PURPOSE-The aim of the present study was to examine whether early adolescent major depressive disorder was associated with negative health outcomes in young adulthood after controlling for depression at the time of follow-up. In addition, indicators of medical and social costs associated with these health consequences were measured. METHODS-705adolescents participating in a longitudinal study of children varying in risk for depression due to maternal depression were assessed for a history of depression at age 15, depressive disorders at age 20, and a variety of health outcomes at age 20. RESULTS-Resultsshowed that even after controlling for the effects of concurrent depression at age 20, early adolescent depression continued to be associated with poorer interviewer-rated health, poorer self-perceived general health, higher health care utilization and increased work impairment due to physical health, although not with limitations to physical functioning or the presence of chronic medical conditions. CONCLUSIONS-Depression during early adolescence has consequences for health and associated costs during young adulthood. The implications of these findings for screening and treatment of adolescent depression are discussed. Keywords depression; adolescence; health outcomes; young adulthood; functional impairment; health care costs Owing to its high prevalence and chronic nature, depression has been ranked by the World Health Organization as the single most burdensome disease in the world [1]. Although part of the burden on society is attributable to direct treatment costs, a significant portion of the cost of depression is indirect, related to the increased costs of treatment and lost productivity resulting from comorbid health conditions associated with depression [2]. Recently, the association between depression and health outcomes has received significant empirical attention, with many studies suggesting that screening and treatment for depression is a costeffective method of limiting expenses for comorbid health conditions [2,3]. Carefully designed studies have established the presence of a bidirectional relationship between depression and chronic illness across a variety of diseases, including cancer, heart disease, diabetes, arthritis, and asthma [4,5,6,7,8,9,10,11]. Several mechanisms that may account for this relationship haveCorrespondence concerning this article should be addressed to Danielle Keenan-Miller, UCLA Department of Psychology, 1285 Franz Hall, Los Angeles, CA 90095. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. However, most of the research on th...

Background-Many recent studies of serotonin transporter gene by environment effects predicting depression have used stress assessments with undefined or poor psychometric methods, possibly contributing to wide variation in findings. The present study attempted to distinguish between effects of acute and chronic stress to predict depressive symptoms at age 20 among 346 youth varying in polymorphisms of the 5HTT gene who had been assessed at ages 15 and 20.

Considerable research has focused on youth depression, but further information is needed to characterize different patterns of onset and recurrence during adolescence. Four outcome groups by age 20 were defined (early onset-recurrent, early-onset-desisting, later-onset, never depressed) and compared on three variables predictive of youth depression: gender, maternal depression, and interpersonal functioning. Further, it was hypothesized that the association between maternal depression and youth depression between 15 and 20 is mediated by early-onset depression and interpersonal dysfunction by age 15. Eight hundred sixteen community youth selected for depression risk by history (or absence) of maternal depression were interviewed at age 15, and 699 were included in the 5-year follow-up. Controlling for gender, early onset and interpersonal dysfunction mediated the link between maternal depression and late adolescent major depression. Different patterns for males and females were observed. For males maternal depression's effect was mediated by early onset but not interpersonal difficulties, while for females maternal depression's effect was mediated by interpersonal difficulties but not early onset. Maternal depression did not predict first onset of major depression after age 15. The results suggest the need for targeting the impact of maternal depression's gender-specific effects on early youth outcomes, and also highlight the different patterns of major depression in youth and their likely implications for future course of depression.

Youth with depression by 15 with recurrence by age 20 may represent a high-risk group, with likely life-course-persistent depression and maladjustment. Community youth whose early depression does not recur by age 20, or who have onset with no recurrence after age 15, may have more benign and possibly limited depressions. Later onset with recurrence is also a group at risk for dysfunctional outcomes, requiring further follow-up.

Adults with bipolar disorder (BD) and major depressive disorder (MDD) have higher circulating levels of proinflammatory cytokines than healthy controls. However, it is not known whether pediatric-onset patients with BD or MDD show increases in levels of inflammation or activation of nuclear factor kappa B (NF-κB), a key transcription factor in inflammatory signaling. Circulating levels of inflammatory cytokines, as well as spontaneous and stimulated levels of activated NF-κB in total peripheral blood mononuclear cells, monocytes and lymphocytes were measured in adolescents with BD (n=18), MDD (n=13), or no psychiatric history (n=20). Participants had a range of mood symptoms at time of testing. Adolescents with BD had significantly higher spontaneous levels of NF-κB in peripheral blood mononuclear cells, monocyte and lymphocyte populations, and higher plasma levels of IL-1β than healthy controls. Following stimulation with recombinant human TNF-α, participants with BD and MDD both had greater increases in NF-κB in monocytes than controls. Further, greater stimulated increases of NF-κB in monocytes were associated with the current severity of depressive symptoms. The results are limited by the small sample and cross-sectional design. Interventions that target early immunological dysregulation should be examined in relation to long-term outcomes in youth with bipolar and depressive disorders.