Evidence map›Paper›PMID 40867540›Full record

SynthesisBiomolecules2025

Vitamin D as a Modifiable Risk Factor in Schizophrenia a Systematic Review.

Jadwiga Mosiołek, Bartosz Mosiołek, Agata Szulc

Abstract readSystematic Review
In one paragraph

Synthesis in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Jadwiga MosiołekFaculty of Health Sciences, Medical University of Warsaw, Żwirki i Wigury 61, 02-091 Warsaw, Poland.
Bartosz MosiołekFaculty of Medicine, Medical University of Warsaw, Żwirki I Wigury 61, 02-091 Warsaw, Poland.ORCID 0009-0006-6090-4783
Agata SzulcFaculty of Health Sciences, Medical University of Warsaw, Żwirki i Wigury 61, 02-091 Warsaw, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology of schizophrenia remains poorly understood. Although certain risk factors have been identified, effective preventive measures are still lacking. This study investigates potential preventive methods while focusing on the role of vitamin D and its status. The role of malnutrition in schizophrenia risk was first identified in studies on the Dutch Hunger Winter. Vitamin D deficiency was hypothesized as a contributing factor shortly thereafter. This review aims to explore the correlations between vitamin D deficiency at various life stages (maternal, neonatal, adult) and schizophrenia risk, as well as its effects on pharmacokinetics, neurobiology, bone health, and metabolic syndrome. The studies were retrieved from two indexed databases, PubMed and Web of Science, following PRISMA guidelines and included studies published between 2000 and 2024. No correlation was found between maternal vitamin D levels and schizophrenia in offspring while a positive correlation was observed between low neonatal vitamin D levels and schizophrenia in later life. Approximately half of the studies on adults reported mean vitamin D concentrations of below 20 ng/mL which were negatively correlated with gray matter volume and bone health while positively correlated with the prevalence of metabolic syndrome. Additionally, vitamin D levels were also found to correlate with antipsychotic drug concentrations.

Indexed as

SchizophreniaVitamin DVitamin D DeficiencyAdultFemaleHumansMetabolic SyndromeRisk FactorsVitamin Dcalcitriolcholecalciferoldeficiencypsychosisschizophreniavitamin D

Identifiers

PMID40867540
PMCPMC12383755

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.