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MyDeficiencies

Bromocriptine

Dopamine Agonist

Also sold as Cycloset, Parlodel.

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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.

Bromocriptine has no classical depletion mechanism. It is not a chelator, not a hepatic enzyme inducer, not renally wasting, and is eliminated mainly through bile (roughly 82% in feces per the Parlodel label, only 2-6% in urine), with the kidney playing a minor role. It is a substrate and, in vitro, a potent inhibitor of CYP3A4, but the Cycloset label reports that in-vivo drug-interaction potential from that inhibition is low at therapeutic exposure. No FDA label, drug-interaction checker (drugs.com, checked against vitamin D3 and folic acid specifically), or pharmacology reference reviewed here documents a mineral, vitamin, or electrolyte depletion effect. This low mechanistic prior sets the headline: nothing in this dossier reaches red, and the one orange entry runs in the protective direction, not the depleting one.

Ergot dopamine agonist · ATC N04BC01 · also sold as Cycloset and Parlodel · reviewed 2026-09-23. 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 Bromocriptine in the research — not how common it is, how serious it would be, and not anything about you personally.

Red — Severe
≥2 independent Tier A sources, this drug in the cohort, consistent direction and clinically meaningful magnitude, named mechanism, no substantial contradicting Tier A evidence.
Orange — Moderate
≥1 Tier A source with this drug in the cohort showing a real effect, but bounded by exposure window, subgroup, frequency, or a functional (not circulating) measure.
Yellow — Low
mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where a class member has real data but this drug does not; also used for context flags and reverse-direction (protective) findings.
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: no Tier B/C evidence to support even yellow, and no circulating claim to rebut as white; a genuine gap in the literature or in what could be accessed during this review, not a finding of safety.

What the research found

Calcium / bone mineral content

Orange — Moderate

See study details

In hyperprolactinemic patients, bromocriptine treatment raises bone mineral content as prolactin normalizes; this is a reverse-direction, beneficial off-target effect bound to the hyperprolactinemia indication, not evidence of calcium depletion, and not relevant to the diabetes (Cycloset) population that is this dossier's primary context.

Full detail, limits and 2 references

What the grade means here: ≥1 Tier A source with this drug in the cohort showing a real effect, but bounded by exposure window, subgroup, frequency, or a functional (not circulating) measure. Orange

Limits on what this shows

  • Key negative/null findings: None located specific to bromocriptine; a third relevant title, "Plasma calcitonin, IGF-I levels and vertebral bone mineral density in hyperprolactinemic women during bromocriptine treatment" (PMID 8317189), was identified but could not be opened during this review (see Sources) and was not used to support this grade.
  • At-risk subgroups: Applies only to patients being treated for hyperprolactinemia/prolactinoma, not to the type 2 diabetes (Cycloset) population, who do not have baseline hyperprolactinemia.
  • Counter-evidence: Both supporting studies are small, uncontrolled (before-after or single case), and confounded by indication: the true cause of any deficit prior to treatment is the disease (hyperprolactinemia/hypogonadism), not the drug, and the "finding" here is the drug removing that disease-driven deficit, not causing one (Hard Rule 6 applies in the opposite sense: the drug is reversing an indication-linked effect).

Regulatory status

Not addressed in either the CYCLOSET or Parlodel FDA label; this is a mechanism/outcome finding from the primary literature on the hyperprolactinemia indication, not a labeled effect.

Population evidence

Small before-after study, 15 hyperprolactinemic women, 6-month dopamine-agonist (bromocriptine, per the study title) treatment: forearm bone mineral content increased significantly (p<0.05) as plasma prolactin fell markedly (p<0.01) (Calcified Tissue International, 1985;37(6):687-689). A separate single case report describes reversal of severe osteopenia in a hyperprolactinemic patient treated with bromocriptine (Western Journal of Medicine, 1988;149(3):341-343, PMID 3176495).

Mechanism

Named: chronic hyperprolactinemia suppresses the gonadal axis and is thought to affect intestinal calcium transport and bone calcium mobilization; normalizing prolactin with bromocriptine removes that suppressive effect, allowing bone mineral content to recover.

Counter-evidence held on record

This is not a reason to add calcium or vitamin D for patients on bromocriptine, in any indication. It is the opposite of a depletion finding: the drug is associated with bone mineral content going up, not down, and only in patients whose baseline problem was untreated hyperprolactinemia. It has no established relevance to the diabetes/Cycloset population. Do not present this to consumers as "bromocriptine depletes calcium." It does not.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

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

Mitochondrial burden

Yellow — Low

See study details

In Goto-Kakizaki diabetic rats and cultured human adipose tissue, bromocriptine activates AMPK-linked catabolic signaling in fat and liver rather than showing evidence of mitochondrial harm; this is animal/ex-vivo mechanism-level evidence, not a clinical mitochondrial-toxicity finding.

Full detail, limits and 1 references

What the grade means here: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where a class member has real data but this drug does not; also used for context flags and reverse-direction (protective) findings. Yellow

Limits on what this shows

  • Key negative/null findings: No effect on skeletal muscle markers in the same study, despite effects in fat and liver; the human component of the study is correlational (baseline adipose dopaminergic markers vs. insulin resistance), not a bromocriptine-intervention arm, so it cannot be used to support a human causal claim.
  • At-risk subgroups: Not applicable; this is a proposed benefit signal, not a risk signal.
  • Counter-evidence: A separate line of evidence (necroptosis of prolactinoma tumor cells via a PGAM5-CypD mitochondrial pathway) was identified in search results as a title only and could not be opened for this review; it was not used to support or contradict this entry and is not listed as a verified source.

Regulatory status

Not addressed in either FDA label.

Population evidence

Molecular Metabolism, 2021 (DOI 10.1016/j.molmet.2021.101241): Goto-Kakizaki type 2 diabetic rats on standard or high-caloric diet, bromocriptine 10 mg/kg/day i.p. for the final month of a 5-month protocol, plus a cross-sectional human visceral-adipose-tissue analysis (n=92 obese patients stratified by insulin sensitivity, not a bromocriptine-treated cohort). In rat peri-epididymal fat: increased AMPK-Thr172 phosphorylation (p<0.05), increased beta-hydroxybutyrate (p<0.01 to p<0.05), increased GLUT4 and PPARgamma, decreased adiposity/adipocyte volume. In liver: reduced hepatic triglycerides/steatosis. No significant change in skeletal muscle.

Mechanism

Named: bromocriptine remodels adipose-tissue and hepatic dopaminergic signaling (increased D1 receptor and tyrosine hydroxylase), driving AMPK-mediated catabolic/lipid-oxidative shifts. This is a proposed biogenesis/catabolic-signaling mechanism, not a direct measurement of mitochondrial membrane integrity or electron-transport-chain activity.

Counter-evidence held on record

This is mechanism-level, animal/ex-vivo evidence in a diabetic rodent model, not a human clinical finding, and it points toward a possible metabolic benefit, not a mitochondrial-toxicity risk. It should not be surfaced to consumers as either a warning or a reason to take a mitochondrial-support supplement.

Oxidative Stress

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

Oxidative stress

Yellow — Low

See study details

In an in vitro phospholipid-liposome system, bromocriptine inhibits lipid peroxidation triggered by DOPA and iron, but the study's own data show this protection is not via classic free-radical scavenging; this is a single in vitro finding, not evidence bromocriptine either causes or reliably prevents oxidative stress in patients.

Full detail and limits

What the grade means here: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where a class member has real data but this drug does not; also used for context flags and reverse-direction (protective) findings. Yellow

Limits on what this shows

  • Key negative/null findings: No superoxide-scavenging activity detected for bromocriptine in the same study, a genuine negative result recorded here rather than omitted.
  • At-risk subgroups: Not applicable; in vitro only.
  • Counter-evidence: Additional titles suggesting broader antioxidant properties of bromocriptine (an isolated hydroxyl-radical-scavenging report, an NQO1/Nrf2 cytoprotection report, and a rodent brain-trauma lipid-peroxidation report) were located via search but could not be opened during this review (PubMed returned repeated 429/bot-verification responses); they are listed in Sources as identified-but-unverified leads and were not used to support this grade.

Regulatory status

Not addressed in either FDA label.

Population evidence

In vitro study (phospholipid liposomes exposed to DOPA and iron complexes; ScienceDirect record, PII 0304394094111286, apparent 1994 publication): bromocriptine "inhibits lipid peroxidation in phospholipid liposomes induced by DOPA and iron complexes." The peroxidation process itself was not mediated by active oxygen species in this model, and bromocriptine showed no superoxide-scavenging activity against hypoxanthine-xanthine-oxidase-generated superoxide by chemiluminescence assay.

Mechanism

Explicitly not classic radical scavenging, per the study's own conclusion; an alternative, unspecified protective mechanism against DOPA/iron-driven lipid peroxidation is proposed but not identified.

Counter-evidence held on record

Shares its underlying source with the Iron entry below (see Overlap map). This is laboratory mechanism evidence only; it does not support an antioxidant-supplement recommendation, and it does not establish that bromocriptine causes oxidative stress either.

Copper and Iron Balance

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

Iron

Yellow — Low

See study details

No evidence found that bromocriptine depletes or alters iron status; the same in vitro study above shows it blunts iron-catalyzed lipid peroxidation, and a separate class-level literature clarifies that in restless legs syndrome the causal arrow runs from brain iron deficiency to dopaminergic dysfunction, not from dopamine-agonist treatment to iron depletion.

Full detail and limits

What the grade means here: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where a class member has real data but this drug does not; also used for context flags and reverse-direction (protective) findings. Yellow

Limits on what this shows

  • Key negative/null findings: A 1978 Neurology study titled "The effect of levodopa, lergotrile, and bromocriptine on brain iron, manganese, and copper" is indexed and drug-specific but could not be opened during this review (paywalled abstract, 402 on Ovid; PubMed and Semantic Scholar both blocked repeated attempts). It is listed in Sources as an identified-but-inaccessible lead and was not used to support any claim in this entry.
  • At-risk subgroups: None identified specific to bromocriptine and iron status.
  • Counter-evidence: No consumer or clinical claim that bromocriptine depletes iron was located in this review, so no white-tier rebuttal was needed; this entry exists to record genuine mechanism-level and direction-clarifying evidence, not to rebut a circulating claim.

Regulatory status

Not addressed in either FDA label; no iron-related warning or monitoring requirement.

Population evidence

Same in vitro liposome study as the Oxidative stress entry (ScienceDirect PII 0304394094111286, 1994): bromocriptine inhibited DOPA/iron-complex-induced phospholipid peroxidation. Separately, a mouse-model study (Sleep Medicine, 2020) of the brain-iron-deficiency pattern of restless legs syndrome shows dopaminergic treatment reduces RLS-like behaviors without correcting the underlying brain iron deficiency; this class-level study did not include bromocriptine specifically (dopaminergic agents generally were studied), so it is Tier C for bromocriptine and used only to clarify mechanism/direction, not to support a bromocriptine-specific claim.

Mechanism

In vitro: inhibition of iron-catalyzed lipid peroxidation by an unidentified, non-radical-scavenging pathway. Direction clarification: iron deficiency is a driver of RLS pathophysiology that dopamine agonists (a class that has included bromocriptine, per a 1988 Annals of Neurology double-blind crossover trial) treat symptomatically; the drugs do not act on iron status itself.

Counter-evidence held on record

Shares its in vitro source with the Oxidative stress entry above (see Overlap map). This is not a reason to supplement iron alongside bromocriptine, and it is not evidence that bromocriptine treats or causes iron-deficiency-related conditions; it only clarifies that where iron and dopamine agonists appear together in the literature, the deficiency drives the disease the drug treats, not the reverse.

Copper

Not graded — disclosed evidence gap

See study details

No Tier B/C evidence usable to support even a yellow grade, and no circulating consumer claim to rebut as white.

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: Both conditions for ungraded are met: no drug-specific or class-level copper evidence could be verified for bromocriptine, and no consumer claim linking bromocriptine to copper status was located. This was not decided after a single blocked attempt: copper-focused searches were run with multiple phrasings ("bromocriptine copper," "bromocriptine ceruloplasmin," "dopamine agonist copper metabolism") across general web search and targeted site fetches.
  • Tooling limitation disclosed: One drug-specific, title-level lead exists: Neurology, 1978;28(7):734, "The effect of levodopa, lergotrile, and bromocriptine on brain iron, manganese, and copper." It could not be opened during this review (Ovid abstract page returned HTTP 402; PubMed and Semantic Scholar both returned repeated 429/bot-verification errors; Europe PMC and NCBI eutils were blocked at this session's network egress policy level with HTTP 403). It is listed in Sources as an identified-but-inaccessible citation. A future revision should re-attempt this specific source before this entry is upgraded.

Gut Microbiome Risk

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

Gut microbiome risk

Not graded — disclosed evidence gap

See study details

No Tier B/C evidence usable to support even a yellow grade, and no circulating consumer claim to rebut as white.

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: Both conditions for ungraded are met. Searches were run with multiple phrasings ("bromocriptine gut microbiome," "bromocriptine intestinal flora," "dopamine agonist gut microbiota composition," "bromocriptine fecal microbiome") across general web search and targeted fetches. The only tangentially related bromocriptine-specific result found was a study on bromocriptine reducing colonic inflammation via IL-1beta in a colitis model, which addresses inflammation, not microbiome composition or diversity, and was not opened or used here. A medRxiv preprint on dopaminergic medication and fecal microbiome changes in Parkinson's disease was identified but not confirmed to include bromocriptine in its cohort and was not opened.
  • Tooling limitation disclosed: The Europe PMC REST API (www.ebi.ac.uk) and NCBI's eutils API (eutils.ncbi.nlm.nih.gov), which would normally be used for a systematic drug-plus-category search of this kind, were blocked at this session's network egress policy level (HTTP 403) for the entire review, which narrowed this category's search to general web search and manual site fetches. A future revision with API access should re-run this category specifically.

Oxygen and ATP Output

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

ATP production

Yellow — Low

See study details

The same diabetic-rat/adipose-tissue study shows bromocriptine increasing beta-hydroxybutyrate and AMPK-linked catabolic markers consistent with increased fatty-acid oxidation and ATP-generating flux, not with impaired ATP synthesis; this is mechanism-level, not a direct ATP-synthesis measurement.

Full detail, limits and 1 references

What the grade means here: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where a class member has real data but this drug does not; also used for context flags and reverse-direction (protective) findings. Yellow

Limits on what this shows

  • Key negative/null findings: No significant change in skeletal muscle markers in the same animals.
  • At-risk subgroups: Not applicable.
  • Counter-evidence: None located specific to reduced ATP production or energy impairment from bromocriptine in any species.

Regulatory status

Not addressed in either FDA label.

Population evidence

Same source as the mitochondrial burden entry above: Molecular Metabolism, 2021 (DOI 10.1016/j.molmet.2021.101241), Goto-Kakizaki diabetic rats, bromocriptine 10 mg/kg/day i.p., 1 month. Increased beta-hydroxybutyrate (a marker of hepatic ketogenesis/fatty-acid oxidation) and increased AMPK-Thr172 phosphorylation, both catabolic, ATP-generating pathways, in peri-epididymal fat.

Mechanism

Named: AMPK activation shifts cellular metabolism toward fatty-acid oxidation and ketogenesis, both ATP-yielding catabolic pathways, rather than toward impaired energy production. No electron-transport-chain flux or direct cellular ATP measurement was reported.

Counter-evidence held on record

Shares its underlying source with the mitochondrial burden entry above (see Overlap map). Do not count these as two independent confirmations of the same finding, and do not present either as a reason for a CoQ10 or ATP-support supplement; no such recommendation is supported by this evidence.

Oxygen delivery / utilization

Yellow — Low

See study details

Bromocriptine is documented to cause cold-sensitive digital vasospasm, reducing peripheral tissue oxygen delivery, in patients treated for acromegaly; this is a labeled vascular adverse reaction at the higher doses used for that indication, not a finding reported for the low-dose Cycloset diabetes regimen, and it is not a nutrient-deficiency finding.

Full detail, limits and 1 references

What the grade means here: mechanistic plausibility only (Tier B), or class extrapolation (Tier C) where a class member has real data but this drug does not; also used for context flags and reverse-direction (protective) findings. Yellow

Limits on what this shows

  • Key negative/null findings: Not reported in the CYCLOSET label's own adverse-reaction tables, which instead emphasize hypotension and orthostatic effects; the CYCLOSET dose range (0.8-4.8 mg/day) is markedly lower than doses used historically for acromegaly, which is consistent with vasospasm being a higher-dose phenomenon.
  • At-risk subgroups: Patients on higher-dose bromocriptine for acromegaly or Parkinsonism; cold exposure appears to be a precipitant per the label language.
  • Counter-evidence: No vasospasm signal was found in the CYCLOSET (diabetes-dose) label's adverse-reaction data reviewed for this dossier.

Regulatory status

Not present in the CYCLOSET (diabetes) label reviewed for this dossier; documented in the professional drugs.com monograph (derived from AHFS/label-level content) specifically for the acromegaly indication: "Cold-sensitive digital vasospasm reported in patients being treated for acromegaly; usually resolves following a reduction in dosage and may be prevented by keeping fingers warm."

Population evidence

Labeled/monograph-level adverse-reaction reporting in the acromegaly-treated population (drugs.com Monograph for Professionals). A separate PubMed-indexed case report, "[Digital ischemia related to bromocriptine]" (PMID 18572278), could not be opened during this review (bot-verification block) and is listed in Sources as an identified-but-inaccessible lead, not used to support this grade.

Mechanism

Named: ergot-derived vasoconstriction/vasospasm, a recognized class effect of ergot alkaloids acting on peripheral vascular alpha-adrenergic and serotonergic receptors, reducing peripheral blood flow and tissue oxygen delivery to the digits.

Counter-evidence held on record

This is a vasoconstrictive adverse drug reaction, not a hemoglobin, hematocrit, or nutrient-deficiency finding, and Hard Rule 2 applies: it must not be filed or presented as a nutrient-deficiency entry. Management per the label-derived language is dose reduction and keeping the affected area warm, not a supplement.

All references used above
  1. CYCLOSET (bromocriptine mesylate tablets) full prescribing information. — FDA-approved labeling, DailyMed setid e42ba916-16b9-4d1c-8d09-9d2fbb1b6c20. Opened and reviewed in full for pharmacokinetics, dosing, adverse reactions.
  2. Parlodel SnapTabs (bromocriptine mesylate) tablets, USP, full prescribing information. — FDA label, accessdata.fda.gov, 2021 revision (017962s083lbl.pdf). Opened and reviewed for pharmacokinetics, elimination, adverse reactions.
  3. Bromocriptine. StatPearls [Internet]. — NCBI Bookshelf NBK555948. Opened for mechanism of action, pharmacokinetics, adverse effects, monitoring.
  4. Bromocriptine. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. — NCBI Bookshelf NBK548601. Opened for hepatotoxicity likelihood score and mechanism.
  5. WHO Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index, N04BC01 bromocriptine. — Opened to confirm ATC code.
  6. Bromocriptine Monograph for Professionals. — Drugs.com, AHFS-derived content. Opened; quoted for cold-sensitive digital vasospasm in acromegaly and CYP3A4 metabolism language.
  7. Drug Interactions Checker: bromocriptine and Vitamin D3. — Drugs.com. Opened; returned "no interactions found." Used as counter-evidence only.
  8. Drug Interactions Checker: bromocriptine and folic acid. — Drugs.com. Opened; returned "no interactions found." Used as counter-evidence only.
  9. Inhibitory effects of bromocriptine on phospholipid peroxidation induced by DOPA and iron. — In vitro study, phospholipid liposomes. ScienceDirect, PII 0304394094111286, apparent 1994 publication (exact journal/volume/page not confirmed from the accessible abstract). Opened; used for Oxidative stress and Iron entries.
  10. Dopamine D2 receptor agonist, bromocriptine, remodels adipose tissue dopaminergic signalling and upregulates catabolic pathways, improving metabolic profile in type 2 diabetes. — Molecular Metabolism, 2021, DOI 10.1016/j.molmet.2021.101241. Goto-Kakizaki diabetic rats plus human adipose cross-sectional analysis. Opened; used for Mitochondrial burden and ATP production entries.
  11. Increased forearm bone mineral content after bromocriptine treatment in hyperprolactinemia. — Calcified Tissue International, 1985;37(6):687-689. n=15 hyperprolactinemic women, 6-month treatment, before-after design. Opened; used for Calcium/bone entry.
  12. Reversal of severe osteopenia in a patient with hyperprolactinemia treated with bromocriptine. — Western Journal of Medicine, 1988;149(3):341-343, PMID 3176495. Case report. Opened (partial: title, journal, year, conclusion confirmed; specific before/after numeric values not available in accessible content). Used for Calcium/bone entry.
  13. Effects of bromocriptine mesylate on homocysteine and high-sensitivity C-reactive protein levels in patients with type-2 diabetes mellitus. — Journal of Cardiovascular and Thoracic Research, 2016, DOI 10.15171/jcvtr.2016.02. Before-after trial, Tabriz University of Medical Sciences, n=46 completers, Cycloset-formulation bromocriptine, 6 months. Opened; used for Monitoring panel homocysteine context note.
  14. Iron-deficiency and dopaminergic treatment effects on RLS-like behaviors of an animal model with the brain iron deficiency pattern of the restless legs syndrome. — Sleep Medicine, 2020. Mouse model (BXD40f), dopaminergic agents studied generally. Opened; used to clarify iron-dopamine direction for the Iron entry.Cohort note: bromocriptine specifically was not confirmed in this study's cohort; treated as Tier C class-level evidence for bromocriptine, not Tier A/B.
  15. The effect of levodopa, lergotrile, and bromocriptine on brain iron, manganese, and copper. — Neurology, 1978;28(7):734.Not opened: Ovid abstract page returned HTTP 402 (paywall); PubMed article page returned repeated HTTP 429 / bot-verification challenges; Semantic Scholar API returned HTTP 429. Listed as an identified-but-inaccessible lead for Copper and Iron; not used to support any claim.
  16. [Digital ischemia related to bromocriptine]. — PubMed PMID 18572278.Not opened: PubMed article page returned a bot-verification (CAPTCHA) challenge on every attempt. Listed as an identified-but-inaccessible lead for Oxygen delivery/utilization; not used to support the grade (the drugs.com monograph citation above was used instead).
  17. Antioxidant properties of bromocriptine, a dopamine agonist. — Yoshikawa et al., Journal of Neurochemistry, 1994, PMID 8113789.Not opened: PubMed article page returned repeated HTTP 429 responses. Listed as an identified-but-unverified lead for Oxidative stress; not used to support the grade.
  18. Bromocriptine activates NQO1 via Nrf2-PI3K/Akt signaling: novel cytoprotective mechanism against oxidative damage. — PubMed PMID 18455424.Not opened: WebFetch proxy returned HTTP 429 (rate-limited). Listed as an identified-but-unverified lead for Oxidative stress; not used to support the grade.
  19. Plasma calcitonin, IGF-I levels and vertebral bone mineral density in hyperprolactinemic women during bromocriptine treatment. — PubMed PMID 8317189.Not opened: PubMed article page returned a bot-verification challenge. Listed as an identified-but-unverified lead for Calcium/bone; not used to support the grade (two other opened sources were used instead).
  20. Drug-Induced Nutrient Depletions: What Pharmacists Need to Know. — U.S. Pharmacist. Opened and searched in full; bromocriptine, dopamine agonists, and Cycloset are not mentioned.
  21. Drug-Induced Nutrient Depletion & Deficiency. — BodyBio blog. Opened; full drug-specific list not present in accessible content, and bromocriptine was not found in what was accessible.