← Medication interactions guide · A · B–C · D–L · M–O · P–S · T–Z
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.
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D
Dantrolene
A direct-acting skeletal muscle relaxant. It is currently the only specific and effective treatment for malignant hyperthermia. Chemically, dantrolene is a hydantoin derivative, but does not exhibit antiepileptic activity like other hydantoin derivates such as phenytoin. Dantrolene depresses excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor 1, and decreasing intracellular calcium concentration. Ryanodine receptors mediate the release of calcium from the sarcoplasmic reticulum, an essential step in muscle contraction. Hepatic, most likely by hepatic microsomal enzymes. Its major metabolites in body fluids are 5-hydroxydantrolene and an acetylamino metabolite of dantrolene. Another metabolite with an unknown structure appears related to the latter. Dantrium may also undergo hydrolysis and subsequent oxidation forming nitrophenylfuroic acid.
More detail and references
The most significant adverse reaction with dantrolene therapy is hepatotoxicity. In humans, this effect is most commonly associated with high-dose chronic therapy but may also be seen after short-term high-dose therapy.
Turmeric will help allay liver damage but may slow excretion.
References
Drugban.ca: https://www.drugbank.ca/drugs/DB01219
Denosumab
Denosumab is a fully human IgG2 monoclonal antibody that blocks RANKL (receptor activator of nuclear factor kappa-B ligand).
Mechanism
- RANKL is produced by osteoblasts and stromal cells. It binds RANK on osteoclast precursors and mature osteoclasts, which drives their formation, activation and survival.
- Denosumab binds RANKL and stops it from reaching RANK. It does the same job as osteoprotegerin (OPG), the body’s natural decoy receptor for RANKL.
- As a result, fewer osteoclasts form and the existing ones are less active and die sooner. Bone resorption falls sharply, bone mineral density rises, and fracture risk drops.
How it differs from bisphosphonates
- It is not incorporated into the bone matrix, so its effect is reversible and lasts only while the drug is circulating.
- When it is stopped, bone turnover rebounds quickly, with BMD loss and a risk of multiple vertebral fractures. Stopping usually needs follow-on therapy, typically a bisphosphonate.
- It is cleared by the reticuloendothelial system, not the kidneys, so no renal dose adjustment is needed. However, hypocalcaemia risk is higher in CKD.
More detail and references
Uses and dosing
- Prolia 60 mg SC every 6 months: postmenopausal and male osteoporosis, glucocorticoid-induced osteoporosis, and bone loss from hormone ablation in prostate or breast cancer.
- Xgeva 120 mg SC every 4 weeks: prevention of skeletal-related events in bone metastases and multiple myeloma, giant cell tumour of bone, and hypercalcaemia of malignancy.
Key adverse effects
- Hypocalcaemia. Correct calcium and vitamin D before starting and supplement during treatment.
- Osteonecrosis of the jaw, which is more common with the oncology dose.
- Atypical femoral fractures.
- Infections such as cellulitis, and dermatitis or eczema.
- Rebound vertebral fractures after stopping.
interaction with curcumin
Checking for a pharmacokinetic link between denosumab and curcumin.
No clinically significant interaction between denosumab and curcumin has been documented, and none would be expected on mechanistic grounds.
Why a pharmacokinetic interaction is unlikely
Curcumin’s interaction potential comes mainly from inhibiting CYP enzymes (CYP3A4, 2C9, 1A2) and drug transporters such as P-gp. Denosumab is a monoclonal antibody that is broken down by protein catabolism in the reticuloendothelial system, like any IgG. It doesn’t pass through those pathways, so curcumin shouldn’t change its levels or half-life.
Theoretical pharmacodynamic overlap
In cell and animal studies, curcumin suppresses RANKL-induced NF-κB signalling and osteoclast formation, so it acts on the same pathway as denosumab, further downstream. In theory this could add a small antiresorptive effect. There are no human data showing this matters clinically, either for benefit or for harm such as oversuppressed bone turnover. Curcumin’s poor oral bioavailability makes a meaningful effect less likely.
Practical points
- Curcumin is not known to worsen hypocalcaemia, ONJ risk or atypical fracture risk.
It has its own cautions that apply regardless of denosumab:
Turmeric and curcumin supplements have been linked to rare cases of liver injury. The TGA has issued safety advice on this, particularly for high-dose or enhanced-bioavailability products.
- It has mild antiplatelet activity, which is relevant if the patient takes anticoagulants or antiplatelets or is having dental or oral surgery.
It may reduce iron absorption.
Calcium and vitamin D supplementation alongside denosumab should continue as usual. Curcumin doesn’t replace it.
Deracoxib
Trade names Deramaxx, Doxidyl
An NSAID that’s primarily a Cox-2 inhibitor. Typically okay with Golden Paste
Desvenlafaxine
Trade name Pristiq
An antidepressant in the SNRI class. Would need physician consent for concurrent use of Golden Paste.
serotonin-norepinephrine reuptake inhibitor (SNRI). It works by helping to restore the balance of certain natural substances (serotonin and norepinephrine) in the brain.
Dexamethasone
A corticosteroid, generally okay with Golden Paste. It is metabolized via CYP3A4 (like all steroids), but clinical experience hasn’t indicated any problems.
Dexlansoprazole
Trade name Dexilant
A proton pump inhibitor, but this is a delayed release formulation. It is also a stronger preparation than some others in the class. Best to have physician approval.
Diazepam
Also called Valium. One of the most widely prescribed sedatives, and one of the benzodiazepines. It’s cleared via CYP3A4, CYP2B6 and CYP2C19. In dogs, it is probably not a problem with Golden Paste, as most dogs metabolize it very fast. In combination with curcumin extract, a potent inhibitor of both CYP3A4 and CYP2C19, that may be a different story. CBD inhibits CYP2B6, and the combination of CBD and either curcumin or Golden Paste may be a problem. Doug has said it’s okay for dogs along with Golden Paste, but is more slowly metabolized in humans. Probably a good idea to suggest checking with the doctor, given the potential for addictive results in humans.
NOTE: We did have one report of a dog that slept for hours after one dose of diazepam. An outlier, no doubt, but something to keep in mind. We were not told what the dosage was, so it’s possible the dog was simply given too much.
Dicyclomine
Trade names Bentyl, others
Also called Dicycloverine, this is an anticholinergic given to reduce gastrointestinal muscle spasms. Since turmeric can work against anticholinergics, this needs to have physician approval.
Diltiazem
Trade name Adizem, Zemtard, Vaso-Card, others
A calcium-channel blocker, but works in a different manner than the typical ones like amlodipine. It is both an inhibitor and a substrate of CYP3A4, so its clearance would be affected by the Golden Paste.
Docetaxel
Trade names Taxotere, others
Chemotherapy medication. There are a couple of considerations with this. It has been trialled with curcumin with positive results–thyroid cancer cells were sensitized to the cytotoxicity of the docetaxel. However, it is also cleared via CYP3A4, and one study with human subjects found that its clearance varied widely with the patients’ individual enzyme activity. High levels of CYP3A4 activity resulted in lower–even possibly suboptimal–levels of docetaxel in the bloodstream, while low levels of activity might cause systemic toxicity to the patient. This should be mentioned to anyone who asks about using it with curcumin or Golden Paste, since the pepper in Golden Paste inhibits that enzyme. Curcumin does as well, but to a lesser extent.
More detail and references
References:
The Effect of an Individual’s Cytochrome CYP3A4 Activity on
Docetaxel Clearance: http://clincancerres.aacrjournals.org/content/clincanres/6/4/1255.full.pdf
Curcumin Enhances Docetaxel-Induced Apoptosis of 8505C Anaplastic Thyroid Carcinoma Cells:
Dorzolamide
Trade name Trusopt
Carbonic anyhydrase inhibitor, eyedrops, should be okay with Golden Paste.
Dosulepin
Trade names dothiepin, prothiaden, others
A tricyclic antidepressant that’s metabolized via glucoronidation, one of the pathways that pepper inhibits. Needs physician okay.
Doxazosin
Trade names Cardura, Cardura XL
Alpha1 blocker, primarily metabolized via CYP3A4, also a PgP substrate, vet or doctor should be consulted.
Doxycycline
Trade names Ronaxan, others
Antibiotic in the tetracycline class, okay with Golden Paste.
Doxyrubicin
Also known as: Adriamycin, Caelyx, Myocet, Rubex
ok in conjunction with turmeric
Curcumin is a potential antitumor phytochemical isolated from Curcuma longawith capacity of suppressing cancer metastasis and proliferation and affecting molecular pathways. Experiments have demonstrated the potential of curcumin for inhibiting chemoresistance by downregulating oncogene pathways such as MMP-2, TGF-β, EMT, PI3K/Akt, NF-κB and AP-1.Furthermore, coadministration of curcumin and DOX potentiates apoptosis induction in cancer cells. In light of this, nanoplatforms have been employed for codelivery of curcumin and DOX. This results in promoting the bioavailability and internalization of the aforementioned active compounds in cancer cells and, consequently, enhancing their antitumor activity. Noteworthy, curcumin has been applied for reducing adverse effects of DOX on normal cells and tissues via reducing inflammation,oxidative stress and apoptosis. The current review highlights the anticancer mechanism, side effects and co-delivery of curcumin and DOX via nanovehicles.
More detail and references
Pharmaceutics 2020,12, 1084; doi:10.3390/pharmaceutics12111084www.mdpi.com/journal/pharmaceutics
DOX is administered in a single dose and repetition occurs after 21 days . DOX interferes with cancer progression via intercalation with DNA and reducing activity of topoisomerase II,
resulting in suppressing DNA replication. Although DOX demonstrated potential antitumor activity against different cancer cells, it was soon found that its efficiency in cancer therapy is restricted by a phenomenon known as chemo resistance.
To date, a high number of molecular pathways and mechanisms have been identified that contribute to DOX resistance. Trefoil factor 3 (TFF3) is a secreted protein with overexpression in small and large intestines and is correlated with enhanced cell migration . Antiapoptotic and proproliferative functions of TFF3 are mediated by its trefoil domain and a cysteine residue (Cys057) incarboxy-terminal . Following doxorubicin administration, an increase occurs in the expression of TFF3 and Akt that are responsible for cancer proliferation and inhibiting apoptosis. It has been reported that downregulation of TFF3 provides the way for enhancing apoptosis and doxorubicin sensitivity .
Uncontrolled proliferation of cancer cells is dependent on glucose uptake and glycolysis. Sphingosine kinase 1 (SphK1) accounts for triggering cancer chemoresistance and also,elevating glycolysis .
A newly published article has shed some light on the relationship between SphK1 and DOX resistance in osteosarcoma (OS) cells. Exposing OS cells to DOX is associated with upregulation of SphK1 and subsequent increase in glucose metabolism, leading to induction of chemoresistance . Noteworthy, non-coding RNAs also play a significant role in DOX resistance. It seems that enhancing expression of oncosuppressor miRNAs such as miRNA-124 and miRNA-223 is of importance in impairing cancer proliferation and migration, and increasing their sensitivity into DOX chemotherapy. Furthermore, reducing activity of drug transporters such as P-gp elevates DOXaccumulation in cancer cells and is of importance in reversing chemoresistance . Overall, studies are in agreement with the fact that different molecular pathways and mechanisms can involve in inducingDOX chemoresistance and phytochemical are potential agents in triggering chemosensitivity .
However, chemoresistance is not the only drawback of DOX. A dose-dependent side effect is another challenge in DOX chemotherapy. Cardiotoxicity, hepatotoxicity and nephrotoxicity are major adverse effects of DOX. Stimulation of molecular pathways such as Akt that promote cell proliferation is of importance in reducing DOX side effects . Non-coding RNAs such asmiRNA-146a are able to prevent apoptotic cell death in improving DOX-mediated cardiotoxicity .
E
Enalapril
Trade names Enacard, Vasotec
An ACE inhibitor for high blood pressure that’s typically okay along with Golden Paste. Often prescribed when poor renal function is present along with hypertension. Used widely for dogs and humans. No metabolic interactions with Golden Paste.
Epilim: see Sodium valproate
Epirubicin, Epirubicin Ebewe
Trade names Ellence, Pharmorubicin
A cancer medication similar to doxorubicin (both are anthracyclines). It is metabolized by both of the major pathways (CYP3A4 and glucorinadation via UGTB7 (unlike doxorubicin which is affected only by CYP3A4). Physician consult required.
Errolon: see Furosemide
Escitalopram
Trade names Lexapro, Cipralex, others–also see citalopram
An SSRI that raises serotonin levels. Escitalopram and citalopram are stereoisomers (meaning that their molecules are mirror images, approximately). There is some controversy over whether escitalopram is actually superior to citalopram or was introduced just to keep a patented drug on the market when citalopram’s patent expired. For the purposes of interactions, they can be considered interchangeable.
Estriol
Also spelled Oestriol, trade names Incurin, Ovestin, Ortho-Gynest, Synapause, others
One form of estrogen, marketed primarily for hormone replacement therapy in humans (in Europe and some other countries, but not in the US or Canada) and for urinary incontinence in dogs (as Incurin). Generally okay with Golden Paste.
Ethambutol
An essential medication in the management of tuberculosis. However, it can cause an optic neuropathy of uncertain etiology.
Optic neuritis: symptoms may include decreased acuity, color blindness or visual defects (usually reversible with discontinuation, though irreversible blindness has been reported)
Peripheral neuritis
Turmeric polyphenols reduce this.
Eurofen: see Carprofen
Eutensin: see Furosemide
Ezetimibe
Also known as: atozet
Inhibits sterol transporter at brush border and, consequently, intestinal absorption of cholesterol, which in turn decreases delivery of cholesterol to the liver and reduces hepatic cholesterol stores.
Metabolized by glucuronide conjugation. Half life 22 hours.
Elimination will be increased when on turmeric.
F
Feldene: see Piroxicam
Fenofibrate
Trade names Lipantil, Tricor and others
For high cholesterol. The FDA has withdrawn approval for use in combination with statins in the US, after several studies showed little cardiovascular benefits and a high incidence of side effects. It’s cleared by one of the metabolic pathways that both turmeric and pepper inhibit (glucoronidation), but is probably okay with Golden Paste.
References:
More detail and references
Drugbank record: https://www.drugbank.ca/drugs/DB01039
Fesoterodine Fumarate
Trade names Toviaz
An antimuscarinic marketed for overactive bladder. Metabolized via CYP3A4 and CYP2D6, so the prescribing physician should probably be consulted before Golden Paste is added. If you also take CBD, checking with your doctor is particularly important, since CBD inhibits both CYP3A4 and CYP2D6.
References:
More detail and references
Drugbank record: https://www.drugbank.ca/drugs/DB06702
Fexofenadine
Trade names Allegra, Fexidine, Flexofen, others
This is a prescription antihistamine. According to the manufacturer (Sanofi-Aventis), “Fexofenadine is a substrate of CYP3A4. However, only about 5% is metabolized by the liver, indicating that the role of hepatic metabolism is relatively minor in its clearance from the body.” So it should be okay with the Golden Paste.
Finasteride
Trade names Propecia, Proscar
An “anti-androgen” prescribed for benign prostate hyperplasia and also for male pattern baldness hair loss. It’s a type 2 5α-Reductase inhibitor, as is curcumin. Like curcumin, it is also metabolized via CYP3A4 and its clearance would therefore be inhibited by Golden Paste. I think it would not be significant, but a physician consult would be best.
Fioricet
This is a combination of butalbital, acetaminophen and caffeine. There is one product that also contains codeine, and that would have the usual cautions about concurrent use of Golden Paste. Otherwise, it’s likely not a problem.
Flagyl: see Metronidazole
Flomax: see Tamsulosin
Florfenicol
Trade names Nuflor, others
A fluorinated synthetic analog of thamphenicol (an antibiotic), used primarily for livestock. Not approved for human use or in any application where its residue might end up in human foods. It is approved in the US for the control of various bacteria in aquaculture. It is metabolized via CYP3A4, so should not be used with Golden Paste without veterinary approval. Florfenicol is an active ingredient in some other preparations, and the small amount present in those may not be a problem, especially in topicals.
Fluoxetine
Trade names Prozac, Sarafem, others
One of the early SSRI’s, still widely used. Golden Paste will inhibit its clearance and increase the amount of serotonin in the bloodstream, so doctor advice is recommended.
References:
More detail and references
Drugbank.ca: https://www.drugbank.ca/drugs/DB00472
PharmGkb: https://www.pharmgkb.org/chemical/PA449673
Paper on curcumin’s interaction with fluoxetine: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4090827/
Flusapex: see Furosemide
Fluticasone/salmeterol
Also known as: Seritide
Seritide is an inhaler for asthmatics. It’s a combination of fluticasone propionate and salmeterol. Fluticasone is a CYP3A4 inhibitor (like pepper) so its metabolism won’t be affected by turmeric or Golden Paste. Salmeterol is a beta2-adrenergic receptor agonist and is not a cytochrome P450 substrate. OK with Golden Paste.
More detail and references
DrugBank record for fluticasone propionate: https://www.drugbank.ca/drugs/DB00588
DrugBank record for salmeterol: https://www.drugbank.ca/drugs/DB00938
Fluxinin Meglumline
Trade name Banamine
An NSAID commonly used for horses, as a topical cream or in their feed. It’s available only by prescription in the US, and labeled for five days use only. Okay with Golden Paste for that time period.
Furosemide
Trade names Aisemide, Apo-Furosemide, Beronald, Desdemin, Discoid, Diural, Diurapid, Dryptal, Durafurid, Edemid, Errolon, Eutensin, Flusapex, Frudix, Frusetic, Frusid, Fulsix, Fuluvamide, Furesis, Furix, Furo-Puren, Furon, Furosedon, Fusid.frusone, Hydro-rapid, Impugan, Katlex, Lasilix, Lasix, Libeo, Lodix, Lowpston, Macasirool, Mirfat, Nicorol, Odemase, Oedemex, Profemin, Rosemide, Rusyde, Salix, Teva-Furosemide, Trofurit, Uremide, Urex and possibly others
A loop diuretic, one of the most frequently prescribed drugs worldwide, usually to assist with hypertension. Generally okay with Golden Paste, though with a caution that turmeric is also a modest diuretic.
Fusid-Frusone: see Furosemide
G
Gabapentin
Trade names Epleptin, Neurontin
Gabapentin gained approval only as an anti-seizure medication. However, it is widely prescribed off-label for a variety of conditions, mostly related to nerve pain and more recently to mood disorders. The evidence for efficacy in these off-label conditions is controversial and not universally accepted.
May be useful in dogs and cats as adjunctive therapy for refractory or complex partial seizures and in many species for the treatment of chronic pain (especially neuropathic pain). The mechanism of action of gabapentin for either its anticonvulsant or analgesic actions is not fully understood, but it appears to bind to CaV α2δ, a subunit of the voltage-gated calcium channels. By decreasing calcium influx, the release of excitatory neurotransmitters (eg, substance P, glutamate, norepinephrine) is inhibited. Although gabapentin is structurally related to γ-aminobutyric acid type A (GABA), it does not appear to alter GABA binding, reuptake, or degradation or to serve as a GABA agonist in vivo.
More detail and references
In dogs, oral bioavailability is ≈80% at a dose of 50 mg/kg. Peak plasma levels occur ≈2 hours after administration. Gabapentin is partially metabolized to N-methyl-gabapentin in dogs; elimination is primarily via renal routes. Elimination half-life is ≈2 to 4 hours.
In general, use of the commercially available human oral solution (Neurontin®) should be avoided in dogs, as it reportedly contains xylitol (300 mg/mL).
There have been reports of excessive sedation in dogs that were given gabapentin along with CBD, so we need to provide that caution if someone asks about Golden Paste and CBD along with gabapentin. Otherwise, it does not appear to be a problem along with Golden Paste or curcumin.
Galliprant: see Grapiprant
Gestakadin: see Norethisterone acetate
Giazo: see Balsalazide and Mesalamine
Glimepiride
We don’t have detailed notes on this medication yet. Ask Dr Doug if you need to know.
Glucophage: see Metformin
Gocovri: see Amantadine
Grapiprant
Trade name Galliprant
A non-steroidal anti-inflammatory, but a different one compared to the typical non-selective COX inhibitors and also the selective COX-2 inhibitors. Grapiprant inhibits the formation of PGE2, one of the prostaglandins involved in pain and inflammation. Quoting the authors of a research article published in Veterinary Medicine and Science, “PGE2 binds to four receptors, of which one, the EP4 receptor, is primarily responsible for the pain and inflammation associated with osteoarthritis (OA). The deleterious and pathologic actions of PGE2 are inhibited in varying degrees by steroids, aspirin and cyclo-oxygenase inhibiting NSAIDs; however, administration of these drugs causes decreased production of PGE2, thereby decreasing or eliminating the homeostatic functions of the molecule. By inhibiting just the EP4 receptor, the homeostatic function of PGE2 is better maintained.“
More detail and references
Bottom line, should be okay with Golden Paste.
References:
Grapiprant: an EP4 prostaglandin receptor antagonist and novel therapy for pain and inflammation: http://onlinelibrary.wiley.com/doi/10.1002/vms3.13/pdf
H
Heartmedin: see Pimobendan
Homatropine
Trade names Equipin, Isopto Homatropine
Homatropine is a potent anticholinergic that is sometimes combined with hydrocodone as a cough suppressant. In the very small amount in the combination, it shouldn’t be an issue with Golden Paste. But the medication itself would still need a 3-4 hour separation from Golden Paste because of the hydrocodone.
Humira: see Adalimumab
Hycamtin: see Topotecan
Hydro-Rapid: see Furosemide
Hydrocodone: see Codeine (for hydrocodone with homatropine, see the entry on homatropine)
Hydroxychloroquine
Also known as: Plaquenil
Decreases activity of immune system. Mechanisms underlying the anti-inflammatory and immunomodulatory effects of hydroxychloroquine are unknown. Peak plasma time: 3.26 hr Half-life: 40-50 days.
Seems ok with turmeric.
Hydroxyzine
Sold in the US as Atarax
Hydroxyzine is prescribed sometimes for panic attacks (and is one of the prescription drugs subject to abuse). It’s also an antihistamine, and is prescribed in veterinary use mostly for that purpose. It’s another one of the CYP3A4 substrates, so it’s metabolized by the same pathway that’s inhibited by pepper. Should be okay with Golden Paste unless it was being abused in larger doses than ordinarily prescribed.
Sources:
More detail and references
Drugbank: https://www.drugbank.ca/drugs/DB00557
Drugbank: https://www.drugbank.ca/drugs/DB00557/biointeractions (for interactions with other drugs)
Hyomax: see Hyoscyamine
Hyoscyamine
Also known as daturine, trade names Symax, HyoMax, Anaspaz, Egazil, Buwecon, Cystospaz, Levsin, Levbid, Levsinex, Donnamar, NuLev, Spacol T/S and Neoquess
An alkaloid of the nightshade family, from a variety of plants including henbane, jimsonweed, deadly nightshade, mandrake and tomatoes. For our purposes, the significance is that it’s a potent anticholinergic, and therefore turmeric is likely to act in opposition to it. Physician consult required.
Hysingla: see Codeine
I
Imidapril Hydrochloride
Trade names Prilium, Tanatril
An ACE inhibitor sold under several brand names. Prilium is approved only for veterinary use in dogs. It’s a pro-drug whose active metabolite is imidaprilat. Like other ACE inhibitors, it can raise potassium levels and lower sodium levels. One caution along with Golden Paste is to avoid dehydration, since that will also result in elevated potassium levels. Increased incidence of angioedema has been noted with concurrent use of NSAIDs (in humans, uncertain if this may also be the case for dogs). Like all the other ACE inhibitors, it’s metabolized at least in part via CYP3A4, but none of the others have so far been a problem with Golden Paste and it seems unlikely that imidapril would be either.
Impugan: see Furosemide
Incruse
Ellipta. See also Anoro, Breo and Trelegy
The Ellipta inhalers generally contain two or three medication strips instead of just one, as in the Diskus and other inhalers. Except that Incruse only contains one, unlike the other Ellipta products. Incruse Ellipta contains umeclidinium by itself. Golden Paste does have a minor interaction with this, but we’ve had no reports of problems.
Incurin: see Estriol
Indapamide
Thiazide-like diuretic often prescribed along with an ACE inhibitor for blood pressure. It’s cleared via CYP3A4, so Golden Paste should be used only with physician approval.
Irbesartan
Trade name Avapro, Aprovel, Karvea, others
An angiotensin receptor II antagonist (similar to an ACE inhibitor) for hypertension. Generally okay with Golden Paste. See also Coaprovel–it is irbesartan combined with hydrochlorothiazide.
K
Kapvay: see Clonidine
Karvea: see Irbesartan
Katlex: see Furosemide
Keflex: see Cephalexin
Kelaprofen: see Carprofen
Kliofem
A combination of estradiol and norethisterone, a progestin. Prescribed primarily as hormone replacement therapy in post menopausal women. Shouldn’t be a problem by itself with Golden Paste. However, it is a potent enough P-glycoprotein inhibitor that in combination with Golden Paste (whose black pepper is also a P-gp inhibitor), it could be an issue with certain medications.
Klonopin: see Clonazepam
L
Labetalol
Also Altol, Latol, Normadate, Normodyne
Combination selective-alpha and non-selective beta adrenergic blocker, for hypertension. Competes with other catecholemines for binding to these sites. Action is potent but reversible. Like the other beta blockers, it should be okay with Golden Paste.
Lacidipine
Trade names Lacipil, Motens
A calcium channel blocker used for hypertension. Probably okay with Golden Paste.
Lacipil: see Lacidipine
Lamictal: see Lamotrigine
Lamisil: see Terbinafine
Lamotrigine
Trade name Lamictal
EDIT–this is a major change.
An anticonvulsant originally sold for epileptic seizures, but now used also as a mood stabilizer. It is widely prescribed off-label for peripheral neuropathy, migraines, cluster headaches and adult ADHD. It’s inactivated by glucoronidation, but is affected primarily by the UGT2B7 isoform and to a lesser extent by UGT1A4. The piperine in pepper is a moderate to potent inhibitor of UGT1A1, but has no significant effect on UGT2B7 and as far as I can determine, no effect on UGT1A4. Therefore, although the side effects of Lamictal overdosage are severe, i don’t think Golden Paste is going to be a problem with it.
Lansoprazole
Trade names Prevacid, others
A proton pump inhibitor used to lower the amount of stomach acid. Commonly prescribed for ulcers, GERD and as an adjunct to antibiotics for H. pylori infections. Usually okay with Golden Paste. Some people have reported that they can’t have it at the same time as Golden Paste. No good logic for that but it’s been reported often enough that whatever the reason is, it seems to be a legitimate problem. A very few people have not been able to use Golden Paste at all when they were taking any of the PPI’s, including lansoprazole.
Lasilix: see Furosemide
Lasix: see Furosemide
Lercanidipine
Trade name Zandip, Lercaril
A calcium channel blocker for hypertension. Like the other drugs in its class, it’s metabolized via CYP3A4. But it is more sensitive to CYP3A4 inhibitors than most of the other drugs in the class, and greatly increased levels have been noted with such moderate inhibitors as grapefruit juice. Best to get the prescribing physician’s consent.
Letairis: see Ambritensan
Levate: see Amitriptyline
Levbid, Levsin, Levsinex: see Hyoscyamine
Levetiracetam
Trade name Keppra
An anti-seizure medication in both veterinary and human use. Its exact mechanism is unknown, but it is thought to work via inhibition of presynaptic calcium channels, reducing neurotransmitter release and slowing impulse conduction across nerve synapses. It is not metabolized via any of the cytochrome P450 pathways and Golden Paste is okay with it.
Levothyroxine, L-Thyroxine
Trade names Eltroxin, Euthyrox, Eutirox, Letrox, Levaxin, Lévothyrox, Levoxyl, L-thyroxine, Thyrax, Thyrax Duotab, Thyrox, Thyronorm, Unithroid, Eutirox, Synthroid, Tirosint, Thyrin, Thyrolar
A synthetic form of the thyroid hormone thyroxine (T4). Widely used in both human and veterinary medicine for hypothyroidism and several other thyroid gland dysfunctions. Okay with Golden Paste, but see below..
NOTE: We’ve had several reports now of increased thyroid hormone levels when people with a still-functioning thyroid added Golden Paste to their diet. So questions about this should include a suggestion for testing thyroid hormones reasonably soon if the individual still has their thyroid.
Lisinopril
Trade names Zestril, Prinivil, Qbrelis
Angiotensin converting enzyme (ACE) inhibitors dilate arteries and veins by competitively inhibiting the conversion of angiotensin I to angiotensin II (a potent endogenous vasoconstrictor) and by inhibiting bradykinin metabolism; these actions result in preload and afterload reductions on the heart ACE inhibitors also promote sodium and water excretion by inhibiting angiotensin-II induced aldosterone secretion; elevation in potassium may also be observed.
ACE inhibitors also elicit renoprotective effects through vasodilation of renal arterioles.
This drug is not metabolised. turmeric will add to drop in blood pressure which needs to be monitored along with dose.
ACE inhibitors reduce cardiac and vascular remodeling associated with chronic hypertension, heart failure, and myocardial infarction
More detail and references
In most cases, Golden Paste is going to be okay with lisinopril.
Loratadine
Trade name Claritin
Loratadine is a former prescription-only antihistamine now sold OTC as Claritin. It is a selective inverse agonist of peripheral histamine H1 receptors. It’s converted to the active metabolite, descarboethoxyloratadine, via CYP3A4. However, at least one clinical study indicated that in the presence of a CYP3A4 inhibitor, it would be metabolized via CYP2D6. No metabolic problem with Golden Paste, in other words.
Sources:
PubMed: Identification of human liver cytochrome P450 enzymes that metabolize the nonsedating antihistamine loratadine. Formation of descarboethoxyloratadine by CYP3A4 and CYP2D6
https://pubmed.ncbi.nlm.nih.gov/8615885/
More detail and references
DrugBank: https://www.drugbank.ca/drugs/DB00455
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
