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Background: The modification of performance following conflict can be measured using conflict adaptation tasks thought to measure the change in the allocation of cognitive resources in order to reduce conflict interference and improve performance. While previous studies have suggested atypical processing during nonsocial cognitive control tasks, conflict adaptation (i.e. congruency sequence effects) for social–emotional stimuli have not been previously studied in autism spectrum disorder. Methods: A total of 32 participants diagnosed with autism spectrum disorder and 27 typically developing matched controls completed an emotional Stroop conflict task that required the classification of facial affect while simultaneously ignoring an overlaid affective word. Results: Both groups showed behavioral evidence for emotional conflict adaptation based on response times and accuracy rates. However, the autism spectrum disorder group demonstrated a speed-accuracy trade-off manifested through significantly faster response times and decreased accuracy rates on trials containing conflict between the emotional face and the overlaid emotional word. Conclusion: Reduced selective attention toward socially relevant information may bias individuals with autism spectrum disorder toward more rapid processing and decision making even when conflict is present. Nonetheless, the loss of important information from the social stimuli reduces decision-making accuracy, negatively affecting the ability to adapt both cognitively and emotionally when conflict arises.

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Though the etiology of autism spectrum disorder (ASD) remains largely unknown, recent findings suggest that hormone dysregulation within the prenatal environment, in conjunction with genetic factors, may alter fetal neurodevelopment. Early emphasis has been placed on the potential role of in utero exposure to androgens, particularly testosterone, to theorize ASD as the manifestation of an “extreme male brain.” The relationship between autism risk and obstetric conditions associated with inflammation and steroid dysregulation merits a much broader understanding of the in utero steroid environment and its potential influence on fetal neuroendocrine development. The exploration of hormone dysregulation in the prenatal environment and ASD development builds upon prior research publishing associations with obstetric conditions and ASD risk. The insight gained may be applied to the development of chronic adult metabolic diseases that share prenatal risk factors with ASD. Future research directions will also be discussed.

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