The Role of Positive and Negative Aspects of Life Events in Depressive and Anxiety Symptoms.

Negative or stressful life events are robust risk factors for depression and anxiety. Less attention has been paid to positive aspects of events and whether positivity buffers the impact of negative aspects of events. The present study examined positivity and negativity of interpersonal and non-interpersonal episodic life events in predicting anxiety and depressive symptoms in a sample of 373 young adults. Regressions tested main and interactive effects of positivity and negativity ratings of events in predicting symptom factors (Fears, Anhedonia-Apprehension (AA), General Distress (GD)) relevant to anxiety and depression. A significant interaction demonstrated that positivity protected against high levels of negativity of non-interpersonal events in predicting GD. A main effect of interpersonal negativity predicting higher AA was observed. Results for Fears were non-significant. Findings suggest that positivity of life events may buffer against negativity in predicting symptoms shared between anxiety and depression.

Independent and relative effects of stress, depressive symptoms, and affect on college students' daily health behaviors.

Stress and depressive symptoms are associated with maladaptive health behavior practices such as unhealthy eating, sedentary behavior, insufficient sleep, and substance use. The relative and interactive effects of stress and depressive symptoms on health behavior practices are less well understood. The present study examined these processes in a daily diary study of 127 college students. Results from hierarchical generalized linear models indicated that depressive symptoms, and chronic and daily stress, but not acute stressful life events, were significantly associated with a composite score of daily maladaptive health behavior engagement (depressive symptoms b = .01, SE= .00, p < .01; chronic stress, b = .03, SE= .01, p < .01; daily stress, b = .01, SE= .01, p = .02); unexpectedly, the effect of stress on health behaviors was not moderated by depressive symptoms. Additionally, results demonstrated that the effect of depressive symptoms on health behaviors was mediated by fluctuations in daily negative affect. These results bear implications for intervention during a crucial period in the development of mental and physical health.

Pathways maintaining physical health problems from childhood to young adulthood: The role of stress and mood.

OBJECTIVE: Poor physical health in childhood is associated with a variety of negative health-related outcomes in adulthood. Psychosocial pathways contributing to the maintenance of physical health problems from childhood to young adulthood remain largely unexamined, despite evidence that factors such as negative mood and stress impact physical health. DESIGN: The current study tested the direct and indirect effects of ongoing health, chronic stress, health-related chronic stress, and depressive symptoms at age 20 on the link between health problems in childhood and young adulthood (age 21) in a longitudinal sample (n = 384). MAIN OUTCOME MEASURES: The hypotheses were tested using a multiple mediation path analysis framework; the primary outcome measure was a composite index of health status markers in young adulthood. RESULTS: The proposed model provided an adequate fit for the data, with significant total indirect effects of the four mediators and significant specific indirect effects of health-related chronic stress and depressive symptoms in maintaining health problems from childhood into young adulthood. CONCLUSIONS: Health problems are maintained from early childhood into young adulthood in part through psychosocial mechanisms. Depressive symptoms and health-related chronic stress have significant, unique effects on the relationship between health problems in early childhood and young adulthood.

Chronic and Episodic Stress in Children of Depressed Mothers.

The goal of this study was to examine chronic and episodic stress in children of mothers with and without a history of major depressive disorder (MDD) during the children's lives. Participants were 255 mothers selected according to their history of MDD (present vs. absent during child's life) and their children (age 8-14; 53% girls, 81% Caucasian). Mothers' and children's histories of MDD were assessed using diagnostic interviews, and their depressive symptoms were assessed via self-report measures. Children's levels of chronic and episodic stress were assessed using a semistructured contextual threat interview. Children of mothers with a history of recurrent MDD, compared to single MDD or no depression, experienced more chronic stress within several domains including peers, mother-child relations, and other family member relations as well as greater episodic dependent interpersonal stress. Each of these group differences was maintained after excluding children with a history of MDD themselves and controlling for their current depressive symptoms. However, only the group difference in chronic peer stress was maintained when controlling for mothers' current depression. The results suggest that children exposed to recurrent maternal MDD experience higher levels of both chronic and episodic stress, at least some of which they contribute to themselves (dependent interpersonal stress) and which is at least partially independent of the effects of children's depression. In addition, much of this stress is associated primarily with current depression in the mother, though it appears that chronic peer stress may remain elevated even after the remission of maternal depression.

Prospective associations between chronic youth sleep problems and young adult health.

OBJECTIVES: The current study investigated prospective associations between youth sleep problems across childhood and adolescence, as well as the relationship between chronic youth sleep problems and young adult health. Exploratory analyses investigated this sleep-health relationship in the context of several established risk factors, including youth depression and environmental stress. DESIGN: This project is an extension of the Mater-University Study of Pregnancy, a longitudinal study that followed more than 7000 children across early development. SETTING: Brisbane, Australia. PARTICIPANTS: Seven hundred ten mother-child dyads assessed from birth to age 20. MEASUREMENTS: We used maternal report measures to assess the persistence of youth sleep problems. We used structural equation modeling to explore the relationship between chronic maternal-reported youth sleep problems and subjective reports of young adult health quality and to assess whether associations remained when other potential health risks were included in the model. RESULTS: Path analyses revealed that sleep problems in early childhood predicted sleep problems in middle adolescence, which predicted sleep problems at age 20. Structural equation models showed that chronic youth sleep problems predicted youth health quality at age 20 (ß = .263, P < .001) over and above the effects of early adversity, chronic childhood illness, maternal depression, lifetime youth depression, and chronic youth stress. CONCLUSIONS: Chronic sleep problems can emerge in childhood and may contribute to negative health outcomes in young adulthood. Chronic youth sleep problems remain a significant predictor of poor health when tested against other known health risk factors, suggesting that sleep may be an important health intervention target.

Close Friends' Psychopathology as a Pathway From Early Adversity to Young Adulthood Depressive Symptoms.

Past research has highlighted the negative impact of early adverse experiences on childhood social functioning, including friendship selection, and later mental health. The current study explored the long-term effects of early adversity on young adults' close friends' psychological symptoms and the impact of these close friendships on later depressive symptoms. A prospective longitudinal design was used to examine 816 youth from a large community-based sample, who were followed from birth through age 25. Participants' mothers provided contemporaneous information about adversity exposure up to age 5, and participants completed questionnaires about their own depressive symptoms at age 20 and in their early 20s. Youth also nominated a best friend to complete questionnaires about his or her own psychopathology at age 20. Individuals who experienced more early adversity by age 5 had best friends with higher rates of psychopathology at age 20. Moreover, best friends' psychopathology predicted target youth depressive symptoms 2 to 5 years later. Results indicate that early adversity continues to affect social functioning throughout young adulthood and that best friendships marked by elevated psychopathology in turn negatively affect mental health. Findings have implications for clinical interventions designed to prevent the development of depressive symptoms in youth who have been exposed to early adversity.

Genetic susceptibility to family environment: BDNF Val66met and 5-HTTLPR influence depressive symptoms.

Functional genetic polymorphisms associated with Brain-Derived Neurotrophic Factor (BDNF) and serotonin (5-HTTLPR) have demonstrated associations with depression in interaction with environmental stressors. In light of evidence for biological connections between BDNF and serotonin, it is prudent to consider genetic epistasis between variants in these genes in the development of depressive symptoms. The current study examined the effects of val66met, 5-HTTLPR, and family environment quality on youth depressive symptoms in adolescence and young adulthood in a longitudinal sample oversampled for maternal depression history. A differential susceptibility model was tested, comparing the effects of family environment on depression scores across different levels of a cumulative plasticity genotype, defined as presence of both, either, or neither plasticity alleles (defined here as val66met Met and 5-HTTLPR 'S'). Cumulative plasticity genotype interacted with family environment quality to predict depression among males and females at age 15. After age 15, however, the interaction of cumulative plasticity genotype and early family environment quality was only predictive of depression among females. Results supported a differential susceptibility model at age 15, such that plasticity allele presence was associated with more or less depressive symptoms depending on valence of the family environment, and a diathesis-stress model of gene-environment interaction after age 15. These findings, although preliminary because of the small sample size, support prior results indicating interactive effects of 5-HTTLPR, val66met, and environmental stress, and suggest that family environment may have a stronger influence on genetically susceptible women than men.

A developmental pathway from early life stress to inflammation: the role of negative health behaviors.

Early life stressors are associated with elevated inflammation, a key physiological risk factor for disease. However, the mechanisms by which early stress leads to inflammation remain largely unknown. Using a longitudinal data set, we examined smoking, alcohol consumption, and body mass index (BMI) as health-behavior pathways by which early adversity might lead to inflammation during young adulthood. Contemporaneously measured early adversity predicted increased BMI and smoking but not alcohol consumption, and these effects were partially accounted for by chronic stress in young adulthood. Higher BMI in turn predicted higher levels of soluble tumor necrosis factor receptor type II (sTNF-RII) and C-reactive protein (CRP), and smoking predicted elevated sTNF-RII. These findings establish that early adversity contributes to inflammation in part through ongoing stress and maladaptive health behavior. Given that maladaptive health behaviors portend inflammation in young adulthood, they serve as promising targets for interventions designed to prevent the negative consequences of early adversity.

Early adversity and health outcomes in young adulthood: the role of ongoing stress.

OBJECTIVE: The current study examined the prospective effects of exposure to stressful conditions in early childhood on physical health in young adulthood, and explored continuing exposure to stressors, as well as depression, in adolescence as possible mechanisms of this relationship. METHOD: A prospective longitudinal design was used to examine 705 mother-child pairs from a community-based sample, followed from offspring birth through age 20 years. Mothers provided contemporaneous assessments of early adverse conditions from offspring birth through age 5. Offspring responses to the UCLA Life Stress Interview, Structured Clinical Interview for DSM Disorders, Physical Functioning subscale of the SF-36 Health Survey, and questions about the presence of chronic disease were used to assess youth stress at age 15, depression from ages 15-20, and physical health at age 20. RESULTS: Early adversity conferred risk for elevated levels of social and nonsocial stress at youth age 15, as well as depression between ages 15 and 20. Social and nonsocial stress, in turn, had effects on physical health at age 20, directly and indirectly via depression. CONCLUSION: Findings suggest that early adverse conditions have lasting implications for physical health, and that continued exposure to increased levels of both social and nonsocial stress in adolescence, as well as the presence of depression, might be important mechanisms by which early adversity impacts later physical health.

Maternal depression and the intergenerational transmission of relational impairment.

Previous research has demonstrated that the offspring of depressed mothers are at greater risk for negative psychopathological and psychosocial outcomes than children of nondepressed mothers. This study specifically examines offspring's romantic relationship quality during the transition to adulthood as a function of maternal depression and 3 putative mechanisms for this association: youth depression history, mother-child relationship discord, and maternal romantic relationship difficulties. The study further explores the role of these factors in the risk for depressive symptoms during the transition to adulthood. Hypotheses were examined longitudinally in a community sample of 182 Australian youth who were followed from birth to age 20 and were in committed romantic relationships at age 20 with romantic partners willing to provide data regarding romantic relationship satisfaction. Structural equation modeling analyses found support for a direct effect of maternal depression on youth romantic relationship quality with significant mediation by mother-child relationship discord, as well as an association between mother-child relationship discord and later depressive symptoms that is mediated by youth romantic relationship quality. Findings also lend support for an indirect effect of maternal depression on youth depressive symptoms via mother-child relationship discord and youth romantic relationship quality. This study provides further evidence for the negative psychosocial and psychopathological outcomes of children of depressed mothers and the intergenerational transmission of relational difficulties.

Cortisol secretion in depressed, and at-risk adults.

Distinct patterns of cortisol secretion have been associated with depression in past research, but it remains unclear whether individuals at-risk for depression may also have similar patterns of cortisol secretion. This is the first study to date of both naturalistic diurnal cortisol secretion and cortisol reactivity to a psychosocial laboratory stressor in depressed and at-risk adults. Cortisol secretion patterns were compared for 57 currently depressed, at-risk (based on trait-level positive and negative affect), and control participants over 5 days and in response to a laboratory stressor. After controlling for potentially confounding biobehavioral variables, the depressed group had a larger cortisol awakening response (CAR) and higher average diurnal cortisol compared to control participants. Individuals at-risk for depression also had significantly higher waking cortisol levels than control participants. Results for the psychosocial laboratory stressor did not show the predicted elevations in cortisol for depressed and at-risk participants compared to controls. The at-risk group recovered more quickly when compared to the depressed group both in levels of cortisol and concurrent measures of negative affect. The at-risk and depressed participants were similar on the diurnal cortisol measures, but differed on response to the laboratory social stressor, suggesting divergence in cortisol secretion patterns between currently depressed and temperamentally at-risk individuals. Further investigation of HPA functioning of individuals at-risk for depression may clarify the stress processes involved in risk for depression onset.

Effects of child psychopathology on maternal depression: the mediating role of child-related acute and chronic stressors.

In light of recent research highlighting the potential effects of children's behavior on mothers' mental health, the current study examined 679 mothers and their adolescent children from a community-based sample to determine the effects of youth psychopathology on maternal depression and levels of child-related stress in mothers' lives. It was hypothesized that the number of past clinical diagnoses in 15-year-old adolescents would predict the presence of maternal depression at youth age 15 and 5 years later, as well as more episodes of maternal depression during the follow-up period. Furthermore, it was hypothesized that increased levels of child-related stress in mothers' lives would mediate these relationships. Regression analyses indicated that past youth diagnoses do confer risk for the presence of current and future maternal depression, as well as more episodes of maternal depression, and mediation analyses revealed that child-related acute and chronic stress were mediators of the relationship between youth diagnoses and the presence of maternal depression at follow-up. Findings suggest that increased levels of child-related objective stress in mothers' lives are one mechanism by which children's psychopathology affects mothers' future risk for depression.

Childhood social withdrawal, interpersonal impairment, and young adult depression: a mediational model.

Building on interpersonal theories of depression, the current study sought to explore whether early childhood social withdrawal serves as a risk factor for depressive symptoms and diagnoses in young adulthood. The researchers hypothesized that social impairment at age 15 would mediate the association between social withdrawal at age 5 and depression by age 20. This mediational model was tested in a community sample of 702 Australian youth followed from mother's pregnancy to youth age 20. Structural equation modeling analyses found support for a model in which childhood social withdrawal predicted adolescent social impairment, which, in turn, predicted depression in young adulthood. Additionally, gender was found to moderate the relationship between adolescent social impairment and depression in early adulthood, with females exhibiting a stronger association between social functioning and depression at the symptom and diagnostic level. This study illuminates one potential pathway from early developing social difficulties to later depressive symptoms and disorders.

Do adolescent offspring of women with PTSD experience higher levels of chronic and episodic stress?

Offspring of mothers with posttraumatic stress disorder (PTSD) are at higher risk for a range of negative developmental outcomes, including differing forms of psychopathology. This study suggests that the multigenerational impact of trauma may be partially attributed to increased levels of stress experienced by these offspring during childhood and adolescence. Diagnostic interviews were conducted with over 800 women and their offspring. Experiences of stress were assessed using multiple measures. Results indicate that offspring of mothers with PTSD or high levels of PTSD symptoms experienced higher levels of lifetime exposure to major stress, η(2) = .02, current chronic stress due to family relations, η(2) = .01, and a higher level of objectively rated recent episodic life stress, η(2) = .01, compared to offspring of women without PTSD. These findings remained significant after controlling for maternal history of depression.

Stressful life events predict delayed functional recovery following treatment for mania in bipolar disorder.

Identifying predictors of functional recovery in bipolar disorder is critical to treatment efforts to help patients re-establish premorbid levels of role adjustment following an acute manic episode. The current study examined the role of stressful life events as potential obstacles to recovery of functioning in various roles. 65 patients with bipolar I disorder participated in a longitudinal study of functional recovery following clinical recovery from a manic episode. Stressful life events were assessed as predictors of concurrent vs. delayed recovery of role functioning in 4 domains (friends, family, home duties, work/school). Despite clinical recovery, a subset of patients experienced delayed functional recovery in various role domains. Moreover, delayed functional recovery was significantly associated with presence of one or more stressors in the prior 3 months, even after controlling for mood symptoms. Presence of a stressor predicted longer time to functional recovery in life domains, up to 112 days in work/school. Interventions that provide monitoring, support, and problem-solving may be needed to help prevent or mitigate the effects of stress on functional recovery.

Interpersonal Style, Stress, and Depression: An Examination of Transactional and Diathesis-Stress Models.

The present study examines a transactional, interpersonal model of depression in which stress generation (Hammen, 1991) in romantic relationships mediates the association between aspects of interpersonal style (i.e., attachment, dependency, and reassurance seeking) and depressive symptoms. It also examines an alternative, diathesis-stress model in which interpersonal style interacts with romantic stressors in predicting depressive symptoms. These models were tested in a sample of college women, both prospectively over a four-week period, as well as on a day-today basis using a daily diary methodology. Overall, there was strong evidence for a transactional, mediation model in which interpersonal style predicted romantic conflict stress, and in turn depressive symptoms. The alternative diathesis-stress model of depression was not supported. These results are interpreted in relation to previous research, and key limitations that should be addressed by future research are discussed.

Longitudinal course of adolescent depression: neuroendocrine and psychosocial predictors.

OBJECTIVE: The study examined whether cortisol measures are associated with the clinical course of depression in adolescents. Furthermore, the study evaluated whether the relationship between cortisol and clinical course is moderated by environmental stress and/or social support. METHOD: Fifty-five adolescents with depression (age range 13-18 years) were recruited. In addition to a systematic diagnostic assessment, information was obtained on environmental stress and social support. Urinary free cortisol measures were collected on three consecutive nights during the index episode. Clinical follow-up evaluations were conducted at regular intervals over a 5-year period, documenting recovery from the index depressive episode and recurrent episodes. Information on environmental stress and social support also was gathered during each follow-up assessment. RESULTS: Consistent with prior reports, the majority of adolescents (92.2%) recovered from the initial depressive episode. A substantial proportion of the recovered youth (42.6%) experienced a subsequent episode during the follow-up period. Higher cortisol levels were associated with a longer time to recovery from the index depressive episode. The effect of cortisol on recovery was moderated by social support. The combination of elevated cortisol and recent stressful experiences predicted recurrence, whereas a higher level of social support was protective against recurrence. CONCLUSIONS: These data, in conjunction with prior literature, suggest that depression reflects an underlying neurobiological vulnerability that may predispose individuals with high vulnerability to chronic, recurrent episodes. Psychosocial factors, independently or in combination with an underlying neurobiological vulnerability, also play an important role in determining the clinical course of depression.

Specificity of Stress Generation: A Comparison of Adolescents with Depressive, Anxiety, and Comorbid Diagnoses.

Individuals with a history of depression experience more stress that is dependent in part on their own actions. However, it is unclear whether stress generation is a unique feature of depression, or a universal process that is also present in other types of psychopathology, such as anxiety disorders. The current study addressed this issue by comparing adolescents with a history of "pure" (i.e., non-comorbid) depressive disorders, pure anxiety disorders, comorbid depression and anxiety, and no disorder, on their levels of dependent and independent stress. Results indicated that adolescents with pure depression experienced more dependent stress than adolescents with pure anxiety, and adolescents with any internalizing diagnosis experienced more dependent stress than controls. Further, adolescents with comorbid depression and anxiety reported the highest levels of stress generation. The results suggest that while stress generation may be more strongly associated with depression than anxiety in adolescence, it is not unique to depression.

Hippocampal changes associated with early-life adversity and vulnerability to depression.

BACKGROUND: Smaller hippocampal volume has been reported in some adult and pediatric studies of unipolar major depressive disorder. It is not clear whether the smaller hippocampal volume precedes or is a consequence of the illness. Early-life adversity is associated with both smaller hippocampal volume and increased vulnerability to depressive disorder. Hippocampal changes may mediate the relationship between early-life adversity and depressive illness in a subset of patients. However, there are no reports of longitudinal clinical studies that have examined this issue. METHODS: Thirty adolescents with unipolar major depressive disorder, 22 adolescent volunteers with no personal history of a psychiatric illness including depression but who were at high risk for developing depression by virtue of parental depression (high-risk group), and 35 adolescent volunteers with no personal or family history of a psychiatric disorder (control subjects) underwent volumetric magnetic resonance imaging studies. Information was also gathered on early and recent adverse experiences with standard interviews. The participants were followed for up to 5 years to assess the onset and clinical course of depression. RESULTS: Depressed and high-risk groups had significantly smaller left and right hippocampal volumes than control subjects. Higher levels of early-life adversity were associated with smaller hippocampal volumes. Smaller hippocampal volume partially mediated the effect of early-life adversity on depression during longitudinal follow-up. CONCLUSIONS: Smaller hippocampal volume in adolescents at high risk for depression suggests that it may be a vulnerability marker for the illness. Early-life adversity may interact with genetic vulnerability to induce hippocampal changes, potentially increasing the risk for depressive disorder.

Ethnic differences in electroencephalographic sleep patterns in adolescents.

The purpose of the study was to evaluate ethnic differences in polysomnography measures in adolescents. Ninety-six volunteers from four ethnic groups (13 African-American, 18 Asian-American, 19 Mexican-American, and 46 Non-Hispanic White) were recruited. The subjects were in good physical and psychological health, and were asymptomatic with respect to sleep/wake complaints or sleep disorders. Polysomnography measures were collected on three consecutive nights. African-Americans manifested lower sleep efficiency, spent proportionately more time in stage 2 sleep, and had less stage 4 sleep compared to the other ethnic groups. In contrast to this, Mexican-Americans had more rapid eye movement (REM) sleep than their counterparts. The observed sleep patterns in the different ethnic groups persisted after controlling for specific demographic, clinical and psychosocial variables that are known to influence sleep measures. Gender had a differential effect on sleep patterns in the various ethnic groups. For instance, differences in non-REM sleep were more evident in African-American males, whereas increased REM sleep was most notable in Mexican-American females. At present, the clinical implications of the observed cross-ethnic differences in sleep physiology among adolescents are not clear. In previous studies, reduced sleep efficiency and stage 4 sleep, as well as increased REM sleep, were associated with psychopathology. It is not known whether the traditionally described sleep profiles, based largely on Non-Hispanic White populations, will generalize to other racial or ethnic groups. In addition to a systematic investigation of this issue, future research should attempt to identify the underlying causes for cross-ethnic variations in sleep physiology.