— January 20, 2026 · Vitamin B1 Linked to How Often the Bowels Move

Table of Contents

1. At a Glance
2. What Was Done
3. What Was Found, Number by Number
4. How Vitamin B1 Could Affect the Gut
5. How It Fits With Earlier Research
6. Where Thiamine Comes From
7. What It Cannot Show
8. What the Researchers and Coverage Said
9. What Remains Unknown
10. Sources and Primary Documents
11. Key Research Papers
12. Connections

At a Glance

• Paper: Díaz-Muñoz C, Bozzarelli I, Lopera-Maya EA, et al. “Genetic dissection of stool frequency implicates vitamin B1 metabolism and other actionable pathways in the modulation of gut motility.” Gut 2026;75(8):1480–1490. Published online January 20, 2026; print issue August 2026. Open access.
• Who: an international team of 17 authors from Spain, Italy, the Netherlands, the United Kingdom, Canada and Australia, coordinated by Mauro D’Amato.
• Design: multi-ancestry genome-wide association study meta-analysis of stool frequency, plus heritability, genetic correlation, Mendelian randomisation, fine-mapping and drug-signature analyses, then a diet–gene test in UK Biobank.
• Size: 268,606 people in six population cohorts: 167,966 of European ancestry in five cohorts and 100,640 East Asians in one cohort. Diet analysis: 98,449 UK Biobank participants.
• Main genetic result: 21 DNA regions linked to stool frequency, 10 of them new. Fine-mapping pointed to single variants near SLC35F3 (thiamine transporter) and XPR1 (phosphate exporter).
• Main diet result: higher dietary thiamine was associated with more frequent bowel movements (p<0.0001), and SLC35F3/XPR1 genotype modified that association (p<0.0001).
• What it is not: not a trial. No thiamine was given to anyone, and the paper makes no claim that thiamine supplements change bowel habits.
• Funding: public research grants from Spain, Italy, the Netherlands and the European Union. Competing interests: “None declared.”

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What Was Done

Measuring how fast material moves through a person’s gut takes special tests in specialist centres, which cannot be run on hundreds of thousands of people. The researchers therefore used stool frequency, the number of bowel movements over a set time, as an indirect stand-in. The paper calls it “an indirect proxy for gastrointestinal transit” and notes that, “although not a perfect proxy for gut motility,” it correlates with how fast material passes through the colon.

Each of the six cohorts asked about bowel habits in its own way. UK Biobank asked, “What is the average number of times you open your bowels per day?” A Dutch cohort (Lifelines) used a 7-day bowel diary. The other cohorts were a Canadian cohort, a Belgian gut-flora cohort, a United States cohort and the China Kadoorie Biobank. Across the cohorts, the average ranged from 0.98 to 1.42 bowel movements per day. IBS was more common at both ends of the range: constipation-predominant IBS (IBS-C) at the low end and diarrhoea-predominant IBS (IBS-D) at the high end.

The team then ran a series of analyses on the combined data:

• Genome-wide association: millions of common DNA variants were tested for a link to stool frequency, first in each ancestry group and then in a combined multi-ancestry meta-analysis.
• Heritability and genetic correlation: how much of the variation the measured DNA explains, and how much the genetics of stool frequency overlaps with 1,461 other traits and diseases.
• Mendelian randomisation: a method that uses genetic variants as natural experiments to test whether one trait may cause another. Here it was run between stool frequency and IBS, diverticular disease and haemorrhoids, using separate data from the FinnGen and Million Veteran Program biobanks.
• Fine-mapping: narrowing each DNA region down to the single variant most likely to be responsible, and the gene that variant probably affects.
• Drug-signature analysis: a computer screen of public databases for medicines whose effects on gene activity mimic or oppose the genetic pattern of stool frequency.
• Diet–gene test: because two fine-mapped genes pointed to thiamine, the team tested dietary thiamine against stool frequency in UK Biobank. According to the online supplement, thiamine intake in milligrams came from UK Biobank’s 24-hour dietary recall data, the model was adjusted for age and sex, and the two gene variants were combined into a score of 0 to 4 “effect alleles” (copies of the variant tied to fewer bowel movements).

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What Was Found, Number by Number

How much of bowel frequency is genetic

• The measured DNA explained about 7.0% of the variation in stool frequency in Europeans and 5.6% in East Asians, a difference the authors describe as not significant. The paper notes that the figure for IBS is in the same range, 5.8% to 10.3% depending on how IBS is defined.
• The genetics of stool frequency looked almost the same in both ancestry groups (genetic correlation 0.88 on a scale where 1.0 means identical).
• Of 1,461 other traits tested, 164 showed a significant genetic overlap with stool frequency, across digestive, heart and blood-vessel, muscle and bone, nervous-system and psychiatric conditions. The abstract gives genetic correlations of 0.18 to 0.47 with digestive and psychiatric disorders, and 0.12 to 0.14 with cardiovascular traits.

The DNA regions

• The European analysis found 12 independent regions (2 new); the East Asian analysis found 3 (2 new); the combined analysis found 18, including 7 seen only when the groups were combined. In total, 21 regions, 10 of them new, “almost doubling” the 14 regions reported by the same group’s earlier study.
• 197 protein-coding genes lie in these 21 regions. Gene-set analysis pointed again to sensory perception, nerve-signalling chemicals (neuropeptides) and ion channels.
• Three regions were fine-mapped to a single likely causal variant: one near SLC35F3 (probability 0.93), one in a poorly understood stretch called ZFHX4-AS1 (0.90, mechanism unknown) and one near XPR1 (0.74). For both B1-related variants, the effect allele was linked to fewer bowel movements.
• Two other strong candidate genes were KLB (klotho-beta), which helps control how much bile acid the liver makes, and COLQ, which anchors the enzyme that breaks down the nerve messenger acetylcholine at nerve endings in the gut wall.

Links with gut diseases

• Mendelian randomisation suggested that the genetics of stool frequency has a causal effect on IBS, “but not vice versa.”
• Stool frequency and diverticular disease showed causal effects in both directions.
• Genetic risk of haemorrhoids was linked to lower stool frequency, which the authors connect to haemorrhoids’ known association with constipation.
• Tests for bias from variants acting through other pathways (MR-PRESSO and Egger tests) did not show a problem (all p>0.05).

The vitamin B1 signal

• In 98,449 UK Biobank participants, higher dietary thiamine was associated with more frequent bowel movements (p<0.0001).
• Adding the SLC35F3/XPR1 gene score to the model “significantly improved the explanatory power of the model” (likelihood ratio test p<0.0001; change in deviance 12.06; change in Akaike Information Criterion −14.9). In plain terms, the link between thiamine intake and bowel frequency was not the same for everyone; it differed with a person’s variants in the two genes, with the combined effect alleles having the strongest negative influence.
• The paper does not give an effect size per milligram of thiamine, so it does not say how many extra bowel movements go with a given amount of the vitamin.

The drug screen

• The computer screen flagged 831 compounds, 538 of them with a known action. They included medicines already used for bowel problems, such as loperamide and pinaverium bromide, and physostigmine, which the paper lists as used for delayed stomach emptying. The authors read these as a check that the method works.
• Calcium channel blockers, a class of blood-pressure medicines, were over-represented (false-discovery-adjusted p=0.023), and protein kinase inhibitors were the most enriched class. 293 compounds had no known target. These are computer leads, not tested effects.

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How Vitamin B1 Could Affect the Gut

The bowel moves its contents by peristalsis, waves of muscle contraction coordinated by the nerve network inside the gut wall. Many of those nerves use acetylcholine as their messenger to tell gut muscle to contract.

The authors propose a chain that links thiamine to that signal. It is a model built from the genetic results and earlier biochemistry; this study did not test it in cells, animals or people:

1. Getting thiamine into place. SLC35F3 is described in the paper as “a transporter regulating thiamine intracellular trafficking and availability.” A 2014 study first identified it as a thiamine transporter, after the human gene made bacteria take up thiamine.
2. Activating it. Thiamine works in the body as thiamine pyrophosphate (TPP), which carries phosphate groups. XPR1 exports inorganic phosphate from cells; the paper calls it “essential for converting thiamine into its active form.”
3. Making the messenger. TPP is a required helper for pyruvate dehydrogenase, the enzyme that makes acetyl-coenzyme A, “the immediate substrate for acetylcholine synthesis in enteric neurons.”
4. The result. In the authors’ words, “Reduced thiamine availability or impaired thiamine utilisation can therefore decrease acetylcholine production and weaken cholinergic tone.”

The COLQ finding fits the same picture, since COLQ helps control how acetylcholine is cleared. The authors describe the thiamine, COLQ and cholinergic findings as pointing “toward a unified mechanism” in which the amount of acetylcholine available in the gut affects peristalsis. A separate pathway runs through bile acids: the variant linked to more frequent bowel movements appears to lower KLB expression, which the authors connect to more bile-acid production and faster colon transit, a mechanism also discussed on the site’s bile acid malabsorption in IBS-D page.

Where gut bacteria come in

Thiamine reaches the body from food and, to an uncertain extent, from bacteria in the colon. A 2014 laboratory study reported that “colonic microbiota synthesize a considerable amount of thiamine in the form of thiamine pyrophosphate” and identified a transporter (SLC44A4) in the lining of the colon that takes up this bacterial TPP; its activity was high in the colon and negligible in the small intestine. A 2015 analysis of the genomes of 256 common gut bacteria predicted that each of eight B vitamins, thiamine among them, can be made by 40% to 65% of these species. The Linus Pauling Institute’s thiamin review states that the colon’s contribution to the body’s thiamine needs “is not clear.”

The Gut study collected no data on the gut microbiome, so it cannot say whether bacterial thiamine plays any part in the link it found. A 2025 review of thiamine and digestion lists exposure of the gut to oral drugs and to the microbiome among the ways thiamine-dependent processes in the gut could be disturbed.

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How It Fits With Earlier Research

The authors write that a role for thiamine in gut motility “finds only scarce prior in previous scientific literature.” The main earlier threads are these:

• The first stool-frequency GWAS (2021). The same research group studied 167,875 people of European ancestry and found 14 DNA regions. The genes were concentrated in nerve-signalling pathways and in the motor nerves that control peristalsis, and people in the top 1% of the genetic score for frequent stools had five times the risk of IBS with diarrhoea. The 2026 study adds an East Asian biobank, 10 new regions and the thiamine genes.
• The largest IBS GWAS (2021). A study of 53,400 people with IBS and 433,201 controls found six risk regions and strong genetic overlap with anxiety, neuroticism and depression. The 2026 paper notes that stool frequency, studied as a measurable trait, produced more signals (21) than IBS itself (6), and that it too overlaps genetically with mood and anxiety disorders, consistent with the gut–brain axis.
• Dietary thiamine and constipation (2024). A cross-sectional study of 10,371 US adults in the National Health and Nutrition Examination Survey (2005–2010), using 24-hour dietary records, found that 1,123 (10.8%) had chronic constipation. Higher thiamine intake was associated with lower odds of constipation (fully adjusted odds ratio 0.87, 95% CI 0.77 to 0.99), and the top third of intake against the bottom third gave an odds ratio of 0.80 (0.65 to 0.99). Its authors called for “additional extensive prospective research.” The Gut paper cites it as being “in line with” its own result.
• Gastrointestinal beriberi. Severe thiamine deficiency (beriberi) is best known for its effects on nerves and the heart, but a digestive form has long been described. The Linus Pauling Institute describes “nausea, vomiting, and severe abdominal pain in a syndrome described as gastrointestinal beriberi.” A 2025 review reports that thiamine deficiency has been linked to impaired stomach and intestinal motility. It also states that thiamine and its drug forms “have been shown to improve symptoms such as nausea, constipation, dysphagia and intestinal dysmotility, in both humans and animals”; that is the review’s summary of earlier reports, not a result of the 2026 study.
• A drug that blocks thiamine uptake. The paper notes that fedratinib, a medicine for the bone-marrow disease myelofibrosis, inhibits another thiamine transporter and caused Wernicke’s encephalopathy, a form of thiamine deficiency that the authors note is “also characterised by constipation.” In their drug screen, fedratinib was anticorrelated with stool frequency.
• The two genes’ earlier history. SLC35F3 was first tied to thiamine in a 2014 blood-pressure study, in which people carrying two copies of its risk variant had lower thiamine in their red blood cells. XPR1 was identified in 2013 as the first known phosphate exporter in animals. The 2026 paper notes that markers in the XPR1 region had been linked to systolic blood pressure, one of several overlaps it reports between bowel habits and cardiovascular traits.
• Fibre, the most studied dietary factor. A 2022 meta-analysis of 16 randomised trials in 1,251 adults with chronic constipation found that 66% responded to fibre supplements against 41% on control (risk ratio 1.48, 95% CI 1.17 to 1.88), with more frequent stools. The benefit was seen with doses above 10 grams a day. This matters for reading the thiamine result, because thiamine-rich whole grains and legumes are also rich in dietary fibre (see the limits below).

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Where Thiamine Comes From

Thiamine is one of the water-soluble B vitamins. The Linus Pauling Institute’s Micronutrient Information Center (updated July 2021) states that “whole-grain cereals, legumes (e.g., beans and lentils), nuts, lean pork, and yeast are rich sources of thiamin,” and that “most of the thiamin is lost during the production of white flour and polished (milled) rice.” Its food table lists, among others:

• Brown rice, long-grain, cooked: 0.18 mg per half cup, against 0.016 mg for unenriched white rice.
• Lentils, cooked: 0.17 mg per half cup; green peas, cooked: 0.21 mg per half cup.
• Whole-wheat bread: 0.13 mg per slice.
• Lean pork loin or tenderloin, roasted: 0.80 mg per 3 ounces (see pork and thiamine).
• Pecans: 0.19 mg per ounce.

The recommended dietary allowance set by the US Food and Nutrition Board in 1998 is 1.2 mg a day for men and 1.1 mg a day for women aged 19 and over, a level based on preventing deficiency. The UK Biobank measure used in the study, as UK Biobank files it, is thiamine estimated from the foods participants reported eating the previous day. The site’s Vitamin B1 food sources page has more detail.

The study did not test any food, amount or supplement, and it did not identify an intake linked to “normal” bowel habits.

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What It Cannot Show

The authors list four limitations in their own words:

1. “we relied on SF derived from questionnaire data, which is only an indirect proxy for gut motility”;
2. “we did not include dietary, medication or lifestyle variables due to inconsistent availability across cohorts and to avoid significant loss of statistical power”;
3. “several SF-associated loci still lack unequivocal identification of causative gene(s), and experimental validation of proposed pathophysiological mechanisms is pending”;
4. “the therapeutic potential of most SF-associated perturbagens requires identification of their molecular targets and further evaluation of druggable pathways in preclinical and clinical settings.”

Other points follow from how the study was built:

• Association is not proof. The diet analysis shows that people who reported more thiamine also reported more frequent bowel movements. It does not show that eating more thiamine, or taking a supplement, changes bowel habits. No intervention was tested.
• Limited adjustment. According to the supplement, the diet model was adjusted for age and sex. The paper does not report adjustment for fibre, total food intake, fluid, physical activity or medicines, all of which can affect bowel habits. Because thiamine-rich foods such as whole grains and legumes also carry fibre, the study cannot separate the vitamin from the foods that contain it.
• Self-report. Both thiamine intake (a recall of the previous day’s food) and bowel frequency (a questionnaire answer) were reported by participants, and both carry recall error.
• More is not always better. The paper shows IBS rising at both ends of the stool-frequency range, with IBS-D at the high end. A link with “more frequent” bowel movements is a statement about direction, not about health.
• Small genetic share. The common DNA variants measured explain about 7% of the variation in stool frequency, so most of the variation is not explained by them. The paper’s introduction names the gut microbiome, diet, physical activity and medications among the other influences on gut motility.
• Two ancestry groups. All participants were of European or East Asian ancestry. The diet analysis used UK Biobank’s European-ancestry participants only.
• No size of effect. The paper reports significance tests and model-fit statistics, not how much stool frequency changes per milligram of thiamine.
• Computer leads only. The drug screen matched gene-activity patterns in databases; it did not test any medicine on bowel habits.

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What the Researchers and Coverage Said

CIC bioGUNE’s press release, dated January 20, 2026, quoted the first author, Cristian Díaz-Muñoz: “We used genetics to build a roadmap of biological pathways that set the gut’s pace. What stood out was how strongly the data pointed to vitamin B1 metabolism, alongside established mechanisms like bile acids and nerve signalling.”

The study’s coordinator, Mauro D’Amato, said in the same release: “Gut motility problems sit at the heart of IBS, constipation and other common gut-motility disorders, but the underlying biology is very hard to pin down. These genetic results highlight specific pathways, especially vitamin B1, as testable leads for the next stage of research, including lab experiments and carefully designed clinical studies.”

In an interview published by a medical news site on January 23, 2026, D’Amato addressed the obvious next question: “I’ve already heard people saying ‘Oh, well, how much vitamin B? What should I eat every day now?’ We’re not there yet, at least this is not what we do in the lab.” The interview summarises him as saying that animal studies and, later, human clinical trials are needed to find out whether vitamin B1 supplementation can improve real-world outcomes. The interview notes that he reports no relevant disclosures.

Most coverage stayed close to the paper, which itself describes “a strong association between dietary vitamin B1 intake and stool frequency.” One national news headline on January 22 went further, saying the vitamin “may control speed of digestion.” The study measured how often people reported opening their bowels, which the authors treat as an indirect proxy for transit, and its diet result is an association, not a demonstration of control. The paper’s own discussion frames supplementation as a question for the future: “future research may explore whether targeted nutritional interventions, such as thiamine supplementation, can alleviate disordered gut motility and IBS symptoms in genetically susceptible individuals.”

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What Remains Unknown

• Whether giving thiamine, through food or supplements, changes stool frequency, constipation or IBS symptoms in anyone. No trial has tested this against these genetic findings.
• Whether people who carry the SLC35F3 and XPR1 variants linked to fewer bowel movements respond differently to thiamine, which is the “genetically susceptible individuals” question the authors raise.
• Whether the proposed chain from thiamine to TPP to acetylcholine in gut nerves actually operates as described. The authors write that “future studies can investigate these interactions at a mechanistic level.”
• How much the thiamine link reflects the vitamin itself rather than the whole grains, legumes and other foods that supply it.
• What part, if any, thiamine made by gut bacteria plays.
• Whether the findings hold in African, South Asian, Hispanic and other populations not included.
• What lies behind the newly found region near ZFHX4-AS1, whose mechanism the authors call “elusive,” and whether any of the drug-screen leads affect gut motility in practice.

For background on the vitamin itself, the site’s thiamine deficiency and vitamin B1 benefits pages cover what is established about thiamine outside this study.

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Sources and Primary Documents

Every figure attributed to the study above was taken from the open-access full text and its online supplement, not from press coverage.

1. Díaz-Muñoz C, Bozzarelli I, Lopera-Maya EA, Belbasis L, Lo Faro V, Camargo Tavares L, et al. (2026). Genetic dissection of stool frequency implicates vitamin B1 metabolism and other actionable pathways in the modulation of gut motility. Gut 75(8):1480-1490. — doi:10.1136/gutjnl-2025-337059 · PubMed PMID: 41558814 · Full text (PMC13479210)
2. CIC bioGUNE (January 20, 2026). DNA ties gut motility to vitamin B1. — Press release
3. ScienceDaily (January 22, 2026). A common vitamin could influence bathroom frequency. — News summary
4. HCPLive (January 23, 2026). From Physiology to Genetics: A New Lens on Gut Motility, with Mauro D’Amato, PhD. — Interview
5. Linus Pauling Institute, Oregon State University. Micronutrient Information Center: Thiamin (updated July 2021, reviewed October 2021). — Thiamin

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Key Research Papers

Background papers on stool-frequency genetics, thiamine and the gut. Each entry was checked against PubMed and Crossref before it was written down.

1. Bonfiglio F, Liu X, Smillie C, Pandit A, Kurilshikov A, Bacigalupe R, et al. (2021). GWAS of stool frequency provides insights into gastrointestinal motility and irritable bowel syndrome. Cell Genomics 1(3):100069. — PubMed PMID: 34957435
2. Eijsbouts C, Zheng T, Kennedy NA, Bonfiglio F, Anderson CA, Moutsianas L, et al. (2021). Genome-wide analysis of 53,400 people with irritable bowel syndrome highlights shared genetic pathways with mood and anxiety disorders. Nature Genetics 53(11):1543-1552. — PubMed PMID: 34741163
3. Du W, Lu L, Liu Y, Yan Y, La R, Wu Q, et al. (2024). The association between dietary vitamin B1 intake and constipation: a population-based study. BMC Gastroenterology 24(1):171. — PubMed PMID: 38760704
4. Overton E, Emelyanova A, Bunik VI (2025). Thiamine, gastrointestinal beriberi and acetylcholine signaling. Frontiers in Nutrition 12:1541054. — PubMed PMID: 40271433
5. Zhang K, Huentelman MJ, Rao F, Sun EI, Corneveaux JJ, Schork AJ, et al. (2014). Genetic implication of a novel thiamine transporter in human hypertension. Journal of the American College of Cardiology 63(15):1542-1555. — PubMed PMID: 24509276
6. Giovannini D, Touhami J, Charnet P, Sitbon M, Battini JL (2013). Inorganic phosphate export by the retrovirus receptor XPR1 in metazoans. Cell Reports 3(6):1866-1873. — PubMed PMID: 23791524
7. Nabokina SM, Inoue K, Subramanian VS, Valle JE, Yuasa H, Said HM (2014). Molecular identification and functional characterization of the human colonic thiamine pyrophosphate transporter. Journal of Biological Chemistry 289(7):4405-4416. — PubMed PMID: 24379411
8. Magnúsdóttir S, Ravcheev D, de Crécy-Lagard V, Thiele I (2015). Systematic genome assessment of B-vitamin biosynthesis suggests co-operation among gut microbes. Frontiers in Genetics 6:148. — PubMed PMID: 25941533
9. van der Schoot A, Drysdale C, Whelan K, Dimidi E (2022). The effect of fiber supplementation on chronic constipation in adults: an updated systematic review and meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition 116(4):953-969. — PubMed PMID: 35816465

PubMed Topic Searches

1. PubMed: Stool frequency and genome-wide association
2. PubMed: Thiamine and constipation
3. PubMed: Thiamine and gastrointestinal motility
4. PubMed: Genetics of irritable bowel syndrome
5. PubMed: Gut microbiota and thiamine synthesis

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Connections

• News Archive
• Vitamin B1 (Thiamine) — the vitamin, its functions and research
• Thiamine Deficiency — symptoms, causes and recovery
• Vitamin B1 Benefits — deep dive on the research
• Vitamin B1 Food Sources — foods and daily intake
• Beriberi and Wernicke-Korsakoff — severe thiamine deficiency
• Constipation — causes and research
• Irritable Bowel Syndrome — the condition and its research
• IBS Subtypes — IBS-C, IBS-D, IBS-M and IBS-U
• Bile Acid Malabsorption in IBS-D — the bile-acid route to faster transit
• Peristalsis — animation of how the gut moves food along
• Bile Acids — animation of bile and fat digestion
• Your Microbiome — the bacteria of the gut
• Dietary Fiber — fibre and bowel function
• The Gut-Brain Axis — how gut and brain signal each other
• Diverticulitis — genetically linked to stool frequency in the study
• Hemorrhoids — linked to lower stool frequency in the study
• Wernicke’s Encephalopathy — the neurological thiamine emergency
• Pork for Thiamine — one of the richest food sources
• Lentils — a legume source of thiamine and fibre
• Brown Rice — the whole grain that keeps its thiamine

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