Evidence map›Paper›PMID 25034760›Full record

ReviewSchizophrenia research2016

Autoimmune diseases, gastrointestinal disorders and the microbiome in schizophrenia: more than a gut feeling.

Emily G Severance, Robert H Yolken, William W Eaton

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Schizophrenia research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 4 pooled it
11.2field-weighted citation impact, top 1% of its field
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

124 citing papers in PubMed, 4 syntheses or guidelines pooled it, 248 citations in OpenAlex.

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64 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Emily G SeveranceStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933 USA. Electronic address: eseverance@jhmi.edu.
Robert H YolkenStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933 USA.
William W EatonDepartment of Mental Health, Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, MD, USA.
Johns Hopkins University · US

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9M
Development for RCT of Gluten Free Diet in Gliadin-Positive SchizophreniaR34MH100776 · NIMH · JOHNS HOPKINS UNIVERSITY · PI EATON, WILLIAM W, KELLY, DEANNA L · 2013 to 2015
$712k
NIMH NIH HHS P50 MH094268NIMH NIH HHS R34 MH100776
6 · The paper itself

Abstract

Autoimmunity, gastrointestinal (GI) disorders and schizophrenia have been associated with one another for a long time. This paper reviews these connections and provides a context by which multiple risk factors for schizophrenia may be related. Epidemiological studies strongly link schizophrenia with autoimmune disorders including enteropathic celiac disease. Exposure to wheat gluten and bovine milk casein also contribute to non-celiac food sensitivities in susceptible individuals. Co-morbid GI inflammation accompanies humoral immunity to food antigens, occurs early during the course of schizophrenia and appears to be independent from antipsychotic-generated motility effects. This inflammation impacts endothelial barrier permeability and can precipitate translocation of gut bacteria into systemic circulation. Infection by the neurotropic gut pathogen, Toxoplasma gondii, will elicit an inflammatory GI environment. Such processes trigger innate immunity, including activation of complement C1q, which also functions at synapses in the brain. The emerging field of microbiome research lies at the center of these interactions with evidence that the abundance and diversity of resident gut microbiota contribute to digestion, inflammation, gut permeability and behavior. Dietary modifications of core bacterial compositions may explain inefficient gluten digestion and how immigrant status in certain situations is a risk factor for schizophrenia. Gut microbiome research in schizophrenia is in its infancy, but data in related fields suggest disease-associated altered phylogenetic compositions. In summary, this review surveys associative and experimental data linking autoimmunity, GI activity and schizophrenia, and proposes that understanding of disrupted biological pathways outside of the brain can lend valuable information regarding pathogeneses of complex, polygenic brain disorders.

Indexed as

Autoimmune DiseasesGastrointestinal DiseasesHumansMicrobiotaSchizophreniaAutoimmunityImmune systemIntestinalMicrobiotaPsychiatryPsychosis

Identifiers

PMID25034760
PMCPMC4294997
OpenAlexW2083667275

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.