Social Anhedonia As a Vulnerability Factor for Depression in Adults with ASD

Background: Deficits in social reward processing have been associated with the onset, severity, and maintenance of depressive symptoms in the general literature. Social anhedonia, or reduced interest or pleasure in social stimuli, may represent a similar vulnerability factor for co-occurring depressive symptoms in individuals with ASD. In the typically developing (TD) population, lack of motivation to engage in rewarding experiences – or disrupted anticipatory (‘wanting’) pleasure – has been associated with increased distress due to perceived social isolation, or loneliness. In ASD, a less established body of work has suggested both decreased social anticipatory (‘wanting’) and consummatory (‘liking’) pleasure compared to TD counterparts, with some studies suggesting a particular deficit in social ‘wanting’ that is related to ASD symptom severity.

Objectives: To examine anticipatory and consummatory social and non-social pleasure as contributors to loneliness and depressed mood in adults with ASD compared to typically developing adults with depressive disorders (TD-dep) and never-depressed controls (TD-con).

Methods: A total of n=101 adults aged 18-35 with verbal IQ>80 were recruited from the three cohorts (ASD, n=44; TD-dep, n=28; TD-con, n=29). All participants completed diagnostic screening and testing, as well as self-report measures of capacity to experience social pleasure (Anticipatory and Consummatory Interpersonal Pleasure Scale; ACIPS), non-social pleasure (Temporal Experience of Pleasure Scale; TES), autism spectrum traits (Social Responsiveness Scale; SRS), loneliness (Loneliness in Context Questionnaire; LiCQ), and depressive symptoms (Beck Depression Inventory-II; BDI).

Results: The ASD and TD-dep groups did not differ significantly on measures of social and non-social pleasure, for both anticipatory and consummatory dimensions. However, both ASD and TD-dep groups showed decreased capacity for social and non-social pleasure compared to TD-con. The ASD cohort reported greater loneliness and depressive symptoms than TD-con, but less than TD-dep. In the whole sample (and replicated in ASD alone), there was a significant cross-over interaction between capacity for social pleasure and ASD traits on loneliness (t(98)=-2.36, p=0.02): individuals with greater capacity for social pleasure demonstrated a positive relation between ASD traits and loneliness, whereas individuals with decreased capacity for social pleasure exhibited the opposite effect (Figure 1). This moderation effect was not present for the measure of non-social pleasure. Finally, the ASD and TD-dep groups were combined to examine predictors of depressive symptoms trans-diagnostically. When controlling for social and non-social pleasure, loneliness, and ASD traits as predictors of depressive symptoms in a multiple regression framework, only loneliness was a significant predictor of BDI-II scores.

Conclusions: Results indicate that individuals with ASD exhibit a similar profile of capacity for social and non-social pleasure compared to TD-dep, in which ‘liking’ and ‘wanting’ components are both diminished compared to TD-con. In our transdiagnostic sample, increased ASD traits were associated with greater loneliness for individuals with greater capacity for social pleasure. Interestingly, the opposite effect occurred for individuals with decreased capacity for social pleasure. These findings suggest that social anhedonia may be a shared mechanism across autism and depression populations which may partially explain the experience of loneliness and prevalence of co-occurring mood disorders in ASD.