Depression rates skyrocket in adolescence, and adolescent-onset depression is associated with increased risk for depression, substance use, suicide, and work-related disability in adulthood. Consistent with NIH objectives of identifying the biobehavioral causes and prospective trajectories of mental disorders, it is imperative that we identify mechanisms that increase individuals' risk for depression. The long-term goal of this study is to identify the pathways linking early risk factors with adolescent-onset depression; this research will provide a foundation for identification of at-risk youth and the development of interventions to prevent the onset or progression of depression. Depression is a mood disorder characterized by high negative affect and/or low positive affect. Extensive research has examined the high negative affect component of depression, articulating how stress, loss, and dysregulation in the negative valence system (NVS) predict adolescent depression. Much less research has examined the low positive affect component of depression, although low positive affect (e.g. anhedonia) is uniquely associated with additional impairment, poor treatment response, and suicidality above and beyond negative affect. The current study will identify pathways linking dysregulation in the positive valence system (PVS) with depressive disorders in adolescence. We hypothesize that youth with trait reward insensitivity, low trait positive affect, and/or deficits in the regulation of positive affect will have difficulty generating and maintaining positive affect when faced with rewarding or positive events. We further hypothesize that these abnormalities will prospectively predict depressive symptoms and disorders in adolescence, and that the effects may be specific to the anhedonia symptoms of depression. Finally, we also hypothesize that these deficits in the positive valence system will be predicted by stress exposure and deficits in the negative valence system (NVS). Study hypotheses will be examined both cross- sectionally and prospectively with assessments at baseline, 4-months, 8-months, and 12-months. An unselected community sample of youth and parents will be invited to participate in the Time 1 laboratory visit during which youth will complete induced reward and stress paradigms before, during, and after which physiological reactivity, state positive and negative affect, and state emotion regulation will be assessed. Following the lab visit, youth will complete a 7-day ecological momentary assessment (EMA) protocol in which the occurrence of positive and negative life events and youths' affective and cognitive responses to these life events will be randomly sampled in the youths' natural environment in real time. Youth and parents will report on depressive symptoms and diagnoses and stress exposure at baseline, 4-months, 8-months, and 12-months. This prospective design will allow us to test if trait dysregulation in the PVS at baseline predicts state affective and cognitive responses to positive life events during the EMA study, and if these in turn mediate the effects of PVS dysregulation on depressive symptoms over time (Aim 1). We will also be able to examine if stress exposure and NVS dysregulation predict PVS dysregulation (Aim 2).
/PUBLIC HEALTH RELEVANCE This research will provide important information about how abnormal emotional, physiological, and cognitive responses to positive events develop in early adolescence that put some youth at risk for the development of depression and anhedonia in adolescence. Knowledge about these risk factors is essential for (1) identifying youth at high risk for adolescent-onset depression and (2) developing effective early preventive interventions for these high-risk youth.
