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In this study, we sought to combine two lines of research to better understand risk for the intergenerational transmission of depression. The first focuses on the role of maternal criticism as a potential mechanism of risk for depression in youth while the second builds from interpersonal and stress generation models regarding the potential impact of youth depression on future escalations in maternal criticism. Specifically, we examined the role of maternal criticism within a transactional mediation model using data from a multi-wave study. Participants were 251 mother–offspring pairs consisting of mothers with (n = 129) and without (n = 122) a history of major depressive disorder (MDD) during their child’s lifetime who completed assessments every 6 months for 2 years. We found support for the hypothesized transactional mediational model in which maternal expressed emotion-criticism (EE-Crit) mediated the link between maternal history of MDD and residual change in youth’s depressive symptoms over the previous 6 months and, reciprocally, youth depressive symptoms mediated the relation between maternal MDD history and residual change in EE-Crit 6 months later. These results indicate that maternal criticism and offspring depressive symptoms may contribute to a vicious cycle of depression risk, which should be considered for interventions targeted toward youth at risk of developing MDD.
Adolescence is characterized by profound change, including increases in negative emotions. Approximately 84% of American adolescents own a smartphone, which can continuously and unobtrusively track variables potentially predictive of heightened negative emotions (e.g. activity levels, location, pattern of phone usage). The extent to which built-in smartphone sensors can reliably predict states of elevated negative affect in adolescents is an open question.
Adolescent participants (n = 22; ages 13–18) with low to high levels of depressive symptoms were followed for 15 weeks using a combination of ecological momentary assessments (EMAs) and continuously collected passive smartphone sensor data. EMAs probed negative emotional states (i.e. anger, sadness and anxiety) 2–3 times per day every other week throughout the study (total: 1145 EMA measurements). Smartphone accelerometer, location and device state data were collected to derive 14 discrete estimates of behavior, including activity level, percentage of time spent at home, sleep onset and duration, and phone usage.
A personalized ensemble machine learning model derived from smartphone sensor data outperformed other statistical approaches (e.g. linear mixed model) and predicted states of elevated anger and anxiety with acceptable discrimination ability (area under the curve (AUC) = 74% and 71%, respectively), but demonstrated more modest discrimination ability for predicting states of high sadness (AUC = 66%).
To the extent that smartphone data could provide reasonably accurate real-time predictions of states of high negative affect in teens, brief ‘just-in-time’ interventions could be immediately deployed via smartphone notifications or mental health apps to alleviate these states.
Anhedonia is a core symptom of depression that predicts worse treatment outcomes. Dysfunction in neural reward circuits is thought to contribute to anhedonia. However, whether laboratory-based assessments of anhedonia and reward-related neural function translate to adolescents' subjective affective experiences in real-world contexts remains unclear.
We recruited a sample of adolescents (n = 82; ages 12–18; mean = 15.83) who varied in anhedonia and measured the relationships among clinician-rated and self-reported anhedonia, behaviorally assessed reward learning ability, neural response to monetary reward and loss (as assessed with functional magnetic resonance imaging), and repeated ecological momentary assessment (EMA) of positive affect (PA) and negative affect (NA) in daily life.
Anhedonia was associated with lower mean PA and higher mean NA across the 5-day EMA period. Anhedonia was not related to impaired behavioral reward learning, but low PA was associated with reduced nucleus accumbens response during reward anticipation and reduced medial prefrontal cortex (mPFC) response during reward outcome. Greater mean NA was associated with increased mPFC response to loss outcome.
Traditional laboratory-based measures of anhedonia were associated with lower subjective PA and higher subjective NA in youths' daily lives. Lower subjective PA and higher subjective NA were associated with decreased reward-related striatal functioning. Higher NA was also related to increased mPFC activity to loss. Collectively, these findings demonstrate that laboratory-based measures of anhedonia translate to real-world contexts and that subjective ratings of PA and NA may be associated with neural response to reward and loss.
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