Medication interactions: A

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General information for discussion with your doctor, pharmacist or vet. It is not medical or veterinary advice. Never stop or change a medication without talking to your prescriber.

A

Abraxane

See also Paclitaxel

A formulation of paclitaxel bound to nano-particles of albumin rather than with Kolliphor EL (a modified form of castor oil). It lacks some of the toxicity of standard paclitaxel.

Terminal half-life: 27 hours

More detail and references

FDA prescriber info: https://www.accessdata.fda.gov/drugsatfda_docs/label/2009/021660s022lbl.pdf

Acardi: see Pimobendan

Aceon: see Perindopril

Acepromazine

Trade names Atravet, Acezine

Acepromazine is an antipsychotic that was originally developed for human use but is now sold almost exclusively for veterinary use. It is cleared via the CYP3A4 pathway, and is thus a potential problem with Golden Paste. Dogs with the MDR1 gene mutation should probably not have acepromazine at all, but should definitely not have it with Golden Paste. Will take longer to clear but always has a hangover effect of a few days anyway.

Acetaminophen, Paracetamol

Trade names Tylenol, Panadol and many others

A non-NSAID pain reliever widely used, available OTC in most locations. It’s often combined with other pain medications such as codeine (such as Pardale-V for dogs). Okay with Golden Paste. Toxic to cats who are unable to metabolize it.

The interaction between paracetamol (acetaminophen / APAP) and curcumin involves two distinct pharmacologic mechanisms: metabolic/hepatoprotective modulation in the liver and pharmacodynamic synergy in pain and inflammatory pathways.

More detail and references

1. Hepatic Metabolism and Toxicological Modulation

Paracetamol clearance depends on three primary metabolic routes:

Glucuronidation & Sulfation (~85–90%): Conjugation by UDP-glucuronosyltransferases (UGT1A1, UGT1A6, UGT1A9) and sulfotransferases (SULT1A1, SULT2A1) into non-toxic, water-soluble metabolites.
CYP-mediated Oxidation (~5–10%): Primarily catalyzed by CYP2E1 (with minor contributions from CYP1A2 and CYP3A4) into the electrophilic reactive intermediate N-acetyl-p-benzoquinone imine (NAPQI).
Detoxification: Under standard doses, hepatic reduced glutathione (GSH) conjugates NAPQI via glutathione S-transferases (GST) into non-toxic mercapturic acid conjugates. In overdose or depleted states, NAPQI binds cellular macromolecules and mitochondrial proteins, triggering mitochondrial permeability transition pore (MPTP) opening, reactive oxygen species (ROS) cascades, and centrilobular hepatic necrosis.

Curcumin’s Hepatoprotective Interventions

In short: Curcumin inhibits CYP2E1 flux while upregulating Nrf2-driven GSH synthesis and Phase II detox.

Inhibition and Downregulation of CYP2E1: Curcumin and its reductive metabolites (e.g., tetrahydrocurcumin) suppress CYP2E1 catalytic activity and gene expression. This reduces the kinetic rate of NAPQI formation from paracetamol.
Nrf2-ARE Pathway Upregulation & GSH Preservation: Curcumin acts as an electrophilic signaling agent that disrupts the Keap1-Cul3 complex, releasing Nrf2 to translocate to the nucleus. This transactivates antioxidant response element (ARE) genes:
Glutamate-cysteine ligase catalytic and modifier subunits: Re-establishes rate-limiting de novo synthesis of GSH, counteracting APAP-induced glutathione depletion.
Glutathione reductase (GR), Glutathione peroxidase (GPx), and GST: Accelerates the catalytic clearance of free NAPQI and scavenges lipid hydroperoxides.
Mitochondrial Protection & Apoptotic Suppression: Curcumin inhibits APAP-induced mitochondrial swelling and membrane potential collapse, prevents Bax translocation to the mitochondrial outer membrane, maintains Bcl-2 levels, and reduces c-Jun N-terminal kinase (JNK) phosphorylation.
Kupffer Cell & Cytokine Attenuation: Suppresses secondary inflammatory injury mediated by hepatic macrophages, downregulating pro-inflammatory cascades (TNF-α, IL-1β, IL-12, IL-18).

2. Pharmacokinetic Clearance & Phase II Conjugation

Curcumin undergoes rapid, high-capacity intestinal and hepatic glucuronidation and sulfation:

Enzyme Competition: Both molecules utilize UGT and SULT isoforms (notably UGT1A1). In cell-free systems, high-dose polyphenols can compete for glucuronidation capacity. However, in vivo oral dosing shows that systemic curcumin bioavailability remains low (low nanomolar plasma ranges without bioenhancers), making saturation-based displacement of paracetamol glucuronidation negligible at standard therapeutic doses.
Bioenhancers (Piperine Caveat): When curcumin is co-formulated with piperine to increase systemic bioavailability, piperine acts as a potent inhibitor of hepatic/intestinal glucuronidation and hepatic CYP enzymes. Co-administering piperine-enhanced formulations slightly delays paracetamol clearance and increases its half-life, but does not induce toxicity given the parallel suppression of CYP2E1-mediated bioactivation.

3. Pharmacodynamic and Analgesic Synergy

Paracetamol and curcumin target distinct, complementary nodes along nociceptive and inflammatory pathways:


Parameter	Paracetamol (Acetaminophen)	Curcumin	Combined Effect
Primary Site of Action	Central Nervous System (CNS)	Peripheral tissues & systemic immune cells	Dual central + peripheral blockade
Prostaglandin Synthesis	Functional inhibition of central COX variants (peroxidase site of COX-1/COX-2 in low-peroxide environments)	Transcriptional suppression of COX-2 via NF-κB inhibition; direct 5-LOX inhibition	Spares gastric COX-1 while suppressing central and peripheral pro-inflammatory eicosanoids
Cannabinoid / TRPV1 Interaction	Metabolized by fatty acid amide hydrolase (FAAH) to AM404, which inhibits anandamide reuptake and activates TRPV1 / CB1	Modulates endocannabinoid receptor sensitivity and downregulates peripheral TRPV1 expression	Enhanced descending serotonergic/cannabinoid pain control
Inflammatory Cytokines	Minimal direct impact on peripheral cytokines	Broad down-regulation of TNF-α, IL-6, and MCP-1	Curcumin supplies the peripheral anti-inflammatory action that paracetamol lacks

The combination exhibits dose-sparing properties, allowing for lower requirements of paracetamol in multimodal pain management protocols while buffering the liver against oxidative stress.

Acitretin

Trade names Soriatane, Neotigason

Oral retinoid used for severe psoriasis that has not responded to other treatment. Interactions with the cytochrome P450 enzymes do not appear in the literature. However, one likely incident of CYP3A4 inhibition was reported in a drug-drug interaction with serolimus (which is metabolized by CYP3A4). This would not necessarily be a caution with Golden Paste or curcumin, but the side effects of acitretin are severe enough that a physician consult is recommended. It is a potent teratogenic and should not be used by women of child-bearing age. Its long half life (2 days minimum) means that it could not be feasibly separated from Golden Paste.

Drugbank: https://www.drugbank.ca/drugs/DB00459Serum Sirolimus Level Elevation Induced by Acitretin: Report of a Novel Drug-Drug Interaction: https://pubmed.ncbi.nlm.nih.gov/26151793/

More detail and references

FDA prescriber info (for Soriatane): https://www.accessdata.fda.gov/drugsatfda_docs/label/2014/019821s024lbl.pdf

Aclasta: see Zolendronic acid

Acticarp: see Carprofen

Actigall: see Ursodeoxycholic acid

Acyclovir, Aciclovir

Trade name Zovirax

Acyclovir is an antiviral widely used against a variety of viral species. In humans, it’s most common use is probably for the herpes viruses that cause shingles and cold sores. It’s effective against the bovine papilloma virus that causes sarcoids. Okay with Golden Paste.

Adalat: see Nifedipine

Adalimumab

Sold as Humira

Adalimumab is a ‘biological’ – that is, it’s manufactured from natural sources, usually human, animal or bacterial, rather than being chemically synthesized. Adalimumab is a human monoclonal antibody against TNF-alpha, produced by recombinant DNA technology. Turmeric is also a TNF inhibitor, and Adalimumab is okay with Golden Paste.

Br J Pharmacol. 2013 Aug;169(8):1672-92. doi: 10.1111/bph.12131. Curcumin: An Orally Bioavailable Blocker of TNF and Other Pro-Inflammatory Biomarkers

More detail and references

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3753829/

Sources:

DrugBank: https://www.drugbank.ca/drugs/DB00051

PharmGKB: https://www.pharmgkb.org/chemical/PA10004

Adizem: see Diltiazem

Aisemide: see Furosemide

Alanase: see Beclometasone

Allegra: see Fexofenadine

Allopurinol

Mechanism of Action: Xanthine oxidase inhibitor; inhibits conversion of hypoxanthine to xanthine to uric acid; decreases production of uric acid without disrupting synthesis of vital purines.

Metabolized in liver. Metabolites: Oxypurinol (active), allopurinol riboside (activity unknown)

Elimination: Half-life: Parent drug, 1-3 hr; active metabolite, 15-20 hr

Fine with turmeric and scientific studies indicate that both together reduce metabolic syndrome, liver inflammation and fatty liver disease

More detail and references

https://pubmed.ncbi.nlm.nih.gov/30248460/

Alna: see Tamsulosin

Alprazolam

Brand name Xanax

Alprazolam is one of the benzodiazepines, and like all the drugs in that class, it’s a CYP3A4 substrate. It is a short-acting drug compared to some of the other benzo’s, and it’s likely that occasional use of it would not be a problem along with Golden Paste. However, it also has a high rate of abuse and mis-use, and I wouldn’t necessarily believe someone who said they were just having it once in a while. To be on the safe side, best to refer the person back to the prescribing physician.

Alzain: see Pregabalin

Amantadine

Trade names Gocovri, Symadine, Symmetrel

Amantadine was originally developed as an antiviral, specifically against type A flu viruses. The viruses quickly developed resistance to it and it is no longer sold for that purpose. It is now prescribed for Parkinsons and some other movement disorders. It increases dopamine release, and blocks dopamine reuptake. Turmeric has the same effect, and elevated dopamine levels have resulted in adverse reactions in many individuals. In addition, it is an anticholinergic, which means that one of its mechanisms acts in opposition to turmeric. It is cleared in part by MAO-B, which is inhibited by both turmeric and pepper. The use of Golden Paste along with it would require physician/vet approval.

antiviral medication: While amantadine may have efficacy and clinical usefulness against some veterinary viral diseases, presently the greatest interest for its use in small animals is as a N-methyl-D-aspartate (NMDA) antagonist in the adjunctive treatment of chronic pain, often in those tolerant to opioids. It is generally used in combination with an NSAID, opioid, or gabapentin/pregabalin. It is also used as an adjunct drug to treat neuropathic pain. It has been suggested for use as an early intervention in the treatment of pain associated with osteosarcomas.

More detail and references

Like ketamine, dextromethorphan, and memantine, amantadine antagonizes the NMDA receptor. amantadine is a weak, noncompetitive NMDA receptor antagonist (N-methyl-D-aspartate receptor (also known as the NMDA receptor or NMDAR), is a glutamate receptor and ion channel protein found in nerve cells. The NMDA receptor is one of three types of ionotropic glutamate receptors. The other receptors are the AMPA and kainate receptors. It is activated when glutamate and glycine (or D-serine) bind to it, and when activated it allows positively charged ions to flow through the cell membrane. The NMDA receptor is very important for controlling synaptic plasticity and memory function.) Within the central nervous system (CNS), chronic pain can be maintained or exacerbated when glutamate or aspartate bind to this receptor. It is believed that this receptor is particularly important in allodynia (sensation of pain resulting from a normally non-noxious stimulus). Amantadine alone is not a particularly good analgesic, but in combination with other analgesics (eg, opiates, NSAIDs), it is thought to help alleviate chronic pain.

There is very limited experience in domestic animals with amantadine and its adverse effect profile is not well described. It has been reported that dogs given amantadine occasionally develop agitation, loose stools, flatulence, or diarrhea, particularly early in therapy.

In dogs, oral bioavailability of amantadine is reportedly very high, and some of the drug is metabolized; elimination half-life is around 5 hours. A study showed that, in greyhounds, an oral dose of 2.8 mg/kg was well tolerated and terminal half-life, time to maximum concentration, and maximum concentration were 5.9 hours, 1-4 hours, and 271 ng/mL, respectively.

Ambrisentan

Trade name Letairis

Ambrisentan is an endothelin receptor antagonist for relief of pulmonary hypertension. It is metabolized primarily via CYP3A4, so a doctor should be consulted before adding Golden Paste.

Terminal half-life: 15 hours

More detail and references

FDA approval letter: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2019/022081Orig1s039.pdf

Amiodarone

An antiarrythmic medication used to treat ventricular fibrillation, ventricular tachycardia, atrial fibrillation and other cardiac rhythm irregularities. It has a wide range of serious side effects and is metabolized via CYP3A4. Physician consult required and it would probably not be approved.

One interesting article that Doug found does indicate that curcumin can help protect against one of the major side effects of amiodarone – pulmonary fibrosis. But the pepper in the Golden Paste would still be a contra-indication. And one of the metabolic pathways for amiodarone is CYP2C9, which is inhibited by curcumin, though not as potently as pepper inhibits CYP3A4.

More detail and references

References:

Protective effects of curcumin against amiodarone-induced pulmonary fibrosis in rats: https://www.ncbi.nlm.nih.gov/pubmed/12890714

Drugbank.ca: https://www.drugbank.ca/drugs/DB01118

Amitriptyline

Trade names Amitrip, Elavil, Levate, others

A tricyclic antidepressant that can increase the amount of serotonin in the bloodstream. Unlike most of the other antidepressants, this one carries a specific warning not to use along with MAO inhibitors. Its main metabolic pathway is CYP2D6, which has a minor inhibition from curcumin. That by itself would probably not be a problem, but the fact that both turmeric and pepper are MAO inhibitors is. Physician consult before use.

Amlodipine

Trade names Nordip, Norvasc, Amodip

A calcium channel blocker used for hypertension. Generally okay with Golden Paste (it’s often prescribed along with an ACE inhibitor, in fact). It’s cleared via CYP3A4, and there have been instances of people with sudden and dangerously low blood pressure because of accidentally over-dosing on amlodipine (and this would probably apply to all the calcium-channel blockers). But many of our group members have been using both amlodipine and Golden Paste without incident, so it appears to be reasonably safe.

Anakinra

Trade name Kineret

A biologic prescribed for rheumatoid arthritis. It’s a human-recombinant variation of an IL-1 receptor antagonist. There are no metabolic interactions with Golden Paste, but the prescriber information warns against its use along with TNF inhibitors. Whole turmeric is probably not a sufficiently potent TNF inhibitor to be a significant problem, but the prescribing physician should be consulted anyway.

Anaspaz: see Hyoscyamine

Anastrozole

Trade names Arimidex, others

Used to treat hormone-receptor-positive breast cancer, and also as a breast cancer preventive in those at high risk. Its metabolism was potently inhibited by CYP3A4 inhibitors, so it should have physician approval for use with Golden Paste.

Metabolized in liver via N-dealkylation, hydroxylation, and glucuronidation (85%)

Metabolite: Triazole (inactive)

Enzymes inhibited: CYP1A2, CYP2C9, CYP3A4 (at high concentrations; inhibition not significant at usual dose)

Anipryl: see Selegiline hydrochloride

Anoro

Ellipta. See also Breo, Incruse and Trelegy

The Ellipta inhalers have two or three medication strips instead of the single medication in the Diskus and other inhaers. Anoro Ellipta contains umeclinidium and vilanterol. There are minor interactions from Golden Paste with both of these, but they do not appear to be significant.

Antisedan: see Atipemazole

Apixaban

Apixaban (brand name Eliquis) is an oral anticoagulant—specifically a direct, selective, reversible inhibitor of Factor Xa (free and clot-bound) as well as prothrombinase activity.

Its effects break down into therapeutic pharmacodynamics, clinical indications, and adverse effects:

More detail and references

1. Primary Pharmacological Mechanism

Inhibition of Thrombin Generation: By selectively blocking Factor Xa, apixaban prevents the conversion of prothrombin (Factor II) into thrombin (Factor IIa).
Thrombus Prevention & Attenuation: Because thrombin activates platelets and converts fibrinogen to fibrin, inhibiting Factor Xa suppresses fibrin clot formation and halts the propagation of preexisting thrombi.
No Direct Antithrombin Dependency: Unlike heparins, it does not require antithrombin III (ATIII) as a cofactor. It also does not directly inhibit platelet aggregation, though thrombin-induced aggregation decreases secondarily.

2. Clinical & Therapeutic Effects

Apixaban is prescribed to manage and prevent thromboembolic conditions:

Stroke & Systemic Embolism Prophylaxis: In patients with non-valvular atrial fibrillation (NVAF).
Deep Vein Thrombosis (DVT) & Pulmonary Embolism (PE): Acute treatment and extended secondary prevention.
Venous Thromboembolism (VTE) Prophylaxis: Postoperative prevention following elective hip or knee arthroplasty.

3. Adverse Effects & Risks


Category	Manifestations
Common / Minor Bleeding	Epistaxis, gingival bleeding, cutaneous hematomas/ecchymosis, prolonged oozing from minor cuts, microscopic hematuria.
Major / Critical Bleeding	Gastrointestinal hemorrhage (melena, hematemesis), intracranial hemorrhage (subdural/subarachnoid), intraocular bleeding, and retroperitoneal hematoma.
Spinal / Epidural Hematoma	Black box risk if neuraxial anesthesia (spinal/epidural) or spinal puncture is performed, potentially causing long-term or permanent paralysis.
Non-Hemorrhagic Effects	Nausea, post-hemorrhagic anemia, elevated hepatic transaminases, minor skin rash.

4. Pharmacokinetic Considerations

Bioavailability & Tmax: Oral bioavailability is approximately 50%, with peak plasma concentrations reached within 3 to 4 hours.
Elimination: Dual clearance pathway—roughly 27% renal clearance, with the remainder metabolized via CYP3A4/5 and excreted via biliary/fecal routes.
Half-life: Approximately 12 hours (steady-state dosing is twice daily).
Reversal Agent: Andexanet alfa serves as a specific decoy receptor to bind and neutralize Factor Xa inhibitors in life-threatening bleeding situations.

The apixaban–curcumin interaction is mainly a potential increase in bleeding risk. It is rated as a moderate, mostly theoretical interaction: it rests on lab and animal data, plus case reports involving other anticoagulants, rather than controlled studies with apixaban.

How it could happen

There are two possible mechanisms, and they can add together:

Additive effects on clotting (pharmacodynamic). Curcumin, the active compound in turmeric, inhibits platelet aggregation in lab studies, for example by interfering with thromboxane A2 and platelet-activating factor. It may also have mild anticoagulant effects. Apixaban blocks factor Xa. Combining an antiplatelet effect with an anticoagulant raises bleeding risk, even if neither drug level changes.
Higher apixaban levels (pharmacokinetic). Apixaban is cleared partly by the liver enzyme CYP3A4 and is pumped out by the transporters P-gp and BCRP. In lab studies, curcumin inhibits CYP3A4, P-gp and BCRP. In theory, this could raise apixaban concentrations.

How much it matters in practice

Plain curcumin is very poorly absorbed, so the effect of normal supplement doses is probably small. Turmeric used in cooking is not considered a concern.
High-dose or “enhanced-bioavailability” products are more concerning. These include products with piperine (black pepper extract), as well as liposomal, phytosome or nanoparticle forms. Piperine itself inhibits CYP3A4 and P-gp, which could further increase apixaban exposure.
There are case reports of raised INR and bleeding when turmeric or curcumin was combined with warfarin. These support the concern, but results from warfarin can’t be applied directly to apixaban.

Usual clinical guidance

Avoid curcumin supplements, especially high-dose or bioavailability-enhanced ones, unless the prescriber agrees.
If they are used together, watch for bleeding. Signs include unusual bruising, nosebleeds, bleeding gums, blood in the urine, black or tarry stools, and prolonged bleeding from cuts.
Supplements like this are generally stopped about 1–2 weeks before surgery or dental procedures.
Bleeding risk is higher in people who also take NSAIDs, aspirin, other antiplatelets or SSRIs, and in older people or those with kidney impairment.

Apo-Furosemide: see Furosemide

Aprinox: see Bendroflumethiazide

Aprovel: see Irbesartan

Arimidex: see Anastrozole

Aspavor: see Atorvastatin

Astrix

Astrix is a 100mg aspirin tablet, technically low-dose (though 80mg is more common for low-dose formulation). Would not typically be a problem along with Golden Paste.

Atarax: see Hydroxyzine

Atenolol, Apo-Atenol

Trade names Tenoretic, Tenormin

Beta blocker to drop blood pressure which turmeric also does. Do not stop Atenolol without physician advice.

Cardioselective inhibitor of beta(1)-adrenoceptor, has no significant intrinsic sympathomimetic activity or membrane stabilizing activity in its therapeutic dosage; exhibits beta(2)-adrenoceptors inhibition and negative chronotropic effect.

Need to monitor blood pressure when taken with turmeric.

Atipemazole

Trade name antisedan

In veterinary use, reverses the sedative effect of dexmedetomidine. Has been investigated as an anti-Parkinson’s drug in humans but is not in clinical use for that purpose.

Atorvastatin

Trade names Lipitor, Aspavor, others

One of the many statins used to reduce plasma cholesterol. It is cleared via CYP3A4, as are all the statins. However, they are in widespread use along with Golden Paste by many group members with no reported adverse effects. So it is generally okay with Golden Paste.

Atovaquone

Also known as: Mepron

An anti-parasitic used for malaria, toxoplasmosis and babesia. Inhibits electron transport chain in Plasmodium. It’s a CYP3A4 inhibitor, so it will further slow the clearance of turmeric, but should otherwise be okay with Golden Paste.

Atozet: see Ezetimibe and Atorvastatin

Atravet: see Acepromazine

Austiofen: see Carprofen

Avandia: see Rosiglitazone

Avapro: see Irbesartan

Avastin: see Bevacizumab

Aygestin: see Norethisterone acetate

Azathioprine

Trade name Imuran

Strong immunosuppressant, metabolized by xanthine oxidase. Turmeric is a potent xanthine oxidase inhibitor, so not a good combination with Golden Paste.

Azilect: see Rasagiline

Azodyl

A probiotic supplement (not a prescription drug) for kidney support. Okay with Golden Paste. Contains Enterococcus thermophilus, Lactobacilus acidophilus, and Bifidobacterium longum and a prebiotic (psyllium).

Can’t find your medication? Ask Dr Doug and it may be added to the guide. A · B–C · D–L · M–O · P–S · T–Z