Thiamine, gastrointestinal beriberi and acetylcholine signaling.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing molecular mechanisms without systematic methodology or primary human trial data
PubMed 40271433 · doi:10.3389/fnut.2025.1541054
What was done
This narrative review analyzed published literature on the molecular mechanisms connecting thiamine deficiency to digestive dysfunction. The authors examined how gastrointestinal-restricted thiamine insufficiency develops through local supply-demand imbalances, microbiome and drug interactions, and disruptions in thiamine-dependent acetylcholine signaling involving coenzyme and non-coenzyme pathways in the enteric nervous system.
What was found
The abstract reports no numerical data or effect sizes. Qualitatively, it reports that thiamine deficiency impairs gastric and intestinal motility, pancreatic exocrine function, gastric acidity, and gut barrier integrity. Thiamine and its derivatives improve symptoms such as nausea, constipation, dysphagia, and dysmotility, acting through thiamine diphosphate-dependent energy and acetylcholine synthesis as well as non-coenzyme modulation of synaptic function.
Why it matters
It highlights gastrointestinal beriberi as a distinct, underappreciated presentation of thiamine deficiency that may contribute to functional gastrointestinal disorders through cholinergic dysfunction.
Limits
The abstract describes a non-systematic narrative review with no quantitative findings, sample size, or formal search strategy reported. The conclusions rely heavily on mechanistic reasoning and mixed preclinical data.
Cited by
- supports Vitamin B1 (thiamine) stimulates and supports gastrointestinal peristalsis.