months later in their first year of secondary school (7th grade). The thesis includes three studies. Study 1 reports the results of multilevel analyses, which showed participation in Tuning in to Teens resulted in significant improvements in parental emotion socialisation and reductions in youth internalising difficulties for the intervention condition. Study 2 examined moderators and mediators of program outcome. Results showed greater program effects for intervention subgroups with high pre-intervention difficulties. Parental education, income, parental internalising difficulties, parental difficulties in emotion awareness and regulation, and attendance rate did not moderate program effects. Mediation analyses supported emotion socialisation theory and showed parents who participated in the Tuning in to Teens parenting program reported improvements in emotion socialisation, which in turn was related to reductions in youth internalising difficulties. Study 3 investigated the relationship between parent emotion socialisation and youth somatic complaints. The study extended the literature on somatic complaints by being the first to consider parents’ emotional competence and emotion socialisation practices as predictors of youth somatic complaints alongside parents’ own somatic complaints. Results indicated that changes in parents’ awareness and regulation of emotion and emotion socialisation practices resulted in reduced youth somatic complaints. These findings have important implications for current aetiological models of somatic complaints and provide support for using an emotion-focused approach to enhance current treatment models of youth somatic complaints. A significant contribution of this thesis is that it presents the first randomised control trial evaluation of a parenting program that utilises research linking parents’ emotion socialisation with young people’s mental health, applying it in practice with a sample of parents of pre-adolescents. The research findings provide support for emotion socialisation theory and for using an emotion focused parenting program to prevent internalising difficulties in early adolescence.
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ItemAdolescent-onset depression: the interplay between family relationships, brain development and inflammation( 2014)Adolescence is an important life phase in which to explore psychological functioning. The emergence of depression during adolescence has been linked to aspects of both the family environment and brain developmental processes, although few studies have explored these two key variables together to prospectively determine adolescent vulnerability to depression. Consequently, the aim of the present thesis was to determine whether volume change in the pre-frontal cortex (PFC), amygdala and hippocampus partially, but significantly, mediate the effects of maternal behaviours on the onset of depression during adolescence. A secondary aim of this study was to explore a specific mechanism through which these changes in the brain may occur; specifically, systemic inflammation as marked via the production of CReactive Protein (CRP). Overall, it was expected that family interactions charaterised by higher rates and longer durations of Aggressive and Dysphoric maternal behaviours would predict the onset of clinical depression. Moreover, it was hypothesized that such maternal behaviours would predict changes in brain volume previously reported in depressed samples, as well as increased levels of CRP. Lastly, it was anticipated that elevated levels of CRP associated with more hostile maternal behaviours would partially, but significantly, mediate the relationship between parenting and structural brain development. Data from the larger Adolescent Development Study (ADS) were used to explore these aims and hypotheses. The ADS is a prospective longitudinal research study that consists of four waves of data collection, with data for this research project drawing on each of these four data collection time points in the following areas; magnetic resonance imaging (MRI) (T1, T3 and T4), family interaction tasks (T1), diagnostic assessment of mental health (T1 -T4) and saliva samples to measure inflammation (T2). As such, participants in this research comprised a smaller sub-sample of the total ADS sample population. This sub-sample consisted of N = 160 adolescents (females = 80), of which N = 32 (females = 22) received a diagnosis of clinical MDD. Path analysis techniques were used to analyse the data. The findings from the present study confirmed that maternal behaviours and changes in brain volume over time both increase vulnerability to MDD onset during adolescence. However, no evidence was found that changes in brain volume across the ages of 12 to 19 years in the PFC, amygdala or hippocampus mediated the effects of these maternal behaviours on mental health outcomes. Moreover, maternal behaviours were also found to result in detectable changes in brain volume over time, highlighting how even subtle variations in parenting behaviour influences biological development. However, when the immune system was included in these analyses, results suggested that CRP did not mediate the influence of maternal behaviours on these structural changes in the brain. The complexities of these interactions and their implications for our understanding of etiological models of depression during adolescence are considered.
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ItemDevelopment of the prefrontal cortex and its relationship to self-regulatory abilities during adolescence( 2014)Adolescence is a period of significant brain maturational changes in regions associated with self-regulation. While normative patterns of cortical thinning are postulated to underlie adaptive functioning, aberrations of this process are thought to result in poor self-regulatory abilities. This study characterises the development of three regions known to underlie regulatory processes, the anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (dlPFC) and ventrolateral prefrontal cortex (vlPFC), during adolescence. The study also examines the relationship between development of these cortical regions with three aspects of self-regulation: i. temperamental effortful control, ii. proactive and reactive forms of cognitive control, and iii. cognitive reappraisal, an adaptive emotion regulation strategy. Ninety-two adolescents (47 females) were examined longitudinally during early (mean age = 12.67), mid- (mean age = 16.42) and late adolescence (mean age = 18.78). Structural MRI scans were obtained at early and mid-adolescence, and cortical thickness of the regions of interest was measured using a semi-automated software (FreeSurfer). Effortful control (measured using the Early Adolescent Temperament Questionnaire-Revised), and proactive and reactive cognitive control (measured using a modified Stroop task), were also examined at early and mid-adolescence. Finally, cognitive reappraisal was measured at late adolescence using the Emotional Regulation Questionnaire. Linear mixed models were employed to analyse brain development between early and mid-adolescence, including sex and hemisphere effects. Subsequently, general linear and linear mixed models were employed to investigate the relationship between change in cortical thickness and change in effortful control/cognitive control over time. Finally, general linear models were employed to investigate the relationship between change in cortical thickness and use cognitive reappraisal strategies during late adolescence. Sex effects were included in all models. Findings revealed that the ACC, dlPFC and vlPFC exhibited significant reductions in cortical thickness between early and mid-adolescence across both hemispheres and sexes. Greater effortful control across time (i.e., averaged across early and mid-adolescence) was related to greater thinning of the left ACC, dlPFC and vlPFC over time, while greater proactive cognitive control across time was related to greater thinning of the right ACC. In addition, greater thinning of the left dlPFC and vlPFC was related to greater engagement in cognitive reappraisal during late adolescence in females. In relation to the development of self-regulation, greater relative increase in effortful control was related to greater thinning of the left dlPFC at trend level. However, greater relative increase in proactive control was related to less thinning of the right vlPFC, and greater relative increase in reactive control was related to less thinning of the left ACC (the latter in males alone). These findings highlight a complicated and dynamic relationship between cortical and self-regulatory development during adolescence, with different patterns of cortical maturation being advantageous for different forms of self-regulation. The importance of investigating sexual dimorphism in brain-behaviour relationships is also emphasised, as different associations were identified between cortical maturation and self-regulation in males and females. These findings suggest that early to mid-adolescence is a developmentally sensitive period for self-regulation, and provide a foundation for understanding abnormal patterns of brain development, and associated behavioural difficulties and psychopathology.
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ItemNeighbourhood disadvantage and internalising symptoms in adolescents: the mediating role of stressful life events, temperament, and maternal aggression( 2013)Purpose of the study: Disadvantaged neighbourhoods are associated with increased risk for anxiety and depression in adolescents. However the mechanisms for this relationship are not fully understood. Using a longitudinal design, I investigated whether several potential mediators, including stressful life events, maternal aggressive, dysphoric and positive behaviour, and adolescent temperament (Surgency, Negative affectivity, Effortful Control, Affiliation), could help explain the relationship between neighbourhood disadvantage and symptoms of anxiety and depression in early- to mid-adolescence. Method: A community sample of 245 adolescents and their parents participated in a range of assessments at baseline (age approximately 12-13 years old), including an observational assessment of parent-adolescent interactions, and a battery of adolescent-rated questionnaires. Neighbourhood disadvantage was assessed by combining Postal Area data collected during this first wave of assessment with a measure of disadvantage called the Socio-Economic Indexes For Areas (SEIFA) developed by the Australian Bureau of Statistics Adolescents were followed-up approximately 4 years later and completed questionnaires assessing depressive and anxious symptoms. Results: Analyses revealed that adolescents from disadvantaged neighbourhoods were more likely to report a greater number of stressful life events, and depressive and anxious symptoms. They were also more likely to score higher on temperament measures of Negative Affectivity, and lower on measures of Surgency and Effortful control. Mothers from disadvantaged neighbourhoods were more likely to display aggressive and dysphoric behaviour for longer periods, and positive behaviour for shorter periods, however no differences were detected in regard to the frequency of these behaviours. Mediational analyses using a bootsrapping approach determined that stressful life events and three temperament dimensions (low Surgency, low Effortful Control, high Negative Affectivity) significantly mediated the relationship between neighbourhood disadvantage and symptoms of anxiety and depression at baseline. Stressful life events and maternal aggression significantly mediated the relationship between neighbourhood disadvantage and change in depressive and anxious symptoms from baseline to follow-up. Conclusion: The research reported in this thesis provides evidence that disadvantaged neighbourhoods differ from less disadvantaged neighbourhoods in several different ways. In addition, various factors were found to partially mediate the relationship between neighbourhood disadvantage and anxiety and depression at different periods during adolescence. Temperament appears to be important earlier in adolescence, maternal affective behaviour seems to be important during mid- to later-adolescence, while stressful life events appear to act throughout adolescence. These findings suggest that the neighbourhood environment is likely to influence adolescents both directly, and indirectly through its effects on more proximal and individual risk factors. It was concluded that prevention and intervention programs targeting a range of risk factors in adolescents from disadvantaged neigbourhoods could be particularly effective at reducing the prevalence of internalising disorders in adolescents.