Ana Alexandra Caldas Osório1, Júlia Horta Tabosa do Egito1, Gabriela Carneiro Martins1, Chong Ae Kim2, Rachel Sayuri Honjo2, Adriana da Conceição Soares Sampaio3, Ana Raquel Marcelino Mesquita3, Elizeu Coutinho Macedo1, Paulo Sérgio Boggio1, Maria Cristina Triguero Veloz Teixeira4.
Abstract
Objective: Fetal testosterone (fT) has organizational effects on the developing human nervous system and can be reliably estimated by the ratio between the length of the second and fourth digits - 2D:4D. Previous studies reported altered patterns of fT in some developmental disabilities (e.g. ASD) relative to typically developing individuals (TD). Williams syndrome (WS) is a rare genetic disorder characterized by exacerbated empathy and social approach and heightened anxiety. Recent reports also highlight the co-occurrence of significant levels of autistic symptoms. Despite constituting an interesting model to study androgenic contributions to social behavior, no studies have sought to explore fT in WS. The main aims of this preliminary study were two-fold: (a) to compare 2D:4D in WS and TD; (b) to analyze the pattern of associations between 2D:4D and hypersociability, affective and cognitive empathy, anxiety and autistic symptoms in WS.
Methods: 2D:4D were measured from digital scans of the ventral surface of the right hand. Hypersociability, empathy, anxiety and autistic symptoms were obtained from parental reports.
Results: There were no significant differences in 2D:4D between WS than TD. In WS lower fT (higher 2D:4D) was significantly associated with hypersociability and affective empathy, as well as marginally associated with anxiety/depression scores. In contrast, cognitive empathy was marginally and negatively associated with 2D:4D, while levels of autistic symptoms were unrelated with this measure.
Conclusion: Our results suggest that fT may be implicated in the emergence of several cardinal features of WS, namely hypersociability, affective empathy and anxiety, but not in ASD symptoms. © The British Society of Developmental Disabilities 2017.
Objective: Fetal testosterone (fT) has organizational effects on the developing human nervous system and can be reliably estimated by the ratio between the length of the second and fourth digits - 2D:4D. Previous studies reported altered patterns of fT in some developmental disabilities (e.g. ASD) relative to typically developing individuals (TD). Williams syndrome (WS) is a rare genetic disorder characterized by exacerbated empathy and social approach and heightened anxiety. Recent reports also highlight the co-occurrence of significant levels of autistic symptoms. Despite constituting an interesting model to study androgenic contributions to social behavior, no studies have sought to explore fT in WS. The main aims of this preliminary study were two-fold: (a) to compare 2D:4D in WS and TD; (b) to analyze the pattern of associations between 2D:4D and hypersociability, affective and cognitive empathy, anxiety and autistic symptoms in WS.
Methods: 2D:4D were measured from digital scans of the ventral surface of the right hand. Hypersociability, empathy, anxiety and autistic symptoms were obtained from parental reports.
Results: There were no significant differences in 2D:4D between WS than TD. In WS lower fT (higher 2D:4D) was significantly associated with hypersociability and affective empathy, as well as marginally associated with anxiety/depression scores. In contrast, cognitive empathy was marginally and negatively associated with 2D:4D, while levels of autistic symptoms were unrelated with this measure.
Conclusion: Our results suggest that fT may be implicated in the emergence of several cardinal features of WS, namely hypersociability, affective empathy and anxiety, but not in ASD symptoms. © The British Society of Developmental Disabilities 2017.
Entities:
Keywords:
2D:4D; ASD; Williams syndrome; affective empathy; anxiety; cognitive empathy; fetal testosterone; hypersociability
Year: 2017
PMID: 34141327 PMCID: PMC8115471 DOI: 10.1080/20473869.2017.1376163
Source DB: PubMed Journal: Int J Dev Disabil ISSN: 2047-3869