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MyDeficiencies

Mirtazapine

Tetracyclic / NaSSA antidepressant

Also sold as Remeron, Remeron SolTab.

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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.

Mirtazapine has essentially no classical depletion machinery. It is extensively metabolized (demethylation and hydroxylation via CYP2D6, CYP1A2, and CYP3A, followed by glucuronide conjugation), but it does not induce those enzymes and a direct pharmacokinetic study found no relevant change in a co-administered CYP2D6 substrate. Absorption is rapid and essentially complete, food has minimal effect on it, and there is no documented chelation, gastric-pH, or antacid-type interaction. Clearance is predominantly renal (about 75%, with 15% fecal) as metabolites, with no labeled tubular-wasting mechanism for any electrolyte or mineral. Nothing in this profile implicates iron, copper, or any classical vitamin through an absorption, catabolism, or renal-wasting pathway, and the literature search below found no red- or orange-grade classical micronutrient deficiency signal for this drug.

Tetracyclic / NaSSA antidepressant · ATC N06AX11 · also sold as Remeron and Remeron SolTab · reviewed 2026-09-29. 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 Mirtazapine 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

Sodium, rare dilutional hyponatremia

Orange — Moderate

See study details

Mirtazapine is labeled as causing hyponatremia very rarely, through a presumed dilutional mechanism, bounded by low frequency and by at-risk subgroups; this is a retention/dilution risk, not a dietary sodium deficiency.

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 negative/null findings: No controlled trial has systematically measured serum sodium change with mirtazapine at scale; the great majority of patients show no detectable sodium disturbance.
  • At-risk subgroups: Elderly patients; patients concomitantly treated with other hyponatremia-associated medications (per label language).

Regulatory status

Labeled precaution. FDA label: "Hyponatremia has been reported very rarely with the use of mirtazapine. Caution should be exercised in patients at risk, such as elderly patients or patients concomitantly treated with medications known to cause hyponatremia."

Population evidence

Human, drug-specific, postmarketing surveillance (Tier A, this drug in the reporting population). No numerator/denominator beyond the "very rare" frequency category is given in the label.

Mechanism

Presumed dilutional/SIADH-type antidiuretic-hormone-potentiation effect, a pattern documented for other antidepressant classes; not a classical renal sodium-wasting or intake-reduction mechanism.

Counter-evidence held on record

No source was found showing mirtazapine protects against or has no sodium effect; the absence of a large systematic study (versus postmarketing case reports only) is itself the evidentiary limitation, disclosed here rather than upgraded past what the data support. This is a retention/dilutional risk, not a dietary sodium deficiency. Do not add sodium or salt supplementation in response to this entry. New hyponatremia in a patient on mirtazapine should prompt a SIADH workup and medication review, not supplementation.

Caloric intake / appetite, reverse-direction context flag

Yellow — Low

Direction: reverse direction (as labelled in the source)

Mirtazapine's hallmark effect is an intake-increasing one, not a depletion signal: it reliably increases appetite and produces clinically meaningful weight gain in a minority of patients via H1 and 5-HT2C receptor antagonism.

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, reverse-direction

Limits on what this shows

  • Key negative/null findings: The majority of patients (over 80% by the appetite-increase figure) do not report a clinically flagged effect; this is not a universal response.
  • At-risk subgroups: Patients with pre-existing obesity, metabolic syndrome, or diabetes risk, where the concurrent lipid effects compound the concern; conversely, underweight or cachectic patients may see this as a clinical benefit rather than a risk.

Regulatory status

Labeled adverse reaction, drawn from placebo- and active-comparator-controlled trials (Tier A, this drug in the cohort).

Population evidence

Appetite increase reported in 17% of mirtazapine patients vs. 2% placebo vs. 6% amitriptyline. Weight gain ≥7% of body weight in 7.5% of mirtazapine patients vs. 0% placebo vs. 5.9% amitriptyline. Nonfasting cholesterol increases ≥20% above the upper limit of normal in 15% of patients; nonfasting triglyceride increases to ≥500 mg/dL in 6%.

Mechanism

Named: potent histamine H1 receptor antagonism plus 5-HT2C receptor antagonism, a well-established combination for appetite stimulation and weight gain in this drug class.

Counter-evidence held on record

No counter-evidence changes the direction; this finding has been replicated consistently across mirtazapine's controlled-trial history since approval. This is an appetite/intake-increasing effect, not a nutrient deficiency, and must never be marketed as one. It should surface only as a metabolic-monitoring prompt (weight, lipids, glucose), never as a supplementation cue, and increased intake does not by itself guarantee improved micronutrient status.

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 drug-specific evidence on mitochondrial structure, membrane integrity, electron transport, or biogenesis was located for mirtazapine, and the only circulating claim touching mitochondrial health for this drug (CoQ10 depletion) is addressed and fails under its own entry.

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: Re-searched on a dedicated pass across PubMed, Crossref, Europe PMC, Semantic Scholar, OpenAlex, Google Scholar, Bing, DuckDuckGo, and BASE, across multiple phrasings (mitochondria, complex I/IV, membrane potential, biogenesis, mitochondrial function, respiratory chain), plus direct text search of the FDA label, the StatPearls mirtazapine monograph, the DrugBank monograph, and the full text of the already-identified 2023/2024 mirtazapine-specific narrative pharmacology review. None of these directly-read, drug-specific sources contains any substantive discussion of mitochondrial structure, membrane potential, or biogenesis; the one incidental hit, a background-section sentence in the NeuroSci 2021 in vitro study noting that oxidative stress generally causes "dysfunction of the mitochondrial membrane potential," is generic scientific background, not a mirtazapine-specific finding, and is not cited as evidence here. The 2019 rodent survey of psychotropic effects on mitochondrial complex I and IV activity across 53 drugs, identified by title in the original review, remained inaccessible on this pass for the same reason: its drug-by-drug results, including whether mirtazapine was among the antidepressants tested, could not be retrieved through any working channel.

Tooling notes

On this dedicated re-pass, Europe PMC's REST API (www.ebi.ac.uk) and the Crossref API were rejected at the proxy level with HTTP 429 on every attempt, across multiple query phrasings and multiple minutes apart; the OpenAlex and Semantic Scholar search endpoints returned HTTP 429 directly from those services (OpenAlex's per-record lookup endpoint, by contrast, worked and was used successfully elsewhere in this pass, confirming the block is specific to search, not the hosts generally); PubMed's search-listing pages were proxy-rejected and individual PubMed article pages returned stub content with no abstract; PMC article pages served a bot-verification challenge; Google Scholar, Bing, and DuckDuckGo search were disallowed by robots.txt; BASE (base-search.net) served an Anubis bot-block page; the general WebSearch tool had exhausted its session query budget before this category was reached. This is the same set of blocks disclosed in the original review, now confirmed fresh and host-by-host under a dedicated budget, so it reflects a persistent access limitation rather than a literature that has been exhausted.

Dual condition check

No Tier B/C mitochondrial-structure evidence located, and the one related circulating claim (CoQ10, a mitochondrial electron carrier) is a distinct nutrient-level claim, addressed and rebutted under its own Fails verification entry. See Overlap map.

Oxidative Stress

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

Oxidative stress, preclinical protective direction, stressor-dependent

Yellow — Low

Direction: reverse direction (as labelled in the source)

Drug-specific animal and in vitro evidence points toward an antioxidant, protective effect for mirtazapine against some oxidative challenges, but not against others, and no human clinical oxidative-stress data exist for this drug.

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, reverse-direction

Limits on what this shows

  • Key negative/null findings: In the same in vitro system, mirtazapine "does not lead to a decrease in cell viability" when applied alone, counteracted H2O2-induced stress (most pronounced in SH-SY5Y cells), but failed to alleviate corticosterone-induced stress, and some mirtazapine/corticosterone combinations worsened outcomes. Direction is stressor-dependent, not uniformly protective.
  • At-risk subgroups: None identified; no human clinical data exist to define a subgroup.

Regulatory status

Not addressed in the FDA label.

Population evidence

In vitro: human SH-SY5Y neuroblastoma and mouse HT-22 hippocampal cell lines, mirtazapine 0.01-20 µM, tested against hydrogen peroxide (50-300 µM) and corticosterone (100-500 µM) stressors (NeuroSci 2021). A 2023/2024 mirtazapine-specific narrative pharmacology review separately states that "numerous in vitro and in vivo investigations have clearly demonstrated the antioxidant and anti-inflammatory properties of MTZ," citing a reproductive-toxicity study in which mirtazapine increased glutathione and decreased lipid peroxidation.

Mechanism

Not fully characterized at the molecular level in what this review could access; described in the narrative review as antioxidant/anti-inflammatory, consistent with reduced lipid peroxidation and preserved glutathione in the cited animal model.

Counter-evidence held on record

The corticosterone-stress arm of the in vitro study is itself a null/negative finding for protection and is recorded here rather than omitted. Two related animal studies on this topic (a cisplatin-induced rat brain oxidative stress model and a rat kidney ischemia-reperfusion model) were located by title and topic during this search but could not be opened in full text during this review (403/paywall); they are listed in Sources as unverified and were not used to support this grade. This is preclinical, animal/in vitro evidence only, in a protective rather than depleting direction. It must never be read as a reason to reduce dietary antioxidant intake, and must never be marketed as a demonstrated clinical antioxidant benefit, which has not been shown in humans taking this drug.

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 mirtazapine-and-copper evidence was confirmed, and no circulating claim names copper specifically for this drug.

Full detail, limits and 1 references

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: Re-searched on a dedicated pass across PubMed, Crossref, Europe PMC, Semantic Scholar, OpenAlex, Google Scholar, Bing, DuckDuckGo, and BASE, across multiple phrasings (serum copper, trace element, ceruloplasmin, copper/zinc ratio, copper homeostasis) combined with mirtazapine, plus direct text search of the FDA label, the StatPearls monograph, the DrugBank monograph, and the mirtazapine-specific narrative pharmacology review, none of which contain the word copper. The previously identified animal trace-element study, "Alterations in serum and brain trace element levels after antidepressant treatment, Part II: Copper" (Biological Trace Element Research, c. 2000, PMID 10949967), was this time confirmed via an OpenAlex single-record lookup (a channel that worked despite the search-endpoint blocks below): its studied cohort was citalopram, imipramine, and fluoxetine in Wistar rats, not mirtazapine. This is now a definite cohort-test failure for this source, not an unverified possibility, and the study remains uncited as evidence for mirtazapine specifically.

Tooling notes

Search-capable channels were blocked in the same pattern disclosed under Mitochondrial burden above: Europe PMC and Crossref proxy-rejected (429) on every attempt; OpenAlex's and Semantic Scholar's search endpoints returned 429 directly from the services; PubMed search pages proxy-rejected and individual PubMed pages returned no abstract; PMC bot-gated; Google/Bing/DuckDuckGo/BASE blocked by robots.txt or bot-verification; WebSearch's session budget was exhausted. OpenAlex's per-record lookup endpoint (by PMID) was the one channel that worked, and it is what resolved the cohort question for the one candidate source above, rather than leaving it unverified.

Dual condition check

No confirmed Tier B/C evidence, and no circulating consumer claim naming copper for mirtazapine was found (the identified consumer depletion claim covers B6, C, D, CoQ10, and sodium only, not copper).

Iron

Not graded — disclosed evidence gap

See study details

No mechanism or evidence was found for mirtazapine causing iron depletion, and no circulating claim names iron for this drug.

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: Re-searched on a dedicated pass across PubMed, Crossref, Europe PMC, Semantic Scholar, OpenAlex, Google Scholar, Bing, DuckDuckGo, and BASE, across multiple phrasings (iron deficiency, anemia mechanism, ferritin, iron absorption, hepcidin, iron and restless legs), plus direct text search of the FDA label (iron appears only once, as the inactive-ingredient colorant "ferric oxide," not as a biological finding), the StatPearls monograph, the DrugBank monograph, and the narrative pharmacology review. The only mirtazapine-and-iron literature located across either pass remains the reverse-direction pediatric case (pre-existing iron deficiency whose periodic limb movements worsened while separately taking mirtazapine for insomnia); this describes iron deficiency affecting symptoms during mirtazapine use, not mirtazapine causing iron deficiency, so per this protocol's direction rule it cannot support a depletion claim.

Tooling notes

Unlike the Mitochondrial burden and Copper categories, the original null result here was not primarily a tooling-block artifact; the FDA label, StatPearls, DrugBank, and narrative-review full-text checks on this pass returned genuinely negative, readable content rather than blocked pages, reinforcing that this is a real evidence gap rather than an access failure. The general PubMed/Crossref/Europe PMC/Semantic Scholar/OpenAlex-search/Google/Bing/DuckDuckGo/BASE blocks described under Mitochondrial burden applied equally here and prevented a fresh literature search beyond the sources already opened.

Dual condition check

No Tier B/C evidence supporting even a yellow grade, and no circulating claim naming iron for mirtazapine specifically. Genuine evidence gap.

Gut Microbiome Risk

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

Gut microbiome risk, in vitro growth inhibition of commensal species

Yellow — Low

See study details

In vitro, mirtazapine inhibits growth of several normal gut commensal species, including beneficial Lactobacillus and Bifidobacterium strains, at pharmacologic concentrations; no human gut-microbiome data exist for this drug.

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 human stool or 16S microbiome study of mirtazapine-treated patients was located. In vitro concentrations tested may not reflect achievable gut luminal drug concentrations in vivo; translatability is unconfirmed.
  • At-risk subgroups: None defined clinically; this remains a theoretical, mechanism-level concern.

Regulatory status

Not addressed in the FDA label.

Population evidence

In vitro antimicrobial susceptibility study, six antidepressants including mirtazapine tested against six organisms representative of normal gut/mucosal microbiota (Staphylococcus aureus, Escherichia coli, Candida albicans, Bifidobacterium bifidum, Enterococcus faecalis, Lactobacillus rhamnosus) (Frontiers in Behavioral Neuroscience, 2023).

Mechanism

Direct antimicrobial/growth-inhibitory activity. At 200 µg/mL, mirtazapine reduced L. rhamnosus growth by 77% and C. albicans growth by 81%; B. bifidum growth was reduced 76% at the same concentration, and E. faecalis growth was reduced 50% at the lowest effective concentration tested. Mirtazapine showed the greatest activity of the antidepressants tested against L. rhamnosus and C. albicans.

Counter-evidence held on record

No in vivo or clinical counter-evidence was located either way; the absence of confirmatory human data is the central limitation and is disclosed rather than glossed over. A separate rat "gut resistome" study of mirtazapine was identified by title during this search but its full content could not be retrieved during this review; it is listed in Sources as unverified. This is in vitro mechanistic evidence only. It has not been shown to translate into a clinically meaningful microbiome disruption in patients taking mirtazapine and should not be marketed as an established gut-health risk.

Oxygen and ATP Output

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

Oxygen delivery/utilization, rare idiosyncratic marrow suppression

Yellow — Low

See study details

Mirtazapine carries a labeled, rare risk of agranulocytosis/severe neutropenia, and an isolated case report describes a rarer bone-marrow-suppression reaction extending to anemia; this is not a systematic hemoglobin or oxygen-delivery deficit.

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: Agranulocytosis/neutropenia is rare and idiosyncratic; it is not a dose-dependent or universal finding, and the overwhelming majority of patients show no hematologic change.
  • At-risk subgroups: Patients with autoimmune disease (the labeled agranulocytosis case had Sjogren's Syndrome); early treatment/dose-titration period, based on the case-report timeline.

Regulatory status

Labeled precaution (Tier A) for agranulocytosis/severe neutropenia: "2 (1 with Sjogren's Syndrome) out of 2796 patients... developed agranulocytosis" plus one severe neutropenia case, a crude incidence of "approximately 1.1 per thousand patients exposed." This figure describes white-cell suppression, not a hemoglobin/oxygen-delivery measure.

Population evidence

Case report (Tier B, this drug specifically): a 71-year-old woman on mirtazapine developed bicytopenia (moderate anaemia and leukopenia) 10 days after dose titration; a Naranjo Adverse Drug Reaction Probability Scale assessment indicated a definite temporal association, and the cytopenias fully resolved after mirtazapine was stopped. The authors note that reported cases of mirtazapine-associated anaemia are otherwise essentially absent from the literature, i.e. this is a rare, not a systematic, signal.

Mechanism

Not established; presumed idiosyncratic, immune-mediated bone-marrow suppression, a pattern seen with other agranulocytosis-associated psychotropics, not a nutrient-pathway (iron, B12, erythropoietin) mediated mechanism.

Counter-evidence held on record

The label itself frames agranulocytosis as a rare idiosyncratic event, not a general population signal, and no large-scale hematologic surveillance data beyond premarketing trials and case reports were located. Two additional case reports (a 2001 bone-marrow-suppression case and a Turkish Journal of Hematology thrombocytopenia/neutropenia case) were identified by title during this search but their full text could not be opened during this review; they are listed in Sources as unverified and were not used to support specific claims above beyond their existence. This is a rare idiosyncratic bone-marrow-suppression risk, not a nutrient-mediated anemia. It should prompt CBC awareness in symptomatic patients (fever, infection, unusual fatigue or pallor), not iron or B12 supplementation, which would not address the underlying mechanism.

ATP production

Not graded — disclosed evidence gap

See study details

No mirtazapine-specific data on ATP synthesis or cellular energy output was located, and labeled somnolence/sedation is the drug's own intended pharmacologic effect, not an ATP-production finding.

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: Re-searched on a dedicated pass across PubMed, Crossref, Europe PMC, Semantic Scholar, OpenAlex, Google Scholar, Bing, DuckDuckGo, and BASE, across multiple phrasings (ATP synthesis, cellular energy, oxidative phosphorylation, energy metabolism, mitochondrial ATP), plus direct text search of the FDA label, the StatPearls monograph, the DrugBank monograph, the narrative pharmacology review, and the NeuroSci 2021 in vitro study, none of which contain the word ATP or any discussion of cellular energy output. No mirtazapine-specific ATP-production study was located on either pass. Labeled somnolence (54% of patients vs. 18% placebo) remains excluded here as the drug's own H1-antihistamine sedative pharmacologic effect, not an ATP-production finding, per the hard rule against filing a drug's intended effect as a nutrient/energy finding.

Tooling notes

The same PubMed/Crossref/Europe PMC/Semantic Scholar/OpenAlex-search/Google/Bing/DuckDuckGo/BASE blocks disclosed under Mitochondrial burden applied to this category; the drug-specific and class-adjacent full texts that were reachable (label, StatPearls, DrugBank, narrative review, NeuroSci 2021) were read in full and returned genuinely negative content rather than blocked pages.

Dual condition check

No Tier B/C evidence, and no circulating claim specifically framed around ATP or cellular energy production for this drug (as distinct from generic sedation/fatigue side-effect commentary) was found. Genuine evidence gap.

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 B6

    Where it comes from: Consumer nutrient-depletion blog post, citing D.W. Tanton, Antidepressants, Antipsychotics & Stimulants (2006), a non-peer-reviewed book: "Remeron depletes... Vit B6."

    Why it fails: No absorption, catabolism, renal-wasting, or cofactor-antagonism mechanism was identified in the FDA label or in a multi-channel peer-reviewed search. The label does not mention pyridoxine. No class-level (Tier C) tetracyclic/NaSSA antidepressant literature connecting this class to B6 status was found.

  • Vitamin C

    Where it comes from: Same blog/book source: "Remeron depletes... vit C."

    Why it fails: No mechanism identified; no Tier B or Tier C literature, drug-specific or class-level, links mirtazapine or NaSSA antidepressants to ascorbic acid status.

  • Vitamin D

    Where it comes from: Same blog/book source: "Remeron depletes... vit D."

    Why it fails: No mechanism identified; mirtazapine is not a CYP-inducer (unlike anticonvulsants, which do have an established vitamin D-catabolism mechanism). General depression/vitamin D association literature exists but does not isolate a mirtazapine-specific causal effect on vitamin D levels.

  • Coenzyme Q10

    Where it comes from: Same blog/book source: "Remeron depletes... coQ10."

    Why it fails: No mechanism identified; mirtazapine does not inhibit HMG-CoA reductase or the mevalonate pathway (the established CoQ10-depletion mechanism for statins). No mirtazapine-specific CoQ10 study was found. This claim is mitochondrial-adjacent (CoQ10 is an electron-transport-chain carrier); see Overlap map for its relationship to the Mitochondrial burden entry.

How the body handles this medication

Metabolism
Extensively metabolized: demethylation and hydroxylation followed by glucuronide conjugation. CYP2D6 and CYP1A2 form the 8-hydroxy metabolite; CYP3A forms the N-desmethyl and N-oxide metabolites.FDA label, Remeron, accessdata.fda.gov 2010
CYP induction / inhibition
No enzyme-induction claim in the label. A direct interaction study found mirtazapine 30 mg/day did not cause relevant changes in steady-state paroxetine (a CYP2D6 substrate/inhibitor) pharmacokinetics, i.e. no clinically relevant CYP2D6 inhibition demonstrated.FDA label, Remeron, accessdata.fda.gov 2010
Elimination
About 75% urinary, 15% fecal (as metabolites); oral bioavailability ~50%; mean half-life 20-40 h (37 h women, 26 h men). Clearance reduced ~30% in moderate and ~50% in severe renal impairment, ~30% in hepatic impairment, and ~40% lower in elderly men vs. younger men.FDA label, Remeron, accessdata.fda.gov 2010
Absorption
Rapid and essentially complete oral absorption, peak plasma level within ~2 h, minimal food effect on rate or extent of absorption, ~85% plasma protein bound. No documented chelation, gastric-pH, or antacid-timing interaction.FDA label, Remeron, accessdata.fda.gov 2010
Renal / electrolyte handling
No tubular electrolyte-wasting mechanism identified. Hyponatremia is labeled as occurring very rarely, with caution in the elderly or in patients on other hyponatremia-associated drugs, a dilutional/SIADH-type pattern, not a classical excretion-driven depletion.FDA label, Remeron, accessdata.fda.gov 2010
Receptor pharmacology relevant to nutrition
Potent H1 antagonist (sedation; somnolence 54% vs. 18% placebo) and potent 5-HT2/5-HT3 antagonist; H1 plus 5-HT2C antagonism together drive appetite increase and weight gain. No significant 5-HT1A/5-HT1B affinity.FDA label; Naunyn-Schmiedeberg's Arch Pharmacol narrative review 2023/2024
All references used above
  1. Remeron (mirtazapine) Tablets, full prescribing information — FDA-approved regulatory label. accessdata.fda.gov, docket 020415s023s024, revised 2010.
  2. Costa, et al. Significant Differences in the Reversal of Cellular Stress Induced by Hydrogen Peroxide and Corticosterone by the Application of Mirtazapine or L-Tryptophan — In vitro study, human SH-SY5Y neuroblastoma and mouse HT-22 hippocampal cell lines, mirtazapine tested directly. NeuroSci, vol. 2, issue 3, article 36, 2021.
  3. Antimicrobial activity of antidepressants on normal gut microbiota: Results of the in vitro study — In vitro antimicrobial susceptibility study, six antidepressants including mirtazapine, six microbial species. Frontiers in Behavioral Neuroscience, 2023. PMID 37035624.
  4. Mirtazapine-Induced Bicytopenia in a Patient With Multifactorial Delirium: A Case Report — Case report, 71-year-old female, this drug specifically. Cureus, 2024/2025. PMID 42181357.
  5. Pharmacological update of mirtazapine: a narrative literature review — Drug-specific narrative pharmacology review. Naunyn-Schmiedeberg's Archives of Pharmacology, 2023/2024. DOI 10.1007/s00210-023-02818-6.
  6. Denutrients (consumer blog): "Mitochondrial damage due to psychiatric [medications]," citing D.W. Tanton, Antidepressants, Antipsychotics & Stimulants (2006) — Tier D consumer source. Origin of the circulating "Remeron depletes B6, C, D, CoQ10, sodium" claim rebutted above.
  7. Drug Nutrient Depleters / Drug Muggers Table — Tier D consumer source, checked and confirmed to NOT list mirtazapine/Remeron individually (only a generic "Anti-Depressants" category covering MAOIs, SSRIs, and tricyclics).
  8. Gulec, et al. Mirtazapine protects against cisplatin-induced oxidative stress and DNA damage in the rat brain — Animal study (rat), title and topic confirmed via journal indexing. Psychiatry and Clinical Neurosciences, 2013. PMID 23279761.Full text not accessible during this review (HTTP 403). Not used to support any specific quantitative claim above; listed for completeness and future verification only.
  9. Effect of Mirtazapine on Oxidative Stress Created in Rat Kidneys by Ischemia-Reperfusion — Animal study (rat), title and topic confirmed via journal indexing. Renal Failure, 2011. PMID 22032749.Full text not opened during this review (paywalled). Not used to support any specific quantitative claim above; listed for completeness only.
  10. Hutchison, L.C., et al. Mirtazapine and bone marrow suppression: A case report — Case report, title and topic confirmed via journal indexing. Journal of the American Geriatrics Society, 2001.Full text not accessible during this review (HTTP 403). Not used to support specific patient-level details above beyond its existence and topic.
  11. Mirtazapine-Induced Thrombocytopenia and Neutropenia — Case report, title and topic confirmed via journal indexing. Turkish Journal of Hematology, vol. 29, issue 3, pp. 297-298.Full text not opened during this review. Not used to support specific patient-level details above beyond its existence and topic.
  12. Schlegel-Zawadzka, M., Nowak, G. Alterations in serum and brain trace element levels after antidepressant treatment. Part II. Copper — Animal study, rat (Wistar). Biological Trace Element Research, vol. 73, issue 1, pp. 37-46, 2000. PMID 10949967.Full text and abstract not directly accessible during either review (PubMed served a bot-verification page in place of content both times). Cohort now confirmed via an OpenAlex single-record lookup (accessed 2026-09-29): the studied antidepressants were citalopram, imipramine, and fluoxetine, not mirtazapine. This is a definite cohort-test failure for mirtazapine, not merely unverified, and the study is not cited as supporting evidence for the Copper entry.
  13. Brain-derived neurotrophic factor modulation in response to oxidative stress and corticosterone: role of scopolamine and mirtazapine — Animal/cell study, title and topic confirmed via journal indexing. ScienceDirect (journal not confirmed further in this review).Full text not opened during this review. Not used to support any specific claim above; listed for completeness only.
  14. Effects of the antidepressant mirtazapine on the gut resistome in rats — Animal study, title and topic confirmed via journal indexing. SciEngine/Acta Microbiologica Sinica, 2025.Only platform metadata was retrievable during this review, not the study content. Not used to support the Gut microbiome risk grade above; listed for completeness and future verification.
  15. World Health Organization Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index — ATC code N06AX11, mirtazapine.