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MyDeficiencies

Meclizine

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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.

Meclizine has no documented classical depletion machinery. The current regulatory label states that it is metabolized by CYP2D6 (the dominant enzyme), has a plasma elimination half-life of about 5 to 6 hours and a median Tmax of 3 hours, and says nothing about CYP induction or inhibition by meclizine, route of excretion, food effects, antacid or mineral interactions, or any vitamin or mineral. A 2004 study found that meclizine activates mouse CAR (and so induces CAR target genes in mice) but acts as an inverse agonist at human CAR, suppressing rather than inducing those genes, which argues against enzyme-induction catabolism of nutrients in people. No mechanism class for classical nutrient loss (absorption interference, induction, renal wasting, cofactor antagonism, dilutional or hormonal disturbance) is supported by the label or by any drug-specific primary study found. That absence is the first finding. No class extrapolation is used anywhere in this dossier.

ATC R06AE05 (WHO index lists the INN as meclozine) · reviewed 2026-10-04. 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 Meclizine 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

Red tier, empty

Red — Severe

Evidence: no red entries

No nutrient or category in this dossier reached the red threshold for meclizine.

Full detail and limits

What the grade means here: 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. no red entries

Limits on what this shows

  • What would fill it: Two independent peer-reviewed human studies (cohort, case-control or trial) that directly measured a specific nutrient level or physiological category in meclizine-treated patients against a comparator, with a named mechanism and consistent direction.

Why empty

Red requires at least 2 independent Tier A, drug-specific sources with the nutrient or category directly measured in people taking the drug. The regulatory label is the only Tier A source located and it addresses no nutrient. No human study measuring a nutrient or any of the seven mandatory categories in meclizine users was found.

Orange tier, empty

Red — Severe

Evidence: no orange entries

No nutrient or category reached the orange threshold for meclizine.

Full detail and limits

What the grade means here: 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. no orange entries

Limits on what this shows

  • What would fill it: A human study measuring a nutrient level or one of the seven categories directly in a defined meclizine-using subgroup (for example long-duration use, hepatic impairment or CYP2D6-inhibitor co-treatment) and showing a bounded, real deficit.

Why empty

Orange requires at least 1 Tier A source with meclizine in the cohort showing a real, bounded deficit. All drug-specific data on mitochondrial respiration, ATP and oxidative markers are cell-culture or rodent studies (Tier B).

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

Yellow — Low

See study details

In cultured human and mouse cells and in mice, meclizine attenuates mitochondrial respiration through a non-canonical route (inhibition of PCYT2 and build-up of phosphoethanolamine), and in animal ischemia models this was protective; there are no human data and no evidence at doses used for vertigo.

Full detail, limits and 1 references

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 negative/null findings: Meclizine did not qualitatively change membrane potential in isolated mitochondria (Nature Biotechnology 2010), and suppressed respiration in intact cells but not in isolated mitochondria (J Biol Chem 2013). The EBioMedicine 2015 page reports reduced oxygen consumption in kidney mitochondria from pretreated animals; how this fits with the 2013 finding of no direct isolated-mitochondria effect was not resolved in this review (one possible explanation, not verified, is ex vivo measurement after in vivo exposure versus drug added directly).
  • At-risk subgroups: None established. Theoretically, patients with higher meclizine exposure (hepatic impairment, or CYP2D6-inhibitor co-treatment, both flagged in the label for raised exposure) would carry more of any concentration-dependent effect; no study tested this.
  • Counter-evidence on record: The original authors state it is an open question whether approved doses reach the concentrations needed. Every positive finding uses pretreatment at 100 mg/kg (intraperitoneal or gavage) or 0.1 to 50 µM in culture, and the animal direction was protective. A pediatric phase 1b pharmacokinetic report lists a mean Cmax of 167 ng/mL at 12.5 mg/day [11]; this review did not make a direct unit comparison to the in-vitro micromolar range.

Regulatory status

The DailyMed label presumes H1 receptor antagonism as the therapeutic mechanism and does not mention mitochondrial effects. Attenuated respiration is therefore not the labeled or intended pharmacology, so this entry does not breach Hard Rule 2.

Population evidence

No human population data. Nature Biotechnology 2010 (Gohil et al.): screen of more than 3,500 small molecules in human fibroblasts grown on galactose versus glucose; meclizine reduced oxygen consumption rate dose-dependently in fibroblasts (10, 25, 50 µM), at 50 µM in mouse striatal cells, HEK293 and HeLa cells, and at 0.1 to 10 µM in cardiomyocytes; mouse plasma of 3 to 5 µM six hours after 100 mg/kg intraperitoneal was reported as sufficient to attenuate respiration in primary cortical neurons; two 100 mg/kg doses before arterial occlusion reduced stroke infarct volume by 23% (P=0.03), and mice tolerated daily 100 mg/kg without weight loss or behavior change. J Biol Chem 2013 (human fibroblasts and mouse striatal cells tested): in fibroblasts meclizine raised phosphoethanolamine about 35-fold (about 1.5 to 4 mM within 5 hours) and was a non-competitive inhibitor of PCYT2 (Ki about 31 µM); phosphoethanolamine inhibited ADP-stimulated respiration in isolated mitochondria (IC50 about 3.13 mM). EBioMedicine 2015 (Kishi et al.): 100 mg/kg in mice 17 to 24 hours before 27 minutes of renal ischemia; 24-hour serum creatinine 0.89 mg/dl versus 1.59 mg/dl in vehicle (sham 0.13), with preserved mitochondrial structure on electron microscopy and inhibition of the Kennedy pathway. 2025 preprint (Ghazal et al.): cardiomyocyte-specific SLC25A3-deleted mice given 100 mg/kg/day by gavage for 12 weeks had damaged mitochondria fall from about 60% to about 10% with MICOS upregulation.

Mechanism

Named: inhibition of PCYT2 in the Kennedy (phosphatidylethanolamine) pathway with accumulation of phosphoethanolamine, which inhibits respiration. See the Overlap map: this single mechanism and evidence cluster underlies the ATP production and Oxidative stress entries too.

Counter-evidence held on record

All data are cell-culture or rodent studies at concentrations and doses not shown to occur with vertigo dosing. This is not evidence of human mitochondrial injury or of any nutrient deficiency, and it is not a basis for recommending coenzyme Q10, ethanolamine, choline or any other supplement. No dose of any supplement appears in this dossier.

Oxidative Stress

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

Oxidative stress

Yellow — Low

See study details

Reverse direction: in a single mouse kidney ischemia-reperfusion study, meclizine pretreatment lowered post-ischemic oxidative injury markers; no study found meclizine depleting antioxidant capacity or raising oxidative damage in people or animals.

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 negative/null findings: No oxidative marker (malondialdehyde, glutathione, SOD, catalase) has been reported as measured for meclizine in any source opened; the 2023 mouse study explicitly did not measure them.
  • At-risk subgroups: None established.
  • Counter-evidence on record: The sole oxidative-marker result is a gene-expression readout (mRNA of two markers) in a pretreatment ischemia model at 100 mg/kg, from one laboratory group; it is not a direct redox or antioxidant-capacity assay.

Regulatory status

Not addressed in the DailyMed label.

Population evidence

No human data. EBioMedicine 2015 (Kishi et al.): in mice given 100 mg/kg meclizine before renal ischemia, post-ischemic mRNA expression of heme oxygenase-1 and inducible nitric oxide synthase (markers of oxidative injury) was significantly lower than in vehicle mice, which the authors interpret as reduced reactive oxygen species generation. Nature Biotechnology 2010 discusses that shifting energy metabolism toward glycolysis can reduce oxidative damage, but the retrieved text reported no direct reactive oxygen species measurement for meclizine. Metabolic Brain Disease 2023 (Mostafa and Asaad): oral meclizine 12.5 and 25 mg/kg for 14 days in LPS-treated mice lowered IL-1β, TNF-α, NF-κB, AKT, ERK and JNK in brain, but did not measure malondialdehyde, glutathione, SOD, catalase or ROS and is therefore recorded as an inflammatory finding only, not an oxidative stress finding.

Mechanism

Proposed, not tested: lower oxidative phosphorylation flux producing less reactive oxygen species. Shares its experiments with the Mitochondrial burden and ATP production entries (Overlap map).

Counter-evidence held on record

This is a reverse-direction animal signal where the drug appears protective. It is not a reason to take meclizine for any redox purpose, and it is not a basis to recommend or withhold antioxidant supplements. No dose appears in this dossier.

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 drug-specific evidence at any tier on meclizine and copper status, and no meclizine-specific circulating claim; a disclosed evidence gap, not a finding of safety.

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 in Step 7 met: no Tier B or Tier C evidence supports even a yellow grade (clean PubMed zero; PubMed-independent channels were blocked, so a Tier B or C source indexed only elsewhere cannot be fully excluded), AND no circulating consumer claim about meclizine and copper exists to rebut as white. This is a literature and access gap. It is not a statement that meclizine does not affect copper.
  • What would fill it: A study measuring serum copper or ceruloplasmin in meclizine users, or an in-vitro or animal study of meclizine and copper handling; a revision should re-run the OpenAlex, Crossref, Semantic Scholar and Europe PMC searches when those channels recover.

Regulatory status

The DailyMed label (a second explicit extraction pass) contains no statement about vitamins, minerals or nutrients.

Research channels and outcome

PubMed listing "meclizine copper": clean zero results (after earlier 429 responses on other PubMed queries, this one returned normally). Channels tried: DailyMed label (opened, no statement); PubMed search-listing pages (clean zero-result queries recorded in this card); WebSearch (consumer-claim audit, before the session search budget of 200 calls was exhausted); direct publisher fetches; OpenAlex search, Crossref search, Semantic Scholar search and Europe PMC REST search (each returned HTTP 429 or a proxy rejection on every attempt, including a second attempt after a long pause; these four are tooling-limited and returned no content); direct curl to every host failed at the proxy (connection refused at CONNECT); Unpaywall was not reachable by curl and was not retried through WebFetch because no candidate paper needed open-access resolution.

Circulating claims checked

Consumer depletion lists were opened (see Sources [12] to [16]). One article lists copper among nutrients that support immune and histamine regulation but does not claim meclizine lowers it, and meclizine is not named in any depletion handbook opened. Nothing to rebut.

Revision re-check

Updated 2026-10-04 pass: no new copper or iron search succeeded. The web search budget was exhausted, and the fetch tool returned HTTP 429 with a request not to retry after the first few pages, so the clean-zero PubMed listings above remain the only drug-specific result. This remains a partly tooling-limited gap.

Iron

Not graded — disclosed evidence gap

See study details

No drug-specific evidence at any tier on meclizine and iron status, and no meclizine-specific circulating claim; a disclosed evidence gap, not a finding of safety.

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 Tier C evidence found, and no meclizine-specific circulating claim. This is a literature and access gap, not reassurance.
  • What would fill it: Ferritin, transferrin saturation or hemoglobin data in meclizine users, or a mechanistic study of meclizine and iron handling.

Regulatory status

The DailyMed label contains no statement about iron, hematologic effects or any mineral interaction.

Research channels and outcome

PubMed listing "meclizine iron": clean zero results (obtained on the second attempt; the first two attempts were rate limited with HTTP 429 and carry no information). Channels tried: DailyMed label (opened, no statement); PubMed search-listing pages (clean zero-result queries recorded in this card); WebSearch (consumer-claim audit, before the session search budget of 200 calls was exhausted); direct publisher fetches; OpenAlex search, Crossref search, Semantic Scholar search and Europe PMC REST search (each returned HTTP 429 or a proxy rejection on every attempt, including a second attempt after a long pause; these four are tooling-limited and returned no content); direct curl to every host failed at the proxy (connection refused at CONNECT); Unpaywall was not reachable by curl and was not retried through WebFetch because no candidate paper needed open-access resolution.

Circulating claims checked

A consumer article lists iron among minerals supporting immune and histamine regulation, in the direction nutrient-to-symptom rather than drug-to-nutrient. No source opened claims meclizine lowers or raises iron.

Revision re-check

Updated 2026-10-04 pass: no new copper or iron search succeeded. The web search budget was exhausted, and the fetch tool returned HTTP 429 with a request not to retry after the first few pages, so the clean-zero PubMed listings above remain the only drug-specific result. This remains a partly tooling-limited gap.

Gut Microbiome Risk

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

Gut microbiome risk

Yellow — Low

See study details

In one in-vitro screen, meclizine changed central carbon metabolism of the gut pathogen Clostridioides difficile without affecting its growth; no study of meclizine on commensal gut bacteria, microbiome composition or human stool was found, and no class extrapolation is used.

Full detail, limits and 1 references

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 negative/null findings: Meclizine did not affect C. difficile growth in this screen. The PubMed listings "meclizine microbiome" and "meclizine gut microbiota" returned zero results, and "meclizine bacteria" returned 12 results of which only the C. difficile screen concerned a gut organism (the others were a travel advice item, a tuberculosis macrophage study, a viral replication study, an antibiotic-combination formulation study, a UV assay method, and unrelated items). Maier 2018 (Nature, more than 1,000 drugs against 40 human gut strains) was re-opened in this revision: the retrieved article text did not mention meclizine or any first-generation H1 antihistamine, and its Supplementary Table 1 could not be opened (the Springer static-content host disallows automated fetches via robots.txt, which was not circumvented). Maier 2018 therefore passes no cohort test for meclizine and is not used for this grade. Zimmermann 2019 (Nature drug metabolism by gut bacteria) could not be opened (HTTP 429).
  • At-risk subgroups: None established.
  • Counter-evidence on record: A single in-vitro screen of one pathogen at 10 to 100 µM, with no growth effect, cannot support a claim about commensal bacteria or about meclizine at vertigo doses. A consumer article (Sources [14]) claims "several types of antihistamines" suppress Bifidobacterium and Lactobacillus citing Maier 2018 without details; it does not name meclizine, and that claim is rebutted under Fails verification. No class extrapolation is made: no first-generation H1 antihistamine could be verified in a published gut-bacteria cohort, so the Tier C route was tested and not available.

Regulatory status

The DailyMed label lists dry mouth and vomiting among adverse reactions and does not address the gut microbiome. Anticholinergic effects on motility are the drug's labeled pharmacology and are not filed here (Hard Rule 2).

Population evidence

No human data. Antimicrobial Agents and Chemotherapy, published 2025-12-17 (PMID 41405459; doi 10.1128/aac.00960-25): a high-throughput reporter screen of the Prestwick Chemical Library at 10 and 100 µM identified meclizine as reducing C. difficile toxins TcdA and TcdB and toxin gene expression "without affecting bacterial growth"; meclizine "significantly altered central carbon metabolism" (increased carbohydrate transport, shifted lactate/pyruvate conversion, accumulation of intracellular metabolites that inhibited toxin synthesis). Only the abstract, as returned by an OpenAlex single-record lookup, was read; the full text was not opened (see Sources [17]).

Mechanism

Named at the level of the single organism: altered carbon metabolism in C. difficile. No mechanism for a community-level change (diversity, commensal growth) is documented for meclizine. This is a functional, single-species effect and not a dysbiosis finding.

Counter-evidence held on record

This is a single-species in-vitro signal, not evidence that meclizine alters the human gut microbiome, and it is not a basis to recommend or withhold probiotics, prebiotics or any supplement. No dose of any supplement appears in this dossier.

Oxygen and ATP Output

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

ATP production

Yellow — Low

See study details

Cellular ATP fell in culture only when cells were forced to rely on oxidative phosphorylation (galactose medium), and in one study only with added ethanolamine; in glucose medium glycolysis compensated, and in one mouse preprint cardiac ATP was preserved. No human ATP data exist.

Full detail, limits and 1 references

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 negative/null findings: Total cardiac ATP was unchanged by meclizine in the 2025 mouse preprint; the ATP decrease required galactose medium, a condition that deliberately removes glycolytic compensation.
  • At-risk subgroups: None established.
  • Counter-evidence on record: The preprint (bioRxiv version opened via PMC; peer-review status unresolved) found the cardiac benefit was independent of ATP and glycolysis. The galactose finding is an artificial stress condition, not a physiologic one.

Regulatory status

Not addressed in the DailyMed label; not labeled pharmacology.

Population evidence

No human data. J Biol Chem 2013: combined meclizine and ethanolamine supplementation synergistically decreased cellular ATP in fibroblasts cultured in galactose. EBioMedicine 2015 (Kishi et al.): meclizine upregulated glycolysis in glucose-containing medium and reduced cellular ATP in galactose-containing medium. 2025 preprint (Ghazal et al.): in SLC25A3-deleted mouse hearts given meclizine 100 mg/kg/day for 12 weeks, total cardiac ATP remained preserved in both vehicle and meclizine groups, meclizine did not raise energy production, and it lowered glycolytic enzyme expression and tissue lactate. The retrieved text of the 2010 Nature Biotechnology paper did not report direct cellular ATP values.

Mechanism

Indirect: attenuated respiration (see Mitochondrial burden) shifts the cell toward glycolysis; ATP falls only where glycolysis cannot compensate. The PCYT2 and phosphoethanolamine mechanism is shared with the Mitochondrial burden entry and is recorded in the Overlap map.

Counter-evidence held on record

This is an in-vitro and rodent signal. The cell-culture synergy with added ethanolamine does not say anything about dietary ethanolamine, choline or any supplement, and no supplement is recommended or discouraged on this basis. No dose appears in this dossier.

Oxygen delivery/utilization

Not graded — disclosed evidence gap

See study details

No drug-specific evidence on meclizine and hemoglobin, hematocrit, red-cell mass or tissue oxygen delivery, and no circulating claim; cell-level oxygen consumption data are filed under Mitochondrial burden, not here.

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 on delivery: no Tier B or Tier C evidence on hemoglobin or tissue oxygen delivery and no circulating claim. The reduced cellular oxygen consumption seen in cell and rodent studies is mitochondrial respiration, is recorded once under Mitochondrial burden, and is deliberately not repeated here so it cannot be counted as a separate oxygen-delivery finding (Overlap map). This is a literature and access gap, not reassurance.
  • What would fill it: Hemoglobin or hematocrit data in meclizine users compared with a matched comparator, or an arterial oxygenation or tissue oxygen study in meclizine-treated animals or people.

Regulatory status

The DailyMed label lists anaphylaxis, drowsiness, dry mouth, headache, fatigue, vomiting and rare blurred vision; no hematologic or oxygen-delivery adverse reaction is listed. Fatigue is a labeled adverse reaction and is not an oxygen-delivery finding.

Research channels and outcome

PubMed listing "meclizine anemia": clean zero results. A first PubMed query joining hemoglobin, anemia and hematocrit with OR returned 338,637 unrelated results because the operators dropped the meclizine term; it was discarded and carries no information. Channels tried: DailyMed label (opened, no statement); PubMed search-listing pages (clean zero-result queries recorded in this card); WebSearch (consumer-claim audit, before the session search budget of 200 calls was exhausted); direct publisher fetches; OpenAlex search, Crossref search, Semantic Scholar search and Europe PMC REST search (each returned HTTP 429 or a proxy rejection on every attempt, including a second attempt after a long pause; these four are tooling-limited and returned no content); direct curl to every host failed at the proxy (connection refused at CONNECT); Unpaywall was not reachable by curl and was not retried through WebFetch because no candidate paper needed open-access resolution.

Circulating claims checked

No meclizine-specific claim about oxygen-carrying capacity or red-cell effects was found; class-level fatigue claims in a consumer article (Sources [13]) cite nothing and name no oxygen mechanism.

Revision re-check

Updated 2026-10-04 pass: PubMed "meclizine hypoxia" was rate limited (HTTP 429, not retried per the tool request) and carries no information; "meclizine hemoglobin" returned 1 result whose title concerns a Wnt inhibitory factor 1 and HIF1α/PFKFB3 glycolysis study in diabetic retinopathy macrophages, not hemoglobin or oxygen delivery (abstract not opened, not cited). Meclizine was found in a 2025 Nature Communications study (Sources [18]; abstract read through OpenAlex) to shift infected macrophage metabolism toward glycolysis and reduce drug tolerance of Mycobacterium tuberculosis in mice; this is cellular energy metabolism, the same behavior already filed under Mitochondrial burden and ATP production, and is not hemoglobin, red-cell mass, arterial oxygenation or tissue oxygen delivery. No drug-repurposing paper testing meclizine on HIF or tissue hypoxia could be opened. The full text of the 2025 study could not be opened (HTTP 429), so it is not added to the graded mitochondrial entries.

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.

  • Vitamin C, magnesium, vitamin D, vitamin B6 and zinc absorption impaired by antihistamines, leading to fatigue, immune and inflammation problems

    Where it comes from: Consumer blog (Sources [13]); class-level, meclizine not named, no primary source cited. Tier D.

    Why it fails: No cited evidence. The meclizine label has no food, antacid, mineral or nutrient statement and no absorption mechanism is documented. PubMed "meclizine vitamin" returned 47 results whose first page was historical meclizine-pyridoxine combination products and pregnancy-nausea items, none reporting a depletion or absorption deficit. Fatigue is a labeled adverse reaction of the drug itself, not proof of nutrient loss. Pyridoxine appears in these historical products as an added ingredient, the opposite direction from depletion.

  • Essential fatty acids depleted by "anti-histamines"

    Where it comes from: Practitioner list of nutrient depletions (Sources [12]) naming Singulair and Zyrtec under antihistamines; meclizine not listed; no study cited. Tier D.

    Why it fails: Meclizine is not named, no primary citation is given, and no fatty-acid mechanism is documented for meclizine. The named brands are not meclizine: Zyrtec is a second-generation antihistamine, which is not a defensible class member for first-generation meclizine, and Singulair is a leukotriene receptor antagonist rather than an H1 antihistamine.

  • Vitamin B6, vitamin C, zinc, magnesium, copper and iron framed as needed for histamine control or motion sickness relief

    Where it comes from: Consumer article on nutrient deficiencies and histamine intolerance (Sources [15]); meclizine not mentioned.

    Why it fails: Direction reversed (Hard Rule 4): the article describes nutrients affecting histamine handling or symptoms, not meclizine affecting nutrient status. No depletion claim for meclizine is made or supported, so nothing is filed as a deficiency.

  • Antihistamines suppress Bifidobacterium and Lactobacillus (gut microbiome disruption)

    Where it comes from: Consumer blog (Sources [14]) citing Maier 2018 without details; class-level, meclizine not named. Tier D.

    Why it fails: Meclizine is not named, and the cited Nature screen [10] did not mention meclizine or any first-generation H1 antihistamine in the text retrieved (its supplementary drug list could not be opened). The only meclizine-specific gut-bacteria study found [17] tested C. difficile, reported no growth effect, and did not test Bifidobacterium or Lactobacillus. The claim as written for these genera has no meclizine support; the C. difficile finding is graded separately and does not rebut or confirm it.

How the body handles this medication

Absorption
Median Tmax 3 hours after an oral dose (range 1.5 to 6 hours). The label contains no food-effect, antacid or mineral interaction statement.DailyMed label [1]
Metabolism
CYP2D6 is the dominant metabolizing enzyme; the label warns of a possible interaction with CYP2D6 inhibitors. The label makes no statement that meclizine induces or inhibits any CYP enzyme. In a 2004 study meclizine activated mouse CAR but was an inverse agonist at human CAR.DailyMed label [1]; Huang 2004 [9]
Elimination
Plasma elimination half-life about 5 to 6 hours. The label has no excretion statement; a StatPearls reference states metabolites are excreted in the urine and unchanged drug in the feces (duration of action 8 to 24 hours).DailyMed label [1]; StatPearls NBK560645 [3]
Accumulation in impairment
Caution in renal impairment and the elderly because of potential drug or metabolite accumulation; hepatic impairment may increase systemic exposure.DailyMed label [1]
Renal tubular handling
No effect on renal tubular handling of water or electrolytes is described in the label, and none was found in the drug-specific literature reviewed.DailyMed label [1]; PubMed listings [16]
Interactions and class pharmacology
Increased CNS depression with other CNS depressants including alcohol; first-generation H1 antagonist with anticholinergic properties, which the label presumes (but does not establish) as the therapeutic mechanism. These are intended or labeled pharmacology and are not graded as nutrient findings.DailyMed label [1]; StatPearls NBK560645 [3]

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.

  • Labs

    No nutrient test is supported by this evidence

    No graded or ungraded entry supports a routine vitamin, mineral or hematologic test because of meclizine. Testing driven by symptoms, age or the underlying condition remains a clinician decision.

  • Labeled safety

    Drowsiness and anticholinergic effects

    The label warns of drowsiness, caution with driving or machinery, and caution in asthma, glaucoma and prostate enlargement. These are the drug's own effects, not nutrient findings.

  • At-risk groups

    Elderly, renal or hepatic impairment

    The label calls for caution in renal impairment, hepatic impairment and the elderly because of higher exposure. Pharmacist review of CYP2D6 inhibitors is warranted.

  • Supplement timing

    No separation interval documented

    The label states no mineral, antacid or food interaction, so no separation interval is required by the evidence reviewed. No supplement is recommended for any entry and no supplement dose appears here.

  • Pregnancy and pediatrics

    Label statements

    Epidemiological studies cited in the label have not identified an association with major birth defects; safety and effectiveness in pediatric patients have not been established.

  • Research gap

    Re-check three ungraded categories and one thin yellow

    Copper, iron and oxygen delivery/utilization should be re-searched when OpenAlex, Crossref, Semantic Scholar and Europe PMC search channels recover. For gut microbiome risk (yellow, single C. difficile abstract), the full text of [17], Zimmermann 2019 and the Maier 2018 supplementary drug list should be checked for meclizine or a first-generation H1 antagonist; the full text of [18] should be checked for oxygen consumption data.

Overlap map, to prevent double counting

  • Mitochondrial burden

    Shares evidence with: ATP production, Oxidative stress

    Note: All three rest on the same small set of Tier B papers: Nature Biotechnology 2010 [4], J Biol Chem 2013 [5], EBioMedicine 2015 [6] and the 2025 preprint [7], and on one mechanism (PCYT2 inhibition and phosphoethanolamine accumulation attenuating respiration). Treat as one line of preclinical evidence, not three confirmations.

  • ATP production

    Shares evidence with: Mitochondrial burden

    Note: The galactose-medium ATP readouts come from [5] and [6]; the preserved-ATP result from [7]. Same experiments as the mitochondrial entry, read for a different outcome.

  • Oxidative stress

    Shares evidence with: Mitochondrial burden, ATP production

    Note: The heme oxygenase-1 and iNOS mRNA finding is from [6], the same ischemia paper used for the mitochondrial structure and ATP findings. The 2023 mouse paper [8] measured inflammatory signaling only and is not counted as oxidative evidence.

  • Oxygen delivery/utilization (ungraded)

    Shares evidence with: Mitochondrial burden, ATP production

    Note: Reduced cellular oxygen consumption in [4], [5] and [6] (and the glycolytic shift in macrophages in [18], read at abstract level only) is mitochondrial respiration and cellular energy metabolism, filed once under Mitochondrial burden. It is deliberately not reused as an oxygen-delivery finding.

  • Copper

    Shares evidence with: Iron

    Note: Independent entries. They share only the same null search approach (separate PubMed queries, each a clean zero) and the same label silence; no evidence is pooled.

  • Gut microbiome risk

    Shares evidence with: Fails verification: antihistamine gut bacteria claim

    Note: The yellow grade rests only on the C. difficile screen [17], which is independent of the mitochondrial evidence cluster [4] to [7], although both describe meclizine shifting carbon metabolism toward or away from glycolysis in different organisms; treat as separate preclinical lines. The consumer microbiome article [14] cites Maier 2018 [10], which could not be shown to include meclizine; it supports no graded entry and is listed only to document the circulating class claim.

All references used above
  1. Meclizine Hydrochloride Tablets, prescribing information (RemedyRepack Inc., effective 2026-09-16; DailyMed setid d53bf04e-5cfc-4974-9b24-2cce545d1bd0). — Tier A regulatory label. Also the DailyMed listing query for brand and product names.Text read through a fetch-and-extract tool, with a second explicit pass for absent statements (excretion, food, mineral, CYP induction, nutrients: none found). A DailyMed query for the brand name Antivert returned zero entries on 2026-10-02 per the API response.
  2. WHO Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index, R06AE05. — ATC code, class (piperazine derivatives, antihistamines for systemic use) and DDD 50 mg; substance listed as meclozine.
  3. Meclizine. StatPearls, NCBI Bookshelf NBK560645. — Tier B established pharmacology reference.
  4. Gohil VM et al. Nutrient-sensitized screening for drugs that shift energy metabolism from mitochondrial respiration to glycolysis. — Nature Biotechnology 2010. Screen of more than 3,500 compounds in human fibroblasts, plus isolated mitochondria, cardiac and stroke mouse models. Tier B, meclizine-specific. PMID 20160716; doi 10.1038/nbt.1606.
  5. Meclizine inhibits mitochondrial respiration through direct targeting of cytosolic phosphoethanolamine metabolism. — Journal of Biological Chemistry 2013. Human fibroblasts and mouse striatal cells; PCYT2 and phosphoethanolamine. Tier B, meclizine-specific. PMID 24142790.Abstract-level content only: the JBC PDF returned HTTP 403 and the PubMed abstract page returned metadata only. Author list not retrieved.
  6. Kishi S et al. Meclizine preconditioning protects the kidney against ischemia-reperfusion injury. — EBioMedicine 2015. Mouse renal ischemia, 100 mg/kg meclizine. Tier B, meclizine-specific. PMID 26501107.
  7. Ghazal et al. Meclizine rescues cardiac function and mitochondrial ultrastructure by ATP- and glycolysis-independent mechanisms in a genetic model of mitochondrial energy dysfunction. — 2025, cardiomyocyte SLC25A3-deleted mice, 100 mg/kg/day for 12 weeks. Tier B, meclizine-specific. PMID 40950028; PMCID PMC12424673.The opened page identifies the work as a bioRxiv preprint; peer-review status was not resolved.
  8. Mostafa RE, Asaad GF. Meclizine moderates lipopolysaccharide-induced neuroinflammation in mice through the regulation of AKT/NF-κB/ERK/JNK signaling pathway. — Metabolic Brain Disease 2023;38(8). 40 male Swiss albino mice, oral meclizine 12.5 and 25 mg/kg for 14 days. Tier B. PMID 37733253; doi 10.1007/s11011-023-01295-3. Measured inflammatory signaling, not oxidative markers.The PMC copy returned a reCAPTCHA page; the Springer page was used. The study is cited to document that oxidative markers were not measured.
  9. Huang W, Zhang J, Wei P, Schrader WT, Moore DD. Meclizine is an agonist ligand for mouse constitutive androstane receptor (CAR) and an inverse agonist for human CAR. — Molecular Endocrinology 2004;18(10):2402. HepG2 transfection, wild-type and CAR-null mice, humanized-CAR mouse hepatocytes. Tier B, meclizine-specific. PMID 15272053.A 2011 J Pharmacol Exp Ther paper on meclizine, human PXR and CAR returned HTTP 403 and was not opened, so it is not cited.
  10. Maier L et al. Extensive impact of non-antibiotic drugs on human gut bacteria. — Nature 2018. More than 1,000 marketed drugs screened against 40 human gut bacterial strains; 24% of drugs with human targets inhibited at least one strain. Tier C at most for meclizine.Cohort excluded or unverified for this drug: meclizine was not mentioned in the content retrieved (re-checked 2026-10-04) and the supplementary drug list was not opened (the Springer static-content supplementary file host disallows automated fetches via robots.txt; not circumvented). Not used to support any graded claim.
  11. Pharmacokinetics of meclizine in children with achondroplasia (phase 1b), figure caption page. — Pediatric patients aged 5 to 10 years, 12.5 and 25 mg/day, 14 days; mean Cmax 167 ng/mL (95% CI 83 to 250) in the 12.5 mg cohort. Context only.Only the figure page was opened, not the full paper; the population is pediatric and off-label. Not used for any grade.
  12. Nutrient depletions from prescription drugs (practitioner list). Dr. Cheryl Kasdorf, ND, 2012. — Tier D. Lists "Anti-histamines" with Singulair and Zyrtec and "Essential Fatty Acids"; meclizine not named; no individual citations.
  13. Do antihistamines affect nutrient absorption? The hidden risks of allergy medications. XLR8 Your Health blog. — Tier D. Claims for vitamin C, magnesium, vitamin D, vitamin B6 and zinc; meclizine not mentioned; no primary sources.
  14. Do antihistamines affect gut bacteria? Microbiome impact. Cymbiotika blog. — Tier D. Class-level claim about antihistamines and gut bacteria citing a Nature screen without details; meclizine not mentioned.
  15. Nutrient deficiencies with histamine intolerance. Fact vs Fitness blog. — Tier D. Nutrient-to-histamine direction; lists B6, C, zinc, magnesium, copper, iron; cites 12 references; meclizine not mentioned.Other depletion handbooks opened with no mention of meclizine or antihistamines: chiropractic-clinic.com nutrient-depletion PDF, mcvitamins.com, coastalpharmacyandwellness.com.
  16. PubMed search-listing pages for meclizine (query results recorded, individual hits not cited as evidence unless listed above). — Queries run: "meclizine microbiome" (zero), "meclizine copper" (zero), "meclizine iron" (zero), "meclizine anemia" (zero), "meclizine deficiency" (7 results; none a nutrient measurement), "meclizine vitamin" (47 results), "meclizine oxidative stress" (6 results), "meclizine mitochondrial" (20 results), "meclizine gut microbiota" (zero). Revision queries: "meclizine bacteria" (12 results), "meclizine hemoglobin" (1 unrelated result), "meclizine hypoxia" (HTTP 429, no information).PubMed listing pages were rate limited (HTTP 429) on roughly half of attempts and succeeded only when spaced by about two minutes.
  17. Development of a high-throughput screening platform for C. difficile toxin synthesis inhibitors unveils meclizine as an antivirulence agent. — Antimicrobial Agents and Chemotherapy, published 2025-12-17. Prestwick Chemical Library screen at 10 and 100 µM with a C. difficile reporter strain; meclizine reduced TcdA and TcdB without affecting growth and altered central carbon metabolism. Tier B, meclizine-specific, in vitro, one gut pathogen. PMID 41405459; doi 10.1128/aac.00960-25.Abstract only, read via the OpenAlex single-record lookup https://api.openalex.org/works/pmid:41405459. The PubMed abstract page returned metadata only and the publisher page returned HTTP 429. Author list and full methods not retrieved.
  18. Bioenergetic reprogramming of macrophages reduces drug tolerance in Mycobacterium tuberculosis. — Nature Communications, published 2025-10-23. Meclizine shifted infected macrophage metabolism toward glycolysis and reduced drug tolerance in infected mice. Tier B, meclizine-specific. PMID 41130947; doi 10.1038/s41467-025-64407-w. Cited only to document that it was found and why it is not counted as oxygen-delivery evidence; overlaps with Mitochondrial burden.Abstract only, read via the OpenAlex single-record lookup https://api.openalex.org/works/pmid:41130947. The nature.com article and PDF returned HTTP 429 and were not retried. Not used to support any graded claim.