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MyDeficiencies

Calcitonin salmon

anti-parathyroid agent, calcium homeostasis (H05)

Also sold as Miacalcin, Fortical.

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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.

Calcitonin salmon is a 32-amino-acid peptide hormone given by subcutaneous or intramuscular injection or as an intranasal spray. It is not appreciably metabolized by hepatic CYP450 enzymes, does not induce or inhibit any CYP isoform, and the only labeled drug interaction on record (increased renal clearance of lithium) runs in the drug-affects-drug direction, not the classical small-molecule depletion machinery of chelation, enzyme induction, or transporter competition. On the pharmacokinetic prescreen alone, this drug has essentially none of the classical mechanisms that produce a nutrient-depletion signal.

anti-parathyroid agent, calcium homeostasis (H05) · ATC H05BA01 · also sold as Miacalcin and Fortical and generic calcitonin salmon · reviewed 2026-09-26. 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 Calcitonin salmon 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

Calcium, direct, label-mandated hypocalcemia risk, bounded to the early-treatment window and inadequately corrected patients

Orange — Moderate

See study details

Calcitonin salmon directly lowers serum calcium through osteoclast inhibition and reduced renal tubular calcium reabsorption; symptomatic hypocalcemia (tetany, seizures) is a named adverse effect, bounded to patients with uncorrected hypocalcemia or vitamin D deficiency and to the early-treatment period.

Full detail, limits and 1 references

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

  • Null / negative findings: None identified in the sources opened during this review. This is expected: calcium lowering is calcitonin's primary intended pharmacology when the drug is used to treat hypercalcemia, so the literature framing is "efficacy for hypercalcemia" rather than "adverse hypocalcemia," even though the mechanism and direction are identical.
  • At-risk subgroups: Pre-existing or uncorrected hypocalcemia; uncorrected vitamin D deficiency; renal impairment (both peptide clearance and mineral handling are renal-dependent); the first several doses of injectable therapy specifically, per the label's standby-parenteral-calcium instruction.
  • Counter-evidence on record: The label's own mandated co-therapy (at least 1,000 mg elemental calcium and at least 400 IU vitamin D per day) is designed to keep this deficit bounded and preventable in adequately supplemented patients; this is not a claim that hypocalcemia occurs universally or independent of correctable risk factors.

Regulatory status

Warnings and Precautions of the Miacalcin (calcitonin salmon) injection label: "Hypocalcemia associated with tetany (i.e., muscle cramps, twitching) and seizure activity has been reported." Hypocalcemia and vitamin D deficiency must be corrected before starting therapy; provisions for parenteral calcium should be available during the first several administrations; serum calcium and symptoms of hypocalcemia should be monitored.

Population evidence

Tier A regulatory label (direct, drug-specific). Jowsey J, Riggs BL, Kelly PJ, Hoffman DL, "Calcium and Salmon Calcitonin in Treatment of Osteoporosis," J Clin Endocrinol Metab 1978;47(3):633-639, confirms this exact combination (salmon calcitonin plus calcium) was studied clinically in an osteoporotic cohort, but this review could not open the full text to verify sample size or effect size, so it is cited only as confirmation that the cohort matches, not as quantitative support.

Mechanism

Named: calcitonin-receptor agonism suppresses osteoclastic bone resorption (reducing calcium efflux from bone) while independently increasing renal tubular calcium excretion. Both actions lower serum calcium regardless of dietary intake.

Counter-evidence held on record

This is a monitoring-and-correction issue, not a reason to add calcium or vitamin D beyond the label's own regimen. Calcium and vitamin D both carry their own tolerable upper intake levels (2,000-2,500 mg/day and 4,000 IU/day respectively per the NIH Office of Dietary Supplements); the label's 1,000 mg/400 IU regimen is well under both, and any change should go through the prescriber, not be self-directed.

Phosphate, direct renal phosphaturic effect, bounded and functional rather than routinely symptomatic

Orange — Moderate

See study details

Calcitonin salmon increases renal phosphate excretion by reducing tubular reabsorption, a direct label-documented effect; clinically symptomatic hypophosphatemia is uncommon in standard use but the phosphaturic action itself is real, direct, and dose-related.

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

  • Null / negative findings: None identified in sources opened; the effect is described in the label as a renal handling change rather than a quantified hypophosphatemia rate, consistent with a bounded, functional finding.
  • At-risk subgroups: Renal impairment; Paget's disease patients (high baseline bone turnover and phosphate flux); concurrent use of other phosphate-wasting agents.
  • Counter-evidence on record: Bounded, functional renal effect; not typically producing symptomatic hypophosphatemia in patients on standard, monitored therapy.

Regulatory status

Same Clinical Pharmacology sentence as the calcium entry: "increases the excretion of filtered phosphate, calcium, and sodium by decreasing their tubular reabsorption."

Population evidence

Tier A regulatory label (direct pharmacodynamic statement). No separately quantified human hypophosphatemia incidence rate was located or opened in this session; this review does not have a second independent Tier A source for phosphate specifically.

Mechanism

Named: calcitonin-receptor-mediated reduction of proximal tubular phosphate reabsorption, functionally parallel to (but independent of) parathyroid hormone's phosphaturic action.

Counter-evidence held on record

No phosphate supplementation is recommended. Serum phosphate should be followed on the same routine metabolic panel used to monitor calcium, not managed by self-supplementation.

Sodium, mechanistically real renal effect, no demonstrated clinical deficit

Yellow — Low

See study details

The same label sentence documenting reduced renal tubular reabsorption names sodium alongside calcium and phosphate, but no clinical hyponatremia signal, incidence figure, or monitoring guidance for sodium specifically was located in this review.

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

  • Null / negative findings: None located; absence of a clinical hyponatremia literature for a drug in wide use for decades is itself informative and is why this stays yellow rather than orange.
  • At-risk subgroups: Theoretical only: patients on concurrent natriuretic agents (for example diuretics) or drugs affecting ADH, where an additive natriuretic effect is mechanistically plausible but not documented for this combination.
  • Counter-evidence on record: No hyponatremia warning appears anywhere else in the label sections reviewed (Warnings and Precautions, Adverse Reactions), which weighs against clinical significance at labeled doses.

Regulatory status

Tier A for the mechanism only: "decreasing their tubular reabsorption" (filtered phosphate, calcium, and sodium), DailyMed SPL, Clinical Pharmacology.

Population evidence

No Tier A or Tier B clinical outcome data (for example, a hyponatremia incidence rate or case series) was found for calcitonin salmon specifically, despite multiple query attempts.

Mechanism

Named at the level of the label statement (reduced tubular sodium reabsorption); no further mechanistic detail (transporter identity, magnitude) was located.

Counter-evidence held on record

No sodium supplementation or restriction is recommended from this entry alone; this is a monitoring-awareness flag, not a demonstrated deficiency.

Magnesium, old, mixed animal renal-physiology literature; direction unresolved

Yellow — Low

See study details

A small set of 1980s rat-nephron studies tested synthetic salmon calcitonin's effect on renal magnesium transport, but this review could confirm only titles and journal metadata, not full findings, and a separate 1987 study used salmon calcitonin therapeutically alongside magnesium rather than describing magnesium loss; direction and human relevance remain unresolved.

Full detail, limits and 3 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

  • Null / negative findings: Marie PJ, Hott M, "Effect of calcitonin on the magnesium-induced bone resorption in the mouse," Magnesium 1987, PMID 3573817, used salmon calcitonin (1 IU/kg/day) concurrently with magnesium loading to inhibit bone resorption, a protective/combination framing rather than a magnesium-wasting concern, direction in this small literature is genuinely mixed, not consistently depletive.
  • At-risk subgroups: None established in humans; this is animal mechanistic literature only.
  • Counter-evidence on record: No magnesium warning or monitoring instruction appears in the modern Miacalcin label, despite decades of clinical use, which argues against a clinically important human magnesium effect at labeled doses.

Regulatory status

Not mentioned in the Miacalcin injection label sections reviewed (magnesium is absent from the Clinical Pharmacology renal-handling sentence, which names only phosphate, calcium, and sodium).

Population evidence

Tier B, animal, drug-specific by title only: Quamme GA, "Effect of calcitonin on calcium and magnesium transport in rat nephron," Am J Physiol 1980, PMID 7386624 (thyroparathyroidectomized rats given synthetic salmon calcitonin); Roy DR, "Acute effect of salmon calcitonin on renal magnesium transport in the magnesium-loaded rat," Can J Physiol Pharmacol 1986, PMID 3955445. Full text of both was not opened in this session (disclosed limitation); direction of the magnesium effect (increased vs. decreased reabsorption) could not be independently verified beyond the PubMed listing metadata.

Mechanism

Proposed but unverified beyond title: calcitonin-receptor-mediated modulation of magnesium transport in the thick ascending limb, tested acutely in rodent models.

Counter-evidence held on record

No magnesium dosing or supplementation guidance is given here; the evidence base is decades-old animal physiology that this review could not independently verify beyond bibliographic metadata.

Vitamin D, label-mandated precondition and co-therapy, not a drug-caused depletion

Yellow — Low

See study details

Calcitonin salmon does not deplete vitamin D. The label requires any existing vitamin D deficiency to be corrected before starting therapy and requires at least 400 IU/day of vitamin D during treatment, because uncorrected deficiency amplifies the drug's own direct hypocalcemia risk (see the calcium entry above).

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, context flag

Limits on what this shows

  • Null / negative findings: Not applicable; this entry exists to prevent this dossier from being read as silent on vitamin D given how prominently the label features it.
  • At-risk subgroups: Patients starting therapy with unrecognized or undertreated vitamin D deficiency, a population with high baseline prevalence in the osteoporosis and Paget's indications independent of calcitonin (confounding by indication).
  • Counter-evidence on record: None needed; this is a context flag by design, not a deficiency claim, per protocol.

Regulatory status

DailyMed SPL, Warnings and Precautions: "Hypocalcemia must be corrected before initiating therapy. Other disorders affecting mineral metabolism (such as vitamin D deficiency) should also be effectively treated." Dosage and Administration requires at least 400 IU vitamin D per day alongside at least 1,000 mg elemental calcium per day in osteoporosis and Paget's patients.

Population evidence

Tier A for the label requirement itself; this is a precondition/co-therapy instruction, not a study measuring vitamin D levels falling as a consequence of the drug.

Mechanism

None applicable in the depletion direction; the relationship runs the other way (adequate vitamin D status is required for the drug's calcium-lowering effect to be tolerated safely).

Counter-evidence held on record

The label's own regimen (at least 400 IU/day) is far below the 4,000 IU/day adult tolerable upper intake level (NIH Office of Dietary Supplements). This entry supports following the label's co-therapy, not exceeding it.

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 or class-level source, and no consumer circulating claim, was found, even after a dedicated re-research pass across additional channels.

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: This revision re-queried Europe PMC ("salmon calcitonin mitochondria") and Crossref ("salmon calcitonin mitochondrial membrane potential biogenesis") independently of the original review. Europe PMC returned only a tangential 2024 paper on calcitonin and aortic smooth-muscle-cell phenotypic switching via the AMPK/mTOR pathway (Liu et al., ACS Pharmacol Transl Sci, PMC10928884), which was opened in full for the ATP production entry above; it does not measure mitochondrial membrane potential, biogenesis markers, or any other mitochondrial-structure endpoint, so it cannot be carried forward here. Crossref returned only unrelated general mitochondrial-biogenesis literature with no calcitonin connection. Osteoclast-mitochondria research, given calcitonin's known osteoclast-suppressing mechanism, was searched specifically in both the original review and this revision and found nothing. No consumer nutrient-depletion claim referencing calcitonin and mitochondrial damage was located. Both conditions for ungraded are met.

Tooling note

NCBI eutils and the EBI/Europe PMC REST API were blocked at the network gateway (HTTP 403) for direct access throughout. During this revision, OpenAlex and Semantic Scholar's search endpoint returned repeated HTTP 429 rate-limit responses for this category specifically and could not be used; Europe PMC and Crossref, by contrast, returned clean on-topic or off-topic result sets rather than errors, so the negative finding above is a genuine search result, not a blocked attempt.

Oxidative Stress

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

Oxidative stress

Not graded — disclosed evidence gap

See study details

Two candidate sources were opened or status-checked this revision and neither could be used as evidence; no other drug-specific or class-level source, and no consumer claim, was found.

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: Taşkıran AS, Özdemir E, "The anticonvulsant effects of salmon calcitonin on pentylenetetrazole-kindled rats," Journal of Cellular Neuroscience and Oxidative Stress 2019;11:16, was opened in full despite its journal title: it measured only seizure stage, spike counts, and myoclonic jerk timing, and explicitly reported no antioxidant biomarkers or oxidative stress indicators. A related paper, Taskıran AS et al., "The effects of salmon calcitonin on epileptic seizures, epileptogenesis, and postseizure hippocampal neuronal damage...," Epilepsy & Behavior 2020;113:107501, remains closed access (no open-access location per Unpaywall) and its title alone does not establish that oxidative markers were measured. This revision's Europe PMC search ("calcitonin oxidative stress") surfaced one new candidate, Mandlik DS, Lavhale MP, Mandlik SK, "Anti-osteoporotic potential of Lawsonia inermis leaf extract: integration of network pharmacology, molecular docking, and experimental validation in ovariectomized rats," Inflammopharmacology 2026;34(7):4783-4809, an ovariectomized-rat osteoporosis study of a plant extract; calcitonin is mentioned in the source listing, plausibly as a positive-control comparator, but the paper is closed access and neither Unpaywall nor Semantic Scholar could supply an abstract, so whether calcitonin salmon was actually dosed in the study cohort and whether oxidative stress markers were measured in that arm could not be confirmed. It is disclosed but not used as evidence. No other salmon-calcitonin source, and no consumer claim, was found.

Tooling note

NCBI eutils and EBI/Europe PMC direct gateway access remain blocked (HTTP 403). During this revision, Europe PMC's search endpoint succeeded for the initial query but returned HTTP 429 on repeat attempts to pull the Mandlik 2026 abstract; Unpaywall and Semantic Scholar single-record lookups for that DOI both succeeded but neither source carries the abstract text. A revision with access to the Mandlik 2026 full text, or to the paywalled 2020 Epilepsy & Behavior full text, should re-check this category before it is assumed still ungraded.

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 or class-level source, and no consumer circulating claim, was found, across both the original review and this revision's independent re-search.

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: The original review's PubMed and Crossref searches returned only unrelated results: a cuproptosis-and-osteoporosis review that does not study calcitonin, a retracted shoulder-hand syndrome article, a thyroid-cancer PET-imaging paper using calcitonin only as an unrelated tumor marker, and general copper-metabolism/ceruloplasmin literature with no calcitonin connection. This revision re-queried Europe PMC ("salmon calcitonin" AND copper) independently and the only salmon-calcitonin-specific result was a buccal-delivery/liposomal drug-delivery paper (Keum et al. 2022, Int J Nanomedicine ) with no copper content at all. No genuine drug-specific or class-level source was found, and no consumer claim circulates linking calcitonin to copper status.

Iron

Not graded — disclosed evidence gap

See study details

No drug-specific or class-level source, and no consumer circulating claim, was found, across both the original review and this revision's independent re-search.

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: The original review's PubMed searches ("calcitonin iron status," "calcitonin hemoglobin hematocrit oxygen") returned only false-positive matches on "procalcitonin," an unrelated sepsis/inflammation biomarker, plus incidental mentions of calcitonin in unrelated leprosy-nutrition and inflammatory-bowel-disease bone-density papers. This revision re-queried Crossref ("salmon calcitonin iron ferritin") independently: of roughly 1.8 million indexed works, the sample returned five unrelated calcitonin pharmaceutical-standards entries and one unrelated iron-absorption paper (Theil et al., dietary ferritin-bound iron absorption in women), with no overlap between the two topics. No genuine drug-specific or class-level iron evidence, and no consumer claim, was found.

Gut Microbiome Risk

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

Gut microbiome risk

Not graded — disclosed evidence gap

See study details

The only hits were for calcitonin gene-related peptide (CGRP), a different gene product with a different receptor and pharmacology that cannot be carried forward to this drug, or for unrelated fish/skin/nasopharyngeal microbiome research; no genuine calcitonin-salmon source, and no consumer claim, was found.

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: The original review's PubMed search ("calcitonin gut microbiome") returned only CGRP studies (microbiome-gut-brain axis, visceral sensitivity, intestinal innate lymphoid cells). CGRP is a distinct alternative splice product of the calcitonin gene with its own receptor and drug class (used in migraine therapeutics) and is not evidence for calcitonin salmon under Hard Rule 4 (different molecule). This revision re-queried Crossref independently ("calcitonin salmon gut microbiome microbiota") across an index of over 350,000 microbiome-related works; the sample returned was dominated by Atlantic-salmon-the-fish gut microbiota and feed-efficiency research (an unrelated homonym collision with "salmon"), plus skin and nasopharyngeal microbiome studies, with no calcitonin-salmon-the-drug connection. OpenAlex and Semantic Scholar search attempts for this category returned rate-limit errors and could not be completed. Route of administration (subcutaneous, intramuscular, or intranasal, with negligible direct gut luminal exposure) lowers prior mechanistic plausibility for a direct microbiome effect, but this reasoning is not itself evidence and does not create a graded entry on its own. No consumer circulating claim was found.

Oxygen and ATP Output

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

ATP production, protective/restorative finding in a vascular-injury model, not a depletion signal

Yellow — Low

Direction: reverse direction (as labelled in the source)

In a rat carotid-injury restenosis model and cultured vascular smooth muscle cells, salmon calcitonin restored ATP levels that had been suppressed by PDGF-BB stimulation, via AMPK activation, while blocking pathological smooth-muscle phenotypic switching. This is a protective, drug-specific mechanistic finding in a disease model, not evidence of a cellular energy deficit caused by the drug.

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, reverse-direction

Limits on what this shows

  • Null / negative findings: The paper does not report mitochondrial membrane potential, mitochondrial biogenesis markers, or reactive-oxygen-species measurements alongside the ATP data, so this finding cannot be extended to the mitochondrial burden or oxidative stress categories (see Overlap map). No quantitative fold-change or absolute ATP value was stated in the accessible text, only the qualitative metabolomic direction.
  • At-risk subgroups: None established in humans; this is a rodent vascular-injury and cell-culture model, not a clinical population, and not the drug's approved indications (osteoporosis, Paget's disease, hypercalcemia of malignancy).
  • Counter-evidence on record: Two additional drug-specific sources were located but their content could not be independently verified: Wielinga PY, Alder B, Lutz TA, "The acute effect of amylin and salmon calcitonin on energy expenditure," Physiol Behav 2007 (title/authors/venue confirmed via Crossref and Semantic Scholar; abstract not accessible, closed access per Unpaywall); Sasaki M, Tanaka K, Nakamuta H, Koida M, "The influence of salmon calcitonin and its analog on the acidity of the osteoclast," Jpn J Pharmacol 1992 (gold open access per Unpaywall metadata, but full text could not be retrieved in this session). Neither is used as evidence for this grade; both are disclosed for a future revision.

Regulatory status

Not addressed in the Miacalcin label; this entry rests entirely on primary mechanistic literature located and opened during this revision.

Population evidence

Tier B, drug-specific: Liu M, Xiang F, Yang T, et al. "Calcitonin Inhibits Phenotypic Switching of Aortic Smooth Muscle Cells and Neointimal Hyperplasia through the AMP-Activated Protein Kinase/Mechanistic Target of Rapamycin Pathway," ACS Pharmacol Transl Sci 2024, PMC10928884. Confirmed by opening the full text: salmon calcitonin specifically (the paper states it is "the most used" of four calcitonin forms), tested in vitro in primary rat vascular smooth muscle cells (VSMCs) and human cell lines (HASMCs, HUVECs) at 600 nmol/L, and in vivo in male Sprague-Dawley rats (350-400 g) using a carotid artery balloon-injury restenosis model at 20 IU/kg/day intraperitoneally for 14 days. LC-MS/MS metabolomics (AB Sciex QTRAP 6500 platform) identified ATP as one of the most differentially expressed metabolites, with PDGF-BB-stimulated VSMCs showing reduced ATP that was restored by calcitonin co-treatment.

Mechanism

Named: calcitonin activates AMPK (phosphorylation at Thr-172), which inhibits mTOR activation; silencing AMPK (si-AMPK) blocked calcitonin's inhibition of mTOR, confirming pathway dependence. The paper frames reduced ATP as an upstream driver of the pathological AMPK/mTOR shift that calcitonin reverses.

Counter-evidence held on record

This is not evidence that calcitonin salmon boosts cellular energy or ATP in general, and it is not a basis for any energy-related supplement claim. It is a mechanistic finding in a rodent vascular-injury model, unrelated to the drug's approved indications, and it does not support any consumer-facing "increases ATP" or "boosts energy" message.

Oxygen delivery / utilization

Not graded — disclosed evidence gap

See study details

No drug-specific or class-level source, and no consumer circulating claim, was found, across both the original review and this revision's independent re-search.

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: The original review's PubMed search ("calcitonin hemoglobin hematocrit oxygen") returned only sepsis-biomarker studies using "procalcitonin" and "red cell distribution width" in critically ill patients, unrelated to calcitonin salmon pharmacology. This revision re-queried Crossref independently ("salmon calcitonin hemoglobin hematocrit oxygen"): the closest matches were an unrelated ischemic-stroke hemoglobin/hematocrit outcomes study and a 1976 dissertation on ammonia's effect on the oxygen-carrying hemoglobin of coho salmon, the fish, not the drug, an unrelated homonym collision. No genuine source on red-cell mass, hemoglobin, or tissue oxygenation under calcitonin salmon therapy, and no consumer claim, was found.
All references used above
  1. DailyMed structured product label, MIACALCIN (CALCITONIN SALMON) INJECTION, SOLUTION, Mylan Institutional LLC — SPL set ID 26caf31f-7f7c-48a8-a1ac-35d2ceefda2b. Used for mechanism of action, pharmacokinetics, renal handling, Warnings and Precautions (hypocalcemia), Dosage and Administration (calcium/vitamin D co-therapy), Drug Interactions (lithium), and Adverse Reactions (nausea, injection-site reaction, flushing, poor appetite).
  2. DailyMed SPL registry search, calcitonin salmon products — Used to enumerate current Miacalcin, Fortical, and generic calcitonin salmon formulations and locate the set ID above.
  3. WHO Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index, code H05BA01 — Used for ATC code, classification (anti-parathyroid agents / calcium homeostasis), and Defined Daily Dose (200 U nasal, 100 U parenteral).
  4. Jowsey J, Riggs BL, Kelly PJ, Hoffman DL. "Calcium and Salmon Calcitonin in Treatment of Osteoporosis." J Clin Endocrinol Metab. 1978;47(3):633-639. — DOI 10.1210/jcem-47-3-633. Confirmed via Crossref metadata (title, authors, journal, year, cohort match: salmon calcitonin plus calcium in osteoporotic patients). Cited only to confirm this drug/cohort was clinically studied for the calcium entry; not used for any unverified quantitative claim.Full text not opened in this session: PubMed individual-article page served a bot-verification challenge instead of content.
  5. Quamme GA. "Effect of calcitonin on calcium and magnesium transport in rat nephron." Am J Physiol. 1980. PMID 7386624. — Rat model, thyroparathyroidectomized rats given synthetic salmon calcitonin. Confirmed via PubMed search-listing metadata only.Full text not opened in this session; direction of the magnesium effect not independently verified beyond title/listing.
  6. Roy DR. "Acute effect of salmon calcitonin on renal magnesium transport in the magnesium-loaded rat." Can J Physiol Pharmacol. 1986. PMID 3955445. — Rat model, magnesium-loaded rats given salmon calcitonin. Confirmed via PubMed search-listing metadata only.Full text not opened in this session.
  7. Marie PJ, Hott M. "Effect of calcitonin on the magnesium-induced bone resorption in the mouse." Magnesium. 1987. PMID 3573817. — Mouse model, salmon calcitonin 1 IU/kg/day used therapeutically alongside magnesium loading. Confirmed via PubMed search-listing metadata only.Full text not opened in this session.
  8. Taşkıran AS, Özdemir E. "The anticonvulsant effects of salmon calcitonin on pentylenetetrazole-kindled rats." Journal of Cellular Neuroscience and Oxidative Stress. 2019;11:16. DOI 10.37212/jcnos.584705. — Opened in full via publisher site (dergipark.org.tr). Confirmed: 48 male Wistar rats, salmon calcitonin 25/50/100 µg/kg vs. saline vs. ethosuximide vs. combination; measured only seizure stage, spike count, and myoclonic jerk timing. No oxidative stress marker was measured despite the journal's name, cited as a documented near-miss for the oxidative stress category, not as supporting evidence.
  9. Taskıran AS, Ozdemir E, Gumus E, Ergul M. "The effects of salmon calcitonin on epileptic seizures, epileptogenesis, and postseizure hippocampal neuronal damage in pentylenetetrazole-induced epilepsy model in rats." Epilepsy Behav. 2020;113:107501. DOI 10.1016/j.yebeh.2020.107501. — Rat model, drug-specific by title. Checked via Unpaywall: closed access, no open-access location available.Paywalled; abstract and full text could not be opened in this session. Disclosed but not used as evidence for any grade.
  10. Filiz AK, Karabulut S. "Involvement of nitric oxide pathway in the acute anticonvulsant effect of salmon calcitonin in rats." Epilepsy Res. 2022;180:106864. DOI 10.1016/j.eplepsyres.2022.106864. — Located via Crossref bibliographic search alongside the two studies above; nitric oxide pathway, not oxidative stress markers, and not opened beyond metadata. Listed for completeness, not used as evidence.Full text not opened in this session.
  11. Avramides A, Baker RK, Wallach S. "Metabolic effects of synthetic salmon calcitonin in Paget's disease of bone." Metabolism. 1974. DOI 10.1016/0026-0495(74)90070-5. — Located via Crossref as the closest candidate for the ATP production category.Publisher page returned HTTP 403; not opened. Disclosed but not used as evidence for any grade.
  12. NIH Office of Dietary Supplements, Calcium, Health Professional Fact Sheet — Tolerable Upper Intake Level: 2,500 mg/day (ages 19-50), 2,000 mg/day (ages 51 and older). Used to check the label's calcium co-therapy dose.
  13. NIH Office of Dietary Supplements, Vitamin D, Health Professional Fact Sheet — Tolerable Upper Intake Level: 100 mcg (4,000 IU)/day for adults 19 and older. Used to check the label's vitamin D co-therapy dose.
  14. PubMed search listings (multiple query phrasings) — Used for the copper, iron, gut microbiome risk, oxygen delivery/utilization, and mitochondrial burden categories, and for a hypocalcemia case-report check; queries returned either zero results or off-topic matches (most often confusion with "procalcitonin" or with calcitonin gene-related peptide), as detailed in each Ungraded entry above.
  15. Liu M, Xiang F, Yang T, Sun YJ, Yang JM, Wang TY, Chen SX, Xu Y, Shan G, Shi YQ, Dong Z, Guo Y. "Calcitonin Inhibits Phenotypic Switching of Aortic Smooth Muscle Cells and Neointimal Hyperplasia through the AMP-Activated Protein Kinase/Mechanistic Target of Rapamycin Pathway." ACS Pharmacol Transl Sci. 2024. DOI 10.1021/acsptsci.3c00288. — Opened in full via PubMed Central (PMC10928884). Confirmed drug-specific: salmon calcitonin, rat carotid balloon-injury restenosis model and cultured rat/human vascular smooth muscle cells. Metabolomics (LC-MS/MS) showed PDGF-BB reduced ATP levels, restored by calcitonin via AMPK activation/mTOR inhibition. Used as primary evidence for the ATP production entry.
  16. Wielinga PY, Alder B, Lutz TA. "The acute effect of amylin and salmon calcitonin on energy expenditure." Physiol Behav. 2007. DOI 10.1016/j.physbeh.2007.02.012. — Located via Crossref and confirmed via Semantic Scholar (title, authors, venue, year). Drug-specific by title, but closed access per Unpaywall; no abstract available from any channel tried in this session.Full text and abstract not opened in this session; disclosed but not used as evidence for any grade.
  17. Sasaki M, Tanaka K, Nakamuta H, Koida M. "The influence of salmon calcitonin and its analog on the acidity of the osteoclast." Jpn J Pharmacol. 1992. DOI 10.1016/s0021-5198(19)49146-4. — Located via Crossref. Unpaywall reports gold open-access status, but the publisher (Elsevier linkinghub) and a J-STAGE search both failed to surface the actual abstract or full text in this session.Full text not opened despite reported open-access status; disclosed but not used as evidence for any grade.
  18. Mandlik DS, Lavhale MP, Mandlik SK. "Anti-osteoporotic potential of Lawsonia inermis leaf extract: integration of network pharmacology, molecular docking, and experimental validation in ovariectomized rats." Inflammopharmacology. 2026;34(7):4783-4809. DOI 10.1007/s10787-026-02290-7. — Located via Europe PMC search for calcitonin and oxidative stress. Ovariectomized-rat osteoporosis model; calcitonin appears in the source listing, plausibly as a comparator drug, but this could not be confirmed.Closed access; Unpaywall and Semantic Scholar both confirmed metadata but neither could supply the abstract. Disclosed but not used as evidence for any grade.
  19. Theil EC, et al. "Absorption of Iron from Ferritin Is Independent of Heme Iron and Ferrous Salts in Women and Rat Intestinal Segments." 2012. DOI 10.4016/39302.01. — Surfaced by a Crossref query cross-referencing calcitonin and iron; confirmed unrelated to calcitonin salmon (no shared cohort or mechanism). Listed to document that the iron category's negative search result was genuine rather than a keyword miss.