Biochemical correlates of social anxiety in subjects with autism spectrum conditions
Benedetta Nardi, Lionella Palego, Chiara Bonelli, Valeria Tognini, Cristiana Pronestì, Matteo Pioltino, Gabriele Massimetti, Stefano Pini, Alessandro Saba, Laura Betti, Gino Giannaccini, Lilliana Dell’Osso, Barbara CarpitaAbstract
Background
Social anxiety disorder (SAD) is a common and debilitating condition marked by intense fear of negative evaluation in social situations. It often co-occurs with other psychiatric disorders, and in particular Autism Spectrum Disorder (ASD). The exact cause of SAD is unclear, though biological, environmental, and genetic factors are believed to contribute. Recent research highlights the involvement of neuropeptides, neurohormones, and immune system components in SAD development, suggesting complex interactions between psychological and biological factors, with a growing focus on inflammation’s role. This study aimed to investigate potential biochemical correlates of SAD in individuals with ASD, their first-degree relatives (BAP group), and healthy controls (HCs), focusing on inflammatory markers, neuropeptides, and growth factors.
Methods
Twenty-four adults with ASD, their relatives, and HCs, for a total of 72 participants, were assessed. Biochemical parameters were analyzed using enzyme-linked immunosorbent assays (ELISA), and social anxiety symptoms were evaluated via the Social Phobia Spectrum—Self Report (SHY-SR) questionnaire.
Results
Individuals with ASD exhibited significantly higher SHY-SR scores compared to the BAP and HCs. Subjects in the ASD group tended to make greater use of anxiolytics in order to improve their social interaction skills. Additionally, a specific pattern of correlation and association was found between biochemical variables and specific SAD symptoms, suggesting a potential role of inflammatory pathways in SAD pathophysiology.
Conclusions
Our results confirm the presence of greater social phobic symptoms in subjects with ASD, and support the hypothesis of a role of the inflammatory cascade in the maintenance of the disorder.