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MyDeficiencies

Methocarbamol

centrally acting skeletal muscle relaxant (carbamic acid ester)

Also sold as Robaxin.

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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.

Methocarbamol has no recognized classical depletion machinery. It is metabolized by dealkylation and hydroxylation with likely conjugation, essentially all metabolites leave in the urine, the half-life is 1 to 2 hours, and the label sections retrieved name no CYP enzyme, describe no enzyme induction or inhibition, and mention no vitamin, mineral or food interaction [1][2][3]. The only interaction page opened lists alcohol and nothing else [17]. Of the nine mechanism classes screened (absorption interference, enzyme-induced catabolism, renal wasting, cofactor antagonism, mitochondrial or conjugation loss, hormonal or dilutional change, microbiome disruption, changed intake, increased demand), none is documented for this drug.

centrally acting skeletal muscle relaxant (carbamic acid ester) · ATC M03BA03 (WHO ATC/DDD Index [4]) · also sold as Robaxin (tablet and injection); many generics; combination products · 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 Methocarbamol 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

Dietary intake: labeled rare appetite loss and nausea, no nutrient or intake measured (context flag)

Yellow — Low

See study details

Regulatory labeling lists loss of appetite (very rare) and nausea among adverse reactions, so a changed-intake mechanism (class H) is documented as present, but no study measured food or nutrient intake in methocarbamol users and no nutrient is implicated.

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: No intake, weight, BMI or nutrient measurement in methocarbamol users was found. The labeled frequency of appetite loss is very rare. LiverTox lists methocarbamol as an unlikely cause of clinically apparent liver injury (likelihood score E) and describes no nutritional effect [22].
  • At-risk subgroups: None identified in retrieved data. The leaflet notes additive effects with CNS depressants and alcohol [19].

Direction

Context flag, neutral. An adverse reaction is not a nutrient deficiency (Hard Rule 2). No nutrient is named and nothing here implies that intake should increase.

Regulatory status

UK patient leaflet for methocarbamol 750 mg tablets (opened, medicines.org.uk): "loss of appetite", "feeling sick" and "vomiting" listed as very rare; "nausea", "diarrhoea" and "fatigue" listed at unknown frequency; "metallic taste" listed as rare; the leaflet also warns that appetite suppressants may have their effect increased [19]. The US tablet labels (read as summaries) list drowsiness, dizziness and nausea [1][3]; anorexia was not seen in the US label summaries.

Population evidence

None on intake. A PubMed listing of 24 methocarbamol records (clinical, pharmacology and analytical papers) showed no record on appetite, weight, food intake or nutrition [23]. The earlier listing (appetite, nutrition, malnutrition, weight loss, food intake) returned 6 records, none measuring intake. Tier D pages repeat the label statement ("Anorexia has been reported after oral administration" on a drug-monograph aggregator; "anorexia" in a drugs.com professional section) [20][21] and are not used to support the grade.

Mechanism

Not stated for the appetite effect in any source opened. Sedation and nausea are plausible routes to reduced eating (mechanism class H); the drug's central action is described as unknown in LiverTox [22].

Counter-evidence held on record

Counter-evidence and limits Graded yellow only as a context flag: the evidence is a labeled adverse reaction (regulatory label, for the reaction itself), not a study of intake or of any nutrient. Confounding by indication (acute pain, injury, immobility, concurrent opioids or other drugs) is not excluded and no comparison with non-users exists. Framing caution Do not present methocarbamol as causing malnutrition or any specific deficiency. A rare labeled appetite or nausea effect is a drug adverse reaction, not a nutrient finding, and no supplement is implied.

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

Not graded — disclosed evidence gap

See study details

No methocarbamol-specific or defensible class-level evidence on mitochondrial structure, electron transport or biogenesis was retrieved.

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. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C source was found to support even a yellow grade, and no circulating consumer claim of methocarbamol mitochondrial damage was found to rebut. This is a disclosed gap, not a finding of safety. Re-check when access is restored.

What was searched

PubMed listings: methocarbamol AND (oxidative stress OR mitochondria): 2 records, a naproxen methemoglobinemia case report [16] and an HPLC method paper, neither mitochondrial. methocarbamol AND (ATP OR respiration OR membrane potential OR phosphorylation OR mitochondrial): 6 records, none on mitochondria (horse pharmacokinetics, cirrhotic cramps review, a synthetic chemistry paper and others). The label sections retrieved contain no mitochondrial content [1][2][3].

Channel outcomes

First pass: PubMed HTML search listings (format=pubmed) opened intermittently; some requests were refused with HTTP 429 and were not retried on the same page. OpenAlex single-record lookups and DailyMed label pages opened. OpenAlex and Crossref search endpoints returned 429. Web search budget was exhausted in that pass. Europe PMC and Semantic Scholar were not attempted through WebFetch because they are on the blocked-host list. Repair pass 2026-10-07: web search worked. Queries "methocarbamol mitochondria OR mitochondrial toxicity OR ATP", "methocarbamol mitochondrial respiration OR oxygen consumption OR membrane potential in vitro" and "Tox21 mitochondrial membrane potential methocarbamol" returned only generic mitochondrial-toxicity reviews and Tox21 screening papers; none named methocarbamol in the result text seen, and the Tox21 papers (per-compound hit lists live in the screening data) were not opened, so a Tox21 hit or miss for methocarbamol is unknown. A PubMed listing of 24 methocarbamol records [23] and the LiverTox monograph [22] contain no mitochondrial content. A repeat PubMed listing restricted to mitochondrial and ATP terms was refused with HTTP 429 and was not retried.

Gap type

Genuine gap on every channel that opened (PubMed listings, web search, LiverTox, label sources). Residual tooling limit: Europe PMC and Semantic Scholar were not used, one repeat PubMed listing returned 429, and Tox21 per-compound data were not accessible.

Oxidative Stress

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

Oxidative stress: reverse direction, in vitro inhibition of hemoglobin pseudoperoxidase activity only

Yellow — Low

See study details

In a cell-free system methocarbamol inhibited the peroxidase-like activity of free human hemoglobin; no study measured systemic redox or antioxidant markers in methocarbamol users.

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: No study of malondialdehyde, glutathione, superoxide dismutase, total antioxidant capacity or reactive oxygen species in methocarbamol-treated humans or animals was found in a PubMed listing for methocarbamol with antioxidant, oxidative, peroxidase or glutathione terms. The abstract does not state the concentrations reached in patients, and the Ki and IC50 are in the millimolar range, so extrapolation to the body is unproven.
  • At-risk subgroups: None identified.

Direction

Reverse (protective-looking in vitro). Not a depletion and not an oxidative-stress burden.

Regulatory status

No oxidative or antioxidant content in the label sections retrieved [1][2][3].

Population evidence

None in humans. Minai-Tehrani et al. (Int J Biol Macromol 2017; online 2016) tested methocarbamol on human red-cell hemoglobin pseudoperoxidase activity: uncompetitive inhibition, both Km and Vmax decreased with drug concentration, Ki 6 mM, IC50 10 mM. Docking placed the carbamate NH2 hydrogen-bonded to Asp126 and the hydroxyl to Ser102 and Ser133, not at the heme group. Abstract read from PubMed listing; full text not opened [9].

Mechanism

Named, in vitro: binding at a non-heme site that inhibits free-hemoglobin peroxidase activity. The paper frames free hemoglobin after hemolysis as a toxic species [9].

Counter-evidence held on record

Counter-evidence and limits Tier B (mechanistic in vitro study using this drug) only. Not a measure of oxidative stress in a person or tissue, and not evidence that methocarbamol lowers or raises oxidative damage in vivo. Related to the hemolysis entry only through hemoglobin biology (see Overlap map). Framing caution Do not present methocarbamol as an antioxidant or as causing oxidative stress. This is a test-tube enzyme-inhibition finding with no clinical support.

Copper and Iron Balance

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

Copper

Not graded — disclosed evidence gap

See study details

No evidence was retrieved that methocarbamol alters copper status, absorption, excretion or ceruloplasmin.

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. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence for copper status, and no circulating copper claim found. The copper(II) complexation paper is disclosed here so a reader cannot mistake it for a hidden signal. Not a finding of safety.

What was searched

PubMed listings: methocarbamol AND (iron OR ferritin OR copper OR ceruloplasmin): 2 records. One is a 2014 Spectrochimica Acta paper on trapping a methocarbamol degradation product by complexation with copper(II), with spectroscopic and quantum chemical methods; only title and bibliographic data were seen and no abstract was available [15]. It is an analytical chemistry study of a degradation product in solution, not a study of the drug in a biological system, so it was not accepted as Tier B mechanistic evidence for copper status. The other record was a parenteral irritation cell-line paper. methocarbamol AND (vitamin OR deficiency OR copper OR iron OR zinc OR magnesium OR folate): 10 records, none measuring a nutrient in methocarbamol users (veterinary tetanus, analytical chemistry, a cirrhotic cramps review, IV magnesium plus methocarbamol for trigeminal neuralgia as a combination treatment).

Channel outcomes

First pass: PubMed HTML search listings (format=pubmed) opened intermittently; some requests were refused with HTTP 429 and were not retried on the same page. OpenAlex single-record lookups and DailyMed label pages opened. OpenAlex and Crossref search endpoints returned 429. Web search budget was exhausted in that pass. Europe PMC and Semantic Scholar were not attempted through WebFetch because they are on the blocked-host list. Repair pass 2026-10-07: web search for methocarbamol with iron, ferritin, copper, nutrient depletion and depletes phrasings returned only generic copper and iron physiology pages, none about methocarbamol. Depletion-handbook style pages opened [26][27] and the drugs.com vitamin D3 interaction page [28] contain no methocarbamol copper claim.

Gap type

Genuine gap on the PubMed channel, partly tooling-limited for other databases. Kept independent of Iron.

Iron

Not graded — disclosed evidence gap

See study details

No evidence was retrieved that methocarbamol alters iron absorption, stores, ferritin or iron-deficiency anemia.

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. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence on iron and no circulating iron claim found. Not a finding of safety.

What was searched

Same iron-and-copper PubMed listing as above (no iron record) and the vitamin and mineral listing (no iron record). The hemolysis listing (methocarbamol AND hemolysis OR methemoglobin OR anemia OR hemoglobin) returned the 1977, 1957 and 1971 hemolysis studies and the pseudoperoxidase paper but no iron indices [6][7][8][9]. The label sections retrieved list no iron interaction [1][3]. The drugs.com food-interaction page lists no mineral interaction [17].

Channel outcomes

First pass: PubMed HTML search listings (format=pubmed) opened intermittently; some requests were refused with HTTP 429 and were not retried on the same page. OpenAlex single-record lookups and DailyMed label pages opened. OpenAlex and Crossref search endpoints returned 429. Web search budget was exhausted in that pass. Europe PMC and Semantic Scholar were not attempted through WebFetch because they are on the blocked-host list. Repair pass 2026-10-07: web searches pairing methocarbamol with serum iron, hemoglobin, hematocrit, drug-induced hemolytic anemia and methemoglobinemia returned generic iron and drug-induced methemoglobinemia pages (not opened; none named methocarbamol in the result text seen) plus the 1977 hemolysis record already cited [6]. Methocarbamol appears nowhere in the LiverTox monograph in connection with iron or hemolysis [22].

Gap type

Genuine gap on the PubMed channel; tooling-limited for other databases. Any hemolysis-related iron turnover is not measured and is not double-counted (see Overlap map). Anemia would be an outcome, not iron deficiency (Hard Rule 2).

Gut Microbiome Risk

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

Gut microbiome risk

Not graded — disclosed evidence gap

See study details

No evidence was retrieved on methocarbamol and gut microbiome composition, diversity or function.

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. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence, and no circulating microbiome claim for methocarbamol found. Metabolism is hepatic and elimination urinary, so no gut-exposure mechanism is documented, but that is not evidence of absence.

What was searched

PubMed listings: methocarbamol AND (microbiome OR microbiota OR dysbiosis) and methocarbamol AND (microbiome OR microbiota) both returned HTTP 404 pages, which PubMed uses for searches with no match; interpreted as zero results but not independently confirmed. methocarbamol AND (feces OR fecal OR gut OR intestinal OR bacteria OR bacterial): 10 records, none on the microbiome; the gut-adjacent items were two case reports of paralytic ileus (1963 and 1964), listed by title only and not opened. They concern motility, not microbial composition, and are not used as evidence.

Channel outcomes

First pass: PubMed HTML search listings (format=pubmed) opened intermittently; some requests were refused with HTTP 429 and were not retried on the same page. OpenAlex single-record lookups and DailyMed label pages opened. OpenAlex and Crossref search endpoints returned 429. Web search budget was exhausted in that pass. Europe PMC and Semantic Scholar were not attempted through WebFetch because they are on the blocked-host list. Repair pass 2026-10-07: web search worked. Class-level and drug-specific phrasings (methocarbamol with gut microbiome or microbiota; skeletal muscle relaxant use with microbiome composition and 16S) returned no methocarbamol study. Two large drug-microbiome resources were opened through the fetch tool and neither mentions methocarbamol or muscle relaxants: Maier et al. 2018 Nature (main article text as rendered; supplementary drug tables were not accessible) [24] and the Vich Vila et al. 2020 population-cohort paper of 41 drug categories [25]. Zimmermann et al. 2019 (drug metabolism by gut bacteria) appeared in search results but was not opened.

Gap type

Genuine gap on the channels that opened, including class-level searches (muscle relaxants and microbiome) run in the repair pass and two broad drug-microbiome resources that do not list this drug. Residual limit: the PubMed 404 reading is not independently confirmed and supplementary drug tables of the microbiome screens were not accessible.

Oxygen and ATP Output

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

Oxygen delivery/utilization: IV route only, transient hemolysis marker signal, mostly vehicle-driven

Yellow — Low

See study details

After intravenous methocarbamol (100 mg/mL in 50% PEG 300), plasma hemoglobin and haptoglobin moved in the direction of mild hemolysis, but within physiologic range, and hemoglobin, hematocrit and tissue oxygen delivery were not reported as changed.

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: The vehicle alone produced the higher peak plasma hemoglobin, so the excipient, not methocarbamol, is the larger contributor in the 1977 model [6]. No retrieved study reported hemoglobin, hematocrit, red-cell mass or arterial oxygenation after methocarbamol by any route. A 2025 to 2026 ICU series of 68 IV users reported creatinine only [11].
  • At-risk subgroups: Plausibly higher-exposure users of the IV form (large volume, repeated days, rapid rate), and people with pre-existing hemolytic disease or renal impairment, where the label already contraindicates the injection for renal pathology [2]. Oral users have no retrieved hemolysis data.

Direction

Context flag, neutral for oxygen delivery. A transient excess of free plasma hemoglobin with haptoglobin consumption on the IV route. Not a depletion and not an oxygen-delivery deficit. Anemia would be an outcome, not a nutrient (Hard Rule 2).

Regulatory status

The injection label retrieved states the vehicle (PEG 300, 0.5 mL per mL), hypertonicity, rate and duration limits, and a renal contraindication [2]. Hemolysis is not mentioned in the label sections retrieved for either form [1][2][3]. The tablet label lists leukopenia under hemic and lymphatic reactions [3]; this is a white-cell event, not an oxygen-carrying measure.

Population evidence

Scott, Tisdale and Cummings 1977 (Clin Pharmacol Ther), human volunteers, methocarbamol and its vehicle (50% PEG 300) versus vehicle alone and saline, high-dose and low-dose regimens. Plasma hemoglobin rose significantly at 30 minutes after methocarbamol or vehicle: maximum about 10 mg/dL with vehicle alone and about 4 mg/dL with methocarbamol added. Serum haptoglobin declined after both doses over 3 days. Authors: detectable but within physiologic levels comparable to exercise, a small fraction of daily erythrocyte turnover. Read as an abstract via OpenAlex; sample size and CIs were not in the text retrieved [6].

Mechanism

Named for the vehicle and compound together: in vitro hemolytic potential of methocarbamol (a compound related to mephenesin) and hypertonic PEG vehicle [6]. A 1957 study found guaifenesin and methocarbamol could be given slowly as saturated aqueous solutions in large doses with little danger of appreciable hemolysis, using serum bilirubin and hemochromogen tests (abstract summary via OpenAlex) [7]. A 1971 in vitro study of 12 agents found concentration-dependent hemolysis reduced by added sodium chloride; methocarbamol appears in its MeSH indexing only, and its per-drug result was not seen [8].

Counter-evidence held on record

Counter-evidence and limits A methemoglobinemia case report (Lee 2014, naproxen in an alcohol-dependent patient) carries methocarbamol only as an indexing keyword; its abstract was not available, so it is not used as evidence for or against methocarbamol [16]. The 1977 study is a short-exposure human volunteer model with markers of hemolysis, which cannot show a lasting fall in oxygen delivery. It was not designed to detect clinically meaningful anemia. Framing caution Do not present this as methocarbamol causing anemia or low oxygen delivery. It is a small, transient laboratory signal on the injectable form, and the vehicle contributed more than the drug. No supplement is implied.

ATP production

Not graded — disclosed evidence gap

See study details

No evidence was retrieved on methocarbamol and cellular ATP synthesis or energy output.

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. Ungraded

Limits on what this shows

  • Why no grade: Dual condition met: no Tier B or C evidence, and no circulating methocarbamol 'low energy' claim found. Muscle weakness or sedation as labeled CNS effects are drug pharmacology, not an ATP finding. Not a finding of safety.

What was searched

The PubMed listing with ATP, respiration, membrane potential, phosphorylation and mitochondrial terms (6 records, none relevant) and the oxidative stress and mitochondria listing (2 records, none relevant). The label sections retrieved contain no energy-metabolism content [1][2][3].

Channel outcomes

First pass: PubMed HTML search listings (format=pubmed) opened intermittently; some requests were refused with HTTP 429 and were not retried on the same page. OpenAlex single-record lookups and DailyMed label pages opened. OpenAlex and Crossref search endpoints returned 429. Web search budget was exhausted in that pass. Europe PMC and Semantic Scholar were not attempted through WebFetch because they are on the blocked-host list. Repair pass 2026-10-07: the same mitochondrial and ATP web queries as for Mitochondrial burden returned no methocarbamol-specific result; a pharmacology aggregator monograph [21] and LiverTox [22] contain no energy-metabolism content. Fatigue is listed on the UK leaflet at unknown frequency [19]; as a labeled CNS or general effect it is not an ATP finding.

Gap type

Genuine gap on the channels that opened; Europe PMC and Semantic Scholar not used. Kept independent of Mitochondrial burden and Oxygen delivery/utilization (Hard Rule 7); the shared empty search is disclosed in the Overlap map.

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.

  • No circulating methocarbamol nutrient-depletion claim located

    Where it comes from: Consumer pages opened: drugs.com food-interaction page (alcohol only), drugs.com monograph (generic statement that vitamins may interact; no depletion claim) and drugs.com methocarbamol with vitamin D3 interaction page (no interaction found) [17][18][28]. Two depletion-overview documents opened in the repair pass, a chiropractic-clinic nutrient-depletion PDF and a US Pharmacist article, do not mention methocarbamol or muscle relaxants [26][27]. Web searches for methocarbamol with depletion, vitamins, magnesium, B vitamins and CoQ10 returned only generic depletion articles. Retailer and handbook sites were not individually enumerated.

    Why it fails: There is nothing to rebut from the sources reached. This is not a finding that no such claim exists elsewhere. If a claim (for example, B vitamins, magnesium or hemolytic anemia) is found later, it should be graded against the evidence recorded here, which currently supports no depletion. Urine discoloration (black, blue or green) is documented in a reference page and a case-report introduction [5][13] and is not a nutrient claim.

How the body handles this medication

Metabolism and enzymes
Metabolized by dealkylation and hydroxylation, with likely conjugation. The label sections retrieved name no CYP enzyme and describe no CYP induction or inhibition. The tablet label notes methocarbamol may inhibit the effect of pyridostigmine bromide (caution in myasthenia gravis).[1][3] DailyMed tablet labels (read via summarizing fetch tool)
Elimination
"Essentially all methocarbamol metabolites are eliminated in the urine." Mean plasma half-life 1 to 2 hours; plasma protein binding 46 to 50%. Elderly: half-life about 1.5 versus 1.1 hours, binding 41 to 43%.[1][2] sec Clinical Pharmacology
Renal impairment
Tablet label (as summarized): clearance reduced about 40% in renal impairment with half-life similar to normal. Injection: contraindicated in known or suspected renal pathology because PEG 300 "is known to have increased pre-existing acidosis and urea retention".[1][2]; Sica 1990 PK study title only, not opened [12]
Hepatic impairment
In 8 patients with alcoholic cirrhosis, mean total clearance was reduced about 70% versus 8 matched controls; half-life 3.38 hours in cirrhosis. Jaundice (including cholestatic) is a listed adverse reaction.[1][3]
Injection vehicle
Each mL contains 100 mg methocarbamol and 0.5 mL polyethylene glycol 300. Solution is hypertonic; rate not to exceed 3 mL per minute; extravasation to be avoided; not more than 30 mL a day for more than 3 consecutive days except in tetanus. Thrombophlebitis and injection-site pain and sloughing are labeled.[2] Hikma Robaxin injection label (read via summarizing fetch tool)
Absorption, food and mineral interactions
Absorption site and any transporter are not stated in the label sections retrieved. No food, antacid, vitamin or mineral interaction appears in the sections retrieved; the drugs.com food-interaction page lists only alcohol (CNS depression). Methocarbamol may cause color interference in 5-HIAA and VMA urine screening tests.[1][3][17]

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.

  • Renal / IV route

    Kidney function before IV use

    The injection is contraindicated in known or suspected renal pathology because of the PEG 300 vehicle, and has labeled duration limits (not more than 3 consecutive days at up to 30 mL a day, except tetanus) [2]. A 68-patient ICU series saw no creatinine change [11], and a 2024 commentary describes the PEG nephrotoxicity evidence as unsettled [10]. This is a drug-safety matter, not a nutrient finding.

  • Lab / only if prompted

    Hemolysis markers after prolonged or high-volume IV use

    Plasma hemoglobin, haptoglobin and a blood count are the measures that moved or could move in the 1977 model [6]. Worth considering only if there is unexplained jaundice, pallor or a drop in hemoglobin after repeated IV dosing. Oral use has no retrieved hemolysis data.

  • Lab test interference

    5-HIAA and VMA screening

    Methocarbamol may cause color interference in certain screening tests for urinary 5-HIAA and VMA [3][14]. Tell the laboratory or prescriber before these tests.

  • Urine color

    Dark, green, blue or black urine

    Urine color change is reported for methocarbamol [5][13] and is not evidence of a vitamin or mineral problem. Unexplained dark urine with jaundice or pallor still warrants clinical evaluation for other causes.

  • Hepatic / CNS

    Liver impairment, alcohol and sedation

    Clearance falls about 70% in alcoholic cirrhosis [1][3]. Alcohol and other CNS depressants add to drowsiness and dizziness [1][17]. Persistent sedation or nausea that reduces eating is worth raising with a prescriber.

  • Pregnancy / nutrient labs

    Pregnancy and routine nutrient testing

    The tablet label advises against use in women who are or may become pregnant [1]. No nutrient lab is indicated by methocarbamol itself on current evidence; baseline testing depends on the person's other drugs and conditions. No supplement separation interval applies because no interaction was found.

Overlap map, to prevent double counting

Entries resting on the same underlying source, mechanism or empty search.

  • Oxygen delivery/utilization

    Shares evidence with: Oxidative stress; Iron

    Note: Both yellow-tier hemoglobin entries concern free hemoglobin in blood, but they rest on different sources (the 1977 human hemolysis-marker study [6] versus the in vitro pseudoperoxidase study [9]). The pseudoperoxidase paper's rationale is hemolysis-released hemoglobin, so the two are not independent confirmation of one effect. Hemolysis would also release heme iron, but no iron indices were measured, so Iron is not supported by the hemolysis study.

  • Mitochondrial burden

    Shares evidence with: ATP production; Oxidative stress

    Note: The ungraded mitochondrial and ATP entries rest on the same empty PubMed listings and the same repair-pass web queries (mitochondrial/ATP terms and oxidative/mitochondria terms), so their shared absence of evidence is one gap, not two. Oxidative stress is yellow on a separate source [9].

  • Copper

    Shares evidence with: Iron

    Note: Both were searched with one combined PubMed listing that returned only one analytical chemistry copper(II) paper [15] and an irrelevant record. Kept as two independent entries (Hard Rule 7).

  • Dietary intake

    Shares evidence with: None

    Note: Rests on the label adverse-reaction list [19][1][3] and empty PubMed listings only. Not shared with any other entry.

All references used above
  1. Methocarbamol tablets, USP, prescribing information (Granulation Technology, Inc.), DailyMed. — Regulatory label (Tier A). Read through a summarizing fetch tool, not the raw text. Source of metabolism, elimination, special populations, adverse reactions and interaction facts.Summarized by the fetch tool; quotations are the tool's rendering of the label.
  2. ROBAXIN (methocarbamol) injection, Hikma Pharmaceuticals USA Inc., DailyMed. — Regulatory label (Tier A). Composition with PEG 300, renal contraindication, rate and duration limits, adverse reactions.Summarized by the fetch tool; a second Hikma injection label (setid a418c43a-afe8-4a19-a57a-95c8dbe3d3d8) was listed but not opened.
  3. ROBAXIN (methocarbamol) tablet, film coated, repackaged label (Direct Rx), DailyMed. — Regulatory label (Tier A). Drug and laboratory test interactions (5-HIAA, VMA), leukopenia, jaundice, cirrhosis clearance, absence of CYP detail.Summarized by the fetch tool.
  4. WHO Collaborating Centre, ATC/DDD Index: methocarbamol, M03BA03, DDD 3 g oral or parenteral. — Reference index. ATC group M03BA, carbamic acid esters, centrally acting muscle relaxants.
  5. Wikipedia: Methocarbamol. — Reference summary (not a primary source). Used for brand names and the statement that urine may turn black, blue or green.Read through a summarizing fetch tool. Not used to support any grade.
  6. Scott RB, Tisdale SA, Cummings WB. Hemolytic potential of methocarbamol. Clin Pharmacol Ther 1977. — Human volunteer intravenous study, methocarbamol in 50% PEG 300 versus vehicle and saline (Tier A for the IV route; this drug in cohort). PMID 837639. DOI 10.1002/cpt1977212208.Abstract only, via a reconstructed OpenAlex record read through a summarizing fetch tool. Sample size not seen.
  7. Truitt EB, Patterson RB. Comparative hemolytic activity of mephenesin, guaiacol glycerol ether and methocarbamol in vitro and in vivo. Proc Soc Exp Biol Med 1957. — In vitro and in vivo comparison (Tier B). PMID 13453457. DOI 10.3181/00379727-95-23240.Abstract summary only, via OpenAlex and a summarizing fetch tool; species and doses not seen.
  8. Fievet CJ, Gigandet MP, Ansel HC. Hemolysis of erythrocytes by primary pharmacologic agents. Am J Hosp Pharm 1971. — In vitro, 12 agents, human and rabbit erythrocytes (Tier B at most). PMID 4400071. DOI 10.1093/ajhp/28.12.961.Methocarbamol appears in MeSH indexing only; the per-drug result was not seen. Abstract via OpenAlex summary.
  9. Minai-Tehrani D, et al. Inhibition of pseudoperoxidase activity of human red blood cell hemoglobin by methocarbamol. Int J Biol Macromol 2017 (online 2016). — Cell-free in vitro enzyme kinetics and docking (Tier B). PMID 27645932. DOI 10.1016/j.ijbiomac.2016.09.049.Abstract read from a PubMed search listing through a summarizing fetch tool; full text not opened. The PubMed article page itself was not opened.
  10. Chan E, Waggoner C, Boylan PM. Commentary: Is polyethylene glycol toxicity from intravenous methocarbamol fact or fiction? J Pain Palliat Care Pharmacother 2024. — Commentary (narrative, not a primary study; context only). PMID 38718034. DOI 10.1080/15360288.2024.2345322.Abstract only, reconstructed via OpenAlex.
  11. Li M, et al. Exploring the link between intravenous methocarbamol and acute kidney injury. J Pharm Pract (OpenAlex dates it 2025; the PubMed listing shows 2026). — Single-center retrospective ICU series, 68 patients, serum creatinine outcome (Tier A for creatinine, not a nutrient). PMID 41151588. DOI 10.1177/08971900251394101.Abstract only, reconstructed via OpenAlex.
  12. Sica DA, et al. Pharmacokinetics and protein binding of methocarbamol in renal insufficiency and normals. Eur J Clin Pharmacol 1990. — PMID 2253675. DOI 10.1007/bf00280060.Not opened: no abstract was available in the record. Title and bibliographic data only; no facts were drawn from it. Metabolism in rat, dog and human (Bruce 1971, PMID 5548215) was in the same position.
  13. Gangwani MK, et al. Green urine and altered mental status: a case of intoxication. J Ayub Med Coll Abbottabad 2019. — Case report whose abstract lists methocarbamol among substances associated with green urine (Tier D/C context only; the case itself was a benzodiazepine-positive intoxication). PMID 31094132.Abstract only, via OpenAlex. Used for urine color context only.
  14. Honet JC, Casey TV, Rumyan JW. False-positive urinary test for 5-hydroxyindoleacetic acid due to methocarbamol and mephenesin carbamate. N Engl J Med 1959. — PMID 13667004. DOI 10.1056/nejm195907232610407.Title and bibliographic data only; no abstract available. The interference itself is confirmed by the label [3].
  15. Mansour AM, Shehab OR. Trapping of muscle relaxant methocarbamol degradation product by complexation with copper(II) ion. Spectrochim Acta A 2014. — Analytical spectroscopic study. PMID 24674917. DOI 10.1016/j.saa.2014.02.142.Not opened beyond title and metadata; no abstract available. Not used as evidence.
  16. Lee WS, et al. Naproxen-induced methemoglobinemia in an alcohol-dependent patient. Am J Emerg Med 2014. — Case report. PMID 24856747. DOI 10.1016/j.ajem.2014.04.027.Not opened beyond metadata: methocarbamol appears as an indexing keyword and no abstract was available. Not used as evidence.
  17. Drugs.com. Methocarbamol food and supplement interactions. — Tier D consumer page. Used only to document the absence of a nutrient interaction or depletion claim.Read through a summarizing fetch tool.
  18. Drugs.com. Methocarbamol monograph. — Tier D consumer page. Used only to document the absence of a nutrient-depletion claim.Read through a summarizing fetch tool.
  19. Methocarbamol 750 mg Tablets, patient information leaflet, medicines.org.uk (electronic medicines compendium). — Regulatory patient leaflet (Tier A for the listed adverse reactions and interactions). Source of loss of appetite, nausea, vomiting, diarrhoea, fatigue, metallic taste and appetite-suppressant interaction statements.Opened 2026-10-07 through a summarizing fetch tool; quotations are the tool's rendering.
  20. Drugs.com. Methocarbamol side effects. — Tier D consumer and professional aggregator page. Lists nausea, loss of appetite and anorexia (professional gastrointestinal section) and leukopenia.Opened 2026-10-07 through a summarizing fetch tool. Not used to support any grade.
  21. MedCentral. Methocarbamol oral monograph. — Tier D drug-monograph aggregator. States anorexia reported after oral use; no mention of anemia, vitamins, minerals, mitochondria or microbiome.Opened 2026-10-07 through a summarizing fetch tool. Not used to support any grade.
  22. Methocarbamol. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury, NCBI Bookshelf (NBK548286). — Established pharmacology reference. Central muscle relaxant by an unknown mechanism; unlikely cause of clinically apparent liver injury (likelihood score E). No mechanism, mitochondrial, nutrient, iron, copper, hemolysis or anorexia content.Opened 2026-10-07 through a summarizing fetch tool.
  23. PubMed search listing for methocarbamol (24 records on the first page, 2026-10-07). — Search listing, not a study. Titles of 24 records reviewed (LactMed, LiverTox, StatPearls, PEG toxicity commentary, pain and opioid-sparing trials, Nav1.4 channel and muscle-spindle pharmacology, analytical methods, tetanus and myasthenia reports); none on mitochondria, ATP, iron, copper, microbiota, oxidative stress, appetite or nutrition.Only the first page of results was seen; the fetch tool's screening of abstract text for the listed terms is a summary.
  24. Maier L, et al. Extensive impact of non-antibiotic drugs on human gut bacteria. Nature 2018. — In vitro screen of marketed drugs against gut bacterial strains (authorship and design as rendered by the fetch tool). Methocarbamol was not found in the article text as rendered. DOI 10.1038/nature25979.Opened 2026-10-07 through a summarizing fetch tool. Supplementary drug tables were not accessible, so absence from the supplement is not confirmed. Not used as evidence for any grade.
  25. Vich Vila A, et al. Impact of commonly used drugs on the composition and metabolic function of the gut microbiota (2020; journal and year taken from the file name and title as supplied, not independently confirmed from the opened text). — Population cohort analysis of 41 drug categories. Methocarbamol and muscle relaxants are not among the drugs analyzed per the fetch tool's reading.Opened 2026-10-07 through a summarizing fetch tool. Methocarbamol not in the cohort; any class statement from this paper would not apply to this drug. Not used as evidence.
  26. Nutrient depletion that arises from using prescribed medications (chiropractic clinic handout, PDF, 2025). — Tier D depletion overview. No mention of methocarbamol, Robaxin or muscle relaxants.Opened 2026-10-07 through a summarizing fetch tool. Used only to document absence of a circulating claim.
  27. Drug-Induced Nutrient Depletions: What Pharmacists Need to Know. US Pharmacist. — Tier D narrative review. No mention of methocarbamol, Robaxin or muscle relaxants.Opened 2026-10-07 through a summarizing fetch tool. Used only to document absence of a circulating claim.
  28. Drugs.com. Drug interactions between methocarbamol and vitamin D3. — Tier D interaction checker page. "No interactions found."Opened 2026-10-07 through a summarizing fetch tool. Not used to support any grade.