Ayurvedic Herb-Drug Interactions

It is always a concern for Ayurvedic and other holistic health care practitioners to be fully informed by their clients as to what pharmaceutical substances, either prescription or over-the-counter medications, they may currently be taking. Nutraceuticals and herbal medicines are also of concern if one is to safeguard against the possibility of adverse events in the form of drug-herb interactions. I routinely ask clients to either produce a list of such substances that they are taking (or have taken within the preceding 6 months) or, better, bring in the actual containers with the substances to their initial consultations so as to eliminate any error on their part in transcribing the names and potencies of their medications.

While such interactions are relatively rare and usually of a mild level of intensity, this is not universally the case. I was taken aback not too long ago when I leaned that one instructor in an Ayurvedic training program had informed her students that Ayurvedic herbs in general, and the herbs that she had taught in her first year course in herbology in particular, had no side-effects, cautions or potential drug interactions. Those herbs included the following, amongst others.

The information below is taken from “Stockley’s Herbal Medicine Interactions” (E. Williamson, et al., eds., RPS-Pharmaceutical Press, Grayslake, Illinois USA: 2009).

Note that the following list is illustrative and not exhaustive: any practitioner suggesting any herb must be thoroughly familiar with potential issues that might arise in the form of interactions, contraindications, cautions and potential adverse events.

ALOE VERA / KUMARI (Aloe vera babadensis): Aloe Vera may have blood-glucose-lowering properties and may therefore be expected to interact with conventional drugs that have the same effect. Aloe Vera also appears to enhance the absorption of some vitamins. An isolated case report tentatively attributed increased surgical bleeding to the concurrent use of Aloe Vera and sevoflurane. Aloe, when administered with Licorice and Senna may potentiate the effects of anthraquinone-containing laxatives. Chronic use of Aloe can lead to potassium loss, which can increase the actions of cardiac glycosides and antiarrhythmic drugs. When administered with thiazide diuretics, loop diuretics, licorice and corticosteroids may engender potassium deficiency.

ASAFETIDA / HING (Asafoetida ferula): In theory the use of Asafetida with conventional antihypertensive may be expected to produce additive hypotensive effects. It has also been suggested that Asafetida may interact with anticoagulants.

ASHWAGANDHA (Withania somnifera): Although Ashwagandha may potentiate the effects of blood-glucose-lowering drugs, and may affect the reliability of digoxin assays and interfere with the control of hypo-and hyperthyroidism. Limited evidence suggests that Ashwagandha increases thyroid hormone levels and therefore interferes with the control of hypo-and hyperthyroidism. Although the evidence is limited, until more is known, it might be prudent to advise caution if clients taking levothyroxine (or other thyroid hormones) want to take Ashwagandha.

BALA (Sida cordifolia): Due to its ephedrine content Bala (Sida cordiflia) may interact with caffeine and MAO inhibitors exacerbating effects and elevating blood pressure, and may reduce the efficacy of Beta blockers. Ephedrine (Sudafed, etc.) by additive sympathomimetic effects inducing further toxicity and arrhythmia and Steroids (dextamethasone) by enhancing clearance levels and thus reducing effectiveness of the drug. Its use is best avoided or curtailed in individuals on such medications.

BOSWELLIA / SHALLAKI (Boswellia serrata): Evidence suggests that food may beneficially increase the bioavailability of boswellic acids, but other interaction data are generally lacking. It seems possible that Boswellia may interact with conventional drugs by inhibiting P-glycoprotein and/or cytochrome P450 isoenzymes.

CAYENNE / MARICH PHALAM (Capsicum spp.): Capsicum has the potential to decrease the absorption of aspirin, increase the absorption of ciprofloxacin and theophylline, and alter the absorption of cefalexin and digoxin. Capsicum may also decrease the metabolism of pentobarbital and phenazone, but it does not alter the metabolism of theophylline or quinine, which suggests that it has selective effects on hepatic enzymes. The interaction between capsicum and aspirin, ciprofloxicin and digoxin, cefalexin and phenozone, pentobarbital and quinine, is suggested.

CINNAMON / TWAK (Cinnamomum spp.): It has been suggested that Cinnamon may interfere with the control of diabetes by conventional antidiabetic drugs, but controlled studies do not appear to support this suggestion. Because of the presence of Coumarin in several strains of Cinnamon, its use with anticoagulant drugs is cautioned.

FENUGREEK / METHI (Trigonella foenum-graecum): Fenugreek saponins may modestly enhance the antidiabetic effects of the sulfonylureas. Fenugreek seed appears to have been widely studied for its blood glucose-lowering properties. It is suggested that fenugreek decreases blood-glucose levels by affecting an insulin signalling pathway.

GARLIC / RASHONA (Allium sativum): Case reports suggest that garlic may have additive blood pressure-lowering effects with Lisinopril, and may cause bleeding in those taking warfarin or fluindione. It has also been suggested that any antiplatelet effects of garlic may be additive with conventional antiplatelet drugs and NSAIDs, and studies suggest that garlic may reduce isoniazid levels. In a single report, a patient taking Lisinopril developed marked hypotension and became faint after taking garlic capsules. Garlic may have antiplatelet properties. It might therefore be expected to increase the risk of bleeding with conventional antiplatelet drugs and other drugs that have antiplatelet adverse effects.

GINGER / SUNTHI, ADRAK (Zingiber officinalis): There are isolated cases of ginger increasing the response to anticoagulant treatment with warfarin and related drugs. One study showed antiplatelet effects for ginger. Ginger (Zingiber officinale) has sometimes been listed as an herb that interacts with warfarin on the basis that in vitro it inhibits platelet aggregation.

GUGGULU (Commiphora mukul): In healthy subjects, the absorption of diltiazem and propranolol was modestly reduced by gugulipid. If the mechanism is confirmed, guggul might interact with a wide range of other drugs. A case of rhabdomyolysis has been attributed to the use of guggul alone, which should be borne in mind if it is combined with the statins, which also, rarely, cause this adverse effect. Limited evidence suggests that guggul modestly reduces the absorption of single-dose diltiazem.

KALAMEGHA (Andrographis panculata): Andrographis may have antidiabetic and antihypertensive effects, and limited evidence suggests that it may interact with conventional drugs with these properties. Andrographis may also have antiplatelet effects, and so it may interact with conventional antiplatelet drugs and anticoagulants. Evidence suggests that andrographis may have hypotensive properties that may be additive if given with conventional antihypertensives.

LICORICE / YASHTI MADHU (Glycorrhiza glabra): Licorice appears to diminish the effects of antihypertensives and may have additive effects on potassium depletion if given in large quantities with laxatives and corticosteroids. Iron absorption may be decreased by licorice, whereas antibacterials may diminish the effects of licorice. Licorice may enhance the effects of warfarin, there appears to be no evidence to support this.

MINT / PEPPERMINT/ SPEARMINT / PUDHINA (Mentha spp.): Food and antacids may compromise the enteric coating of some commercially available peppermint oil capsules. Peppermint oil appears to increase ciclosporin and felodipine levels and topically, in high doses, it may also enhance the skin penetration of some topical medicines. Peppermint tea contains digoxin-like constituents, but the clinical relevance of this is unclear. It may also impair iron absorption. Peppermint oil capsules appear to increase the bioavailability of felodipine, and therefore may increase the incidence of adverse effects such as headache, light-headedness and flushing. In vitro experiments suggest that peppermint oil is a moderate inhibitor of nifedipine metabolism.

PEPPER / MARICH (Piper nigrum): Both long pepper and black pepper are important ingredients of many Ayurvedic herbal medicines where they are intended to enhance absorption of other medicines, for example in the traditional formula known as Trikatu. Various animal studies have shown increased levels of amoxicillin, barbiturates, NSAIDs and oxytetracycline have been coincident with piperine intake. Piperine also had an antithyroid effect in animals.

SENNA / SWARNPATRI (Senna alexandrina): Senna has been predicted to interact with a number of drugs that lower potassium (such as the corticosteroids and potassium-depleting diuretics), or drugs where the effects become potentially harmful when potassium is lowered (such as digoxin). Senna may slightly reduce quinidine levels.

SHATAVARI (Asparagus racemosus): Shatavari may have additive effects with conventional antidiabetic drugs, and may alter the absorption of a number of drugs by delaying gastric emptying. Shatavari contains phytoestrogens and therefore has the potential to be antagonistic or synergistic with estrogens or estrogen antagonists. Limited evidence suggests that Shatavari increases the gastric emptying rate similarly to metoclopramide, which is known to decrease the absorption of atovaquone, digoxin and ketoprofen, and increase the absorption of ciclosporin, dantrolene, morphine, and paracetamol (acetaminophen).

TURMERIC / HARIDRA (Curcuuma longa): Turmeric or its constituent curcumin affects the absorption of some beta blockers, increases the absorption of midazolam. In a clinical study, curcumin, a major constituent of turmeric, decreased the absorption of talinolol, a P-glycoprotein substrate.

Article provided by William Courson, BVSA, Dpl. Ayur., C.H. an Ayurvedic Practitioner, faculty member and the College Dean of Institutional Development at Sai Ayurvedic College & Ayurvedic Wellness Center.

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