Melbourne School of Psychological Sciences

Early Pregnancy Loss (EPL), a loss occurring before 14 weeks gestation, is a relatively common event, occurring in about 20% of pregnancies. Although many women and their partners do not experience psychological difficulties associated with this loss, a significant minority experience intense and sustained grief, depression and anxiety symptoms. Reliable prevalence rates of serious psychological consequences for women are not well established, and those of partners are largely unknown. Furthermore, it is unclear what factors increase the risk for developing serious psychological symptoms. A range of potential risk factors have been identified, but remain under-researched and have not been rigorously studied. According to Cognitive Behavioural Theory, it is possible that cognitions surrounding the loss may be a particularly relevant risk factor. Yet this topic has rarely been examined and the studies that have are characterised by major methodological shortcomings. Importantly, partners are rarely included in these studies. This study aimed to determine prevalence rates for grief depression and anxiety over the first three and a half months after EPL. It also investigated cognitions after EPL through the Common-Sense Model of Illness Representation, and their link with grief, depression and anxiety symptoms. This study included 28 male partners and 68 women diagnosed with EPL who attended the Early Pregnancy Assessment Service at the Royal Women’s Hospital in Melbourne, Australia. Participants completed self-report measures two weeks (T1), and three months (T2) post-loss. These included the Perinatal Grief Scale, the Centre for Epidemiological Studies-Depression scale, the State Trait Anxiety Inventory, and the Illness Perception Questionnaire-Revised. Results showed that the prevalence of grief, depression and anxiety symptoms for women at T1 were 20.6%, 54.4%, and 52.9%, respectively. For partners, the prevalence rates were 0% for grief, 32.1% for depression, and 25% for anxiety. These rates decreased by T2. Illness perceptions were found to significantly predict grief, depression and anxiety. Unexpectedly, it was often better perceptions of the loss that predicted worse psychological outcomes. These findings provide new information about the experience of EPL and suggest that critical timing for assessment and treatment would be within the first 3 months after EPL. Treatment options, particularly in terms of grief theories presented in the introduction, are discussed. Considering the surprising results and that this is the first study to examine illness perceptions among this sample, replication of these results is needed.

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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