INTERGENERATIONAL DEPRESSION AND ADOLESCENT INSULIN REGULATION: A PSYCHOPHYSIOLOGICAL PERSPECTIVE

Abstract

Rates of type 2 diabetes (T2D) continue to rise in adolescents and young adults, with serious costs to public health and deleterious consequences for the emotional well-being and health of individuals, families, and society. Social adversity and mental health concerns are modifiable factors that may play a role in worsening insulin resistance, a primary precursor to T2D onset, through stress-mediated physiological factors like inflammation and cortisol dysregulation. Yet, limited research has addressed this constellation of risk factors comprehensively, and even fewer studies have considered the contextual roles of social adversity and familial depression in adolescent T2D risk. Participants were N=147 adolescent (12-17y) girls with elevated depression symptoms (CES-D≥21), BMI (≥85th%ile), and family diabetes history. Puberty was assessed with Tanner staging and adiposity via dual energy x-ray absorptiometry. Adolescents completed questionnaires to measure depression symptoms (CES-D) and social adversity (Adverse Childhood Experiences [ACEs]). Parents reported their own depression symptoms (CES-D). Adolescents provided blood samples to evaluate metabolic health and inflammation (C-reactive protein [CRP]) and urine and salivary samples to evaluate total and latent trait cortisol, respectively. Using path analysis within structural equation modeling, the direct, indirect, and moderating associations among ACEs, adolescent/parent depression, CRP, total/latent trait cortisol, and metabolic health, accounting for age, puberty, racial/ethnic minority status, and body adiposity were explore. Parent and adolescent depression interacted to explain adolescent CRP, such that greater adolescent depression symptoms were related to greater inflammation, only when parents also had elevated depression. There was a three-way interaction with racial/ethnic minority status, such that the combination of concurrently high parent and teen depression related to the highest adolescent CRP in racial/ethnic minority youth. More adolescent depression was associated with elevated CRP among adolescents with higher ACEs. More parent depression also was associated with more CRP in adolescents with more ACEs, but negatively associated with CRP in adolescents with fewer ACEs. In youth with high ACEs, the interaction between adolescent/parent depression was associated with LTC, such that higher adolescent depression was associated with lower LTC when parents had elevated depression, but not in youth with low ACEs. Higher parent depression symptoms were related to adolescents’ lower insulin resistance in youth with fewer ACEs. Findings suggest that social adversity, intergenerational depression, and stress physiology may be important considerations in the context of T2D risk in adolescent girls.