Poverty Potentiates the Association of Parental Conflict with Elevated Cytokines and Depression in Mexican-Origin Adolescents

• In Event: 3-211 - How Does Parenting Become Biologically Embedded? Integrating Insights from Neuroimaging, Immunology, and Electrophysiology

Integrative Statement

Experiences of chronic and multiple stressors in adolescence have been associated with heightened inflammation, which poses risk for multiple health problems. In this study, family poverty during adolescence was examined as a moderator of the relations between cytokine responses to lab challenges, family relationship quality, and depressive symptoms.

Hypothesis: Chronic poverty was expected to exacerbate relations between poorer relationship quality and elevated cytokines, and between elevated cytokines and depression.

Method: 223 Mexican-origin youths (108 cisgender female; 115 cisgender male) reported parent support and conflict at 10, 12, 14, and 16 years; provided saliva samples at 17; and reported depressive symptoms at 17 and 19. Their parents reported annual family income each year from 10 through 16; 108 youths lived in poverty throughout adolescence (Mean income-to-needs < 1). Interleukin-6 (IL6) and C-reactive protein (CRP) were assayed from saliva samples collected in a lab visit involving a social exclusion cognitive challenge (1 baseline sample; 5 samples at 10m, 20m, 30m, 40m and 50m post-challenge).

Analyses: (A) Youths’ cytokine responses were modeled and (B) predicted from trajectories of support and conflict, with intercepts modeled as the average across waves and slopes as change from 10 to 16 years, and income-to-needs. (C) Depressive symptoms at 17 and 19 were predicted from cytokine responses at 17, family relationship characteristics, and income-to-needs.

Results: (A) IL6 and CRP increased significantly (both paired t > 4.00, p < .001) from baseline to 10m post-challenge, then decreased non-significantly over subsequent samples. Lower baseline IL6 predicted stronger IL6 reactivity (b = -.324, p < .001) and recovery (b = -.356, p < .001). Lower baseline CRP predicted stronger CRP recovery only (b = -.180, p = .003). (B) Higher baseline IL6 was predicted by higher average conflict (b = .15, p < .10) which decreased from 10 to 16 (b = -.19, p < .05). Higher baseline CRP was predicted by higher average conflict, but only for youths living in poverty (b = .446, p < .01) (see Figure 1). Poverty did not directly predict cytokines. (C) At 17, more depressed youths had less IL6 recovery, or prolonged elevation, post-challenge (b = .181, p < .05), and decreasing support (b = -.227, p < .05); high average conflict predicted depression only for youths in poverty (b = .395, p < .01), whereas increasing conflict over adolescence predicted depression only for youths not in poverty (b = .563, p < .001). Greater increases in depression from 17 to 19 were predicted by stronger CRP reactivity (b = .227, p < .05), and decreasing family support from 10 to 16 (b = -.197, p < .10).

Discussion: Chronically high levels of conflict with parents predicted mildly elevated inflammation in adolescents, especially in families experiencing chronic poverty. As baseline cytokines predicted greater cytokine reactivity, which in turn predicted increased depressive problems, disruptions to inflammatory processes may be one pathway by which Mexican-origin adolescents’ experiences of multifaceted and chronically stressful family contexts contribute to increased depression in emerging adulthood.

Authors

• Paul Hastings, University of California, Davis
  Presenting Author

• Luis A. Parra, University of California, Davis
  Non-Presenting Author

• Lisa E. Johnson, University of California, Davis
  Non-Presenting Author

• David Gerrick Weissman, Harvard University
  Non-Presenting Author

• Richard W. Robins, University of California, Davis
  Non-Presenting Author

• Amanda Guyer, University of California, Davis
  Non-Presenting Author