Reishi
Botanical Name: Ganoderma lucidum (W. Curtis.: Fr.) P. Karst.
Pharmacopoeial Name: Fructus ganodermi.
Synonym: Boletus lucidus Fr.
Common Names: Reishi, reishi mushroom, red reishi; Ling Zhi. ( Ganoderma japonicum = black reishi; Ganoderma applanatum = artist’s conk).
| Drug/Class Interaction Type | Mechanism and Significance | Management | Acyclovir, cefazolin
Antimicrobials
Antivirals
| Synergistic effects (greater than additive) have been observed with antimicrobial and antiviral combinations. Significance not established generally. | Consider coadministration, especially for immunocompromised patients with chronic viral and microbial infection. | Immunosuppressive, myelosuppressive chemotherapy
/ 
| Multifactorial interaction between reishi and chemotherapy; combination may improve therapeutic outcomes. Clinical significance anecdotally established.
Related mushroom polysaccharides also effective.
| Consider pretreatment, coadministration, and posttreatment with chemotherapy. |
Family
Ganodermataceae (Polyporaceae).
Related Species
Ganoderma japonicum (Fr.) Lloyd. (synonym, G. sinense Zhao, Xu et Zhang.), Ganoderma applanatum (Pers.) Pat, Ganoderma tsugae Murrill.
Habitat and Cultivation
A woody shelf-fungus that grows on rotting tree stumps and fallen logs in temperate forests throughout much of North America, most of Europe, South America and Asia, typically affecting oak trees. Reishi is now rare in the wild in China and rarer in Japan but has been under widespread industrial-scale cultivation in China for several years, which constitutes the bulk of commercial reishi supply internationally.
Parts Used
Fruiting body. Spore and mycelium preparations exist but have limited commercial availability; they are not identical to the fruiting body in composition or activity.
Common Forms
Dried whole fruiting body, by decoction (or very finely powdered).
- Tincture: Traditionally, rice wine extract.
- Standardized Solid Extract: Concentrates available greater than 20:1.
Strategic Considerations
Traditional Chinese use of reishi includes stand-alone herb for various conditions (Chinese syndrome-patterns), including heart (Xin) qi and lung (Fei) qi deficiencies. In modern Western usage, reishi is primarily considered as a safe and virtually nontoxic immunomodulatory agent. It is primarily used in the clinical context of immunocompromise, such as chronic fatigue immune dysfunction syndrome (CFIDS), or as an adjunct in integrative cancer protocols to support patients undergoing myelosuppressive conventional therapies. Pharmacological data suggest four primary areas of activity for reishi extracts: immune enhancing and antitumorigenic, cardiovascular regulatory, hypoglycemic, and hepatoprotective. Of these, interactions with pharmaceuticals are suggested primarily by the immunomodulatory data.
Support for use of reishi in oncological settings is largely derived from experimental studies on the biological activities of its polysaccharide and triterpene compounds. These have direct antitumor activity mediated by several pathways, notably the inhibition of the key transcription factors nuclear factor-kappa B (NF-κB) and activating protein 1 (AP-1). The indirect anticancer effects are mediated by promotion of mixed-lymphocyte responses, including enhancement of cytotoxic activity of monocyte-macrophages, natural killer (NK) cells, and lymphokine-activated killer (LAK) cells and increased secretion of cytokines such as interleukin-1 (IL-1), IL-6, and interferon gamma (IFN-γ). Protection against myelosuppression from chemotherapeutic agents and radiation therapy has moderate experimental and anecdotal clinical support; however, clinical trials are required to establish the efficacy of reishi for this purpose. Although some sources have cited Chinese-language clinical studies in support of these uses, full translations are unavailable, and evaluation of these trials by these secondary sources is typically schematic.
More substantial clinical data are available for related mushrooms, such as Coriolus, Polyporus, and Lentinus, and medicinal mushroom polysaccharides, particularly the branched (1→3)-beta-Dglucans, are thought to be broadly similar in their general immunomodulatory and anticancer effects. Additive interactions with antimicrobial pharmaceutical agents have been reported (see later), but these probably are also indirect results from a general enhancement of cell-mediated immunity and antiviral activity by reishi compounds, rather than specific herb-drug interactions. The long-term use of immunomodulating herbs in patient populations dependent on immunosuppressive therapies (e.g., to prevent graft rejection) is de facto contraindicated, and reishi extracts have been shown to reverse immunosuppressive effects of morphine.
Cardiovascular drug interactions seem unlikely given the mild cardiotonic effects of reishi despite suggestions in secondary literature of possible potentiating interactions with cholesterol-lowering and anticoagulant drugs. These interactions have not been demonstrated or reported, and claims of their likelihood are classified as “speculative” here, along with equally hypothetical suggestion of interactions with hypoglycemic drugs, as discussed later.
Effects on Drug Metabolism and Bioavailability
Pharmacokinetic interactions between reishi and pharmaceutical drugs have not been reported, and studies on the effects of the herb on drug-metabolizing systems have not been conducted to date. Induction of human hepatic glutathione- S-transferase in vitro by reishi polysaccharide has been recorded in one in vitro study. Inhibition of beta-glucuronidase in vitro by the triterpene constituent ganoderenic acid A was demonstrated in vitro, and the same constituent had a potent inhibitory effect against carbon tetrachloride (CCl4)–induced hepatotoxicity in a rodent model.
The hepatoprotective effects of the herb may counter solvent and other chemical or solvent-induced hepatotoxicity. These effects on drug-metabolizing enzymes may contribute, along with the antioxidant effects of the herb, to the established hepatoprotective properties of reishi observed in some studies. From these limited data, the potential theoretically exists for some modulation of clearance of glucuronide prodrugs, as well as accelerated clearance of glutathione and glucuronated drug conjugates. The effects of variation in activity of beta-glucuronidase on drug metabolism have not been systematically studied to date, but it may be a clinically significant determinant of variability of individual response to pharmaceuticals.
- Evidence: Acyclovir (Zovirax), cefazolin (Ancef, Kefzol).
- Extrapolated, based on similar properties: Cephalosporin antibiotics: Aztreonam (Azactam injection), cefaclor (Ceclor), cefadroxil (Duricef), cefamandole (Mandol), cefdinir (Omnicef), cefepime (Maxipime), cefixime (Suprax), cefoperazone (Cefobid), cefotaxime (Claforan), cefotetan (Cefotan), cefoxitin (Mefoxin), cefpodoxime (Vantin), cefprozil (Cefzil), ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime), ceftibuten (Cedax), ceftizoxime (Cefizox), ceftriaxone (Rocephin), cefuroxime (Ceftin, Kefurox, Zinacef), cephalexin (Keflex, Keftab), cephapirin (Cefadyl), cephradine (Anspor, Velocef), imipenem combination drug: imipenem and cilastatin (Primaxin I.M., Primaxin I.V.); loracarbef (Lorabid), meropenem (Merrem I.V.); possibly many other antimicrobial and antiviral agents.
- Similar properties but evidence lacking for extrapolation: Nucleoside (analog) reverse-transcriptase inhibitors (NRTIs or NNRTIs): Abacavir (Ziagen), didanosine (ddI, dideoxyinosine; Videx); dideoxycytidine (ddC, zalcitabine; Hivid), lamivudine (3TC, Epivir), stavudine (D4T; Zerit), tenofovir (Viread), zidovudine (azidothymidine, AZT, ZDV, zidothymidine; Retrovir); combination drugs: zidovudine and lamivudine (Combivir); abacavir, lamivudine and zidovudine (Trizivir).
- Similar properties but evidence indicating no or reduced interaction effects: Vidarabine (Ara-A, arabinoside; Vira-A).
| | Potential or Theoretical Beneficial or Supportive Interaction, with Professional Management |
Probability:
4. PlausibleEvidence Base:
PreliminaryEffect and Mechanism of Action
Synergy between reishi extracts or polysaccharides with acyclovir and cefazolin have been demonstrated in vitro. These effects are greater than linear additive effects but may be augmented in vivo by general enhancement of T helper cell type 1 (Th1) immune responses by reishi. The clinical significance of the interaction or general applicability to other antimicrobial or antiviral agents has not been established.
Research
An in vitro study measured the minimum inhibitory concentration (MIC) of an aqueous extract of Ganoderma alone and in combination with several antibiotics (ampicillin, cefazolin, oxytetracycline, chloramphenicol) against a variety of gram-negative and gram-positive bacteria. In combination with cefazolin against Klebsiella oxytocaand Bacillus subtilis, synergistic versus linear additive reductions in MIC were observed. Oh et al. used an in vitro model of human herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) in culture and examined the effects of acyclovir and vidarabine nucleoside agents, alone and in combination, on viral plaque size with an acidic protein-bound polysaccharide extract of reishi. They found a synergistic antiviral effect with acyclovir and reishi extract against both types. With vidarabine, however, there was an antagonistic effect against HSV-2 but a synergistic effect against HSV-1, suggesting that results may not generally be applicable to other nucleoside antivirals or specific viruses. Several reishi triterpene compounds have also been found to exhibit anti–human immunodeficiency virus (HIV) activity in one in vitro study.
Clinical Implications and Integrative Therapeutics
Reishi extracts alone have in vitro antiviral effects against both HSV-1 and HSV-2. The antiviral effects mechanism is not thought to directly involve cytokine such as IFN, but rather an interaction between reishi polysaccharides and the HSV glycoproteins involved in binding to host cell membranes. In addition, reishi polysaccharides enhance Th1 immunity, including the promotion of Th1 cytokines such as IFN-γ and IL-12, as well as NK cell activity. Clinically, the experimental data suggest that herpetic viral conditions may benefit from reishi coadministered with acyclovir, but extrapolations to other antivirals or other viral infections cannot reliably be made. However, reishi polysaccharides enhance cell-mediated immunity, tending to induce increased antimicrobial and antiviral aspects of immune responses, and can be administered to maintain immunocompetence before or after drug administration. Also, reishi extracts are effective in controlling postherpetic pain.
- Evidence: Cyclophosphamide (Cytoxan, Endoxana, Neosar, Procytox), doxorubicin (Adriamycin, Rubex).
- Extrapolated, based on similar properties: Daunorubicin (Cerubidine, DaunoXome), epirubicin (Ellence, Pharmorubicin), idarubicin (Idamycin, Zavedos), mitoxantrone (Novantrone, Onkotrone).
| | Potential or Theoretical Beneficial or Supportive Interaction, with Professional Management | | Prevention or Reduction of Drug Adverse Effect |
Probability:
4. PlausibleEvidence Base:
PreliminaryEffect and Mechanism of Action
Reishi extracts may protect against immunosuppressive aspects of antineoplastic therapies and improve therapeutic outcomes. Mechanisms are multifactorial and include protection against specific toxicities, reversal of leukopenia, and preservation of cell-mediated immune responses; antioxidant scavenging of free radicals; inherent anticancer activity resulting from inhibition of transcription factors NF-κB, AP-1, and free-radical reactive oxygen species (ROS); and other mechanisms.
Research
Reishi (Ganoderma japonicum)increased white blood cell (WBC) count in 72.5% of 175 leukopenic patients, according to a Chinese study cited by Chen and Chen. A Chinese rodent study of doxorubicin (Adriamycin) toxicity by Hongwei and colleagues, cited in detail by Upton, found that oral pretreatment with reishi extract at 500 mg/kg body weight for 14 days significantly reduced histological parameters of doxorubicin-induced toxicity in cardiac, hepatic, and renal cells, compared with controls receiving doxorubicin alone. An unrelated study demonstrated dose-dependent cardioprotective activity of hot-water reishi extracts against ethanol-induced heart toxicity in rodents through antioxidative protection against lipid peroxidation. This is the established mechanism of anthracycline-induced cardiotoxicity. Lu and Lin demonstrated reversal of B-cell and T-cell response suppression by morphine after administration of a polysaccharide reishi extract to morphine-dependent mice. Animal studies have demonstrated radioprotective effects of reishi in recovering immunocompetence after radiation exposure. However, this includes protection against deoxyribonucleic acid (DNA) strand breakage. A murine model showed that oral pretreatment with reishi enabled a significant reduction in cyclophosphamide toxicity in terms of preventing leukopenia. An in vitro study found that reishi may inhibit the angiogenic vascular endothelial growth factor (VEGF), and theoretically, angiogenesis inhibition may interfere with postsurgical wound repair.
McKenna et al. reviewed two small human studies from conference reports relating to Ganodermause in a clinical oncology setting. The first, an open-label trial by Kupin of 48 patients with advanced cancer (renal, gastric, breast), examined the effects of coadminstering reishi extracts during chemotherapy and radiation. The WBC levels were normalized in those taking reishi compared with controls, and treatment-induced leukopenia was rapidly ameliorated in the reishi group, who also had greater appetite and higher levels of general vigor than the controls. Of those patients requiring surgery, the reishi subjects experienced faster recovery and improved wound healing compared with the control group surgical candidates. A smaller study of patients with acute myelogenous leukemia (AML) or nasopharyngeal carcinoma who were pretreated with reishi extracts for 1 week before chemo/radiotherapy, contining the extracts for 3 months after the treatments, reported similar findings in terms of increased efficacy of treatment and reduction of treatment-induced adverse effects.
Clinical Implications and Integrative Therapeutics
The pluripotent anticancer effects of reishi polysaccharides and triterpenes have been subject of extensive experimental study, but to date, clinical trials have not confirmed these in vivo. Evidence for other mushroom beta-glycans is perhaps more compelling, but reasonable rationale appears to exist for combining reishi extracts into protocols designed for therapeutic protection against myelosuppression as a dose-limiting toxicity of chemotherapy. If the antiangiogenic effects of reishi are confirmed, combination with monoclonal antibody drugs targeting VEGF is theoretically a reasonable strategy.
Anisindione (Miradon), dicumarol, ethyl biscoumacetate (Tromexan), nicoumalone (acenocoumarol; Acitrom, Sintrom), phenindione (Dindevan), phenprocoumon (Jarsin, Marcumar), warfarin (Coumadin, Marevan, Warfilone).
Limited experimental data from aggregometry studies suggest that water extracts of reishi have some potential to induce aggregation in vitro, possibly because of an adenosine component in the extracts. The effects may be related to anti-inflammatory properties of reishi acting through a thromboxane A 2 (TXA 2 ) pathway. One small human study showed inhibition of adenosine diphosphate (ADP)–induced aggregation in healthy volunteers, as well as antithrombotic potential (measured by size of extracorporeal thrombi) resulting from oral administration of reishi extracts in atherosclerotic patients. The authors did not speculate on the possible mechanisms of these observed results. This has led to cautions about possible interactions with anticoagulants. However, recent data suggest a lack of effect on hemostatic parameters in healthy volunteers, and adverse interaction with antiplatelet or anticoagulant drugs seems unlikely.
Amphetamine aspartate monohydrate, amphetamine sulfate, dextroamphetamine saccharate, dextroamphetamine sulfate; D-amphetamine, Dexedrine.
There are limited reports that reishi extracts may exert a partial antagonism to the central stimulant effects of amphetamines as well as potentiation of the sedating effects of reserpine and chlorpromazine and increase phenobarbital-induced sleeping times. Reishi is not known clinically for its sedative effects in Western use, although it is incorporated into formulae for certain patterns of insomnia in Chinese herbal medicine. The limited available data do not suggest a straightforward pharmacological mechanism that enables extrapolation to an interaction at this time.
- Atorvastatin (Lipitor), fluvastatin (Lescol, Lescol XL), lovastatin (Altocor, Altoprev, Mevacor), combination drug:
lovastatin and niacin (Advicor); pravastatin (Pravachol), rosuvastatin (Crestor), simvastatin (Zocor), combination drug: simvastatin and extended-release nicotinic acid (Niaspan).
Recent experimental evidence has confirmed the modern Chinese medical use of reishi extracts for reducing cholesterol levels, although this is not an established use in Western botanical medicine. The mode of action is partially through the mevalonate pathway, possibly at the level of 3-hydroxy-3-methylglutaryl (HMG)–coenzyme A (CoA), but is likely multifactorial, with a beta-sitosterol–like effect on cholesterol absorption. These data have been used by secondary sources to suggest an interaction with HMG-CoA reductase inhibitor drugs (statins). Reverse extrapolation from a therapeutic effect to suggest that drugs with the same action may be clinically problematic is not evidence of an interaction. The combination of statins and reishi has not been studied, although Shiao suggests this combination may have an anticancer effect (presumably via farnesyl protein transferase). If used for hypocholesterolemia, the statin-reishi combination would probably have an additive effect on cholesterol levels, but to date an interactive synergy has not been demonstrated.
- Evidence:
Animal-source insulin (Iletin); human analog insulin (Humanlog); human insulin (Humulin, Novolin, NovoRapid, Oralin).
- Extrapolated, based on similar properties:
Buformin (Andromaco Gliporal, Buformina), chlorpropamide (Diabinese), glimepiride (Amaryl), glipizide (Glucotrol; Glucotrol XL), glyburide (glibenclamide; Diabeta, Glynase, Glynase Prestab, Micronase, Pres Tab), metformin (Dianben, Glucophage, Glucophage XR); combination drugs: glipizide and metformin (Metaglip), glyburide and metformin (Glucovance); phenformin (Debeone, Fenformin), tolazamide (Tolinase), tolbutamide (Orinase, Tol-Tab).
Hypoglycemic effects of reishi triterpenes have been established in animal studies. The effect partly results from reishi-induced increases in insulin secretion and partly from effects on hepatic glucose metabolism. An open-label study in eight diabetic patients reported by Teow and reviewed by McKenna apparently found that 1 g reishi extract daily was comparable in effect to the hypoglycemic effect of insulin (100 IU/mL) or oral hypoglycemic agents. Details were not supplied, and additional human trials are unavailable. Corroboration of hypoglycemic effects in vivo by controlled studies is required, together with analysis of the mechanism, before theoretical extrapolations to interactions can be considered more than speculative.
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