Some studies suggest that individuals with autism spectrum disorder have reduced emotional empathy while others do not. The presence of co-occurring alexithymia in autism spectrum disorder and differences in interoception have been associated with reductions in empathic ability. To fully explore the relationships between interoception, alexithymia, and emotional empathy, we collected self-report and interview data in 35 youth with autism spectrum disorder and 40 typically developing controls (ages 8–17 years). The autism spectrum disorder sample had increased alexithymia and physiological hyperarousal compared to typically developing controls, but there were no group differences in interoception or emotional empathy. Alexithymia severity correlated with higher personal distress in both groups and with lower empathic concern in the autism spectrum disorder group. Within the autism spectrum disorder group, higher incidence of reports of bodily sensation when describing emotional experience correlated with lower personal distress and lower alexithymia. In addition, although empathic concern was negatively correlated with alexithymia in the autism spectrum disorder group, across groups, the alexithymia hypothesis was supported in only the personal distress domain of emotional empathy. These results suggest emotional empathy; personal distress, in particular, is not intrinsically impaired in autism spectrum disorder. Lay abstract Empathy, the ability to understand and share the emotions of others, is a necessary skill for social functioning and can be categorized into cognitive and emotional empathy. There is evidence to suggest that individuals with autism spectrum disorder have difficulties with cognitive empathy, the ability to imagine how another person is thinking or feeling. However, it is unclear if individuals with autism spectrum disorder struggle with emotional empathy, the ability to share and feel emotions others are experiencing. Self-report and interview data were collected to explore the relationships between interoception (individuals’ self-reported awareness of sensation from their body such as thirst, heartbeat, etc.), alexithymia (an individual’s ability to describe and distinguish between their own emotions), and emotional empathy in 35 youth with autism spectrum disorder and 40 typically developing youth. Greater personal distress to others’ emotions and greater difficulty describing and recognizing self-emotions were associated with reporting fewer physical sensations in the body when experiencing emotion in the autism spectrum disorder group. The results of this study suggest that while autism spectrum disorder youth with concomitant alexithymia may experience emotional empathy differently, it should not be characterized as an absence of a capacity for emotional empathy.

Gastrointestinal dysfunction is one of the most prevalent physiological symptoms of autism spectrum disorder (ASD). A growing body of largely preclinical research suggests that dysbiotic gut microbiota may modulate brain function and social behavior, yet little is known about the mechanisms that underlie these relationships and how they may influence the pathogenesis or severity of ASD. While various genetic and environmental risk factors have been implicated in ASD, this review aims to provide an overview of studies elucidating the mechanisms by which gut microbiota, associated metabolites, and the brain interact to influence behavior and ASD development, in at least a subgroup of individuals with gastrointestinal problems. Specifically, we review the brain-gut-microbiome system and discuss findings from current animal and human studies as they relate to social-behavioral and neurological impairments in ASD, microbiota-targeted therapies (i.e., probiotics, fecal microbiota transplantation) in ASD, and how microbiota may influence the brain at molecular, structural, and functional levels, with a particular interest in social and emotion-related brain networks. A deeper understanding of microbiome-brain-behavior interactions has the potential to inform new therapies aimed at modulating this system and alleviating both behavioral and physiological symptomatology in individuals with ASD.