Adult Depression
Reciprocal effects of interpersonal life stress and tri-level symptoms of depression and anxiety: A random intercept cross-lagged panel analysis.
Kaylee E. Null, M.A.
Clinical Psychology PhD Student
University of California Los Angeles
Los Angeles, California, United States
Christine Eun, None
Undergraduate Student
University of California, Los Angeles
Los Angeles, California, United States
Richard E. Zinbarg, Ph.D.
Professor
Northwestern University
Evanston, Illinois, United States
Robin Nusslock, Ph.D.
Associate Professor
Northwestern University
Evanston, Illinois, United States
Michelle G. Craske, Ph.D.
Distinguished Professor
University of California, Los Angeles
Los Angeles, California, United States
Background: Prior research has linked acute and chronic stress with the development of depression, as well as blunted reward processing. The stress generation hypothesis proposes a reciprocal relationship such that social stress contributes to later depression, and vice versa. Extensions of this theory have implicated reward processing in stress generation, where impaired reward processes contribute to interpersonal stress, leading to increased depressive symptoms. Here, we investigated reciprocal relationships between chronic interpersonal life stress and anhedonia (which is associated with reward hyposensitivity) in young adults.
Methods: We utilized data from the Brain, Motivation, and Personality Development (BrainMAPD) Project, a multisite, longitudinal study conducted at UCLA and Northwestern (N=320 at T1). Participants ages 18-19 were recruited to represent high, middle, and low levels of trait neuroticism and reward sensitivity. The UCLA Life Stress Interview (LSI) was used to measure chronic interpersonal life stress. Confirmatory factor analyses were used to generate dimensional tri-level factors of depression and anxiety, including General Distress and Anhedonia-Apprehension, from self-report questionnaires. Random intercept cross-lagged panel models (RI-CLPM; constrained and free) were estimated using lavaan in R to assess reciprocal relationships across 4 timepoints spanning 30 months. To test whether the results are specific to Anhedonia-Apprehension, we also tested reciprocal effects of General Distress and social stress. Model fit was assessed using conventional thresholds.
Results: Participants were 51.4% non-Hispanic white, 28.8% Asian, 9.7% Black, 2.2% Native American, 7.5% multiracial, and 0.3% declined to report race. Additionally, participants were 74.7% non-Hispanic/Latinx, and 67.2% female. Using data at each timepoint, we tested two separate RI-CLPMs with free and constrained parameters. Constraints did not degrade the models, so, in favor of parsimony, results are from the constrained models. Preliminary analyses demonstrated that chronic social stress predicted Anhedonia-Apprehension at later timepoints (ps < 0.05). There were no lagged effects between General Distress and interpersonal life stress (ps > 0.05).
Discussion: Partially consistent with hypotheses, we found that chronic interpersonal stress predicted later Anhedonia-Apprehension, a factor corresponding to reduced positive affect. However, Anhedonia-Apprehension did not predict subsequent social stress. This is consistent with previous research finding that stress contributes to the development of anhedonia and provides evidence that anhedonia may not contribute to the generation of subsequent social stress. Additionally, General Distress, a broad factor of negative affect shared between symptoms of anxiety and depression, was not reciprocally related to social stress over time. Our findings are limited by use of self-report to construct the tri-level factors and by the non-treatment seeking nature of the sample. To our knowledge, this is the first test of stress generation using tri-level factors, and results suggest that chronic interpersonal life stress may confer risk for later anhedonia.