Longitudinal Associations of Social Problem-Solving and Emotion Regulation on Depression and Anxiety in Adults with High-Functioning Autism

Background:  High-Functioning Autism-Spectrum Disorder (HFASD) is associated with increased susceptibility to depression and anxiety. It has been suggested that ASD-related social communication/interaction deficits, and resultant isolation/loneliness, and perceived social inadequacy could be at fault. Two studies have modeled the specific role of social problem-solving (SPS) deficits on this susceptibility by examining autistic-trait expression levels in neurotypical samples. Between these studies, it was found that SPS deficits play the role of a significant mediator between autistic-trait expression and both depressive and anxious symptomology.

Objectives:  The current study aims to: (i) explore whether these findings will persist in a HFASD sample; (ii) utilize a longitudinal design to assess the directionality of the relationship between SPS and depression/anxiety; and (iii) examine what role, if any, emotion regulation plays in these relationships.

Methods:  The study sample consists of 65 HFASD adults from the US (n=42) and the UK (n=24). Participant age ranged from 19-52 (M=31.51, SD=8.58). The study had two sessions (completed online), separated by three months. Participants were assessed on ASD-related social deficits (Social Responsiveness Scale, 2^ndEdition), SPS ability (Social Problem-Solving Inventory, Revised), depressive/anxious symptomology (Depression Anxiety and Stress Scale), and emotion regulation (Difficulties in Emotion Regulation Scale).

Results: Session 1 data support findings of high rates of depression/anxiety in HFASD, with 80% of participants reporting at least one episode of diagnosed depression, and 72.3% reporting at least one episode of diagnosed anxiety in their lifetime. Consistent with neurotypical sample findings, increased ASD-related social deficits were significantly associated with increases in depressive (r=.39, p<.001) and anxious (r=.40, p<.001) symptomology, as well as poorer SPS skills (r=-.32, p<.01). While a significant negative association between SPS and depressive symptoms was found (r=-.29, p<.05), there was essentially no association found with symptoms of anxiety (r=.01, p=.95). Mediation analysis results suggest that deficient SPS accounts for approximately 38% of the variance in depressive symptoms initially predicted by ASD-related social deficits. This mediation, however, did not reach statistical significance (Z=1.35, SE=.05, p=.18). Consistent with neurotypical models, ASD-related social deficits were found to be associated with increased utilization of impulsive (r=.25, p<.05) and avoidant (r=.25, p<.05) problem-solving styles, and a negative problem-solving orientation (r=.52, p<.001). The role of emotion regulation, and assessment of the SPS/depressive symptoms relationship directionality will be examined following the collection of Session 2 data (scheduled for completion by February, 2015).

Conclusions:  This study provides further support to the increased susceptibility of HFASD populations to episodes of depression/anxiety. The finding that deficient SPS was significantly associated with increased depressive symptoms suggests that targeted therapies directed at the improvement of this skillset could be a beneficial treatment option for depressive vulnerability in HFASD. Recently, a pilot-study examining the feasibility of Problem-Solving Therapy (PST) for HFASD adults showed promise with regard to participant skill acquisition. In other populations, PST has been shown to be an effective treatment option for reducing depressed mood. Hopefully the results from this study can provide further support and insight for the use of PST to help alleviate the depressive vulnerability in HFASD populations.