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BackgroundDepression is thought to generate stressful life events. However, other internalizing symptoms such as anxiety or post-traumatic stress and individual difference variables such as personality traits and alcohol use may contribute to stressful life events. Whether stress generation is specific to depression or generalized to these other variables is unclear. Therefore, we tested whether stress generation was depression specific or generalizable to anxiety, PTSD, alcohol use, neuroticism, and extraversion.DesignTwo-wave longitudinal study with a five-year follow-up.Methods917 young adults completed measures of internalizing symptoms, alcohol use, neuroticism, and extraversion during college and five years later along with an interview-based measure of life events.ResultsSymptoms of depression, anxiety, PTSD, and neuroticism exhibited bivariate predictive effects on interpersonal-dependent events. When considering internalizing symptoms in the aggregate, stress generation was specific to symptoms rather than neuroticism. Furthermore, interpersonal-dependent life events mediated Time 1 internalizing symptoms predicting Time 2 symptoms.ConclusionOur results indicate that stress generation applies to internalizing symptoms broadly rather than specifically to depression. Moreover, neuroticism was no longer a significant predictor of life events when examined with internalizing symptoms simultaneously. These results support the value of integrative models that test numerous factors predicting stressful life events.

BackgroundStressful life experiences and personality can influence one another. Personality may contribute to the amount and type of stress individuals experience, which is referred to as a selection effect. Life stress may also impact one's personality, which is referred to as a socialization effect. It was hypothesized that neuroticism would predict increased chronic and episodic stress (selection effect) and that chronic and episodic stress would predict increased neuroticism (socialization effect).MethodsThe current study investigated selection and socialization effects of neuroticism and life stress over a three-year period in 627 adolescents. Life stress data were examined in terms of duration (chronic versus episodic) and type (interpersonal versus non-interpersonal). Episodic stress data were examined as dependent or independent.ResultsThe results from ten cross-lagged panel models provided some evidence for significant selection and socialization effects depending on stress type. Over three years, we observed that neuroticism increases interpersonal chronic stress and non-interpersonal stressful events (selection effects) and that dependent non-interpersonal stressful events and chronic stress increase neuroticism (socialization effects).LimitationsStudy limitations include a lack of a lifespan perspective and a statistical approach that does not differentiate between- from within-person variance.ConclusionsFindings suggest the value of attending to stress response as well as targeting neuroticism in prevention and intervention approaches in adolescents.

Maternal stress during pregnancy can cause alterations to the fetal hypothalamus-pituitary-adrenal (HPA) axis, a phenomenon known as fetal programming that may have lasting effects on offspring outcomes, including depression. Evidence suggests that these effects may vary with respect to the offspring's genetic risk. Nonetheless, few studies have examined these effects into adulthood, when risk for depression onset is highest. The present study builds upon the extant literature by examining the interaction of maternal prenatal perceived stress (MPPS) and offspring HPA-axis polygenic risk to predict offspring depression in early adulthood. A total of 381 mother-child dyads participated in a prospective, longitudinal study that spanned from pregnancy until offspring were 20 years of age. Polygenic risk was defined by a multilocus genetic profile score (MGPS) that reflected the additive risk of three HPA-axis candidate genes. The results indicated that the interaction of MPPS and HPA-axis MGPS confers risk for offspring depression at age 20, in line with the differential susceptibility model. This interaction may be specific to prenatal stress, as maternal stress during early childhood did not interact with genetic risk to predict depression. These findings provide the first evidence that genetic variants that are associated with the HPA axis may act in a polygenic, additive fashion to moderate the association between fetal programming and adult depression.

BACKGROUND: After cancer diagnosis, depressive symptoms are elevated on average and decline over time, but substantial variability is apparent. Few studies have examined to what extent chronic stress in distinct life domains affects depressive symptoms. PURPOSE: Chronic stress in vocational and intimate partner life domains, and their interaction, were tested as predictors of depressive symptoms after breast cancer diagnosis. METHODS: Women (N = 460) completed validated interviews regarding chronic stress in specific life domains shortly after diagnosis and a measure of depressive symptoms every 6 weeks for 6 months. RESULTS: In latent growth curve modeling analyses, greater chronic stress in work (b = 2.90; p < .001) and intimate partner domains (b = 1.38, p = .02) was associated with higher depressive symptoms at study entry (intercept), and greater work stress predicted faster recovery from depressive symptoms over time (b = -0.10; p = .01). The two domains of chronic stress also interacted significantly on depressive symptoms at study entry (b = -1.54; p < .02) and over time (b = 0.14; p < .001). Greater work stress was associated with higher depressive symptoms at study entry regardless of intimate partner stress, but greater intimate partner stress was associated with higher depressive symptoms when work stress was low. The decline over 6 months in initially elevated depressive symptoms predicted by high work stress was significantly steeper when intimate partner stress was low. CONCLUSIONS: Targeting interventions to recently diagnosed breast cancer patients living with chronically stressful vocational and intimate partner life circumstances could be worthwhile.

BackgroundAfter cancer diagnosis, depressive symptoms are elevated on average and decline over time, but substantial variability is apparent. Few studies have examined to what extent chronic stress in distinct life domains affects depressive symptoms.PurposeChronic stress in vocational and intimate partner life domains, and their interaction, were tested as predictors of depressive symptoms after breast cancer diagnosis.MethodsWomen (N = 460) completed validated interviews regarding chronic stress in specific life domains shortly after diagnosis and a measure of depressive symptoms every 6 weeks for 6 months.ResultsIn latent growth curve modeling analyses, greater chronic stress in work (b = 2.90; p < .001) and intimate partner domains (b = 1.38, p = .02) was associated with higher depressive symptoms at study entry (intercept), and greater work stress predicted faster recovery from depressive symptoms over time (b = -0.10; p = .01). The two domains of chronic stress also interacted significantly on depressive symptoms at study entry (b = -1.54; p < .02) and over time (b = 0.14; p < .001). Greater work stress was associated with higher depressive symptoms at study entry regardless of intimate partner stress, but greater intimate partner stress was associated with higher depressive symptoms when work stress was low. The decline over 6 months in initially elevated depressive symptoms predicted by high work stress was significantly steeper when intimate partner stress was low.ConclusionsTargeting interventions to recently diagnosed breast cancer patients living with chronically stressful vocational and intimate partner life circumstances could be worthwhile.

BackgroundAfter cancer diagnosis, depressive symptoms are elevated on average and decline over time, but substantial variability is apparent. Few studies have examined to what extent chronic stress in distinct life domains affects depressive symptoms.PurposeChronic stress in vocational and intimate partner life domains, and their interaction, were tested as predictors of depressive symptoms after breast cancer diagnosis.MethodsWomen (N = 460) completed validated interviews regarding chronic stress in specific life domains shortly after diagnosis and a measure of depressive symptoms every 6 weeks for 6 months.ResultsIn latent growth curve modeling analyses, greater chronic stress in work (b = 2.90; p < .001) and intimate partner domains (b = 1.38, p = .02) was associated with higher depressive symptoms at study entry (intercept), and greater work stress predicted faster recovery from depressive symptoms over time (b = -0.10; p = .01). The two domains of chronic stress also interacted significantly on depressive symptoms at study entry (b = -1.54; p < .02) and over time (b = 0.14; p < .001). Greater work stress was associated with higher depressive symptoms at study entry regardless of intimate partner stress, but greater intimate partner stress was associated with higher depressive symptoms when work stress was low. The decline over 6 months in initially elevated depressive symptoms predicted by high work stress was significantly steeper when intimate partner stress was low.ConclusionsTargeting interventions to recently diagnosed breast cancer patients living with chronically stressful vocational and intimate partner life circumstances could be worthwhile.

The serotonin transporter-linked polymorphic region (5-HTTLPR) is associated with caregiving in nonhuman animals and with affective and cognitive correlates of human parenting, yet its association with human parenting is largely unknown. Using a well-characterized sample of parents and offspring, we evaluated the association of parental 5-HTTLPR with observed positive and negative parenting behavior, as well as its biologically plausible moderation of child-related stress and disruptive child behavior as predictors of parenting. One hundred and sixty-two parents (86% mothers) and their 6- to 9-year-old children with and without attention-deficit/hyperactivity disorder were ascertained using multiple methods including structured interviews, rating scales, and observed parent-child interaction, yielding strong measures of key constructs. Controlling for multiple youth-level (e.g., sex, 5-HTTLPR genotype, disruptive behavior) and parent-level (e.g., demographics, depression, attention-deficit/hyperactivity disorder) factors, parents with an S allele exhibited significantly less observed positive parenting than those with the LL genotype. Significant Gene × Environment interactions were also observed: Child-related stress was negatively associated with observed parental negativity among SS/SL genotype parents but not LL genotype parents; next, observed disruptive child behavior was positively associated with parental negativity for both genotypes, but the effect was strongest in SS/SL parents. These preliminary findings suggest that parental 5-HTTLPR is uniquely associated with positive and negative parenting behavior, with more specific patterns according to child-related stress and disruptive child behavior. We consider implications for future research evaluating genetic influences on parenting as well as considerations for designing and delivering parenting-based interventions.

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

Objectives The present study sought to examine the association between maternal depressive symptoms and characteristics of offspring physical health, including health status, health behaviors, and healthcare utilization, among low-income families. Maternal engagement was explored as a mediator of observed effects. Methods Cross-sectional survey data from a community sample of 4589 low-income women and their preschool-age children participating in the WIC program in Los Angeles County were analyzed using logistic, Poisson, and zero-inflated negative binomial regression. Mediation was tested via conditional process analyses. Results After controlling for the effects of demographic characteristics including maternal health insurance coverage, employment status, education, and preferred language, children of depressed women (N = 1025) were significantly more likely than children of non-depressed women (N = 3564) to receive a "poor" or "fair" maternal rating of general health (OR 2.34), eat fewer vegetables (IRR: 0.94) more sweets (IRR: 1.20) and sugary drinks daily (IRR: 1.32), and consume fast food more often (OR 1.21). These children were also less likely to have health insurance (OR 1.59) and more likely to receive medical care from a public medical clinic or hospital emergency room (OR 1.30). Reduced maternal engagement partially mediated associations between maternal depressive symptoms and several child health outcomes including poor diet, health insurance coverage, and use of public medical services. Conclusions for Practice Maternal depressive symptoms are associated with poor health among preschool-age children in low-income families. Prevention, screening, and treatment efforts aimed at reducing the prevalence of maternal depression may positively affect young children's health.

Breast cancer patients often experience adverse physical side effects of medical treatments. According to the biobehavioral model of cancer stress and disease, life stress during diagnosis and treatment may negatively influence the trajectory of women's physical health-related adjustment to breast cancer. This longitudinal study examined chronic and episodic stress as predictors of bothersome physical symptoms during the year after breast cancer diagnosis. Women diagnosed with breast cancer in the previous 4 months (N = 460) completed a life stress interview for contextual assessment of chronic and episodic stress severity at study entry and 9 months later. Physical symptom bother (e.g., pain, fatigue) was measured at study entry, every 6 weeks through 6 months, and at nine and 12 months. In multilevel structural equation modeling (MSEM) analyses, both chronic stress and episodic stress occurring shortly after diagnosis predicted greater physical symptom bother over the study period. Episodic stress reported to have occurred prior to diagnosis did not predict symptom bother in MSEM analyses, and the interaction between chronic and episodic stress on symptom bother was not significant. Results suggest that ongoing chronic stress and episodic stress occurring shortly after breast cancer diagnosis are important predictors of bothersome symptoms during and after cancer treatment. Screening for chronic stress and recent stressful life events in the months following diagnosis may help to identify breast cancer patients at risk for persistent and bothersome physical symptoms. Interventions to prevent or ameliorate treatment-related physical symptoms may confer added benefit by addressing ongoing non-cancer-related stress in women's lives.

ObjectivePoor 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.DesignThe 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 measuresThe 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.ResultsThe 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.ConclusionsHealth 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.

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.

ObjectivesThe 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.DesignThis project is an extension of the Mater-University Study of Pregnancy, a longitudinal study that followed more than 7000 children across early development.SettingBrisbane, Australia.ParticipantsSeven hundred ten mother-child dyads assessed from birth to age 20.MeasurementsWe 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.ResultsPath 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 (β = .263, P < .001) over and above the effects of early adversity, chronic childhood illness, maternal depression, lifetime youth depression, and chronic youth stress.ConclusionsChronic 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.

Few studies comprehensively evaluate which types of life stress are most strongly associated with depressive episode onsets, over and above other forms of stress, and comparisons between acute and chronic stress are particularly lacking. Past research implicates major (moderate to severe) stressful life events (SLEs), and to a lesser extent, interpersonal forms of stress; research conflicts on whether dependent or independent SLEs are more potent, but theory favors dependent SLEs. The present study used 5 years of annual diagnostic and life stress interviews of chronic stress and SLEs from 2 separate samples (Sample 1 N = 432; Sample 2 N = 146) transitioning into emerging adulthood; 1 sample also collected early adversity interviews. Multivariate analyses simultaneously examined multiple forms of life stress to test hypotheses that all major SLEs, then particularly interpersonal forms of stress, and then dependent SLEs would contribute unique variance to major depressive episode (MDE) onsets. Person-month survival analysis consistently implicated chronic interpersonal stress and major interpersonal SLEs as statistically unique predictors of risk for MDE onset. In addition, follow-up analyses demonstrated temporal precedence for chronic stress; tested differences by gender; showed that recent chronic stress mediates the relationship between adolescent adversity and later MDE onsets; and revealed interactions of several forms of stress with socioeconomic status (SES). Specifically, as SES declined, there was an increasing role for noninterpersonal chronic stress and noninterpersonal major SLEs, coupled with a decreasing role for interpersonal chronic stress. Implications for future etiological research were discussed.

Depression carries serious psychosocial, physical, and economic consequences for cancer survivors. Study goals were to characterize patterns and predictors of depressive symptoms and major depressive episodes in recently diagnosed breast cancer patients. Consecutively recruited women (N = 460) completed a validated interview (CIDI) and questionnaire measure (CES-D) of depression within 4 months after invasive breast cancer diagnosis and at six additional assessments across 12 months. Outcomes were major depressive episodes, continuous symptom scores, and latent symptom trajectory classes. Across 12 months, 16.6 % of women met criteria for a major depressive episode. Unemployment predicted depressive episodes after other correlates were controlled. Distinct trajectory classes were apparent: an estimated 38 % of women had chronically elevated symptoms (High trajectory), 20 % recovered from elevated symptoms (Recovery), and 43 % had lower symptoms (Low and Very Low trajectories). Although 96 % of episodes occurred in the High or Recovery classes, 66 % of women in the High trajectory did not have an episode. Women in the Low (vs High) trajectory were more likely to be older, retired, more affluent, and have fewer comorbid diseases and briefer oncologic treatment. Women in the Recovery trajectory (vs High) were more likely to be married and more affluent and have fewer comorbid diseases. Assuming available therapeutic resources, assessment of both depressive symptoms and episodes over several months after diagnosis is important. Identification of patients at risk for persistently high depressive symptoms (e.g., younger, longer treatment course) opens targeted opportunities to prevent and promote rapid recovery from depression.

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.

After decades in which diatheses dominated research on the diathesis-stress models of depression, increasing attention to stress and stress-depression mechanisms is in the forefront of efforts to understand depression and treat it effectively. Supplementing research on known risk factors and moderators (such as demographic, cognitive, relational, family, and personality characteristics) of the stress-depression association, much work now focuses on experiences of early life stress, acute stressors, and chronic stress and their developmental features and neurobiological mechanisms relevant to depression. The review briefly highlights the current status of risk factors, HPA axis, neural, and genetic approaches, noting conceptual and methodological challenges.

AimsClose to one third of patients with major depression show increases in pro-inflammatory cytokines, which are in turn associated with risk for inflammatory disease. Genetic variants that enhance immune reactivity may thus enhance inflammatory and depressive reactions to stress. The aim of the present study was to investigate a trio of functional SNPs in the promoter regions of IL6 (-174G>C, rs1800795), IL1β (-511C>T, rs16944), and TNF (-308G>A, rs1800629) as moderators of the relationship between chronic stress exposure and elevations in depressive symptoms.MethodsParticipants were 444 Australian youth (mean age=20.12) whose exposure to chronic stress in the past 6months was assessed using the semi-structured UCLA Life Stress Interview, and who completed the Beck Depression Inventory II at ages 15 and 20. Between ages 22 and 25, all participants in the selected sample provided blood samples for genotyping.ResultsIn line with a hypothesized moderation effect, -174G allele carriers at IL6 had fewer depressive symptoms following interpersonal stress, relative to C/C homozygotes with equal interpersonal stress exposure. However, IL6 genotype did not moderate the effects of non-interpersonal stress exposure (i.e., financial, work and health-related difficulties) on depression. Also in line with hypotheses, the -511C allele in IL1β, previously associated with higher IL-1β expression, was associated with more severe depression following chronic interpersonal stress exposure, relative to T/T homozygotes. Again, the moderating effect was specific to interpersonal stressors and did not generalize to non-interpersonal stress. TNF was not a moderator of the effects of either interpersonal or non-interpersonal stress on later depression outcomes.ConclusionFindings were consistent with the hypothesis that pro-inflammatory genetic variation increases the risk of stress-induced depression. The present results provide evidence of a genetic mechanism contributing to individual differences in depressive symptomatology following interpersonal stress exposure.

Oxytocin appears to be centrally involved in socioemotional functioning, and is hypothesized to be relevant to the severe disruption in close relationships characteristic of borderline personality pathology. We examined whether a polymorphism of the oxytocin receptor gene (OXTR rs53576) interacts with quality of family functioning to predict borderline personality disorder (BPD) symptomatology in a sample of youth at age 20. A total of 385 youth from a longitudinal study of offspring of depressed or nondepressed mothers who were well characterized with respect to their family conditions and BPD symptomatology provided DNA for genotyping. Analyses revealed a significant moderation of the link between early family quality and later BPD symptoms by OXTR rs53576, and the pattern was consistent with differential susceptibility (plasticity). Whereas A-allele carriers had high levels of BPD symptoms under negative family conditions and low levels under positive conditions, GG homozygotes had average levels of BPD symptoms regardless of their family quality.

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.

Childhood and adolescent adversity is of great interest in relation to risk for psychopathology, and interview measures of adversity are thought to be more reliable and valid than their questionnaire counterparts. One interview measure, the Childhood Trauma Interview (CTI; Fink et al., 1995), has been positively evaluated relative to similar measures, but there are some psychometric limitations to an existing scoring approach that limit the full potential of this measure. We propose several new summary indices for the CTI that permit examination of different types of adversity and different developmental periods. Our approach creates several summary indices: one sums the severity scores of adversities endorsed; another utilizes the number of minor and major (moderate to severe) adversities. The new indices were examined in association with first onsets of major depressive disorder (MDD) and anxiety disorders across a 5-year period using annual clinical diagnostic interviews (Structured Clinical Interview for DSM-IV-TR). Summary scores derived with the previously used approach were also examined for comparison. Data on 332 participants came from the Youth Emotion Project, a longitudinal study of risk for emotional disorders. Results support the predictive validity of the proposed summary scoring methods and indicate that several forms of major (but typically not minor) adversity are significantly associated with first onsets of MDD and anxiety disorders. Finally, multivariate regression models show that, in many instances, the new indices contributed significant unique variance predicting disorder onsets over and above the previously used summary indices.

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.

ObjectiveThe 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.MethodA 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.ResultsEarly 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.ConclusionFindings 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.

Meta-analytic evidence supports a gene-environment (G×E) interaction between life stress and the serotonin transporter polymorphism (5-HTTLPR) on depression, but few studies have examined factors that influence detection of this effect, despite years of inconsistent results. We propose that the candidate environment (akin to a candidate gene) is key. Theory and evidence implicate major stressful life events (SLEs)-particularly major interpersonal SLEs-as well as chronic family stress. Participants (N = 400) from the Youth Emotion Project (which began with 627 high school juniors oversampled for high neuroticism) completed up to five annual diagnostic and life stress interviews and provided DNA samples. A significant G×E effect for major SLEs and S-carrier genotype was accounted for significantly by major interpersonal SLEs but not significantly by major non-interpersonal SLEs. S-carrier genotype and chronic family stress also significantly interacted. Identifying such candidate environments may facilitate future G×E research in depression and psychopathology more broadly.

PurposeCross-sectional and retrospective studies have highlighted the long-term negative effects of maternal depression on offspring physical, social, and emotional development, but longitudinal research is needed to clarify the pathways by which maternal depression during pregnancy and early childhood affects offspring outcomes. The current study tested one developmental pathway by which maternal depression during pregnancy might negatively impact offspring mental health in young adulthood, via poor physical health in early childhood.MethodsThe sample consisted of 815 Australian youth and their mothers who were followed for 20 years. Mothers reported on their own depressive symptoms during pregnancy and offspring early childhood. Youth completed interviews about health-related stress and social functioning at age 20 years, and completed a questionnaire about their own depressive symptoms 2 to 5 years later.ResultsPath analysis indicated that prenatal maternal depressive symptoms predicted worse physical health during early childhood for offspring, and this effect was partially explained by ongoing maternal depression in early childhood. Offspring poor physical health during childhood predicted increased health-related stress and poor social functioning at age 20. Finally, increased health-related stress and poor social functioning predicted increased levels of depressive symptoms later in young adulthood. Maternal depression had a significant total indirect effect on youth depression via early childhood health and its psychosocial consequences.ConclusionsPoor physical health in early childhood and its effects on young adults' social functioning and levels of health related stress is one important pathway by which maternal depression has long-term consequences for offspring mental health.

Children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for the development of depression, with evidence that peer and academic difficulties mediate predictions of later depression from ADHD. In the present study, we hypothesized that parent-child relationship difficulties may be an additional potential mediator of this association. Academic, peer, and parent-child functioning were tested as mediators of the association of attention problems and depression in two distinctly different yet complementary samples. Study 1 was a cross-sectional sample of 5- to 10-year-old children (N = 230) with and without ADHD. Study 2 was a prospective longitudinal sample of 472 youth, followed prospectively from birth to age 20 years, at risk for depression. Despite differences in age, measures, and designs, both studies implicated peer and parent-child problems as unique mediators of depressive symptoms, whereas academic difficulties did not uniquely mediate the ADHD-depression association. Furthermore, inattention symptoms, but not hyperactivity, predicted depressive symptoms via the disruption of interpersonal functioning. The inclusion of oppositional defiant disorder into models impacted results and supported its independent role in parent-child problems. Implications include support for interventions that target interpersonal competence, which may effectively reduce the risk of depression among children with ADHD.

Children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for the development of depression, with evidence that peer and academic difficulties mediate predictions of later depression from ADHD. In the present study, we hypothesized that parent-child relationship difficulties may be an additional potential mediator of this association. Academic, peer, and parent-child functioning were tested as mediators of the association of attention problems and depression in two distinctly different yet complementary samples. Study 1 was a cross-sectional sample of 5- to 10-year-old children (N = 230) with and without ADHD. Study 2 was a prospective longitudinal sample of 472 youth, followed prospectively from birth to age 20 years, at risk for depression. Despite differences in age, measures, and designs, both studies implicated peer and parent-child problems as unique mediators of depressive symptoms, whereas academic difficulties did not uniquely mediate the ADHD-depression association. Furthermore, inattention symptoms, but not hyperactivity, predicted depressive symptoms via the disruption of interpersonal functioning. The inclusion of oppositional defiant disorder into models impacted results and supported its independent role in parent-child problems. Implications include support for interventions that target interpersonal competence, which may effectively reduce the risk of depression among children with ADHD.

Although tobacco smoking, which has been linked to depression, is a major public health problem, little is known about the neurobiological factors that confer vulnerability to smoking in youngsters and the effects of adolescent smoking on the course of depression. This study examined whether hypothalamic-pituitary-adrenal (HPA) activity and stressful life experiences are related to smoking behavior in depressed and non-depressed adolescents, and whether smoking predicts a worsening course of depression. Smoking history and stressful experiences were assessed in 151 adolescents (48 with no personal or family history of psychiatric disorder, 48 with no psychiatric history, but at high risk for depression by virtue of parental depression, and 55 with current major depressive disorder). Evening salivary cortisol and nocturnal urinary-free cortisol were measured for three consecutive evenings. The participants were then followed at regular intervals for up to 5 years to assess smoking history, clinical course of depression and stressful experiences during the follow-up period. Increased evening/night-time cortisol levels were associated with both initiation and persistence of smoking during follow-up. Stressful life experiences further increased the risk for smoking in depressed as well as non-depressed youth. Smoking was also associated with a higher frequency of depressive episodes during follow-up. A model that included stressful experiences and cortisol levels reduced the contribution of smoking per se to depression. High evening/night-time cortisol level appears to be a vulnerability marker for smoking in adolescents, with stressful experiences further increasing the risk for smoking in vulnerable youth. High evening/night-time cortisol levels and stressful experiences accounted, at least partially, for the association between depressive illness and smoking behavior.

Previous work has demonstrated reliable electroencephalographic (EEG) sleep and hypothalamic-pituitary-adrenal (HPA) changes associated with adult major depressive disorder. These changes might be evident before clinical manifestation of the illness in at-risk persons. The aim of the study was to identify depression-related EEG sleep and HPA changes in healthy adolescents at high risk for depression, and to examine the relationship between EEG sleep (or HPA) changes and the onset of depression. Forty-eight 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 48 adolescent volunteers with no personal or family history of a psychiatric disorder (normal controls) were recruited. EEG sleep and HPA measures were collected on three consecutive evenings and nights at baseline. Clinical follow-up evaluations were conducted at regular intervals over a 5-year period. Compared with normal controls, adolescents at high risk for depression had shorter latency to rapid eye movement (REM) sleep, increased phasic REM sleep, more REM sleep and elevated nocturnal urinary-free cortisol (NUFC) excretion at baseline. Shorter REM latency, higher REM density and elevated NUFC (measured at baseline) were associated with the development of depression during follow-up. The findings that REM sleep abnormalities and elevated HPA activity occur before the onset of depression in at-risk adolescents suggest that these variables serve as vulnerability markers for the illness.