Colchicine

antigout preparation, antimitotic (microtubule inhibitor)

Also sold as Colcrys, Mitigare.

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Colchicine has little of the classical depletion machinery (no enzyme induction or renal tubular wasting was described in the label sections read) but it has one real, drug-specific mechanism: it inhibits beta-tubulin polymerization into microtubules [1], and in humans and animals that is associated with disordered small-intestinal mucosal function. The label sections read do not mention vitamin B12, malabsorption, folate or any other nutrient [1], so the literature, not the label, carries the nutrient signal. Two entries reach orange. Vitamin B12 is the strongest: colchicine reduced B12 absorption in human Schilling-test experiments with a localized ileal effect and normal intrinsic factor [4], and a prospective pediatric FMF cohort reported falling B12 over 6 months [8]. It stops at orange because long-term adult cohorts disagree: mean B12 did not differ from controls in 95 FMF patients on colchicine for 2 or more years, although B12 deficiency was more common (12 vs 3, p=0.021) [7], and serum B12 was normal in all 12 patients on 1 to 2 mg/day for 3 or more years [9]. Lactose malabsorption is the second orange entry, a functional carbohydrate effect measured by breath test in FMF patients [10]. No red entry is supportable.

antigout preparation, antimitotic (microtubule inhibitor) · ATC M04AC01 (WHO ATC/DDD Index [2]) · also sold as Colcrys and Mitigare; many generics · reviewed 2026-10-06. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Colchicine in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe: Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow — Low: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded — disclosed evidence gap: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Vitamin B12: reversible ileal malabsorption in human experiments; serum deficiency inconsistent and limited to subgroups of long-term FMF users

Orange — Moderate

See study details

Colchicine reduces B12 absorption at the ileal mucosa without disturbing intrinsic factor, and some, not all, long-term users develop low serum B12.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. Orange

Limits on what this shows

Key null findings: Mean serum B12 did not differ between treated FMF patients and controls [7]. Mean B12 of 15 colchicine-naive FMF patients was not different from treated patients (p=0.356), underpowered [7]. Serum B12 was normal in all 12 patients on 1 to 2 mg/day for 3 or more years [9]. The authors of [7] concluded they did not observe significant B12 deficiency among treated patients.
At-risk subgroups: Long-term FMF users (2 or more years at FMF-range doses) and children in the first 6 months of therapy, per the studies above. Gout-prophylaxis doses (0.6 to 1.2 mg/day [1]) were not studied for B12 in any source retrieved.
Counter-evidence on record: Confounding by indication: untreated FMF controls were few (n=15) [7], and Kaba has no unexposed comparator [8]. Inflammation is not a plausible explanation for the fall in Kaba: in a Behcet cohort CRP correlated negatively with B12 and folate [12], which would predict B12 rising as inflammation resolves (context only, different disease, colchicine effect not isolated). The experimental Webb data measure absorption, not body stores, and are decades old.

Direction

Depletion pathway (reduced absorption). Functional and reversible in the experimental data; no retention or excess effect.

Regulatory status

Not mentioned in the colchicine label sections read [1] (read via a summarizing tool: the first 100,000 of 115,450 characters of the label XML and the clinical pharmacology and toxicology sections of the label page; nutrient interactions were asked for and none were reported). The label does list diarrhea and blood dyscrasias [1].

Population evidence

Webb 1968 [4], human Schilling-test experiments: colchicine substantially reduced B12 absorption in most healthy subjects, with the largest effect when delivered into the ileum; gastric histology and intrinsic factor activity were normal; colchicine did not block B12 binding to intrinsic factor; malabsorption was reversible. Sample size, dose and duration were not visible in the abstract text retrieved (reconstructed abstract only; full text not opened). Race 1970 [5] is a companion human study, but no abstract was available and its findings were not seen, so it supports nothing here. Gemici 2013 [7], case-control: 95 adult FMF patients on colchicine for 2 or more years vs 90 matched controls; mean B12 352 vs 361 pg/mL (p=0.71); B12 deficient 12 vs 3 (p=0.021); 3 of the 12 had megaloblastic anemia, no deficient control was anemic; no other cause was identified. Kaba 2026 [8], prospective cohort of 46 children with newly diagnosed FMF measured at baseline, 3 and 6 months: B12 declined (p<0.001) and folate declined (p=0.001) while hemoglobin rose; absolute values and doses were not visible in the abstract-level text.

Mechanism

Present and named at the tissue level. Webb localizes the defect to ileal mucosal function, not gastric secretion or intrinsic factor binding [4]. In guinea pig ileal tissue colchicine produced a dose-related, reversible fall in intrinsic factor-B12 receptor binding (5.78 to 1.3 ng B12 bound) with malabsorption in treated animals [6] (Tier B). A link to the drug's tubulin-polymerization inhibition [1] is plausible but the receptor-trafficking explanation is an inference, not shown in any source opened.

Why orange, not red

One prospective Tier A cohort with a measured decline (abstract-level) plus one Tier A absorption experiment, against two Tier A cohorts with normal mean or normal serum B12. Clinical magnitude is shown only by 3 anemic cases in [7].

Counter-evidence held on record

Framing caution This is a reduced-absorption effect seen in experiments and in some long-term users, not in everyone. Many users have normal B12. This page gives no supplement advice; a B12 check with a prescriber is the appropriate step if symptoms or macrocytic anemia appear.

Lactose absorption: functional malabsorption by breath test in a 23-patient FMF series, with high baseline prevalence in comparison groups

Orange — Moderate

See study details

Colchicine induces or aggravates lactose malabsorption in FMF patients; this is a functional digestive effect, not depletion of a vitamin or mineral.

Full detail and limits

Limits on what this shows

Key null findings: Malabsorption was already common without colchicine (65% untreated FMF, 42% non-FMF) [10]. No randomized or large controlled study was retrieved.
At-risk subgroups: FMF patients on long-term colchicine with abdominal symptoms; the intra-patient retest (7 of 12) supports a drug effect beyond baseline FMF status [10].
Counter-evidence on record: Small n, unrandomized, three non-matched comparison groups; confounding by FMF itself (65% baseline) is only partly excluded by the within-patient retest.

Direction

Functional malabsorption of a macronutrient (carbohydrate). Not a store depletion and not a micronutrient deficiency.

Regulatory status

Lactose is not mentioned in the label sections read; diarrhea is the most common adverse reaction [1].

Population evidence

Fradkin 1995 [10]: lactose breath testing in 23 FMF patients on colchicine (0.25 to 15 years, mean 3.16 years). Malabsorption in 87% of treated patients vs 65% of untreated FMF controls vs 42% of non-FMF controls. Of 12 patients retested at 3 months, 7 showed induction or aggravation of lactose malabsorption. A lactose-free diet produced partial symptom improvement. Abstract-level read; doses and test thresholds not visible.

Mechanism

Plausible, partly shown. Jejunal biopsies from patients on long-term colchicine showed normal histology but reduced (Na+ K+)-ATPase activity in 4 examined [9]; colchicine produced atrophic jejunal mucosal change in rats [26]. Lactase activity itself was not measured in any source opened.

Counter-evidence held on record

Framing caution A tolerance problem for milk sugar, not a vitamin or mineral deficiency. Diarrhea on colchicine has several causes and is dose-related per the label [1]; this entry should not be read as advice to change diet.

Folate: decline in one uncontrolled pediatric FMF cohort

Yellow — Low

See study details

Serum folate fell over 6 months of colchicine in newly diagnosed FMF children, but magnitude, deficiency prevalence and mechanism are not established.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. Yellow

Limits on what this shows

Key null findings: None measured directly. A Behcet cohort found CRP negatively correlated with folate and B12 [12], so inflammation, not the drug, could lower folate; it would predict a rise on treatment, which Kaba did not see.
Counter-evidence on record: No unexposed comparator in [8]; adult folate result in [7] not seen. A dedicated PubMed search for colchicine with folate or folic acid was rate-limited (429) and never completed, so this entry is partly tooling-limited. Why yellow and not orange: the one Tier A source did not show a deficit, only a mean decline, and was read at abstract level.

Direction

Depletion signal (circulating decline), unconfirmed.

Regulatory status

Not mentioned in label sections read [1].

Population evidence

Kaba 2026 [8]: 46 children, folate fell at 6 months (p=0.001), abstract-level; values and deficiency rates not visible. Gemici 2013 [7] measured folic acid in 95 colchicine-treated adults and 90 controls but the abstract reports only B12 results; the folate result was not seen.

Mechanism

Not shown for folate. Jejunal mucosal dysfunction [9][26] is a plausible route for a jejunally absorbed vitamin, but no colchicine folate-absorption study was retrieved.

Counter-evidence held on record

Framing caution A monitoring prompt at most, never a deficiency claim. Shares its source with the B12 entry (see Overlap map).

Fat absorption: mild steatorrhea in a small FMF series and gout case reports

Yellow — Low

See study details

Mild fat malabsorption occurred in some long-term colchicine users, with normal serum carotene and calcium; no fat-soluble vitamin deficiency was documented.

Full detail and limits

Limits on what this shows

Key null findings: Serum carotene and calcium normal in all 12 [9]. No fat-soluble vitamin status (A, D, E, K) was reported in any source opened.
Counter-evidence on record: Orange was considered and rejected: n=12 with no controls, mild values, and the one companion functional marker (carotene) normal. Steatorrhea is an outcome of absorption, not a vitamin deficiency (Hard Rule 2).

Direction

Malabsorption (functional); no retention effect.

Regulatory status

Not mentioned in label sections read; the label lists diarrhea [1].

Population evidence

Ehrenfeld 1982 [9]: 12 FMF patients on 1.0 to 2.0 mg/day for 3 or more years; 3 had mild steatorrhea (7.5, 7.9, 9.9 g/day), D-xylose absorption normal in 11 of 12, serum B12, calcium and carotene normal in all. Boucher 1973 [11]: a second case report of steatorrhoea after long-term colchicine for gout, with the authors discussing a possible link to jejunal reticulum cell sarcoma (causality not established). Race 1970 [5] exists but its findings were not seen.

Mechanism

Plausible: jejunal biopsy showed reduced (Na+ K+)-ATPase with normal histology [9]; rat jejunal atrophy with reduced absorption [26].

Counter-evidence held on record

Framing caution Mild and unconfirmed. Not evidence that fat-soluble vitamins are low.

Sodium and potassium: diarrheal disturbance, mechanistic and toxicity data only

Yellow — Low

See study details

Colchicine reduces intestinal water, sodium and potassium absorption in animals and diarrhea is common, but serum sodium and potassium were not shown to fall at therapeutic doses.

Full detail and limits

Limits on what this shows

Counter-evidence on record: No human therapeutic-dose electrolyte measurement either way. Poisoning data cannot be extrapolated to prophylactic dosing.

Direction

Disturbance through diarrheal loss, not dietary deficiency (Hard Rule 5). Raising salt or potassium intake is not the remedy implied.

Regulatory status

Diarrhea 23% at the gout flare treatment dose; GI effects up to 20% in FMF, usually mild, transient and reversible on dose reduction [1]. Electrolytes are not named in the sections read.

Population evidence

Goulston 1966 [26], rats at 80 micrograms per 100 g, day 3 perfusion: significant reductions in water, sodium and potassium absorption and in bidirectional sodium fluxes (reconstructed abstract; Tier B). Ehrenfeld 1982 [9]: reduced jejunal (Na+ K+)-ATPase activity in 4 patients. Sheibani 2022 [27]: 34 colchicine poisoning cases, hypokalemia among factors associated with mortality; this is overdose toxicity, not therapeutic use. No study measuring serum sodium or potassium in therapeutic users was found (PubMed queries returned none).

Mechanism

Present (mucosal transport impairment, [9][26]).

Counter-evidence held on record

Framing caution Excess-loss and disturbance framing only. Persistent diarrhea on colchicine is a reason to contact the prescriber, not to add supplements.

No ungraded entries

Not graded — disclosed evidence gap

See study details

Every classical nutrient and all seven physiological categories reached at least a Tier B source and so are graded; none met the dual ungraded condition.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. None

Limits on what this shows

Why no grade: Not applicable. The two lowest-evidence entries, Copper (one rat study, [28]) and ATP production (conflicting cell studies, [24][25]), each have a Tier B source, so the dual condition in Step 7 (no Tier B or C evidence and no circulating claim) was not met and yellow was required.

Channels tried

PubMed search-listing pages (fetch tool): colchicine with B12, cobalamin, FMF B12, folate (blocked by rate limit, not repeated), microbiota, mitochondria, ATP, oxidative stress, malabsorption, myopathy, bone marrow, iron, copper, ceruloplasmin, trace elements (zero results), electrolytes, hypokalemia, hemolysis, methemoglobin (zero results), erythrocytes. OpenAlex single-record lookups for abstracts. DailyMed label via fetch tool. WHO ATC index and Wikipedia. Blocked or unavailable: WebSearch (budget exhausted), OpenAlex and Crossref search endpoints (429), Springer and MDPI search pages (robots disallowed), PubMed record pages (bot verification or empty on some attempts).

Tooling note

A genuine gap versus tooling-limited split cannot be fully made for human folate, fat-soluble vitamin, zinc and hemolysis data: those searches ran once with narrow phrasings under heavy rate limiting. Re-check when access is restored.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden: cell and animal studies at colchicine concentrations not compared with clinical exposure

Yellow — Low

See study details

Colchicine impaired mitochondrial function in mouse muscle and depolarized mitochondria in cultured cells; no human mitochondrial measurement exists in the sources retrieved.

Full detail and limits

Limits on what this shows

Key null findings: PubMed title search for colchicine and mitochondrial returned 6 records, none human clinical; no human muscle or blood mitochondrial measurement in colchicine users was found. Concentration check: the label's peak plasma level after one 0.6 mg dose is 2.5 ng/mL [1], roughly 6 nanomolar by simple arithmetic (molecular weight of about 399 g/mol assumed, not retrieved), so 0.1 micromolar is about 16 times higher; cancer cell concentrations in [23] were not seen.
Counter-evidence on record: Chen's liver cells and Singh's cancer cells are cytotoxicity models; Buch's design was acute and used colchicine as a tool, not as a therapeutic model.

Direction

Burden (adverse effect on mitochondria) in vitro and in vivo animal; human relevance unknown.

Regulatory status

Not mentioned; the label describes cytoskeletal disruption and notes aneuploidy and micronucleus formation [1].

Population evidence

Buch 2020 [21], mice: colchicine injected on two consecutive days as an autophagy inhibitor impaired muscle mitochondrial function including reduced ADP sensitivity in young and aged mice, and reduced insulin sensitivity in aged mice. Chen 2012 [22], human L-02 liver cells: dose-dependent loss of viability, early cell death at 0.1 micromolar, with loss of mitochondrial membrane potential and caspase-9 activation. Singh 2026 [23], MCF7 and MDA-MB-231 breast cancer cells: depolarized mitochondrial membrane potential, reduced oxygen consumption and complex I-driven respiration.

Mechanism

Present in vitro and animal; plausibly downstream of microtubule and autophagy disruption, not shown to be a direct electron transport effect.

Counter-evidence held on record

Framing caution Experimental toxicology, not a finding in patients. Shares sources with the ATP entry.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress: reverse direction, lower markers in treated FMF remission, confounded by disease activity

Yellow — Low

See study details

The sources retrieved show colchicine associated with lower, not higher, oxidative stress markers; no antioxidant depletion by colchicine was found.

Full detail and limits

Limits on what this shows

Counter-evidence on record: All comparisons are confounded by disease activity (attack vs remission). Singh 2026 [23] reported reduced ROS production in cancer cells, again consistent with lower, not higher, ROS. No study reported glutathione or antioxidant enzyme depletion attributable to colchicine.

Direction

Reverse (protective or neutral association).

Regulatory status

Not mentioned [1].

Population evidence

Sahin 2011 [14]: 24 subjects (18 FMF in four groups, 6 controls); remission patients on colchicine 1.5 mg/day had reduced PMN lipid peroxidation and lower intracellular calcium than attack groups, with colchicine associated with modulated vitamin E, beta-carotene and calcium release. Gulbahar 2007 [15], Behcet disease: baseline protein carbonyl and MDA were elevated vs controls and no longer different at study end in the colchicine and vitamin E treatment groups (sample size not stated in the abstract; colchicine effect not separable from vitamin E). Bettiol 2021 [16], 160 subjects: in vitro colchicine pretreatment reduced oxidation-induced neutrophil extracellular trap production and apoptosis.

Mechanism

Anti-inflammatory and neutrophil-directed effects reduce ROS-linked injury; not an antioxidant chemistry claim.

Counter-evidence held on record

Framing caution Not a depletion claim and not a reason to take antioxidant supplements. Supplementation would not be the remedy here.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Copper: one acute rat study of serum ceruloplasmin, copper itself not measured

Yellow — Low

See study details

Colchicine lowered serum ceruloplasmin acutely in rats; this is a protein-level effect, not evidence of copper depletion.

Full detail and limits

Limits on what this shows

Key null findings: PubMed title search "colchicine AND copper" returned 10 records (analytical chemistry and tubulin-complex papers, none on copper status); "colchicine ceruloplasmin" returned 3 (one rat study above; one primary sclerosing cholangitis trial with no ceruloplasmin result; one hepatocyte paper not opened). No human copper measurement found.
Counter-evidence on record: The dose is a toxic dose associated with deaths, and serum protein concentration is not body copper.

Direction

Unclear (acute fall in a copper-binding protein); no copper retention or loss was measured.

Regulatory status

Not mentioned [1].

Population evidence

Pribyl 1976 [28], rats: colchicine at 0.3 mg/100 g body weight (as the demecolcine dose; colchicine "equivalent") lowered serum ceruloplasmin within 2 to 3 hours in both sexes; females began recovering at 8 hours, males did not, and male mortality was higher (reconstructed abstract; Tier B).

Mechanism

Not described in the abstract. An effect on secretion of a hepatic protein through microtubule disruption is an inference, not stated in the source.

Counter-evidence held on record

Framing caution No evidence of copper deficiency or excess in patients; not a basis for any copper-related advice.

Iron: anemia in FMF is indication-linked and improves on colchicine

Yellow — Low

See study details

Low iron indices in untreated FMF reflect inflammation; the retrieved cohorts show iron and hemoglobin rising, not falling, after colchicine starts.

Full detail and limits

Limits on what this shows

Counter-evidence on record: PubMed queries for colchicine with iron deficiency and hemoglobin in FMF returned only these two studies; no iron-absorption study with colchicine was found.

Direction

Neutral to reverse; confounding by indication (Hard Rule 6). No iron-depleting effect of colchicine was found.

Regulatory status

Iron not mentioned. The label's blood dyscrasia warning is handled under Oxygen delivery, as drug toxicity [1].

Population evidence

Celkan 2005 [13], 172 children: anemia in 53% of newly diagnosed FMF, 31% of colchicine-treated patients and 5% of controls; anemic patients had low transferrin saturation with high ferritin, iron indices tracked inflammatory markers, and anemia resolved with disease control (reconstructed abstract). Kaba 2026 [8], 46 children: at 6 months of colchicine hemoglobin rose (p=0.027), iron rose (p<0.001) and ferritin fell (p=0.002).

Mechanism

Absent for iron depletion in the sources retrieved. The pattern (low saturation, high ferritin) is an anemia of inflammation, which regresses as inflammation is controlled.

Counter-evidence held on record

Framing caution Do not infer iron deficiency or an iron supplement need from colchicine use. Ferritin in FMF is an inflammatory marker as well as a store marker.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk: mixed human data, dose-dependent dysbiosis in mice

Yellow — Low

See study details

Colchicine perturbs the gut microbiota in mice at 2.5 mg/kg/day; a small human randomized-trial analysis found no diversity change, and an FMF cohort associated colchicine with anti-inflammatory taxa.

Full detail and limits

Limits on what this shows

Key null findings: Kisimba is a direct null in humans on a therapeutic dose, though underpowered and in a non-FMF, non-gout population [17]. Colchicine-associated taxa in [18] are anti-inflammatory, not dysbiotic.
Counter-evidence on record: Mouse doses (0.1 to 2.5 mg/kg/day) are far above human prophylactic exposure and the dose-response was incremental. Delplanque is cross-sectional with FMF disease effects entangled. One further FMF metabolome paper [Ktsoyan 2013, PMID 23373011] had no abstract text and was not used.

Direction

Mixed; composition change possible, adverse direction unproven in humans.

Regulatory status

Not mentioned [1].

Population evidence

Kisimba 2023 [17], secondary analysis of a double-blind randomized trial: colchicine 0.6 mg twice daily or placebo for 3 months in adults with obesity and metabolic syndrome; stool pairs from 15 colchicine and 12 placebo subjects; inflammatory markers fell but Chao1, Shannon and Pielou alpha diversity and ASV counts did not change; only Oscillibacter nominally changed. Delplanque 2024 [18]: 119 FMF patients vs 61 controls, 16S sequencing; models adjusted for colchicine intake and resistance; colchicine treatment was associated with expansion of Faecalibacterium and Roseburia; FMF patients had more Enterobacter, Klebsiella and Ruminococcus gnavus group. Shi 2020 [19] and 2021 [20], mice at 0.1, 0.5 and 2.5 mg/kg/day for 7 days: profound intestinal microbiota remodeling and increased permeability at 2.5 mg/kg/day, and gastric microbiota diversity reduced with gastric mucosal injury.

Mechanism

Mucosal injury and permeability change in mice [19][20]; not shown to drive nutrient synthesis loss in humans.

Counter-evidence held on record

Framing caution A research signal, not a clinical finding of dysbiosis. No probiotic or dietary action is supported by these data.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

ATP production: conflicting cell results, respiration reduced, no human data

Yellow — Low

See study details

One cell study reported lower ATP pools and others reduced oxygen consumption, while a frog nerve study found ATP unchanged; none is a human or therapeutic-dose measurement.

Full detail and limits

Limits on what this shows

Key null findings: Edström 1979 [25] is a direct null for ATP. No human ATP or phosphocreatine measurement in colchicine users was found (a PubMed search for colchicine in the title with ATP returned 115 records; on inspection of titles none was a human energy-metabolism study, and the listing summarizer flagged only cell-level ones).
Counter-evidence on record: Surrogate respiration data are not ATP output; cell systems differ (fibroblast line, nerve, cancer lines).

Direction

Mixed; possible reduction in cellular energy output in vitro.

Regulatory status

Not mentioned [1].

Population evidence

Chou 1984 [24], 3T3 cells: colchicine or vinblastine expanded UTP pools while reducing ATP pools (reconstructed abstract). Edström 1979 [25], isolated frog sciatic nerve: colchicine did not reduce ATP and creatine phosphate, so energy loss did not explain transport inhibition (reconstructed abstract). Singh 2026 [23]: reduced oxygen consumption and oxidative phosphorylation in cancer cells. Buch 2020 [21]: reduced ADP sensitivity in mouse muscle mitochondria.

Mechanism

Not established; contradictory between systems.

Counter-evidence held on record

Framing caution Not a finding of low energy in patients. Fatigue or weakness on colchicine should be assessed clinically for toxicity (see monitoring), not attributed to ATP loss.

Oxygen delivery/utilization: label-listed myelosuppression is drug toxicity, not a nutrient deficiency; FMF hemoglobin improves

Yellow — Low

See study details

Colchicine carries labeled hematologic toxicity, which must not be filed as iron or B12 deficiency; in FMF children hemoglobin rose on treatment.

Full detail and limits

Limits on what this shows

Counter-evidence on record: Anemia in untreated FMF is more common than on treatment [13]. Overdose reports of pancytopenia (Folpini 1995, Brvar 2004) appeared in listings only and were not opened.

Direction

Neutral for nutrient status. Drug toxicity (myelosuppression) is a separate adverse-effect category.

Regulatory status

Warnings: "Myelosuppression, leukopenia, granulocytopenia, thrombocytopenia, pancytopenia, and aplastic anemia have been reported with colchicine used in therapeutic doses" [1]. Frequency not captured in the sections read.

Population evidence

Kaba 2026 [8]: hemoglobin rose at 6 months (p=0.027). Celkan 2005 [13]: anemia prevalence 53% before vs 31% on colchicine in FMF. Isikay 2013 [31], 88 children, mean 28 months: 11% had side effects including leukopenia, with no raised neuromyopathy risk. Hemolysis and red cell effect searches ("colchicine hemolysis methemoglobin", "colchicine erythrocytes hemolysis") returned no clinical records.

Mechanism

Antimitotic activity on marrow precursors is the drug's pharmacology [1], not a nutrient pathway. Iron, B12 and folate pathways are in their own entries.

Counter-evidence held on record

Framing caution New anemia or low blood counts on colchicine need clinical evaluation as possible drug toxicity; they are not to be self-treated with nutrient supplements. Kept separate from ATP production (Hard Rule 7).

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

Carotene (vitamin A precursor) depletion or malabsorption
Where it comes from: Named in the commissioning brief as a malabsorption angle; the drug-induced malabsorption reviews (Kendall 1973, Longstreth 1975) appeared in PubMed listings, titles only, not opened. Origin not traced to a consumer page.
Why it fails: This drug's own Tier A data contradict it: serum carotene was normal in all 12 long-term FMF users on 1 to 2 mg/day [9], and beta-carotene was modulated upward, not down, in colchicine-treated FMF remission patients [14]. Mild steatorrhea in 3 of 12 [9] keeps a fat absorption entry yellow but does not support carotene loss. Race 1970 [5] was not read.
Myopathy or neuropathy as a nutrient deficiency
Where it comes from: Named in the commissioning brief; mis-filing of a clinical outcome (Hard Rule 2).
Why it fails: Colchicine neuromyopathy is a drug toxicity. In 143 reviewed cases mean dose was 1.25 mg/day, 48% occurred after more than 12 months, 82% had a significant comorbidity or a possible drug interaction, 70% resolved completely in a median 21 days after stopping, and 73% did not recur on reduced-dose rechallenge [30]. The original 12-case series linked it to raised plasma levels from altered renal function [29]. No nutrient was measured in these series; 88 FMF children had no raised risk [31]. This is an outcome entry and no nutrient link is supported.
Anemia or bone marrow toxicity as iron, B12 or folate deficiency
Where it comes from: Named in the commissioning brief; mis-filing of a clinical outcome or the drug's pharmacology (Hard Rule 2).
Why it fails: The label lists myelosuppression, pancytopenia and aplastic anemia as drug effects [1]. In FMF children anemia was more common before colchicine and iron indices and hemoglobin rose on treatment [8][13]; iron saturation was low with high ferritin, an inflammatory pattern [13]. B12 anemia occurred in 3 of 95 long-term users [7], handled in the B12 entry, not as a general anemia claim.

How the body handles this medication

Absorption and distribution: Absolute bioavailability about 45%. A single 0.6 mg fasting dose peaks at 2.5 ng/mL in 1 to 2 hours. Food lowers extent by about 15%, judged clinically insignificant. Volume of distribution 5 to 8 L/kg; protein binding 39%. A named absorption transporter is not given in the label sections read, but the label warns of life-threatening interactions with P-glycoprotein inhibitors.[1] DailyMed Colcrys label sec 12.3, 7
Metabolism and enzymes: Demethylated to 2-O-, 3-O- and 10-O-demethylcolchicine; CYP3A4 is the primary enzyme. Strong CYP3A4 and P-gp inhibitors raise exposure (clarithromycin, ketoconazole, cyclosporine named). No CYP induction or inhibition by colchicine itself was reported in the sections read.[1] sec 12.3, 7
Elimination: In healthy volunteers 40 to 65% of a 1 mg oral dose was recovered unchanged in urine. Half-life 26.6 to 31.2 hours at steady state. Not removed by hemodialysis. (A Wikipedia summary lists 65% fecal and 10 to 20% renal [3]; the label figure is used here and the discrepancy is not resolved.)[1][3]
Renal and hepatic impairment: End-stage renal disease: clearance 75% lower (0.17 vs 0.73 L/hr/kg) and half-life 18.8 vs 4.4 hours. Clearance is significantly reduced in chronic liver disease. Colchicine is contraindicated with P-gp or strong CYP3A4 inhibitors in renal or hepatic impairment.[1] sec 12.3, 4
Mechanism of action and GI tolerability: Disrupts cytoskeletal function by inhibiting beta-tubulin polymerization into microtubules and may interfere with inflammasome assembly. Diarrhea is the most common adverse reaction: 23% at the gout flare treatment dose, and cramping, nausea, diarrhea, abdominal pain or vomiting in up to 20% of FMF patients.[1] sec 12.1, 6
Renal tubular and food or mineral effects: No effect on renal tubular handling of water or electrolytes and no food, antacid or mineral interaction with nutrient consequence was reported in the label sections read. Label dosing: gout prophylaxis 0.6 mg once or twice daily (maximum 1.2 mg/day); FMF 0.3 to 2.4 mg/day by age. Aneuploidy and micronucleus findings are noted in label section 13.1.[1] sec 2, 13.1

What the research says is worth watching

General information from the medication label and the studies above. It is not personal medical advice, and any change belongs with your prescriber.

Lab / long-term use
Vitamin B12 status
Worth considering a serum B12, with methylmalonic acid if borderline, in people on colchicine for 2 or more years, especially at FMF-range doses, and promptly if macrocytic anemia, numbness or fatigue appears [4][7][8]. This is a monitoring prompt, not a finding that every user is deficient. No supplement dose is given here.
Lab / label
Complete blood count
The label lists myelosuppression and aplastic anemia [1]. A falling white cell, platelet or hemoglobin result should be read as possible drug toxicity first, with B12 and folate as a secondary check.
Symptoms / lab
Neuromuscular toxicity
Proximal weakness, myalgia or numbness with raised creatine kinase warrants prescriber review, particularly with renal impairment or a P-gp or strong CYP3A4 inhibitor, or a statin or fibrate [1][29][30]. Most cases resolved after stopping [30].
Symptoms / dose
Diarrhea and electrolytes
Diarrhea is the most common adverse reaction and usually settles on dose reduction [1]. If it is persistent or severe, a prescriber may check serum sodium and potassium; the evidence for electrolyte change at therapeutic doses is absent [26][27].
At-risk groups
Renal, hepatic, children, pregnancy
Renal and hepatic impairment lower clearance (ESRD 75% lower) and raise toxicity risk [1]. Children with FMF showed B12 and folate declines in one cohort [8]. Colchicine crosses the placenta and enters breast milk [1]; no nutrient-specific pregnancy data were retrieved.
Supplement separation
Timing intervals
No supplement separation interval is required by the label sections read [1]. Food lowers absorption extent by about 15%, which the label judges insignificant [1].

Overlap map, to prevent double counting

Entries that rest on the same underlying source or mechanism. Do not count these as independent confirmation.

Vitamin B12
Shares evidence with: Folate; Iron; Oxygen delivery/utilization
Note: Kaba 2026 [8] supplies the measured B12 decline, the folate decline, and the iron and hemoglobin rise in one cohort of 46. Gemici 2013 [7] measured B12 and folic acid together.
Vitamin B12; Lactose absorption; Fat absorption; Sodium and potassium
Shares evidence with: Each other
Note: One underlying mechanism: small-intestinal mucosal dysfunction from colchicine (ileal for B12 [4][6], jejunal for the rest [9][26]). Ehrenfeld 1982 [9] is the shared source for the biopsy and the fat and normal B12 and carotene results. Together they are one pathway, not four independent confirmations.
Mitochondrial burden
Shares evidence with: ATP production; Oxidative stress
Note: Singh 2026 [23] (respiration, membrane potential and ROS) and Buch 2020 [21] (mitochondrial function and ADP sensitivity) support both the mitochondrial and ATP entries. The ATP entry also uses Chou [24] and Edström [25].
Iron
Shares evidence with: Oxygen delivery/utilization
Note: Celkan 2005 [13] and Kaba 2026 [8] underlie both; the oxygen entry adds the label myelosuppression warning [1] as drug toxicity.
Oxidative stress
Shares evidence with: Carotene (Fails verification)
Note: Sahin 2011 [14] gives both the lower lipid peroxidation and the beta-carotene finding used to rebut the carotene claim.
Gut microbiome risk
Shares evidence with: Sodium and potassium (mechanism only)
Note: Mouse intestinal injury and permeability [19][20] and rat jejunal absorption data [26] describe the same mucosal toxicity at different levels (microbiota vs transport).

All references used above

Colchicine

Findings for this medication

What the research found

Vitamin B12: reversible ileal malabsorption in human experiments; serum deficiency inconsistent and limited to subgroups of long-term FMF users

Lactose absorption: functional malabsorption by breath test in a 23-patient FMF series, with high baseline prevalence in comparison groups

Folate: decline in one uncontrolled pediatric FMF cohort

Fat absorption: mild steatorrhea in a small FMF series and gout case reports

Sodium and potassium: diarrheal disturbance, mechanistic and toxicity data only

No ungraded entries

The five body-system areas

⚡Mitochondrial Burden

Mitochondrial burden: cell and animal studies at colchicine concentrations not compared with clinical exposure

💥Oxidative Stress

Oxidative stress: reverse direction, lower markers in treated FMF remission, confounded by disease activity

⚖️Copper and Iron Balance

Copper: one acute rat study of serum ceruloplasmin, copper itself not measured

Iron: anemia in FMF is indication-linked and improves on colchicine

🌿Gut Microbiome Risk

Gut microbiome risk: mixed human data, dose-dependent dysbiosis in mice

💨Oxygen and ATP Output

ATP production: conflicting cell results, respiration reduced, no human data

Oxygen delivery/utilization: label-listed myelosuppression is drug toxicity, not a nutrient deficiency; FMF hemoglobin improves

Claims checked and not supported

Carotene (vitamin A precursor) depletion or malabsorption

Myopathy or neuropathy as a nutrient deficiency

Anemia or bone marrow toxicity as iron, B12 or folate deficiency

How the body handles this medication

What the research says is worth watching

Overlap map, to prevent double counting

Mitochondrial Burden

Oxidative Stress

Copper and Iron Balance

Gut Microbiome Risk

Oxygen and ATP Output