Melbourne School of Psychological Sciences - Theses

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    Assessing the relationship between executive function, coping, stress, depression, anxiety and quality of life in multiple sclerosis
    GRECH, LISA ( 2014)
    Background: Compared to healthy controls, people with multiple sclerosis (PwMS) use fewer adaptive and more maladaptive coping strategies when managing stressors and they experience higher rates of depression, anxiety and adjustment disorders. In addition, PwMS experience a high prevalence of cognitive impairment, including executive dysfunction, which has been linked to depression and anxiety. Aims: The current study examined the relationship between executive function, coping strategy use and psychosocial adjustment outcomes including stress, depression, anxiety and quality of life (QoL) in PwMS. The research assessed i) the ability of coping strategies and executive function to predict maladaptive and adaptive adjustment outcomes, and ii) the relationship between executive function and coping and whether there is a moderating and mediating relationship of different coping strategies between executive function and psychosocial adjustment in PwMS. Methods: Participants (N=107) with relapsing remitting or secondary progressive multiple sclerosis were administered tasks of executive function and completed self-report measures of stress, depression, anxiety, QoL and coping. Results: Consistent with expectations, stress, depression, anxiety and QoL were predicted by adaptive and maladaptive coping styles. Similarly, coping strategies, total coping and an adaptive coping index were predicted by tasks of executive function. Lower scores on tasks of executive function best predicted higher use of maladaptive strategies, but also adaptive strategies, while higher scores were limited in their ability to predict adaptive coping strategies. Tasks of executive function that most often predicted coping strategies included tasks of working memory, cognitive flexibility, information processing and attention. However, contrary to expectations, there was limited support for a relationship between tasks of executive function and psychosocial adjustment outcomes. An indirect relationship was found between executive function performance and adjustment through individual maladaptive coping strategies and adaptive coping strategies, as well as for an index of adaptive coping. Higher executive function performance was related to better adjustment via lower venting and behavioral disengagement, as well as higher scores on the adaptive coping index, whereas lower executive function performance was related to better adjustment via higher growth and acceptance. In general, better executive function and psychosocial adjustment was associated with minimal use of adaptive coping strategies, or greater use of maladaptive coping strategies. Conclusion: Executive function and psychosocial adjustment is mediated and moderated by coping strategies used by PwMS. Well-preserved executive function provides relative protection from poorer adjustment in the presence of high maladaptive or low adaptive coping. PwMS who perform poorly on tasks of executive function benefit from using less cognitively demanding coping strategies to enhance adjustment outcomes and this area that would benefit from further research to underpin effective intervention strategies. Findings from this study will assist with development of patient resources and patient management aimed at enhancing adaptive psychosocial adjustment in PwMS.
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    Parental psychological distress following very preterm birth: impact on infant social-emotional development and parent-child interaction
    PACE, CARMEN ( 2014)
    It is known that there are high rates of psychological distress in parents of very preterm infants, but previous researchers examining parental mental health after preterm birth have usually assessed mental health at one point in time. As such, little is known about the evolution of parental distress, particularly during the inpatient period in the Neonatal Intensive Care Unit (NICU). Parental distress can negatively impact parent-child relationships, which can then affect longer term child social-emotional development. Furthermore, children born very preterm have higher rates of early social-emotional difficulties, and are more likely to experience suboptimal parent-child interaction. These problems are likely to be compounded by parental mental health difficulties. Understanding these issues in the first year of life is vital to guide appropriate intervention, both for the wellbeing of mothers and fathers during this difficult period, and for the optimal development of their very preterm infants. This study aimed to describe the trajectory of psychological distress (depression, anxiety and post-traumatic stress symptoms) in mothers and fathers of very preterm infants at several key time points from birth to 12 months corrected age. It also investigated how this distress influenced parent-child interaction and the infant’s social-emotional development at 12 months corrected age. Finally, it examined whether parent-child interaction explained the relationship between maternal psychological distress during the first 12 months and infant social-emotional development at 12 months corrected age. Participants included 96 mothers and 86 fathers of 127 infants (99 families including 26 sets of twins and one set of triplets) born prior to 30 weeks gestational age and admitted to the Royal Women’s Hospital NICU in Melbourne, Australia. A subset of families of 55 infants were followed up at 12 months corrected age. Mothers and fathers completed measures assessing depression (The Centre for Epidemiological Studies Depression Scale) and anxiety (The Hospital Anxiety and Depression Scale) fortnightly from birth until the infant reached term equivalent age, and at three, six and 12 months corrected age. In addition, parents completed the Post-traumatic Stress Disorder Checklist Specific Version at term equivalent age and 12 months corrected age to assess post-traumatic stress symptoms. At 12 months corrected age the mothers and infants participated in the Emotional Availability Scales, an observational task assessing parent-child interaction, and mothers completed the Infant-Toddler Social and Emotional Assessment to assess infant social-emotional development. Overall, results showed that symptoms of depression, anxiety and post-traumatic stress were initially high for both mothers and fathers, and reduced in severity over time between the birth of their infant and 12 months corrected age. However, rates of clinically significant symptoms of depression remained above levels that would be expected in the general population at 12 months corrected age. Psychological distress in parents at various time points was predictive of certain infant social-emotional development and parent-child interaction outcomes. When these associations were examined more closely, it was found that the relationships between maternal mental health predictors and infant social-emotional development could not be explained by the influence of parent-child interaction. The findings of this study represent a substantial advance in the understanding of parental mental health following very preterm birth, especially in fathers. Additionally, the results may help identify the optimal timing of assessment and intervention to improve mothers’ and fathers’ wellbeing, and thus their infants’ development.
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    Tuning in to teens: examining the efficacy of an emotion-focused parenting intervention in reducing pre-adolescents’ internalising difficulties
    Kehoe, Christiane Evelyne ( 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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    Adolescent-onset depression: the interplay between family relationships, brain development and inflammation
    Jackson, Jennifer Sun-Fah ( 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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    Older parent-child relationships and their associations with older people’s psychological wellbeing: a comparison of Australian-born people and Chinese immigrants
    LIN, XIAOPING ( 2014)
    Parent-child relationships are one of the most fundamental types of family relationships. Against the background of population ageing in Australia and many other Western countries, the present study explored the nature of these relationships in later life and their associations with older people’s psychological wellbeing. Alongside population ageing, Australian populations are becoming culturally diverse. To enhance our understanding of cultural diversity in these issues, the study focused the differences between older Australian-born people and older Chinese immigrants. Older Chinese immigrants were included in the present study because there are some unique features in the nature of parent-child relationships in this group, such as the concept of filial piety. A convenience sample of 122 participants were recruited in the present study, comprising 60 Australian-born people and 62 Chinese immigrants. These participants were interviewed using a standardized interview schedule. Three groups of measures were used, assessing socio-demographic factors, the nature of parent-child relationships, and psychological wellbeing. The solidarity–conflict model and the concept of ambivalence were used to operationalize the nature of parent-child relationships, and four indicators (i.e., depression, anxiety, loneliness, and quality of life) were used to present a broad picture of older people’s psychological wellbeing. Most participants reported relatively high levels of solidarity in their relationships with adult children. Specifically, the majority lived close to, had frequent contact with, and were involved in some kind of exchange relationships with their children. Most participants felt close to their children, believed that their children’s opinions and values were relatively similar to their own, and had some kind of filial expectations. However, conflict and ambivalence were common, albeit, of low intensity, in participants’ relationships with adult children. The study further found that these relationship dimensions were significantly associated with the four wellbeing indicators and that most of these associations persisted when socio-demographic variables were considered. There were both similarities and differences in the nature of older parent-child relationships between Australian-born people and Chinese immigrants. For example, participants from both groups preferred to live independently and to receive help from professional aged care services than from their children. However, older Chinese immigrants were more likely to live with children and reported higher levels of ideal filial expectations. There were also stronger associations between depressive symptoms and the nature of older parent-child relationships among Chinese participants. These findings highlight the complexity of parent-child relationships in contemporary multicultural Australian society and suggest that using a comprehensive model, such as the solidarity-conflict model, helps to present a more complete picture of these relationships. They also provide evidence for the importance of these relationships to older people’s psychological wellbeing. Finally, these findings have important implications for policy development and service planning and provision for older people, in particular, those for older Chinese immigrants.
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    Sleep, mood, and cognitive vulnerability in adolescents: a naturalistic study over restricted and extended sleep opportunities
    BEI, BEI ( 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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    Neighbourhood disadvantage and internalising symptoms in adolescents: the mediating role of stressful life events, temperament, and maternal aggression
    SPEAR, OWEN ( 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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    Childhood maltreatment and structural neuroanatomy as risk factors for adolescent onset depression
    Barrett, Anna ( 2012)
    This thesis concerns three broad subjects – childhood maltreatment, structural neuroanatomical features in early adolescence, and depressive symptoms in mid-adolescence – with the aim of examining predictive relationships between them. The core focus of the thesis was on investigating relationships between the volumes of key brain structures implicated in emotion regulation, and adolescent onset depression. The measurement of brain structures in a psychiatrically healthy sample of children aged 11-12 years, and the use of these measurements to predict onset of depressive symptoms 2-3 years later, allowed for contribution to theoretical debate about the timing of structural alterations previously associated with depression – specifically, whether observed alterations formed risk factors for depression, or whether they were outcomes of disease-related processes. The evidence of premorbid structural alterations demonstrated by this thesis suggests that there are vulnerability biomarkers for depression, and may assist in better understanding the mechanisms of depressive illness as well as identifying individuals at risk. The secondary focus of the thesis was on retrospectively examining relationships between maltreatment in childhood and structural neuroanatomical features in adolescence, with the aim of identifying effects of childhood adverse experience on brain development. Previous studies have largely utilised adult populations with maltreatment-related psychiatric illness, and therefore have not been able to conclude whether structural alterations following childhood maltreatment only occur in those individuals who later develop psychopathology, or whether these changes occur before the onset of any psychopathology. This thesis investigated whether structural changes were associated with childhood maltreatment in a healthy sample of young adolescents, allowing the separation of early experiential effects from later psychopathological processes. This research also explored whether the volumes of selected brain structures mediated relationships between childhood maltreatment and adolescent onset depression, however no such relationships were detected. As this was an exploratory measure secondary to the key themes of the thesis, and interpretations were constrained by issues of sample size, it is not dealt with in detail. The most robust aspect of this research design was the examination of neurostructural risk factors for depression, and this formed the central content of the thesis. There is also a large extant body of research and literature on depression and brain development, from which to gain a strong theoretical grounding on the role of each brain structure examined in terms of the cognitive and affective processes it is thought to subserve. For this reason, material on the epidemiology and neurobiological models of depression form the first three chapters. An exploration of the emerging body of literature on the relationships between childhood maltreatment and brain development is contained subsequently. Chapter 1 provides an introduction to the epidemiology and selected etiological influences on adolescent depression. Chapter 2 gives an overview of the current understanding of brain development in adolescence, and describes some of the key theoretical models linking brain development to adolescent onset depression. Key structures highlighted in these models were selected for investigation within this thesis, and detailed examination of the evidence and resultant hypotheses for each of five selected structures’ relationships with depression is contained in Chapter 3. The focus then turns to childhood maltreatment as a second major contributor to adolescent onset depression; Chapter 4 summarises research on the prevalence and types of childhood maltreatment and the relationships between childhood maltreatment and adverse outcomes including the development of depression. Chapter 5 reviews literature from the emerging field of developmental traumatology, drawing inferences from the body of work examining neuroendocrinological sequelae of childhood maltreatment and bringing together preliminary findings from a range of sources to form hypotheses regarding potential relationships between childhood maltreatment and the brain structures discussed in previous chapters. Chapter 6 gives detail on the design and methodology of the thesis, and Chapter 7 explains the data analysis used and reports on the results. Interpretation of findings, discussion of strengths and limitations of the research, and implications for future work are contained in Chapter 8.
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    Getting to the heart of teen depression: the relationship between depression and cardiovascular risk in adolescents during wakefulness and sleep
    Waloszek, Joanna Maria ( 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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    A diathesis-stress approach to the development of adolescent depression: a prospective, longitudinal assessment of the relative contribution of neurobiological and socio-environmental risk factors
    Lichter, Renée Stefania ( 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.