Our Health Library information does not replace the advice of a doctor. Please be advised that this information is made available to assist our patients to learn more about their health. Our providers may not see and/or treat all topics found herein. This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER. This cancer information summary provides an overview on cancer therapy interactions with different foods and dietary supplements. This summary contains the following key information: For adult cancer patients in the United States, the frequency of complementary and alternative medicine (CAM) use is approximately 36%.[1] It is possible that the combination of cancer drugs taken by these patients and the CAM they use may interact, causing adverse outcomes.[2,3,4] When dietary supplements /herbs and cancer drugs are taken together, there is always a risk of the supplement having an impact on the pharmacokinetics (PK) or pharmacodynamics (PD) of the drug. Many drug interactions occur from the effects of the supplement on specific enzymes or on components involved in the PK of the drug, such as how the drug is metabolized and transported. Reporting and studying these interactions is important, so health care professionals can help patients navigate CAM usage with standard cancer therapies, thus avoiding preventable adverse outcomes. Integrative oncology consultations available in a number of cancer care settings can engage patients in evidence-based discussions about recommending or stopping supplements, as well as addressing questions about alternative therapies.[5] In the United States, dietary supplements are regulated by the U.S. Food and Drug Administration (FDA) as a separate category from foods, cosmetics, and drugs. Unlike drugs, dietary supplements do not require premarket evaluation and approval by the FDA unless specific disease prevention or treatment claims are made. The quality and amount of ingredients in dietary supplements are also regulated by the FDA through Good Manufacturing Practices (GMPs). The FDA GMPs requires that every finished batch of dietary supplement meets each product specification for identity, purity, strength, composition, and limits on contamination that may adulterate dietary supplements. Because dietary supplements are not formally reviewed for manufacturing consistency every year, ingredients may vary considerably from lot to lot and there is no guarantee that ingredients claimed on product labels are present (or are present in the specified amounts). The FDA has not approved the use of dietary supplements as a treatment for cancer patients. Cytochrome P450 Inhibitors/Inducers One of the main group of enzymes involved in the metabolism of many cancer drugs is the cytochrome P450 (CYP) superfamily of enzymes. These enzymes play an important role in the activation and inactivation of various drugs. Another component involved in the metabolism and excretion of many drugs is the transport protein, P-glycoprotein (P-gp). P-gp works in the intestine as a drug efflux pump regulating the bioavailability of the drug. Various anticancer drugs are substrates of P-gp; thus, if P-gp or any CYP enzyme is impacted, the drug it is processing will also be impacted. The PK of a drug predicts therapeutic outcomes for the patient. Various herbs and dietary supplements are known to influence the PK of certain drugs, such as St. John's wort. Currently, research on dietary supplement and cancer drug PK interactions is limited, but there is evidence for several possible interactions and adverse reactions.[1,6,7] References: General Information Some common dietary antioxidants include the following: Numerous anticancer agents generate reactive oxygen species, which cause decreased levels of antioxidants, deoxyribonucleic acid damage, and cancer cell death. Antioxidants are taken by many cancer patients because it is thought that the substances will protect and repair healthy cells damaged by cancer therapy.[1] There is insufficient information for many specific antioxidant supplements to determine if they are safe and effective as a complementary therapy to standard cancer treatment. Laboratory/Animal/Preclinical Studies A study published in 2018 examined the pharmacokinetic interactions between imatinib (25 mg /kg orally) and vitamin A (12 mg retinol /kg orally), vitamin E (400 IU /kg orally), vitamin D3 (100 IU/kg orally), and vitamin C (500 mg/kg orally) when coadministered in rat animal models. The results showed that there was an increase in the bioavailability of imatinib with vitamins A, E , and D, and a decrease in the bioavailability of imatinib with vitamin C.[2] A study that examined the oxidized form of ascorbate, dehydroascorbate, as a complementary supplement with chemotherapeutic drugs (i.e., doxorubicin, cisplatin, vincristine, methotrexate, and imatinib) initially found that dehydroascorbate given before doxorubicin treatment caused a reduction of therapeutic efficacy in mice with lymphoma (RL) cell–derived xenogeneic tumors. This form of ascorbate is not generally available as a dietary supplement and is not used clinically, and it has different properties and pharmacology from unoxidized or reduced ascorbate; thus, the potential clinical implications of these findings are unknown.[3] An in vivomouse model study observed a possible interaction between vitamin C (40 mg/kg/d) and bortezomib. There was a significant reduction in bortezomib's anticancer activities with consumption of vitamin C.[4] Human/Clinical Studies A study examined pre- and post-diagnosis antioxidant dietary supplement (selenium; multivitamins; zinc; and vitamins A, C, and E) use in postmenopausal breast cancer survivors. The results showed an increased risk of total mortality and worsened recurrence -free survival with antioxidant dietary supplement use during chemotherapy or radiation therapy.[5] A similar study investigated the outcomes for breast cancer patients using antioxidant supplements (vitamins A, C, and E; carotenoids; and coenzyme Q10) before and during treatment with cyclophosphamide, doxorubicin, and paclitaxel. The results showed an increase in hazards of recurrence and death in these patients. Though these hazard ratios are not statistically significant, they both trended in the same direction as those seen in the previous study.[6] This evidence does give reason to use these supplements with caution and indicates that more research on this topic is needed. Alpha-tocopherol, one of eight vitamin E compounds, was investigated in a clinical trial for its impact on adverse effects from chemotherapy and radiation therapy. Initially, some research suggested that alpha-tocopherol may reduce toxicity caused by radiation therapy for head and neck cancer. Two randomized, controlled clinical trials of patients with head and neck cancer who received vitamin E supplementation at a dose of 400 IU/day have shown an association with a higher risk of tumor relapse and a decrease in cancer-free survival.[7,8] References: Ginseng General information Ginseng root has commonly been used as a dietary supplement in traditional Asian medicine. There are several types of ginsengs. While there is no conclusive evidence for the health benefits of ginseng, people currently use it for the following reasons:[1,2] Laboratory/animal/preclinical studies Most in vitro research on ginseng's pharmacokinetic (PK) interactions found little evidence of any effects, determining a low risk of cytochrome P450 (CYP)-dependent herb -drug reactions. Overall, the evidence is mixed and inconclusive.[3,4,5] Case study Ginseng was suspected of being responsible for an incident of hepatotoxicity that occurred in a 26-year-old male taking imatinib. The hypothesized mechanism for this interaction was inhibition of hepatic CYP3A4, the enzyme primarily responsible for metabolizing imatinib. The ginseng was ingested through a ginseng energy drink, which creates uncertainty about whether the ginseng or the other ingredients in the drink caused the adverse effect. Clinical research is needed to confirm if there are any PK interactions between imatinib and ginseng.[6] Scutellaria baicalensis/wogonin General information Scutellaria baicalensis, also known as wogonin, Chinese skullcap, or Huang Qin, is a plant used in traditional Chinese medicine to treat various medical conditions, such as the following:[7] In traditional Chinese medicine, there are some herbal mixtures that contain Scutellaria baicalensis, one being Huang Qin Tang. PHY906, a patented formula derived from Huang Qin Tang, is being studied as a potential adjuvant for cancer therapy; there is some evidence that this herbal mixture potentiates the anticancer effects of certain cancer drugs such as sorafenib.[8] Some research has shown the inhibitory effect of wogonin on the activity of CYP, but more research is needed to determine interactions with specific drugs.[9] Laboratory/animal/preclinical studies A 2016 study investigated the effects of a Scutellariae radix decoction on methotrexate pharmacokinetics in rats. The study revealed an increased systemic methotrexate exposure when given together with the Scutellariae radix decoction. Giving them together is thought to have effects on multidrug resistance –associated proteins and breast cancer resistance protein.[10] A 2018 study examined the PK profile and herb-drug interactions of oral wogonin and intravenous docetaxel in rats with mammary tumors. The investigators found that in rats receiving oral wogonin and docetaxel, the area under the concentration versus time curve (AUC), initial peak serum concentration (Cmax), and half-life for docetaxel increased. The investigators speculated that these increases resulted from the inhibitory effect of wogonin on CYP3A and P-glycoprotein (P-gp). More research is needed with human clinical trials, but these results suggest a possible interaction between wogonin and docetaxel.[11] St. John's Wort General information The flower of the St. John's wort (SJW) (Hypericum perforatum) plant is used traditionally for wound healing, insomnia, and kidney and lung problems, and most commonly today for depression. This flower can be taken through teas, tablets, capsules, and extracts. Currently, the evidence for the clinical efficacy of SJW is varied, but there have been reports of interactions and adverse effects with several drugs.[12] Laboratory/animal/preclinical studies A 2012 study observed the effects of SJW on the PK of methotrexate in a rat animal model. After coadministration of SJW (300 mg /kg and 150 mg/kg) and methotrexate, animals that received 300 mg/kg of SJW had a 163% increase in AUC and a 60% increase in Cmax for methotrexate. For animals that received 150 mg/kg of SJW, an increase in AUC (55%) for methotrexate was observed. Overall, the mortality of the rats treated with SJW combined with methotrexate was higher. The researchers suggested using extreme caution if coadministering these two substances.[13] Human/clinical studies There are two well-known examples of herb-drug interactions impacting drug PK that have clinical evidence. These two interactions are between SJW and both irinotecan and imatinib. After patients were treated with both irinotecan (350 mg/m2) and SJW (900 mg/d), one study found a 42% decrease in plasma levels of SN-38, the active metabolite of irinotecan. The researchers hypothesized that components of SJW extract, pseudohypericin and hyperforin, interacted with CYP3A4 isoform and P-gp, causing reduction in SN-38. This interaction may cause a loss of irinotecan efficacy.[14] A similar outcome occurred in two studies that examined treatment with imatinib (400 mg) and SJW (300 mg 3 times a day). In one study, SJW caused a 32% decrease in AUC, a 29% decrease in Cmax, and a 21% decrease in half-life after two weeks of combined treatment with SJW and imatinib.[15] The second study found that SJW use caused a 43% increase in the clearance of imatinib and a 30% decrease in AUC. This interaction is also thought to be caused by the impact of SJW on CYP3A4, the major enzyme that metabolizes imatinib.[16] Another CYP3A4 substrate that may be impacted by SJW is docetaxel. A 2014 study with ten cancer patients investigated the PK interactions of docetaxel (135 mg IV for 60 min) in combination with SJW (300 mg orally for 14 days). The results showed a statistically significant decrease of 12% in mean AUC and an increased clearance of docetaxel.[17] Although there is a lack of published research, the use of SJW in patients undergoing treatment with ixabepilone is not recommended. SJW may cause a decrease in plasma concentrations of ixabepilone. The drug label for ixabepilone states a warning for this possible interaction.[18] Thunder God Vine General information Thunder god vine, also known as Tripterygium wilfordii Hook f, is an herb traditionally used in Chinese medicine for its possible anti-inflammatory, immunosuppressant, and anticancer effects.[19] Studies have found that triptolide and celastrol, the active components of thunder god vine, are responsible for these possible effects. Clinical observations, mostly from China, reported significant multiorgan toxicities from the traditional raw material or the extracts. Deaths associated with ingesting these materials have been frequently reported.[20,21] Frequency of severe-grade adverse events from the extracts ranged from 5% to 8%,[22,23] with the global incidence of adverse events at 30.8% (95% confidence interval, 21.2–40.3).[23] The most frequently reported adverse events are intestinal toxicity (13.9%), reproductive toxicity (10.2%), hepatotoxicity (6.8%), nephrotoxicity (13.6%), hematotoxicity (5.7%), and cutaneous toxicity (<5%).[23] Evidence varies for herb-drug interactions and toxicity, which are potentially caused by inhibiting effects on the activity of the CYP450 enzyme system.[24] Specifically, celastrol inhibits five cytochrome P450 isoenzymes (CYP1A2, CYP2C19, CYP2D6, CYP2E1, and CYP3A4) in vitro.[25] In addition, a study also found that the coadministration of the CYP3A4 inhibitor, ritonavir, or the inducer, dexamethasone, leads to a significant increase or decrease of the plasma concentration levels of triptolide.[26] Laboratory/animal/preclinical studies A 2017 study investigated the effects of triptolide (10 mg/kg) on the PKs of three different sorafenib doses (20, 50, and 100 mg/kg) in rats. The results showed an increase in Cmax and AUC for each sorafenib dose and a decrease in clearance with pretreatment of triptolide. It is hypothesized that this interaction occurred due to triptolide's possible inhibiting effects on P-gp and CYP3A4 enzymatic activity.[27] References: Grapefruit General information Grapefruit and other similar fruits, such as Seville orange, pomelo, and lime, have been known to interact with a variety of drugs, including some anticancer drugs. These pharmacokinetic interactions may be caused by the furanocoumarin components found in the seeds of grapefruit. These components have been observed impacting the metabolism of substrates of CYP3A4.[1,2,3] Laboratory/animal/preclinical studies Grapefruit and its furanocoumarin components have been studied for their potential antioxidative, anti-inflammatory, and anticancer effects in in vitro and in vivo studies.[4] Human/clinical studies Some research has shown a dietary supplement/food and drug PK interaction between grapefruit juice and imatinib. Grapefruit juice may cause plasma levels of imatinib to increase by inhibiting CYP3A4, in turn triggering organ toxicity.[5] An interaction has been observed between grapefruit juice and etoposide. A randomized, crossover, pilot study of six participants examined the bioavailability of the oral chemotherapy drug etoposide after coadministration of grapefruit juice. The data showed a decrease in bioavailability between the control group and the experimental group, who were treated with etoposide and grapefruit juice. The bioavailability of etoposide (50 mg orally) reduced from approximately 73% to 52% after pretreatment with grapefruit juice (100 mL). This resulted in a decrease in the area under the concentration versus time curve (AUC) by 26% for etoposide with grapefruit juice, compared with etoposide alone.[6] Other studies have found an increase in the bioavailability of sunitinib with grapefruit juice exposure,[7] and an increase in AUC by 29% and an increase in peak serum concentration (Cmax) by 60% for nilotinib (400 mg orally) was also observed when combined with grapefruit juice (240 mL).[8] Green Tea General information Green tea, green tea extract, and products of green tea components are commonly taken as foods, dietary supplements, and herbal therapies. Some of the traditional and modern uses of green tea include the following: Research has been mixed on whether green tea is safe or effective for these uses as well as for coadministration with anticancer drugs.[9] Current research shows that green tea and the polyphenol epigallocatechin gallate (EGCG), an antioxidant component of green tea, can impact the PK or pharmacodynamics (PD) of certain drugs, thus impacting the metabolism and effectiveness of these drugs.[10] Laboratory/animal/preclinical studies As seen in the literature, green tea and its constituent EGCG may be involved in both PK and PD interactions. An interaction between green tea and bortezomib was examined in an in vitro study with human multiple myeloma and glioblastoma cell lines. EGCG blocked bortezomib's protease inhibitory function by binding to the boronic acid structure in bortezomib, causing the inability to induce cancer cell death and consequently blocking its anticancer abilities. The second portion of this study investigated this interaction within a plasmacytoma xenograft nude mouse model. Bortezomib's cancer cell apoptosis -inducing effect was completely prevented with intragastric EGCG administration (50 mg/kg).[11] This interaction was also reported in another animal study that examined human prostate cancer xenografts in immune-deficient mouse models. High intravenous (IV) doses of EGCG along with the coadministration of bortezomib resulted in the abrogation of bortezomib's anticancer effects.[12] Human studies should be conducted to determine clinical significance. The impact of green tea and EGCG on fluorouracil PK was studied in rats. The results of these studies showed a 151% increase in Cmax and a 425% increase in AUC for fluorouracil. The researchers concluded that green tea greatly impacted the PK of fluorouracil.[13] A similar study examined the PK of irinotecan (10 mg/kg IV) given in combination with EGCG (20 mg/kg IV) in rats and found that EGCG caused elevated plasma levels and reduced hepatobiliary excretion of irinotecan and its metabolite SN-38. This is possibly because of EGCG's inhibitory effects on P-glycoprotein (P-gp).[14] A 2019 study evaluated the effects of green tea extract on the PK of palbociclib in a rat animal model. The data showed a decrease in the oral bioavailability of palbociclib when it was coadministered with green tea extract, but there was no impact on the elimination of palbociclib. The altered PK was thought to be the result of interference in the absorption of palbociclib. The authors recommended against the coadministration of these compounds.[15] Research on rat animal models investigated the impact of green tea extract on the oral bioavailability of erlotinib and lapatinib. A decrease in the oral bioavailability for erlotinib and lapatinib was observed after consumption of green tea extract (200 mg/kg). There was a decrease in AUC by 68% for erlotinib and 70% for lapatinib with short-term administration of green tea extract, and a decrease in AUC by 16% for erlotinib and 14% for lapatinib with long-term administration of green tea extract.[16] An in vivo and in vitro study examined the impacts of intragastric coadministration of sunitinib with EGCG. Coadministration of these two solutions resulted in the formation of a precipitate in the stomachs of the mice, thus decreasing its bioavailability. It was also reported that a decrease in the AUC and Cmax of plasma sunitinib with EGCG administration in rats resulted in reduced sunitinib absorption.[17] A possible interaction was also found between EGCG and tamoxifen. A 2009 study assessed the bioavailability and PK of tamoxifen (2 mg/kg) and its metabolite, 4-hydroxytamoxifen, with coadministration of EGCG (0.5 mg/kg, 3 mg/kg, and 10 mg/kg) in Sprague-Dawley rats. The coadministration of EGCG at doses of 3 mg/kg and 10 mg/kg caused a 49% to 78% increase in the bioavailability of tamoxifen. In addition, EGCG significantly impacted the formation of 4-hydroxytamoxifen. It is believed that this reaction was caused by EGCG's inhibitory effect on P-gp and CYP3A.[18] However, a subsequent study analyzed the effect of a green tea extract (1 g twice daily, 300 mg EGCG) on endoxifen (active metabolite of tamoxifen) levels. The study did not demonstrate a PK interaction between the green tea supplement and endoxifen levels.[19] The findings of the preclinical studies provide a justification and motivation for human studies to determine appropriate clinical recommendations. Case study In addition to the in vitro and in vivo EGCG and sunitinib study mentioned above, the same researchers published a case study that might demonstrate a possible adverse effect of green tea consumption with sunitinib treatment. A male patient with metastatic renal cell carcinoma who received sunitinib reported worsened symptoms of hyperemia and eye swelling near the site of a metastatic lesion when drinking green tea; the symptoms improved when he stopped taking green tea. The authors hypothesized that the lack of symptom control may result from EGCG's effects on sunitinib's anticancer abilities.[17] References: References: To assist readers in evaluating the results of human studies of integrative, alternative, and complementary therapies for cancer, the strength of the evidence (i.e., the levels of evidence) associated with each type of treatment is provided whenever possible. To qualify for a level of evidence analysis, a study must: Separate levels of evidence scores are assigned to qualifying human studies on the basis of statistical strength of the study design and scientific strength of the treatment outcomes (i.e., endpoints) measured. The resulting two scores are then combined to produce an overall score. For an explanation of the scores and additional information about levels of evidence analysis, see Levels of Evidence for Human Studies of Integrative, Alternative, and Complementary Therapies. The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above. General Information Revised text to state that in the United States, dietary supplements are regulated by the U.S. Food and Drug Administration (FDA) as a separate category from foods, cosmetics, and drugs. Unlike drugs, dietary supplements do not require premarket evaluation and approval by the FDA unless specific disease prevention or treatment claims are made. Also added text to state that the quality and amount of ingredients in dietary supplements are also regulated by the FDA through Good Manufacturing Practices (GMPs). The FDA GMPs requires that every finished batch of dietary supplement meets each product specification for identity, purity, strength, composition, and limits on contamination that may adulterate dietary supplements. This summary is written and maintained by the PDQ Integrative, Alternative, and Complementary Therapies Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® Cancer Information for Health Professionals pages. Purpose of This Summary This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about cancer therapy interactions with foods and dietary supplements in people with cancer.. It is intended as a resource to inform and assist clinicians in the care of their patients. It does not provide formal guidelines or recommendations for making health care decisions. Reviewers and Updates This summary is reviewed regularly and updated as necessary by the PDQ Integrative, Alternative, and Complementary Therapies Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH). Board members review recently published articles each month to determine whether an article should: Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary. Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries. Levels of Evidence Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Integrative, Alternative, and Complementary Therapies Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations. Permission to Use This Summary PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]." The preferred citation for this PDQ summary is: PDQ® Integrative, Alternative, and Complementary Therapies Editorial Board. PDQ Cancer Therapy Interactions With Foods and Dietary Supplements. Bethesda, MD: National Cancer Institute. Updated <MM/DD/YYYY>. Available at: https://www.cancer.gov/about-cancer/treatment/cam/hp/dietary-interactions-pdq. Accessed <MM/DD/YYYY>. [PMID: 33079503] Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images. Disclaimer The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page. Contact Us More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website's Email Us. Last Revised: 2024-04-05 This information does not replace the advice of a doctor. Ignite Healthwise, LLC disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use and Privacy Policy. Learn how we develop our content. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Ignite Healthwise, LLC.Cancer Therapy Interactions With Foods and Dietary Supplements (PDQ®): Integrative, alternative, and complementary therapies - Health Professional Information [NCI]
Overview
General Information
Antioxidants
Herbs
Foods
Foods, Dietary Supplements, and Cancer Drug Interaction Tables
Herbal /Dietary Supplement Anticancer Therapy Effect Study Type AUC = area under theconcentrationversus time curve; Cmax = peakserumconcentration; EGCG = epigallocatechin gallate; SJW = St. John's wort. SJW Irinotecan Increased activity of CYP3A4 and decreased AUC of activemetaboliteSN38 Clinical trial [1] SJW Imatinib Increased clearance and decreased AUC of imatinib Clinical trial[2] SJW Methotrexate Increased AUC and Cmax of methotrexate Animal study [3] SJW Docetaxel Increased clearance and decreased AUC of docetaxel Clinical trial[4] SJW Ixabepilone May decreaseplasmaconcentrations of ixabepilone Label warning for ixabepilone[5] Green tea Sunitinib Decreaseddrug absorptionandbioavailabilityof sunitinib Animal study andcase report [6] Green tea Palbociclib Decreasedoralbioavailability of palbociclib Animal study[7] Green tea extract Erlotinib Decreased AUC and oral bioavailability of erlotinib Animal study[8] Green tea extract Lapatinib Decreased AUC and oral bioavailability of lapatinib Animal study[8] EGCG Tamoxifen Increased bioavailability of tamoxifen Animal study[9] EGCG Irinotecan Increased plasma concentration of irinotecan and decreasedhepatobiliary excretionof drug and its metabolite SN-38 Animal study[10] Green tea and EGCG Fluorouracil Increased AUC and Cmax of fluorouracil Animal andin vitro study[11] Grapefruit Imatinib May increase plasma levels of imatinib by inhibiting CYP3A4 Review[12] Grapefruit Etoposide Decreased AUC and bioavailability of etoposide Randomized,crossover,pilot study [13] Grapefruit Sunitinib Increased bioavailability of sunitinib Clinical trial[14] Grapefruit Nilotinib Increased AUC and Cmax of nilotinib Clinical trial[15] Vitamin A Imatinib Increased bioavailability of imatinib Animal study[8] Vitamin E Imatinib Increased bioavailability of imatinib Animal study[8] Vitamin D3 Imatinib Increased bioavailability of imatinib Animal study[8] Vitamin C Imatinib Decreased bioavailability of imatinib Animal study[8] Scutellaria baicalensis Docetaxel Increased AUC of drug and exposure to both drug and herb Animal study[16] Anticancer Therapy Herbal/Dietary Supplement Effect Study Type AUC = area under the concentration versus time curve; Cmax = peak serum concentration; EGCG = epigallocatechin gallate; SJW = St. John's wort. Docetaxel Scutellaria baicalensis Increased AUC of drug and exposure to both drug and herb Animal study[16] Docetaxel SJW Increased clearance and decrease AUC of docetaxel Clinical trial[4] Erlotinib Green tea extract Decreased AUC and oral bioavailability of erlotinib Animal study[8] Etoposide Grapefruit Decreased AUC and bioavailability of etoposide Randomized, crossover, pilot study[13] Fluorouracil Green tea and EGCG Increased AUC and Cmax of fluorouracil Animal andin vitro study[11] Imatinib Grapefruit May increase plasma levels of imatinib by inhibiting CYP3A4 Review[12] Imatinib Vitamin A Increased bioavailability of imatinib Animal study[8] Imatinib Vitamin E Increased bioavailability of imatinib Animal study[8] Imatinib Vitamin D3 Increased bioavailability of imatinib Animal study[8] Imatinib Vitamin C Decreased bioavailability of imatinib Animal study[8] Imatinib SJW Increased clearance and decreased AUC of imatinib Clinical trial[2] Irinotecan SJW Increased activity of CYP3A4 and decreased AUC of active metabolite SN38 Clinical trial[1] Irinotecan EGCG Increased plasma concentration of irinotecan and decreased hepatobiliary excretion of drug and its metabolite SN-38 Animal study[10] Ixabepilone SJW May decrease plasma concentrations of ixabepilone Label warning for ixabepilone[5] Lapatinib Green tea extract Decreased AUC and oral bioavailability of lapatinib Animal study[8] Methotrexate SJW Increased AUC and Cmax of methotrexate Animal study[3] Nilotinib Grapefruit Increased AUC and Cmax of nilotinib Clinical trial[15] Palbociclib Green tea Decreased oral bioavailability of palbociclib Animal study[7] Tamoxifen EGCG Increased bioavailability of tamoxifen Animal study[9] Sunitinib Grapefruit Increased bioavailability of sunitinib Clinical trial[14] Sunitinib Green tea Decreased drug absorption and bioavailability of sunitinib Animal study and case report[6] Herbal/Dietary Supplement Cancer Therapy Adverse Reaction Study Type EGCG = epigallocatechin gallate. Vitamin C Doxorubicin,cisplatin,vincristine, methotrexate, and imatinib Dose-dependentdecrease inapoptosiswith allchemotherapeutic drugstested Animal study[17] Vitamin C Bortezomib Decreased bortezomib's anticancer activities Animal study[18] Dl-alpha-tocopherol (vitamin E) Radiation therapy Higher risk oftumor relapseand increased all-causemortality Clinical trial[19,20] Ginseng Imatinib Incident of hepatotoxicity Case report[21] EGCG or green tea extract Bortezomib Decreased anticancer effect by neutralizing effects of bortezomib In vitro and animal study[22] EGCG Bortezomib Decreased bortezomib's anticancer effect Animal study[23] Green tea Sunitinib Decreased anticancer effect, worsenedsymptoms Preclinical researchand case report[6] Summary of the Evidence for Cancer Therapy Interactions With Foods and Dietary Supplements
Latest Updates to This Summary (04 / 05 / 2024)
About This PDQ Summary
Our Health Library information does not replace the advice of a doctor. Please be advised that this information is made available to assist our patients to learn more about their health. Our providers may not see and/or treat all topics found herein. This information does not replace the advice of a doctor. Ignite Healthwise, LLC disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use and Privacy Policy. Learn how we develop our content. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Ignite Healthwise, LLC.Cancer Therapy Interactions With Foods and Dietary Supplements (PDQ®): Integrative, alternative, and complementary therapies - Health Professional Information [NCI]