Ivermectin

avermectin (macrocyclic lactone) antiparasitic

Also sold as Stromectol.

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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.

Ivermectin has no classical depletion machinery. It is cleared by hepatic metabolism (primarily CYP3A4) and excreted almost entirely in feces over about 12 days, with under 1% in urine, and neither U.S. label retrieved mentions any vitamin, mineral or other nutrient as an adverse effect or interaction [1][2]. It inhibits no major CYP enzyme at clinical concentrations in vitro. The one well-measured nutrient relationship runs from nutrient to drug: a high-fat meal raises ivermectin exposure, with an AUC ratio of 2.57 (95% CI 2.16 to 3.05) in a placebo-controlled Merck study of 68 volunteers [4], while a pooled population-PK analysis of 15 volunteers estimated only 1.18 (95% CI 1.10 to 1.67) [5]. Under Hard Rule 4 this is a dosing-timing interaction (the label says take on an empty stomach with water), not a depletion, and it is graded yellow.

avermectin (macrocyclic lactone) antiparasitic · ATC P02CF01 (WHO ATC/DDD Index [3]) · also sold as Stromectol and Mectizan; many generics · reviewed 2026-10-09. 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 Ivermectin 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 fat and food: timing interaction (nutrient affects the drug), exposure rises with a high-fat meal

Yellow — Low

See study details

A high-fat meal raises ivermectin exposure by an amount that differs between two human studies (2.57-fold versus 1.18-fold); this is a dosing-timing issue, not a nutrient depletion.

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

At-risk subgroups: Not defined. The label records neurotoxicity as a warning; whether food-raised exposure alters that risk was not studied in anything opened.

Direction

Nutrient (dietary fat) affects the drug. Hard Rule 4 applies: filed as a timing interaction, not a depletion. Ivermectin does not deplete fat or any fat-soluble nutrient in any source opened.

Regulatory status

Both labels: a 30 mg dose after a high-fat meal (48.6 g fat) gave about 2.5-fold higher bioavailability than fasting; tablets are to be taken on an empty stomach with water [1][2].

Population evidence

Guzzo 2002 [4] (double-blind, placebo-controlled, Merck-sponsored, 68 enrolled, 30 mg fed n=11, 30 mg fasted n=15): AUC fed/fasted geometric mean ratio 2.57 (95% CI 2.16 to 3.05), fed Cmax roughly 3-fold, half-life about 15 hours fed versus about 20 hours fasted. Duthaler 2020 [5] (pooled population-PK of two earlier trials, 15 healthy volunteers, 12 fed and 3 fasted, single 12 mg dose, high-fat breakfast 30 minutes before): model-based food effect 1.18 (95% CI 1.10 to 1.67), which the authors called minimal. The two Tier A sources agree on direction but not on size. Differences in dose (30 mg versus 12 mg), meal timing, and a 3-person fasted arm in [5] may explain part of the gap; the sources do not say which factor matters.

Other beverages

A mini-review [7] reports that 750 mL of orange juice lowered exposure versus water and 750 mL of beer raised plasma levels; the units in the retrieved summary were swapped and internally inconsistent, so no numbers are used. The primary orange-juice report is a 2003 meeting abstract [6] whose text could not be opened.

Mechanism

Not stated in any source opened. A food-driven rise in absorption of a lipophilic drug is plausible but was not demonstrated mechanistically here.

Separation or timing

The label instructs an empty stomach with water but names no hour interval. In the trials, fasted dosing was followed by a meal at about 4 hours [4][20]. The interval is therefore trial practice, not a label rule.

Counter-evidence held on record

Counter-evidence [5] found only a minimal food effect; a protocol document advises taking ivermectin with a meal [28], which is opposite to the label. The disagreement is real and unresolved in the sources opened. Framing caution Timing note only, not a deficiency claim and not a reason to add any nutrient. Follow the prescriber and the label; do not change how ivermectin is taken based on this entry.

Albumin and plasma protein binding: context flag, nutritional state affects free drug, disease lowers albumin

Yellow — Low

See study details

About 93% of ivermectin is protein bound; malnutrition or low albumin could raise the free fraction, and strongyloidiasis itself can lower albumin, but no source shows ivermectin lowering albumin.

Full detail and limits

Limits on what this shows

Null findings: No albumin change is reported in the label adverse reaction tables [1][2]. Guzzo [4] did not report albumin in the text read.

Direction

Protein or nutritional status affects the drug (Hard Rule 4), plus a disease effect (Hard Rule 6). Not a depletion by ivermectin.

Regulatory status

Albumin is not mentioned among adverse reactions on either label [1][2]; the Merck page retrieved did not state protein binding.

Population evidence

Klotz 1990 [8]: equilibrium dialysis in 5 healthy people, binding 93.2% (SD 4.4); the authors suggest the strong binding matters in malnutrition or diseases that lower plasma protein because the free fraction could rise (their inference; free fraction was not measured in such patients). Mini-review [7]: 93.1% in onchocerciasis patients, mainly albumin. Case [25]: a man with lepromatous leprosy and strongyloides hyperinfection, albumin 1.7 g/dL and hemoglobin 7.2 g/dL on admission, 2.8 and 8.8 at discharge after oral ivermectin 12 mg for 3 days plus transfusions and albumin infusions; the authors attribute both to the infection by clinical course, not by direct proof.

Mechanism

High-affinity albumin binding [7][8]. No mechanism by which ivermectin would reduce albumin synthesis or raise loss was found.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication is presumed: the diseases treated cause anemia, protein loss and malnutrition. One case report cannot separate disease from drug. Framing caution Context flag, not a deficiency claim. Do not recommend protein or albumin interventions from this entry.

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: in vitro only, at concentrations far above label plasma levels

Yellow — Low

See study details

Ivermectin lowers mitochondrial membrane potential and respiration in cultured cells at micromolar concentrations; no human measurement exists in anything retrieved.

Full detail and limits

Limits on what this shows

Null findings: No study measuring mitochondrial function in humans given ivermectin was located. ATP was preserved, not reduced, in one cardiomyocyte study (see ATP entry).

Direction

Possible drug-caused organelle effect (excess toxicity signal), not a nutrient deficiency (Hard Rule 2). No nutrient is implicated by these studies.

Regulatory status

No mitochondrial content in either label [1][2].

Population evidence

None in humans. Zhang 2022 [16] (Tier B): human SH-SY5Y neuroblastoma cells, 2.5 to 15 micromolar for 24 hours; ROS rose about 1.3 to 4.2-fold and membrane potential fell (JC-1 green/red ratio up about 1.5-fold at 10 micromolar, p<0.01); ATP and oxidative phosphorylation were not measured. Lee 2022 [17]: pancreatic cancer cells; the ivermectin-plus-gemcitabine combination lowered oxygen consumption rate versus gemcitabine alone, ivermectin concentrations not stated in the retrieved text, and complex I and ATP were not measured. Liu 2020 review [18] (secondhand): dose-dependent falls in basal and maximal oxygen consumption attributed to complex I in U87, T98G and HBMEC cells, concentrations not given; mitochondrial effects were greater in leukemia progenitor cells than in normal marrow cells.

Concentration check

The label peak after a fasting 12 mg dose is 46.6 ng/mL [1], about 0.05 micromolar (molar mass 875.1 g/mol [29]), and protein binding is about 93% [8]. Cell studies used 2.5 to 15 micromolar, about 50 to 280 times higher. The review [18] says 5 micromolar is clinically achievable, citing a 120 mg dose study; by simple linear scaling of the label peak that dose gives about 0.5 micromolar, still about tenfold lower (my arithmetic, not a measured value).

Mechanism

Proposed complex I inhibition and membrane depolarization in cancer cell lines [18]. Not shown in human tissue, blood cells or at clinical exposure.

Counter-evidence held on record

Counter-evidence Supraclinical concentrations, cancer or neuronal cell lines, and combination designs limit relevance. [16] also has an internal inconsistency: one section describes SOD and CAT as decreased while the reported values rise. Framing caution Mechanistic signal only. Not a statement that ivermectin damages mitochondria in patients, and not a reason to take mitochondrial supplements.

Oxidative Stress

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

Oxidative stress: in vitro and animal, mixed direction, no human marker data

Yellow — Low

See study details

Cell and animal studies show pro-oxidant effects at high doses, with mixed antioxidant-enzyme patterns; no study measured oxidative stress markers in people given ivermectin.

Full detail and limits

Limits on what this shows

Null findings: A PubMed search for ivermectin with malondialdehyde, serum and patients returned zero results [30]. The fish study [24] shows lower lipid peroxidation at higher exposure, not higher.

Direction

Drug-caused pro-oxidant signal in models (excess toxicity), not a nutrient depletion. Hard Rule 2 applies.

Regulatory status

No oxidative-stress statement in either label [1][2].

Population evidence

None in humans. [16] (in vitro): MDA rose to 0.25 and 0.76 nmol/mg protein at 10 and 15 micromolar; ROS rose in a dose-dependent way. El-Shobokshy 2023 [23] (animal): 72 male rabbits, 18 per group, ivermectin 0.2 mg/kg subcutaneously weekly for 5 weeks; testicular MDA higher, SOD and CAT lower, and GSH reported lower in ivermectin groups; zinc nanoparticles in the diet reduced the changes (abstract and summary read; exact values not captured). Ogueji 2020 [24] (animal): juvenile catfish, 9 to 25 micrograms/L for up to 4 days; SOD, CAT and GR rose, GPx fell, and lipid peroxidation fell at the higher concentrations, which the authors still read as oxidative stress.

Mechanism

ROS generation tied to mitochondrial depolarization in vitro [16]; not shown in vivo in humans.

Counter-evidence held on record

Counter-evidence The rabbit dose is close to the human antiparasitic dose by weight but is repeated weekly in a toxicity design; fish and cell data are not human exposure. A related rat study ([22], B12 and folic acid co-treatment) reported toxicity at an unstated dose. Framing caution Not an antioxidant-depletion claim and not a recommendation to take antioxidants. Antioxidant supplements are not indicated by this entry.

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 found that ivermectin changes copper status, binds copper in a physiologically relevant way, or is claimed to do so.

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 for ivermectin and copper, and no circulating claim linking ivermectin to copper was found. A disclosed gap, not a finding of safety. Kept independent of Iron (Hard Rule 7).

What was searched

Web search "ivermectin serum copper OR ceruloplasmin OR copper chelation OR copper complex ivermectin": results were generic copper-chelation and copper-lab pages, none on ivermectin. PubMed listing "ivermectin copper": 32 results, first 10 reviewed from snippets; all were nanomaterial, veterinary or receptor pharmacology records, none measured copper status in people or animals given ivermectin, and none reported copper-ivermectin chemistry [30]. Both labels were read; magnesium stearate and colloidal silicon dioxide appear only as excipients [1][2]. The 2021 protocol document [28] cautions that prolonged high-dose zinc is associated with copper deficiency; that statement concerns zinc, not ivermectin.

Channel outcomes

Web search: open phrasing, zero relevant hits; search budget later exhausted. PubMed listing: opened once for page 1 only (pages 2 to 4 not read). PMC pages: reCAPTCHA. Europe PMC, Crossref: 429. This is a mix of a clean zero on open web search and limited database depth, so a genuine gap with a tooling-limited tail.

Iron

Not graded — disclosed evidence gap

See study details

No study measuring iron, ferritin or transferrin in people given ivermectin was found, and no circulating claim links ivermectin to iron.

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 ivermectin and iron and no circulating claim to rebut. A disclosed gap, not reassurance. Any anemia signal is held in the Oxygen delivery entry and not counted twice (see Overlap map).

What was searched

Web search "ivermectin iron ferritin transferrin serum iron effect randomized OR cohort OR rats": no iron-measuring ivermectin study. Web search "ivermectin treatment haemoglobin anaemia iron status ferritin cohort strongyloidiasis OR onchocerciasis OR scabies": dosing and guideline pages only. PubMed listing "ivermectin ferritin": 10 results, none measured ferritin or iron indices in people given ivermectin (snippets only; several were COVID-19 outcome papers and veterinary records) [30]. The hemoglobin studies in the Oxygen delivery entry measured hemoglobin, not iron indices [20][21]. Cohort-level nutrition searches (vitamin A, zinc, iron in onchocerciasis) returned parasite-and-nutrition reviews not specific to ivermectin; none was opened.

Channel outcomes

As for Copper. Strongyloides-associated iron deficiency and anemia exist as disease reports seen only as titles in search results (not opened) and in one opened case [25] with no iron indices; these are indication-linked context, not evidence about the drug. Genuine gap with a tooling-limited tail.

Gut Microbiome Risk

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

Gut microbiome risk: small human data, mostly combination regimens, effect not attributable to ivermectin alone

Yellow — Low

See study details

Human data show no significant overall microbiome change with ivermectin alone in a tiny cohort, and small functional shifts in a combination trial; the stronger finding is the reverse, that baseline microbiome predicts treatment response.

Full detail and limits

Direction

Possible drug-to-microbiome effect (small), plus a microbiome-to-drug effect (baseline community predicts cure). Neither is a nutrient deficiency.

Regulatory status

No microbiome statement in either label [1][2]. Fecal elimination over about 12 days implies gut-lumen exposure [1].

Population evidence

Jenkins 2018 [9] (Tier A, ivermectin given): 20 Strongyloides-infected volunteers in northern Italy versus 11 uninfected; 13 sampled 6 months after treatment. No significant change in overall composition; alpha diversity showed a non-significant downward trend; Turicibacter fell and Enterobacteriales rose. No untreated infected control. Dommann 2026 [10] (randomized trial, secondary microbiome analysis, ivermectin only in combination with albendazole): 204 paired samples, albendazole alone n=67, ivermectin plus albendazole n=69 (low dose 3 to 12 mg n=44, high dose 15 to 21 mg n=25, a post hoc split), moxidectin plus albendazole n=68; sampled at baseline and 2 to 3 weeks. Albendazole alone shifted the community slightly (PERMANOVA R2 0.0079, p=0.032). The high-dose ivermectin subgroup had the largest functional shift (R2 0.0403, p=0.004). Schneeberger 2022 [11]: 80 people (albendazole 41, albendazole plus ivermectin 39); baseline enterotype predicted cure, for example T. trichiura cure odds ratio 0.03 (95% CI 0.01 to 0.2) for one enterotype versus another in the combination arm; this is microbiome affecting the drug.

Non-human data

Chinchilla [12]: 10 animals, single 0.4 mg/kg injection, no significant change in alpha or beta diversity at day 14, one phylum (Cyanobacteria) lower. A USDA dataset page [13] describes a human-donor in vitro gut simulator study with ivermectin (the paper itself was not opened). A bacterial passage study [14] (in vitro, status unconfirmed) found E. coli insensitive and streptococci adapting at up to 10 micromolar.

Class cohort test

Not a class extrapolation. Ivermectin was in the cohorts of [9], [10] and [11]. A 2026 Ethiopian albendazole study [15] did not include ivermectin and is excluded.

Mechanism

Antibacterial activity of ivermectin in vitro is cited by [14]; clearance of helminths itself changes the gut community, which none of the human designs can separate from a direct drug effect.

Counter-evidence held on record

Counter-evidence and confounding [9] has 13 paired samples, no control, and parasite cure as a confounder. [10] has no ivermectin-only arm, low cure rates, a post hoc dose split, and several borderline findings after correction. Most community-level effect sizes were small (R2 0.008 to 0.040). Framing caution This is not a claim of dysbiosis. Do not extend antibiotic microbiome findings to ivermectin, and do not infer that probiotics are needed.

Oxygen and ATP Output

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

ATP production: in vitro, mixed direction, cell-type dependent

Yellow — Low

See study details

One review reports lower ATP in several cancer cell types, while a cardiomyocyte study found mitochondrial ATP preserved under hypoxia; no human ATP data exist.

Full detail and limits

Limits on what this shows

Null findings: [19] is itself a contrary finding. No human ATP, lactate or phosphorus-spectroscopy study was located.

Direction

Neutral to possibly lower, depending on cell type. An energy-output effect of the drug on cultured cells, not a nutrient deficiency.

Regulatory status

Not mentioned in either label [1][2].

Population evidence

None in humans. Liu 2020 review [18] (secondhand, concentrations not given): glioblastoma, HBMEC and chronic myeloid leukemia cells showed increased ROS and mitochondrial superoxide and decreased ATP; acetyl-L-carnitine and N-acetylcysteine reversed effects in renal cell carcinoma cells. Nagai 2017 [19] (read through a figure caption page; values only in the figure image): primary neonatal mouse cardiomyocytes with a mitochondrial ATP sensor, ivermectin 2 or 5 micromolar for 24 hours before hypoxia/reoxygenation; the accompanying text says mitochondrial ATP fell in hypoxia and ivermectin prevented that fall, with Cox6a2 induction proposed in HL-1 cells. ATP was not measured in [16] or [17].

Mechanism

Complex I inhibition (decrease) [18] versus Cox6a2 induction (preservation) [19]. The two are not reconciled in the sources opened.

Counter-evidence held on record

Counter-evidence Cell models at 2 to 15 micromolar, well above label peak levels; the review's concentration data were not retrievable. Graded separately from Mitochondrial burden per Hard Rule 7, though the evidence overlaps (see Overlap map). Framing caution Do not describe this as ivermectin lowering energy in patients. "Low energy" is not supported by any human measurement.

Oxygen delivery/utilization: reverse direction, hemoglobin gains in a placebo-controlled trial

Yellow — Low

See study details

Hemoglobin rose more with repeated ivermectin than placebo in children in one trial; small falls in unblinded volunteer data are confounded; no oxygen-carrying deficit attributable to ivermectin was found.

Full detail and limits

Limits on what this shows

At-risk subgroups: Strongyloides hyperinfection can itself cause anemia and hypoalbuminemia (case in [25]); that is the disease, not the drug.

Direction

Reverse (favorable) in the largest trial; neutral or slightly lower in smaller uncontrolled data. Anemia is an outcome, not a nutrient (Hard Rule 2).

Regulatory status

Merck label: in 963 adults with onchocerciasis, hemoglobin increase 1% and eosinophilia 3%; in 109 patients with strongyloidiasis, decreased leukocyte count 3%, with leukopenia and anemia in one patient [1].

Population evidence

Somé 2025 (RIMDAMAL II) [21]: double-blind placebo-controlled cluster-randomized trial, 14 clusters in Burkina Faso, about 300 micrograms/kg daily for 3 days monthly, up to 8 rounds per season, over two seasons. In 2020, children aged 10 or under in the ivermectin arm had a greater hemoglobin increase than controls (p=0.007). The numeric difference and confidence interval could not be retrieved (abstract only; PMC and the journal page were not readable; OpenAlex abstract field empty). Muñoz 2018 [20]: crossover phase I trial, 54 completers, single fasting doses; mean hemoglobin fell from 142.8 g/L at screening to 137.1 (weight-based), 136.5 (18 mg) and 135.4 g/L (36 mg), all p<0.001, no clinical anemia noted, no placebo arm, and repeated blood sampling for PK was not excluded as an explanation (my inference). Guzzo 2002 [4] collected hemoglobin but the text read did not report it.

Animal data

Mosa 2025 [22] (28 rats, 7 per group, subcutaneous ivermectin for 30 days, dose not stated, abstract and metadata only): slight decrease in hemoglobin, RBC and hematocrit, significant decrease in MCH and MCHC; B12 or folic acid co-treatment restored values. Toxicity design, not a deficiency finding.

Mechanism

None named for a hemoglobin fall. The gain in [21] is not explained in the abstract; reducing co-infection burden is a candidate that the trial does not test.

Counter-evidence held on record

Counter-evidence [21] reports possible confounders (unexpectedly low incidence, government bed nets mid-trial, cluster overdispersion). The hemoglobin result was a secondary outcome reported for one year. Framing caution Not a finding that ivermectin raises or lowers oxygen-carrying capacity in individuals. Do not link this entry to iron or B12 supplementation.

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.

Ivermectin feeds Bifidobacteria and boosts the microbiome
Where it comes from: Hazan 2022, Frontiers in Microbiology, a hypothesis article proposing that ivermectin breakdown products (oleandrose) feed Bifidobacterium [26].
Why it fails: No original data: the author says supporting data are "soon to publish" and none is included. The retrieved copy is marked RETRACTED. No Bifidobacterium measurement in people given ivermectin was found in any opened source, and the human data [9][10] show no such enrichment. White. The article's COVID-19 framing was not evaluated.
Ivermectin kills gut bacteria and damages the microbiome
Where it comes from: Commercial probiotic retailer blog (Tier D) citing no named studies and an unattributed "Triple-SHIME" lab model [27].
Why it fails: Not white: Tier A human data exist but show no significant overall change with ivermectin alone [9] and small shifts in combination regimens [10]. The retailer text itself says changes were "minor and temporary." Carried in the microbiome entry as a weak yellow, not as dysbiosis.
Take ivermectin with a meal for better absorption
Where it comes from: Protocol document, 2021 (Tier D for evidence) [28].
Why it fails: Half true, half contrary to the label. Exposure does rise with a high-fat meal (2.57-fold [4], 1.18-fold [5]), but both labels direct an empty stomach with water [1][2], and higher exposure is not a nutritional benefit. Handled in the Dietary fat entry.
Quercetin, zinc, vitamin D and vitamin C must be taken with, or separated from, ivermectin
Where it comes from: Same protocol document [28], which advises separating quercetin from ivermectin "due to the possible drug interaction" and lists zinc, vitamins D and C beside ivermectin.
Why it fails: No label statement [1][2] and no pharmacokinetic study of any of these nutrients with ivermectin was opened; the document's numbered references were cut off in the retrieved text. The relationship would be nutrient to drug, so it could only be a timing issue (Hard Rule 4), never a depletion. No mechanism evidence was retrieved either way, so it is held out for re-check, not graded white.

How the body handles this medication

Metabolism and enzymes: Hepatic. In vitro, primarily CYP3A4, with CYP2D6 and CYP2E1 contributing to a much lower extent. Clinically relevant concentrations did not significantly inhibit CYP3A4, 2D6, 2C9, 1A2 or 2E1 in vitro. No CYP induction is described. Rare post-marketing INR increases with warfarin.[1][2] DailyMed labels, clinical pharmacology and drug interactions
Elimination: Almost exclusively in feces over an estimated 12 days; under 1% in urine. Plasma half-life about 18 hours on the labels. A 2018 fixed-dose study reported 81 to 91 hours across weight groups, and a mini-review tabulates 5 to 55 hours, so the figure varies by study and method.[1][2][7][20]
Absorption: Peak of the major component (H2B1a) about 46.6 ng/mL (range 16.4 to 101.1) after a fasting 12 mg dose, at about 4 hours. No named absorption transporter is given in the label sections retrieved. Exposure is roughly dose-proportional from 30 to 120 mg with high variability.[1][4]
Food interaction: A 30 mg dose after a high-fat meal (48.6 g fat) gave about 2.5-fold higher bioavailability than fasting. Both labels direct tablets to be taken on an empty stomach with water. The label gives no hour interval; in trials the fasted dose was followed by a meal at about 4 hours.[1][2][4][20]
Distribution and protein binding: Plasma protein binding 93.2% (SD 4.4) in 5 healthy people, reported as mainly to serum albumin in a mini-review. Central volume of distribution 3.1 to 3.5 L/kg in healthy men. Does not readily cross the blood-brain barrier in humans per the label.[2][7][8]
Renal, hepatic, pregnancy, pediatric: No specific renal or hepatic impairment guidance on the Merck label; caution in the elderly for reduced hepatic, renal or cardiac function. Not to be used in pregnancy (safety not established). Safety not established under 15 kg. Orange juice and beer co-administration changed exposure in a 2003 healthy-volunteer study known to this review only as a title and by secondhand summary.[1][6][7]

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.

Timing / label
Dosing relative to meals
Both labels direct tablets on an empty stomach with water. No hour interval is given. Food (especially high fat) raised exposure in human studies, so a prescriber or pharmacist should be asked before changing how doses are taken [1][2][4].
Lab / clinical context
Hemoglobin and CBC
Not routinely required by the label. Worth checking when anemia or leukopenia is suspected in strongyloidiasis, where the disease itself can cause anemia and protein loss [1][25].
Lab / nutritional state
Albumin and nutrition
Relevant in malnourished or hypoalbuminemic patients because ivermectin is about 93% protein bound [8]. This is a drug-handling context, not a deficiency finding.
Lab / label
Liver enzymes
ALT and AST elevation occurred in 2% of strongyloidiasis patients; hepatitis is a post-marketing report [1]. This is drug toxicity, not a nutrient finding.
Timing
Supplement separation
No supplement separation interval is stated on either label [1][2]. No supplement dose is recommended or appears in this dossier, so no upper-limit comparison was needed.
Special populations
Pregnancy, pediatrics, older adults
Not for use in pregnancy (safety not established); not established under 15 kg; caution in older adults for reduced hepatic, renal or cardiac function. Warfarin users have rare INR increases [1].

Overlap map, to prevent double counting

Mitochondrial burden
Shares evidence with: ATP production; Oxidative stress
Note: Same in vitro cancer-cell literature [16][17][18]; ROS and membrane potential from [16] appear in both Mitochondrial burden and Oxidative stress. One body of Tier B evidence viewed three ways, not three confirmations.
ATP production
Shares evidence with: Mitochondrial burden
Note: Relies on the same review [18]. The contrary cardiomyocyte study [19] appears only in ATP.
Oxygen delivery/utilization
Shares evidence with: Albumin and plasma protein binding
Note: The strongyloides case [25] supplies hemoglobin and albumin values to both entries. A single disease-driven case, not two findings.
Oxygen delivery/utilization
Shares evidence with: Iron; Copper (ungraded)
Note: Any anemia would be mediated by these nutrients; hemoglobin changes are held in Oxygen delivery and not counted as iron or copper evidence.
Dietary fat and food
Shares evidence with: PK basis; Albumin
Note: [4] supplies the PK-basis figures and the food effect; [7] supplies beverage and protein-binding statements. Same sources, different statements.
Gut microbiome risk
Shares evidence with: None
Note: [10], [11] and [14] share authors (Keiser and Schneeberger, University of Basel) and are drawn from related trial programs. Treat as related, not independent confirmations.
Copper; Iron
Shares evidence with: Each other (tooling)
Note: Same searches and access limits; no shared evidence. Graded separately per Hard Rule 7.

All references used above

Ivermectin

Findings for this medication

What the research found

Dietary fat and food: timing interaction (nutrient affects the drug), exposure rises with a high-fat meal

Albumin and plasma protein binding: context flag, nutritional state affects free drug, disease lowers albumin

The five body-system areas

⚡Mitochondrial Burden

Mitochondrial burden: in vitro only, at concentrations far above label plasma levels

💥Oxidative Stress

Oxidative stress: in vitro and animal, mixed direction, no human marker data

⚖️Copper and Iron Balance

Copper

Iron

🌿Gut Microbiome Risk

Gut microbiome risk: small human data, mostly combination regimens, effect not attributable to ivermectin alone

💨Oxygen and ATP Output

ATP production: in vitro, mixed direction, cell-type dependent

Oxygen delivery/utilization: reverse direction, hemoglobin gains in a placebo-controlled trial

Claims checked and not supported

Ivermectin feeds Bifidobacteria and boosts the microbiome

Ivermectin kills gut bacteria and damages the microbiome

Take ivermectin with a meal for better absorption

Quercetin, zinc, vitamin D and vitamin C must be taken with, or separated from, ivermectin

How the body handles this medication

What the research says is worth watching

Overlap map, to prevent double counting

Mitochondrial Burden

Oxidative Stress

Copper and Iron Balance

Gut Microbiome Risk

Oxygen and ATP Output