531 - Underlying biological mechanisms of persistent depressive symptoms in adolescence and young adulthood: A role for leptin?
Friday, April 22, 2022
6:15 PM – 8:45 PM US MT
Poster Number: 531 Publication Number: 531.107
Samantha Scott, University of Denver, Denver, CO, United States; Jenalee Doom, University of Denver, Denver, CO, United States; Patricia East, University of California, San Diego School of Medicine, La Jolla, CA, United States; Paulina Correa, Universidad de Chile (INTA), Santiago, Region Metropolitana, Chile; Raquel Burrows, Universidad de Chile (INTA), Santiago, Region Metropolitana, Chile
PhD Student Clinical Psychology University of Denver Denver, Colorado, United States
Background: Depression is a debilitating, common mental health disorder that is persistent in adolescents and young adults (YAs). Understanding biological correlates of persistent depressive symptoms across development is important for informing etiological models. Less research has examined metabolic protein correlates, such as leptin. Leptin is a proinflammatory, cell-signaling metabolic protein secreted by adipose tissue that signals energy availability and is considered an “upstream” driver of important health indicators. Higher levels of leptin have been cross-sectionally associated with depressive symptoms in youth with diabetes and in adult samples. Less is known about longitudinal associations between leptin and depressive symptoms from adolescence into young adulthood.
Objective: We aimed to understand whether depressive symptoms at age 14 predicted leptin at age 16, whether leptin at age 16 predicted depressive symptoms at age 22, and whether leptin mediated the association between depressive symptoms at age 14 and 22.
Design/Methods: Adolescents from working-class families in Chile (Nf636, Mage=14.1 years, 52% female, all Spanish/Indigenous descent) completed a self-report measure of depression (Youth Self-Report; Achenbach, 2000). Two years later, they underwent a fasting blood draw measuring peripheral inflammation (C-Reactive protein; CRP) and leptin (Mage=16.8 years). At age 22 (Nf479, Mage=22.9 years), participants completed a self-report depression measure (Adult Self Report; Achenbach, 2003). All models controlled for adolescent body mass index (BMI), income, sex, age, CRP, and waist-to-hip ratio. The model with YA depressive symptoms also included adolescent depressive symptoms and YA age and income as covariates.
Results: Greater depressive symptoms at age 14 predicted greater leptin at age 16 (B=0.45, SE=0.13, p< .001). Greater leptin predicted greater depressive symptoms in young adulthood (B=0.04, SE=0.02, p=.025). Leptin mediated the association between depressive symptoms at age 14 and age 22 (BIndirect=0.02, SE=0.02, 95% CI: 0.00, 0.04). Sensitivity analyses indicated these findings are stronger for females. Conclusion(s): Leptin mediated the positive association between depressive symptoms in adolescence and young adulthood, such that the association between depressive symptoms in adolescence and young adulthood was partially explained by leptin. Greater depressive symptoms in adolescence predicted greater leptin 2 years later, and greater leptin predicted greater depressive symptoms in young adulthood, controlling for peripheral inflammation and BMI. Underlying biological mechanisms of persistent depressive symptoms in adolescence and young adulthood: A role for leptin?Samantha Scott CV.pdf