BACKGROUND
Evidence indicates that Internet addiction (IA) is associated with depression, but longitudinal studies have rarely been reported, and no studies have yet investigated potential common vulnerability or a possible specific causal relationship between these disorders.
OBJECTIVE
To overcome these gaps, the present 12-month longitudinal study based on a large-sample employed a cross-lagged panel model (CLPM) approach to investigate the potential common vulnerability and specific cross-causal relationships between IA and CSD (or depression).
METHODS
IA and clinically-significant depression (CSD) among 12 043 undergraduates were surveyed at baseline (as freshmen) and in follow-up after 12 months (as sophomores). Application of CLPM revealed two well-fitted design between IA and CSD, and between severities of IA and depression, adjusting for demographics.
RESULTS
Rates of baseline IA and CSD were 5.47% and 3.85%, respectively; increasing to 9.47% and 5.58%, respectively at follow-up. Among those with baseline IA and CSD, 44.61% and 34.48% remained stable at the time of the follow-up survey, respectively. Rates of new-incidences of IA and CSD over 12 months were 7.43% and 4.47%, respectively. Application of a cross-lagged panel model approach (CLPM, a discrete time structural equation model used primarily to assess causal relationships in real-world settings) revealed two well-fitted design between IA and CSD, and between severities of IA and depression, adjusting for demographics. Models revealed that baseline CSD (or depression severity) had a significant net-predictive effect on follow-up IA (or IA severity), and baseline IA (or IA severity) had a significant net-predictive effect on follow-up CSD (or depression severity).
CONCLUSIONS
These correlational patterns using a CLPM indicate that both common vulnerability and bidirectional specific cross-causal effects between them may contribute to the association between IA and depression. As the path coefficients of the net-cross-predictive effects were significantly smaller than those of baseline to follow-up cross-section associations, vulnerability may play a more significant role than bidirectional-causal effects.
CLINICALTRIAL
Ethics Committee of West China Hospital, Sichuan University (NO. 2016-171)
