Gut microbiome differences in children with Attention Deficit Hyperactivity Disorder and Autism Spectrum Disorder and effects of probiotic supplementation: A randomized controlled trial

IF 2.6 2区医学 Q1 EDUCATION, SPECIAL

Research in Developmental Disabilities Pub Date : 2025-04-04 DOI:10.1016/j.ridd.2025.105003

Nil Novau-Ferré , Christopher Papandreou , Meritxell Rojo-Marticella , Josefa Canals-Sans , Mònica Bulló

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引用次数: 0

Abstract

Background

Emerging evidence suggests a significant role of gut microbiota on neurodevelopmental disorders, including Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorder (ASD).

Aims

Our study aimed to compare gut microbiota composition between these disorders and evaluate the effect of probiotic supplementation.

Methods

We conducted a 12-week randomized, double-blind, placebo-controlled trial with 80 children aged 5–14 years (39 with ADHD, 41 with ASD). Baseline and post-intervention fecal samples were analyzed using 16S rRNA gene sequencing to identify changes in gut microbiota composition.

Results

We identified 22 taxa differentiating ADHD and ASD (AUC = 0.939), characterised by increased presence of Clostridia, Ruminococcaceae, and Lachnospiraceae in ADHD, and Bacteroides, Bacilli and Actinobacteria in ASD. These differences remained after accounting for potential confounders. ASD children receiving probiotics had significant increases in Chao 1, Fisher's alpha, and Shannon indices whereas no significant differences in α and β-diversity were found in ADHD. In ADHD, bacteria with potential adverse effects were under-represented. In ASD, the abundance of Eggerthellaceae, and other taxa associated with gastrointestinal problems and anxiety was decreased.

Conclusion

Variations in gut microbiota may influence responses in ADHD and ASD. Probiotic supplementation favorably altered gut microbiota composition, offering insights for future therapeutic strategies targeting the microbiome in neurodevelopmental disorders.

What this paper adds

Recent research underscores the role of gut microbiota in ADHD and ASD, indicating that diet can significantly influence microbiota composition and potentially manage these neurodevelopmental disorders. This study reveals distinct differences in gut microbiota composition between children with ADHD and ASD and demonstrates that probiotic supplementation can modulate specific microbial genera in each disorder. These findings pave the way for the development of innovative microbiome-targeted therapies, offering a new avenue for the treatment of neurodevelopmental disorders. Understanding this relationship is crucial for designing future interventions.

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注意缺陷多动障碍和自闭症谱系障碍儿童肠道微生物组差异及益生菌补充的影响：一项随机对照试验

背景：越来越多的证据表明，肠道微生物群在神经发育障碍（包括注意缺陷多动障碍（ADHD）和自闭症谱系障碍（ASD））中发挥着重要作用。目的本研究旨在比较这些疾病的肠道菌群组成，并评估益生菌补充的效果。方法我们对80名5-14岁的儿童进行了为期12周的随机、双盲、安慰剂对照试验（其中39名患有ADHD， 41名患有ASD）。使用16S rRNA基因测序分析基线和干预后的粪便样本，以确定肠道微生物群组成的变化。结果共鉴定出22个区分ADHD和ASD的分类群（AUC = 0.939）， ADHD中梭状芽孢杆菌、瘤胃球菌科和毛螺杆菌科的存在增加，ASD中拟杆菌、芽胞杆菌和放线菌的存在增加。在考虑了潜在的混杂因素后，这些差异仍然存在。服用益生菌的ASD儿童Chao 1、Fisher’s α和Shannon指数显著升高，而ADHD儿童α和β多样性无显著差异。在ADHD中，具有潜在不良反应的细菌未被充分代表。在ASD中，蛋菜科和其他与胃肠道问题和焦虑相关的分类群的丰度下降。结论肠道菌群的变化可能影响ADHD和ASD的反应。补充益生菌有利于改变肠道微生物群组成，为未来针对神经发育障碍微生物群的治疗策略提供见解。最近的研究强调了肠道微生物群在ADHD和ASD中的作用，表明饮食可以显著影响微生物群的组成，并有可能控制这些神经发育障碍。这项研究揭示了ADHD和ASD儿童肠道微生物群组成的明显差异，并表明益生菌补充剂可以调节每种疾病的特定微生物属。这些发现为开发创新的微生物组靶向疗法铺平了道路，为治疗神经发育障碍提供了新的途径。了解这种关系对于设计未来的干预措施至关重要。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Research in Developmental Disabilities Multiple-

CiteScore

5.50

自引率

6.50%

发文量

178

期刊介绍： Research In Developmental Disabilities is aimed at publishing original research of an interdisciplinary nature that has a direct bearing on the remediation of problems associated with developmental disabilities. Manuscripts will be solicited throughout the world. Articles will be primarily empirical studies, although an occasional position paper or review will be accepted. The aim of the journal will be to publish articles on all aspects of research with the developmentally disabled, with any methodologically sound approach being acceptable.