Evidence map›Paper›PMID 30158857›Full record

ReviewFrontiers in cellular neuroscience2018

Early Disruption of the Microbiome Leading to Decreased Antioxidant Capacity and Epigenetic Changes: Implications for the Rise in Autism.

Rebecca S Eshraghi, Richard C Deth, Rahul Mittal, Mayank Aranke, Sae-In S Kay, Baharak Moshiree, Adrien A Eshraghi

Abstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed.

  1. Trial
  2. DecodingJournal of clinical medicine · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. The Human Gut Microbiome as a Potential Factor in Autism Spectrum Disorder.International journal of molecular sciences · 2022
    Review
  11. CouldJournal of clinical medicine · 2022
    Review
  12. Role of Gut Microbiome in Autism Spectrum Disorder and Its Therapeutic Regulation.Frontiers in cellular and infection microbiology · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Rebecca S EshraghiDivision of Gastroenterology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL, United States.
Richard C DethDepartment of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL, United States.
Rahul MittalDepartment of Otolaryngology, Miller School of Medicine, University of Miami, Miami, FL, United States.
Mayank ArankeDepartment of Otolaryngology, Miller School of Medicine, University of Miami, Miami, FL, United States.
Sae-In S KayDr. Kiran C. Patel College of Osteopathic Medicine, Nova Southeastern University, Fort Lauderdale, FL, United States.
Baharak MoshireeDivision of Gastroenterology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL, United States.
Adrien A EshraghiDepartment of Otolaryngology, Miller School of Medicine, University of Miami, Miami, FL, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently, 1 out of every 59 children in the United States is diagnosed with autism. While initial research to find the possible causes for autism were mostly focused on the genome, more recent studies indicate a significant role for epigenetic regulation of gene expression and the microbiome. In this review article, we examine the connections between early disruption of the developing microbiome and gastrointestinal tract function, with particular regard to susceptibility to autism. The biological mechanisms that accompany individuals with autism are reviewed in this manuscript including immune system dysregulation, inflammation, oxidative stress, metabolic and methylation abnormalities as well as gastrointestinal distress. We propose that these autism-associated biological mechanisms may be caused and/or sustained by dysbiosis, an alteration to the composition of resident commensal communities relative to the community found in healthy individuals and its redox and epigenetic consequences, changes that in part can be due to early use and over-use of antibiotics across generations. Further studies are warranted to clarify the contribution of oxidative stress and gut microbiome in the pathophysiology of autism. A better understanding of the microbiome and gastrointestinal tract in relation to autism will provide promising new opportunities to develop novel treatment modalities.

Indexed as

autismdysbiosisepigeneticsgut microbiotaoxidative stress

Identifiers

PMID30158857
PMCPMC6104136

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.