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Social media addiction (SMA) is becoming increasingly prevalent and, particularly among adolescent girls, is associated with depression and other adverse mental health outcomes. Social Media delivers frequent social feedback. Social feedback is particularly salient to adolescents and neural responsivity to social rewards is thought to increase following puberty onset. However, developmental differences in neural social reward processing mechanisms that may be risk-factors for SMA have not been delineated. We hypothesized that differential social reward responsivity across pubertal development would be associated with later SMA and, in turn, depressive symptoms.
Within a longitudinal design, 100 adolescents (49 girls) completed a social incentive delay task during 1 to 3 fMRI scans (6th-9th grade), and a follow-up self-report assessment (10th-11th grade). The Social Incentive Delay task allowed us to measure brain responsivity to the receipt of social rewards (adolescent smiling faces). At the follow-up timepoint (~2 years after the final fMRI scan), participants self-reported depressive symptoms and SMA symptoms. We used SMA symptoms to classify adolescents into either a SMA (n=53) or non-SMA group (n=47) based on Diagnostic Statistical Manual (DSM) drug addiction severity coding. We examined SMA-group effects on brain responsivity to social rewards over pubertal development, while controlling for biological sex via a 3-way SEX SMA-Group PUBERTY interaction on the social reward outcome vs. neutral outcome contrast in the task (AFNI’s 3dlmer; pvoxel=0.005, pcluster=0.05, min cluster: 211 voxels), within a small volume corrected mask (36,386 voxels) defined via NeuroSynth’s meta-analysis of the term “social”. We went on to assess relationships between pubertal changes in brain responsivity, SMA symptoms, and depressive symptoms.
We observed significant SMA-Group PUBERTY interactions (Figure 1) on social reward responsivity in the ventral media prefrontal cortex (vmPFC; 397 voxels), dorsal media prefrontal cortex (dmPFC; 599 voxels), and posterior cingulate cortex (PCC; 406 voxels). Before puberty onset, adolescents in the non-SMA group displayed relatively lower responsivity to social rewards that increased with pubertal development. Whereas adolescents in the SMA group displayed hyper-responsivity before puberty onset that decreased with pubertal development. While we did not observe significant sex differences in SMA-group counts, girls reported higher depressive symptoms than boys, in 10th-11th grade (Figure 2A). Further, higher SMA symptoms were significantly associated with higher depressive symptoms among girls but not among boys (Figure 2B). A significant moderated mediation model (PROCESS v.4, model 14) indicated that among girls (but not boys), the association between decreasing vmPFC responsivity across pubertal development and increased depressive symptoms two years later (10th and 11th grade) was mediated by increasing SMA symptoms (Figure 2C). This same model was significant for PCC slopes but not dmPFC slopes.
Findings suggest that initial hyper-responsivity to social rewards (before puberty onset) may represent a risk factor for later SMA while gradual decreases in this response over pubertal development could suggest atypical development of social reward processing linked with SMA. Further, these developmental differences in social reward processing may lead to depressive symptoms among adolescent girls through their relationship with increased SMA symptoms.
Jessica S. Flannery, University of North Carolina at Chapel Hill
Presenting Author
Seh-Joo Kwon, University of North Carolina at Chapel Hill
Nathan Jorgensen, University of North Carolina at Chapel Hill
Mitchell J Prinstein, University of North Carolina at Chapel Hill
Kristen A Lindquist, University of North Carolina at Chapel Hill
Eva H Telzer, University of North Carolina at Chapel Hill