Melbourne School of Psychological Sciences - Theses
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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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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.
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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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ItemA diathesis-stress approach to the development of adolescent depression: a prospective, longitudinal assessment of the relative contribution of neurobiological and socio-environmental risk factors( 2013)Parsimonious evidence emphasises depression as one of the leading causes of disability worldwide (World Health Organiszation, 2012a). Further, research suggests that the peak incidence of depression occurs during the adolescent period (Hazell, 2008; Kessler et al., 2012; Kessler et al., 2005; Kim-Cohen et al., 2003), a time marked by significant changes in development of brain regions associated with cognition and emotion regulation (Steinberg, 2005), along with exposure to an increasingly complex social world (Nelson, Leibenluft, McClure, & Pine, 2005; Whittle, Allen, Lubman, & Yucel, 2006). Although recent studies have focused on characterising individual antecedents and consequences to adolescent onset depression, few have integrated neurobiological and socio-environmental factors, within prospective longitudinal designs. The present study therefore utlised a diathesis-stress approach to investigate the contribution of relatively stable neurobiological factors and easily identifiable and/or potentially modifiable socio-environmental factors to the emergence of depression during early to mid-adolescence. Further, taking advantage of the unique prospective design, the current study sought to ascertain if changes in specific brain structures, namely the hippocampus and the amygdala, are present prior to, or occur as a result of, the experience of major depressive disorder during adolescence. The present research incorporated a prospective design to follow a cohort of adolescents with an even representation of low, mid, and high risk of developing psychopathology (based on affective temperament). In the first set of analyses, identified as Study A, the current thesis assessed diathesis-stress models that integrated early neurobiological vulnerability markers, namely temperament (i.e., Negative Affectivity, Effortful Control, and Surgency) and the volumes of specific brain structures (i.e., hippocampus, amygdala, anterior cingulated cortex, and orbitofrontal cortex), with socio-environmental risk factors, namely gender, stressful life events, and socio-economic status, which have independently been found to be robust predictors of the onset of depressive symptoms. Initial hypotheses related to whether specific vulnerability markers previously identified in the literature, exert independent influence on the emergence of depressive symptoms within the current cohort. To that end, it was expected that higher levels of stressful life events, female gender, and lower socio-economic status would each be independently and prospectively associated with the emergence of depressive symptomatology. Further, it was hypothesised that higher levels of Negative Affectivity, as well as lower levels of Effortful Control and Surgency, would each independently and prospectively be associated with the emergence of depressive symptomatology. Finally, it was anticipated that reduced volumes of the hippocampus, medial and lateral orbitofrontal cortex, and anterior cingulated cortex, would each independently and prospectively be associated with the emergence of depressive symptomatology. Given the contradictory evidence regarding the amygdala volumes, an exploratory style of analyses was adopted to determine the direction of the relationship between amygdala volumes and the onset of depressive symptoms. Consistent with the diathesis-stress approach, a number of moderation models were also examined. It was anticipated that socio-environmental risk factors (i.e., gender, stressful life events, and socio-economic status), would independently moderate the relationship between temperament factors (i.e., Effortful Control, Negative Affectivity, and Surgency) and the emergence of depressive symptoms over time. Further, it was predicted that socio-environmental risk factors (i.e., gender, stressful life events, and socio-economic status), would independently moderate the relationship between brain volumes (i.e., hippocampus, amygdala, anterior cingulated cortex, and medial and lateral orbitofrontal cortex) and the emergence of depressive symptoms over time. The results did not support hypothesis relating to the diathesis-stress models assessed within the current thesis, however, some hypotheses regarding the main effects of temperament on the emergence of depressive symptoms were supported. Thus, the utility of investigating temperament as potential proximal factors of depression was confirmed. Further, socio-environmental factors of stressful life events and socio-economic status were shown to have cross-sectional influence on depressive symptoms during early-adolescence. Finally, gender was significantly associated with the development of major depressive disorder, but not with depressive symptoms. While many researchers have speculated that volume changes in the hippocampus and amygdala may increase vulnerability for depression, this is the first known study to date that provides prospective assessment of such a relationship in adolescents. The second set of analyses, identified as Study B, therefore measured brain volumes before and after the onset of a depressive disorder, in order to determine whether aberrant volumes in the hippocampus and the amygdala were antecedents or consequences of the depressive illness. Outcomes of Study B suggested that volume changes in the hippocampus and the amygdala may not be evident premorbidly, or in the early stages following the initial onset of a depressive episode. Indeed, results provided support for the assertion that changes in hippocampal and amygdala volumes commonly observed in those with depression may result only as a long-term consequence of the illness, as opposed to a premorbid vulnerability. The present research contributed to the literature on the pathogenesis of depression during adolescence in a variety of ways. It is hoped that the knowledge gained from the present research will add to the growing body of literature attempting to increase the effectiveness of identifying vulnerable individuals, as well as guide preventative intervention strategies to assist those who are at high risk of depression.