Analysis reveals reduced vitamin A absorption and enterochromaffin cell density in children with ASD, suggesting GI dysfunction.
Abstract Gastrointestinal (GI) symptoms and micronutrient deficiencies are frequently reported in children with Autism Spectrum Disorder (ASD), yet their underlying mechanisms remain poorly understood. Vitamin A deficiency, commonly attributed to selective eating, can lead to severe complications such as vision impairment. In this study, we investigated whether impaired duodenal absorption contributes to hypovitaminosis A in ASD. We also examined GI dysmotility, particularly constipation, hypothesizing a role for serotonin-producing enterochromaffin cells. Duodenal biopsies from 20 children with ASD and 20 age-matched neurotypical controls were analyzed using immunohistochemical staining to assess Retinol Binding Protein 2 (RBP2) expression in enterocytes and quantify enterochromaffin cell density. RBP2 expression was significantly reduced in the ASD group, indicating a potential absorption defect beyond dietary limitations. Additionally, enterochromaffin cell density per gland was markedly lower in ASD samples, suggesting impaired serotonin signaling may contribute to intestinal hypomotility. These findings support the inclusion of vitamin A screening in the standard care of children with ASD and highlight a potential histopathological basis for GI dysfunction in this population.
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Kassandra Wolfsteiner (2025) studied this question.
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