Bipolar Disorders
Mackenzie Maddox, B.S.
Graduate student
Temple University
Philadelphia, Pennsylvania, United States
Rachel Walsh, M.A. (she/her/hers)
Graduate Student
Temple University
Philadelphia, Pennsylvania, United States
Phyllis Zee, Ph.D.
Professor
Northwestern University Feinberg School of Medicine
Chicago, Illinois, United States
Robin Nusslock, Ph.D.
Associate Professor
Northwestern University
Evanston, Illinois, United States
Lauren B. Alloy, Ph.D.
Laura H. Carnell Professor
Temple University
Philadelphia, Pennsylvania, United States
Early-onset bipolar spectrum disorders (BSD) are associated with more severe prognoses including greater comorbidity, increased rates of rapid cycling, and greater risk for suicidality. Adolescence is a crucial developmental period that includes changes in the reward and circadian systems. Reward and circadian rhythms both have been linked to BSD independently in that those diagnosed with BSD tend to display a hypersensitivity to reward and also have irregular circadian rhythms. However, less is known about the associations between the reward system and circadian disruption preceding onset. The goal of this study was to elucidate potential associations between trait reward sensitivity and circadian disruption while examining the moderating impact of pubertal development. Participants were a community-based sample of adolescents (n = 302, 59.3% Female, 56.6% White) recruited from the Philadelphia area for longitudinal studies assessing risk factors for first-onset depression and BSD. During screening phases, participants completed the Behavioral Activation System scale (BAS) as an indicator of trait reward sensitivity. Concurrently at baseline, participants completed the Pubertal Development Scale (PDS) and one week of actigraphy (Actiwatch). Non-parametric circadian analyses were conducted using the ‘nparACT’ package in R to generate three circadian indices: Relative amplitude (RA), Intradaily variability (IV), and Interdaily stability (IS). Because circadian rhythms regulate sleep, participants also completed the Pittsburgh Sleep Quality Index (PSQI) as an indicator of sleep quality. We predicted higher BAS would be associated with greater circadian and sleep disruption as indicated by a flatter RA, a lower IS, a higher IV, and a greater PSQI score. Given that puberty has been associated with changes in reward responsiveness and sleep and circadian functioning, we also predicted that greater pubertal development would amplify these associations. Hierarchical multiple regression was used to examine main and interaction effects across four models while controlling for related covariates. Consistent with hypotheses, higher BAS was significantly associated with lower IS (B = -0.18, p < .01), and greater pubertal development amplified this association (B = -0.14, p = .02) after controlling for biological sex. Simple slopes revealed that this negative association was seen at both advanced and moderate stages of pubertal development but not at early stages. BAS scores were not associated with RA, IV, or PSQI alone or in interaction with pubertal development. These findings show that circadian patterns of instability observed in clinical populations (e.g., individuals with BSD) also were present in a non-clinical sample of adolescents with elevated reward sensitivity, an established risk factor for BSD. In addition, pubertal development moderated this association, suggesting that the strength of this association increases as adolescent development progresses. It is possible this interactive effect between reward and circadian rhythms may contribute to the increased incidence of mental health difficulties in adolescence. More longitudinal research is needed to evaluate this possibility.