Supplements

WHAT THE EVIDENCE SAYS

The decisive study for this entry is MISTRAL (Palliative Medicine, July 2026): a phase 3, multicentre, randomised, double-blind, placebo-controlled trial in which 290 patients with advanced pancreatic cancer received standard treatment plus either subcutaneous mistletoe extract or placebo ^[1]. The primary focus was health-related quality of life, measured with the EORTC QLQ-C30 and QLQ-PAN26 questionnaires ^[1]. The result: no statistically significant differences between the arms in either quality of life or body weight ^[1]. In the nested biomarker study, the only significant change was a rise in eosinophils in the mistletoe group, with no clinical correlate; there were no differences in blood counts, lymphocyte subpopulations, C-reactive protein, albumin or Ca19-9 ^[1]. The authors' conclusion, verbatim: "Since no benefit was observed, there is no clinical reason to recommend mistletoe extract in patients with advanced pancreatic cancer ^[1]."

WHY WE PUT THIS SO PLAINLY WHEN OTHER SOURCES READ DIFFERENTLY.

This is a point where two credible sources diverge, and readers deserve to know what the difference rests on. The National Cancer Institute summary reports older work with mixed results: in pancreatic cancer, longer survival was described in people given mistletoe extract; in melanoma there was no increase in survival time; in lung cancer no differences were found ^[2]. We do not settle the contradiction by picking the more convenient sentence, but on methodological grounds. The earlier studies suggesting benefit in pancreatic cancer were neither blinded nor placebo-controlled, and in quality-of-life research that is decisive: a patient who knows they are receiving an "extra treatment" rates how they feel differently from one who does not ^[2]. MISTRAL tested precisely the setting in which the earlier data looked most promising, in a design immune to that effect, and found no benefit ^[1].

STRENGTH OF THE EVIDENCE

Moderate for the topic as a whole, high for one specific question. High: adding mistletoe to standard treatment in advanced pancreatic cancer does not improve quality of life — that comes from a large trial with the strongest available design ^[1]. Moderate for the rest: mistletoe preparations differ from one another (host tree species, manufacturer, method of preparation), they are used across many diagnoses and schedules, and most remaining data come from unblinded, small or observational studies ^[2]. This must not be read as "absence of effect has been proven in every cancer"; the correct statement is that where it has been tested most rigorously no benefit was shown, and elsewhere high-quality evidence is lacking.

WHAT READERS MAY NOT KNOW ABOUT HOW IT IS GIVEN.

Mistletoe in oncology is usually not a tablet or a tea. According to the National Cancer Institute, extracts are most often given by injection under the skin, and less commonly by mouth, into a vein, into the pleural cavity, or directly into a tumour ^[2]. This has two practical consequences. First, it is not a "dietary supplement" in the everyday sense and should not be thought of like a vitamin from the pharmacy. Second, reported side effects include soreness and inflammation at injection sites, headache, fever, chills, nausea and severe tiredness, and a few cases of severe allergic reactions, including anaphylactic shock, have been reported ^[2].

INTERACTIONS WITH CANCER TREATMENT

In the reference sources available to us there is no documented pharmacokinetic interaction between mistletoe and any specific anticancer drug — and we say so plainly rather than implying an interaction that has not been demonstrated ^[2][3]. The real problems lie elsewhere, and there are three.

• Fever, chills and injection-site inflammation can be mistaken for signs of infection. In a patient undergoing chemotherapy, particularly during neutropenia, fever is a state requiring urgent medical assessment — and a preparation that itself causes fever blurs that signal.
• Mistletoe extracts are immunologically active (MISTRAL recorded a rise in eosinophils) ^[1]. Data on combining them with modern immunotherapy, including checkpoint inhibitors, simply do not exist. Absence of data is not evidence of safety and should not be read as such.
• The risk of a severe allergic reaction, though rare, is real and independent of the cancer itself ^[2].

The general rule the National Cancer Institute states without exceptions: tell your doctor about every preparation you are taking, including those regarded as natural and safe ^[3].

THE SCOPE OF WHAT WE WRITE HERE

We give no doses, brand names or administration schedules, and we do not decide whether any individual should stop or continue mistletoe — that is a decision for their treating team, and cancer3.ai is an information portal, not a clinic. We describe the state of knowledge: what has been tested, how strong the test was, and what it showed.

Sources

1. Wode K et al. — Mistletoe extract in patients with advanced pancreatic cancer: Health-related quality of life in a double-blind, randomized, placebo-controlled trial (MISTRAL), Palliative Medicine 2026: europepmc.org ↗
2. National Cancer Institute — Mistletoe Extracts (PDQ®), Patient Version, updated 2023: cancer.gov ↗
3. National Cancer Institute — Complementary and Alternative Medicine (CAM), updated 2024: cancer.gov ↗

WHY THIS ENTRY EXISTS

Cannabis is among the most widely self-administered products used by people with cancer, and the information circulating outside medicine blends two entirely different claims: that it helps tolerate treatment, and that it treats the cancer. The first has partial support in evidence; the second has none ^[1][2]. That distinction is the substance of this entry.

SYMPTOMS: WHERE THE EVIDENCE IS STRONGEST. The 2024 American Society of Clinical Oncology (ASCO) guideline reviewed 13 systematic reviews and 5 additional primary studies ^[1]. The highest quality of evidence (moderate) was found for cannabinoids in refractory chemotherapy-induced nausea and vomiting, and specifically for licensed drugs rather than herbal cannabis ^[1].

• Dronabinol (synthetic THC) was approved for this indication in 1986 ^[2].
• Nabilone is a second available synthetic THC analogue ^[2].
• Nabiximols (Sativex, 1:1 THC:CBD) are approved in Canada for symptomatic relief of pain in advanced cancer ^[2].

For herbal cannabis itself, rigorous clinical trial data in these indications are lacking - what exists is largely patient surveys ^[2].

APPETITE AND WASTING

Here the picture is weaker than common belief suggests. Dronabinol's indication was extended in 1992 to anorexia associated with HIV infection, but clinical trials showed no statistically significant weight gain - patients did report improved appetite ^[2]. Improved hunger and weight gain are not the same thing, and in cancer cachexia it is the latter that counts (see the separate entry on nutrition in cachexia).

TREATING THE CANCER

NO DATA. The US National Cancer Institute PDQ summary states plainly that clinical trials of medicinal cannabis are limited and that the FDA has not approved cannabis as a treatment for any medical condition ^[2]. Evidence of antitumour activity comes exclusively from laboratory and animal work (apoptosis, inhibition of angiogenesis in glioma, breast and colorectal models) and has not been confirmed in humans ^[2]. On that basis the ASCO guideline strongly recommends against using cannabis or cannabinoids as cancer-directed treatment outside a clinical trial, citing very low quality evidence and poorer outcomes observed in patients using these products during immunotherapy ^[1].

INTERACTIONS WITH CANCER TREATMENT - THE ESTABLISHED PART

Cannabinoids interact with the hepatic cytochrome P450 enzyme system, through which a large share of anticancer drugs is metabolised ^[2]. The NCI warns that highly concentrated CBD oils could through this mechanism increase toxicity or decrease the effectiveness of treatment ^[2]. For a sense of scale: in a study of 24 patients receiving irinotecan or docetaxel, cannabis herbal tea did not significantly influence exposure to or clearance of these drugs ^[2] - so the risk concerns concentrated preparations above all, not every form of cannabis. The practical conclusion is single: cannabinoid use must be disclosed to the treating team, because without that information the interaction risk cannot be assessed.

INTERACTIONS WITH IMMUNOTHERAPY - THE CONTESTED PART

Here the data are outright contradictory and must be presented as such.

• The biological premise raises concern: THC produced immunosuppression and enhanced tumour growth in immunocompetent mice ^[2].
• The ASCO guideline cites poorer clinical outcomes in patients using cannabis during immunotherapy ^[1].
• Yet a pooled analysis of individual patient data from four Canadian Cancer Trials Group studies (684 patients on durvalumab plus tremelimumab, with or without chemotherapy; 65 patients, 9.5%, used cannabinoids and 32 did so at baseline) found no harm: immune progression-free survival was longer in cannabinoid users (10.91 versus 8.31 months; HR 0.60; 90% CI 0.36-1.00; p=0.05), overall survival did not differ significantly (14.23 versus 11.30 months; HR 0.81; 90% CI 0.51-1.27; p=0.35), and there were no differences in response rate or in immune-related adverse events ^[3]. The authors write that the finding supports the safe use of cannabinoids alongside combination immune checkpoint inhibitor therapy ^[3].

WHAT THESE DATA DO NOT SAY

The CCTG analysis is retrospective: dose, route and THC-to-CBD ratio were unknown, the number of users was small and most likely understated through under-reporting ^[3]. Most users had non-small cell lung cancer (41.5%) or pancreatic cancer (40.0%), so the result does not transfer automatically to other diagnoses ^[3]. A positive association between cannabinoid use and longer time to progression does NOT mean cannabinoids improve immunotherapy outcomes - they may simply not harm them, and the difference may reflect the characteristics of patients who reach for them. Nor did any of the cited studies examine whether cannabis affects survival under other treatment regimens.

WHAT THIS MEANS FOR THE READER

Cannabinoids in licensed drug form have a documented place in symptom control, above all in refractory nausea and vomiting ^[1][2]. They are not a cancer treatment and must not replace or delay cancer treatment ^[1][2]. Decisions on starting or continuing them, on the form of the preparation and on interaction risk belong to the physician managing the treatment, who knows the patient's full regimen.

Sources

1. Braun IM, Bohlke K, Abrams DI i wsp. — Cannabis and Cannabinoids in Adults With Cancer: ASCO Guideline, Journal of Clinical Oncology 2024;42(13):1575-1593: ascopubs.org ↗
2. National Cancer Institute — Cannabis and Cannabinoids (PDQ), Health Professional Version: cancer.gov ↗
3. Effects of cannabinoids on immune checkpoint inhibitor response: CCTG pooled analysis of individual patient data, Immunotherapy 2025 (PMID 40184324): pubmed.ncbi.nlm.nih.gov ↗

WHAT THE LARGEST TRIAL SHOWED

• a multicentre double-blind trial conducted in the URCC CCOP network; 576 patients entered the analysis (91% women, mean age 53) ^[1];
• patients were randomised to placebo or ginger at 0.5 g, 1.0 g or 1.5 g daily; the preparation was taken for 6 days, starting 3 days BEFORE chemotherapy ^[1];
• all participants received standard antiemetic treatment with a 5-HT3 receptor antagonist - ginger was studied as an ADDITION, never as a replacement ^[1];
• all ginger doses significantly reduced the severity of acute nausea on day 1 of chemotherapy compared with placebo (p=0.003); the largest reductions were at 0.5 g and 1.0 g (p=0.017 and p=0.036 respectively) ^[1];
• anticipatory nausea, arising before the drug was given, was an independent predictor of nausea (p<0.0001) ^[1].

STRENGTH OF EVIDENCE - MODERATE

MSKCC summarises the literature as mixed but generally supportive: ginger may reduce nausea and vomiting, while a systematic review pointed to the need for further confirmation and some studies showed no additional benefit when standard antiemetics were already in use ^[2]. The result is therefore not uniform: one large positive trial alongside a set of smaller studies with divergent outcomes.

WHAT THESE DATA DO NOT COVER

• the trial assessed ACUTE nausea on day 1; it is not evidence of efficacy in delayed nausea or in vomiting;
• the study population was 91% women and the abstract gives no breakdown by diagnosis, so transferring the result to any given cancer is extrapolation;
• there are no data here on any effect of ginger on the course of cancer, the efficacy of chemotherapy or survival.

INTERACTIONS AND SAFETY - THIS IS THE MOST IMPORTANT PART:

• BLEEDING: ginger inhibits thromboxane formation and platelet aggregation, and so significantly increases bleeding risk in people taking anticoagulant and antiplatelet drugs, including warfarin ^[2]. A fatal bleeding event has been reported in an elderly patient taking dabigatran after consuming a ginger and cinnamon mixture ^[2];
• SURGERY: because of bleeding risk, MSKCC advises stopping ginger 2 weeks before an operation ^[2];
• BLEEDING DISORDERS: a contraindication to use ^[2];
• OTHER DRUGS: potential interactions are described with non-steroidal anti-inflammatory drugs, insulin and tacrolimus ^[2];
• ADVERSE EFFECTS: most commonly heartburn and skin irritation ^[2];
• PREGNANCY: MSKCC advises avoiding it ^[2].

THE SCOPE OF WHAT WE WRITE HERE

We give the doses that WERE STUDIED, because they are part of describing the trial - this is not a dosing recommendation for an individual. Patients undergoing cancer treatment very often take anticoagulants (prophylaxis and treatment of venous thromboembolism is typical in oncology, not exceptional), have thrombocytopenia after chemotherapy, or are being prepared for surgery - in each of those situations the bleeding risk described above is real. Whether to take any plant preparation during treatment is decided by the treating physician, who should be told about ALL supplements being taken. This page describes the state of knowledge and is not advice for any individual.

Sources

1. [1] Ryan JL i wsp. — Ginger (Zingiber officinale) reduces acute chemotherapy-induced nausea: a URCC CCOP study of 576 patients, Supportive Care in Cancer 2012 (PMID 21818642): europepmc.org ↗
2. [2] Memorial Sloan Kettering Cancer Center — About Herbs: Ginger (podsumowanie kliniczne, działania niepożądane, interakcje z lekami przeciwkrzepliwymi): mskcc.org ↗

WHY PEOPLE REACH FOR IT

Green tea is a beverage, not a drug, and that is precisely why its extract feels like a risk-free choice. Preparations standardised for epigallocatechin gallate (EGCG) are sold over the counter as antioxidants and weight-loss support ^[1]. A patient drinking a few cups a day and a patient taking an extract capsule are in two different situations — and that distinction is the core of this entry.

WHAT THE ONCOLOGICAL EVIDENCE SHOWS — SIGNALS IN BOTH DIRECTIONS:

• prevention: data are mixed, with possible benefit suggested for oral premalignant lesions and in populations at high risk of liver and colorectal cancer ^[1];
• prostate cancer: a blend containing green tea showed protective effects after treatment, but high-dose combination supplementation was associated with an ELEVATED incidence of prostate cancer in high-risk men ^[1]; long-term EGCG did not prevent recurrence ^[1];
• breast cancer: reduced recurrence risk has been reported, but regular consumption may elevate risk in some postmenopausal women ^[1];
• ovarian cancer: EGCG did not prevent recurrence ^[1];
• treatment side effects: limited data indicate EGCG may reduce radiation-induced oesophagitis in lung cancer patients and radiation dermatitis ^[1].

WHAT FOLLOWS FROM THIS PICTURE

This is not the profile of a preparation with proven anticancer activity. It is the profile of a substance whose effect depends on dose, formulation and clinical setting, and which in part of the research turned out opposite to expectation.

INTERACTIONS WITH CANCER TREATMENT — THE MOST IMPORTANT PART:

• BORTEZOMIB and other boronic acid-based proteasome inhibitors: EGCG and other polyphenols can inhibit their therapeutic effect ^[1]. This concerns the backbone of multiple myeloma treatment, so the supplement may reduce the efficacy of therapy;
• IRINOTECAN: EGCG inhibits biliary elimination, prolongs half-life and increases the risk of toxicity ^[1];
• PALBOCICLIB: decreased bioavailability in animal models ^[1];
• TAMOXIFEN: increased oral bioavailability, although a clinical trial did not confirm the interaction ^[1];
• NINTEDANIB: 21% reduction in bioavailability ^[1];
• anticoagulants and antiplatelet drugs: vitamin K antagonism at high intake ^[1];
• CYP3A4 and UGT substrates, verapamil, nadolol, rosuvastatin and atorvastatin — documented changes in drug exposure ^[1].

SAFETY: Common effects are nausea, stomach pain, sleep disruption and headache ^[1]. The serious concern is liver injury: hepatotoxicity has been documented at doses from 800 mg EGCG daily, with case reports of jaundice and acute hepatitis after green tea extracts ^[1]. At high doses (800–1600 mg EGCG daily) elevated liver enzymes, rectal bleeding and indigestion have also been described ^[1]. MSKCC lists contraindications: pregnancy and breastfeeding, stomach ulcers, and use on an empty stomach; the preparation should be discontinued if liver symptoms develop ^[1].

WHAT THIS ENTRY DOES NOT SAY

We give no doses and no regimen — any decision about a supplement during cancer treatment belongs to the treating physician, who knows the regimen and the patient's liver status. Nor do we claim that green tea as a drink is harmful: the reported liver events and most interactions concern concentrated EXTRACTS, not an ordinary infusion.

WHAT TO TELL THE TREATING TEAM

That an extract is being taken, the EGCG dose stated on the packaging, and every other supplement — especially before starting bortezomib, irinotecan or the targeted agents listed above.

Sources

1. [1] Memorial Sloan Kettering Cancer Center — About Herbs: Green Tea (dowody kliniczne, hepatotoksycznosc od 800 mg EGCG na dobe, interakcje z bortezomibem, irynotekanem, palbocyklibem, tamoksyfenem i nintedanibem): mskcc.org ↗

WHAT LAETRILE IS

Laetrile is a purified form of amygdalin, a cyanogenic glycoside found in the pits of many fruits and in raw nuts ^[1]. It is sometimes sold as vitamin B17, although no vitamin classification recognises that designation ^[1]. The cyanide released from the molecule is regarded by advocates of the preparation as its principal anticancer component ^[1].

WHAT THE CLINICAL TRIAL SHOWED

The decisive data come from an NCI-sponsored phase II trial that enrolled 179 patients with various cancers, predominantly of the breast, colon and lung ^[1]. Among the 178 treated patients:

• ONE patient met response criteria, with a partial response lasting 10 weeks ^[1];
• 54% had measurable disease progression by the end of the intravenous course ^[1];
• seven months after completing therapy, ALL patients had disease progression ^[1];
• 7% reported improved work capacity and 20% reported symptomatic relief, but that relief did not persist ^[1].

Laetrile has shown little anticancer activity in animal studies and none in human clinical trials ^[1].

WHY THE ROUTE OF ADMINISTRATION CHANGES THE RISK

Cyanide is released from the molecule only under the action of beta-glucosidase enzymes, present in intestinal bacteria and in some commonly eaten plants ^[1]. Blood cyanide levels were therefore not elevated after intravenous administration but were elevated after oral therapy, and poisoning occurs far more frequently with oral use ^[1]. In animal studies, germ-free rats showed no effects from oral laetrile, whereas animals with normal gut flora showed signs of cyanide poisoning including lethargy and convulsions ^[1].

INTERACTIONS THAT INCREASE THE DANGER

Toxicity rises with concurrent consumption of ^[1]:

• raw almonds and crushed fruit pits,
• foods containing beta-glucosidase: celery, peaches, bean sprouts, carrots,
• high-dose oral vitamin C.

A case of life-threatening cyanide toxicity following ingestion of amygdalin together with vitamin C has been reported ^[1]. This combination is particularly troubling because both substances tend to be taken by the same people, as two elements of a single self-treatment strategy — precisely where the risk is greatest.

WHAT POISONING LOOKS LIKE

Adverse effects mirror the picture of cyanide poisoning: nausea, vomiting, headache, dizziness, liver damage, low blood pressure, fever, ataxic neuropathies, drooping eyelids, mental confusion, coma and death ^[1].

LEGAL STATUS

Laetrile is not approved for use in the United States; in 1980 the Supreme Court upheld a federal ban on interstate shipment ^[1]. It continues to be manufactured and administered, mainly in Mexico and in some clinics in the United States ^[1].

WHAT THIS ENTRY DOES NOT SAY

It is not a recommendation for any individual, nor a judgement on decisions already taken. Anyone taking laetrile, or considering taking it, should tell their treating physician — not least because the symptoms of cyanide poisoning can be mistaken for side effects of cancer treatment, and telling them apart determines what is done next. Decisions about cancer treatment are made by the specialist physician.

Sources

1. National Cancer Institute — Laetrile/Amygdalin (PDQ) Health Professional Version: cancer.gov ↗

WHAT IT IS AND WHY IT CONCERNS ONCOLOGY

St John's wort is a herb used for mild to moderate low mood, sold over the counter as capsules, tablets and infusions. It appears in this catalogue not because it has antitumour activity, which has not been demonstrated, but because it is one of the best documented herbs causing drug interactions. The indication for which people take it overlaps with a common experience during cancer treatment, so the risk of concurrent use is real rather than theoretical.

MECHANISM OF THE INTERACTION

St John's wort induces the CYP3A4 enzyme in the liver and the membrane transporter P-glycoprotein ^[1]. Both systems clear drugs from the body. Inducing them means a drug is broken down and excreted faster, so its blood level is lower than assumed when the dose was set. The direction of this interaction runs against everyday intuition: the problem is not overdose but LOSS OF TREATMENT EFFICACY.

WHAT HAS BEEN MEASURED IN PEOPLE

• Irinotecan (used among others in colorectal cancer): in a crossover study in 5 cancer patients taking St John's wort 300 mg three times daily for 18 days, plasma levels of the active metabolite SN-38 fell by 42%, and markedly deeper suppression of bone marrow function was described alongside it ^[1][2].
• Imatinib: in two independent studies enrolling 12 and 10 subjects, at the same herb dose for 14 days, the area under the concentration curve, the maximum concentration and the half-life all decreased; the estimated magnitude is a 30-40% reduction in drug exposure ^[1].

WHY THIS IS MORE DANGEROUS THAN IT LOOKS

The interaction does not produce a new complaint the patient could report — only a silent fall in drug levels. Neither the patient nor the treating team has a symptom prompting them to look, unless the herb is asked about directly. St John's wort is also often regarded as harmless precisely because it is natural and sold without prescription, so it frequently goes unmentioned when medication is reviewed.

HOW LONG THE EFFECT LASTS AFTER STOPPING

Enzyme induction does not stop overnight. CYP3A4 activity returns to baseline roughly one week after St John's wort is discontinued, with an estimated half-life of this effect of about 46 hours ^[1]. Stopping the herb on the day the drug is given therefore does not remove the problem.

LIMITS OF THE EVIDENCE, STATED PLAINLY. The studies in cancer patients are SMALL: five people in the irinotecan study, ten and twelve in the imatinib studies. Groups that size cannot tell us how large the fall in drug levels will be in any individual, or in whom it will be greatest. What is strong is the MECHANISM itself and its direction, confirmed across many drugs and not only anticancer ones. Herbal preparations also vary in active content between manufacturers, so the potency of one package need not match another.

SCOPE OF THIS ENTRY

This entry describes a documented pharmacological phenomenon and contains no recommendations for any individual and no management schedules. Decisions about what to take and what to stop during cancer treatment belong to the treating physician, who knows the full medication list. The one point that matters for the reader: taking St John's wort or other herbal preparations is worth telling the treating team about, because without that information the interaction cannot be anticipated.

Sources

1. Borrelli F, Izzo AA. Herb-Drug Interactions with St John's Wort (Hypericum perforatum): an Update on Clinical Observations. AAPS Journal 2009 (przeglad; PMC2782080): pmc.ncbi.nlm.nih.gov ↗
2. Mathijssen RHJ i wsp. Effects of St John's wort on irinotecan metabolism. Journal of the National Cancer Institute 2002 (PMID 12189228): pubmed.ncbi.nlm.nih.gov ↗

WHY PEOPLE TAKE IT

Silymarin, a mixture of flavonolignans from milk thistle seeds, has a firm reputation as a liver-protective agent. Patients most often start it on their own initiative when liver function tests rise during chemotherapy ^[1].

WHAT THE EVIDENCE SHOWS

Memorial Sloan Kettering summarises the data cautiously: these are SMALL studies rather than decisive clinical trials ^[1]. They suggest:

• reduced chemotherapy-induced liver injury in children with acute lymphoblastic leukaemia and in patients with non-metastatic breast cancer,
• reduced radiotherapy-induced mucositis in patients with head and neck cancer,
• reduced chemotherapy-induced peripheral neuropathy and hand-foot syndrome (oral and topical forms),
• benefit in radiodermatitis in patients with breast cancer (topical form).

What the evidence does NOT show: silymarin does not treat cancer, does not replace any part of oncological treatment, and there are no data that it improves survival.

INTERACTIONS WITH CANCER TREATMENT

This is the most important part of this entry:

• milk thistle INHIBITS cytochrome CYP3A4, the enzyme that metabolises a large share of anticancer drugs, and can therefore change their concentrations ^[1];
• it modulates UGT enzymes, which per MSK may increase side effects of drugs metabolised by that route ^[1];
• it may decrease the clearance of sirolimus ^[1];
• a case of INR rising from 2.64 to 4.12 was reported in a patient on warfarin ^[1];
• cases of pancreatitis were reported with concomitant haloperidol or risperidone ^[1].

CONTRAINDICATIONS AND ADVERSE EFFECTS

Do not use if allergic to plants of the daisy/ragweed family. At high doses, increases in bilirubin and liver enzymes have been described — the opposite of the expected effect. Cutaneous reactions have also been reported: pruritus, rash, urticaria ^[1].

WHAT THIS MEANS

A supplement that looks like a neutral herbal add-on sits directly on the metabolic pathway of cancer drugs. Whether to take it during treatment is decided by the treating physician, who knows the full medication list. This entry is not medical advice.

Sources

1. Memorial Sloan Kettering Cancer Center — About Herbs: Milk Thistle: mskcc.org ↗

WHY PEOPLE TAKE IT

Reishi (lingzhi) is the best known of the so-called medicinal mushrooms, sold as an “immune-boosting” product and as “support during cancer”. It comes as powder, capsules and spore extracts ^[1].

WHAT THE EVIDENCE SHOWS

Memorial Sloan Kettering summarises the data as SMALL clinical studies in which reishi increased plasma antioxidant capacity and affected immune and tumour responses ^[1]. That is not enough to claim efficacy: there is no evidence that reishi treats cancer, prolongs survival, or replaces any part of oncological treatment. MSK also notes findings in the opposite direction — a reishi extract showed toxic effects in leukocytes ^[1].

A SIGNAL THAT MUST NOT BE OVERLOOKED

Patients undergoing treatment for gastrointestinal cancer who took reishi spore supplements had HIGHER levels of the tumour marker CA72-4 ^[1]. In practice this means the supplement may distort the follow-up tests the physician uses to judge how treatment is going.

INTERACTIONS WITH CANCER TREATMENT

• anticoagulants and antiplatelet drugs — reishi can increase bleeding risk ^[1];
• immunosuppressants — reishi enhances the immune response, working against the purpose of such treatment ^[1];
• drugs metabolised by cytochrome P450 — in vitro, reishi polysaccharides inhibited CYP2E1, CYP1A2 and CYP3A ^[1].

SAFETY. Cases of liver injury after powdered reishi have been reported, including one DEATH from fulminant hepatitis ^[1]. Reported adverse effects include nausea, insomnia, dry mouth, constipation, pruritus and vertigo ^[1].

WHAT THIS MEANS

“Natural” and “immune-boosting” does not mean neutral for treatment. Any decision about taking a mushroom preparation during cancer treatment belongs to the treating physician, who knows the full medication list. This entry is not medical advice.

Sources

1. Memorial Sloan Kettering Cancer Center — About Herbs: Reishi Mushroom: mskcc.org ↗

WHAT THIS ENTRY IS ABOUT

Oral mucositis is the painful inflammatory reaction that develops during radiotherapy to the head and neck region and during some chemotherapy regimens, and it can make eating impossible. It is among the most common and most burdensome complications of treatment in this region; a scoping review of 151 studies on the oral consequences of irradiation lists, alongside mucositis, dental caries, periodontitis, xerostomia, candidiasis, trismus, dysphagia and osteoradionecrosis ^[4].

WHAT THE GUIDELINES SAY

• MASCC/ISOO (the Multinational Association of Supportive Care in Cancer with the International Society of Oral Oncology) reviewed 78 papers, of which 49 entered the analysis, and made a NEW SUGGESTION in favour of honey delivered topically COMBINED with systemic delivery, for the PREVENTION of oral mucositis in head and neck cancer patients receiving radiotherapy with or without chemotherapy ^[1];
• in the same paper, for the remaining interventions in the "natural and miscellaneous agents" group — herbal compounds, probiotics, saliva stimulants — no guideline was possible because the evidence was insufficient ^[1];
• separately, chewing gum was found NOT to be effective for the prevention of oral mucositis in paediatric patients with haematological or solid cancers treated with chemotherapy ^[1].

WHAT THE QUANTITATIVE REVIEWS SHOW

• a network meta-analysis of 36 randomised trials compared 13 mouthwashes in use in different countries and ranked them by SUCRA; from best downwards: aloe vera juice, Chinese herbal medicine, Bing Peng San, HONEY, Lactobacillus, chamomile, riboflavin, rehabilitation solution, benzydamine, turmeric, aluminium sulfide, povidone-iodine, chlorhexidine — honey came fourth ^[2];
• the authors of that meta-analysis state plainly that the conclusion still needs to be verified by randomised trials with larger samples ^[2];
• an umbrella review of eight systematic reviews covering 257 primary studies identified honey among the agents showing consistent improvement in quality of life across pain relief, oral function and emotional well-being ^[3].

HOW TO READ THIS HONESTLY

The strength of this recommendation is moderate and worth knowing before buying anything. A "Suggestion" on the MASCC/ISOO scale means the evidence points in a direction but is not strong enough to constitute a Recommendation. A SUCRA ranking orders interventions relative to one another and does NOT say by how much honey reduces risk — the meta-analysis abstract reports no effect size and no confidence intervals ^[2]. Note also that the guideline concerns PREVENTION, that is use from the start of treatment, not the relief of mucositis that has already developed.

WHAT IS NOT KNOWN

• no single dose or schedule has been established: the guideline speaks of topical combined with systemic delivery, without specifying the type of honey ^[1]; trials use various honeys, manuka among them, and none has been shown to be superior;
• the evidence concerns primarily head and neck cancer treated with radiotherapy; extending it to other diagnoses and other treatments is unsupported;
• in children, a review of nutritional interventions describes honey-based results as promising but without pooled data ^[5].

SAFETY POINTS TO KEEP IN MIND

• honey is high in sugars, and irradiation of the head and neck region leads to a dry mouth and radiation caries ^[4] — which is why the decision to use it, and the accompanying dental care, is taken together with the treating team and a dentist, not alone;
• honey is not a sterile product; in a patient with profound neutropenia everything taken by mouth is decided by the treating team;
• in people with diabetes, regular honey intake affects glycaemic control and needs to be discussed with the treating physician.

WHAT THIS ENTRY DOES NOT SAY

It is not a recommendation for any individual, it gives no dose or route, and it replaces neither dental prophylaxis nor pain management. It describes only where the evidence stands: there is a positive guideline suggestion of moderate strength, concerning prevention, in one specific diagnosis and one specific treatment modality.

Sources

1. [1] Yarom N i wsp. — Systematic review of natural and miscellaneous agents for the management of oral mucositis in cancer patients and clinical practice guidelines, part 2: honey, herbal compounds, saliva stimulants, probiotics and miscellaneous agents, Support Care Cancer 2020 (78 prac zidentyfikowanych, 49 wlaczonych; nowa Sugestia za miodem w profilaktyce OM w raku glowy i szyi; PMID 32056010): europepmc.org ↗
2. [2] The effect of different mouthwashes to prevent oral mucositis in patients with radiotherapy and chemotherapy: a network meta-analysis, BMC Complement Med Ther 2025 (36 badan randomizowanych, 13 plukanek, ranking SUCRA — miod na 4. miejscu; PMID 40611101): europepmc.org ↗
3. [3] Therapeutic Interventions to Manage Oral Mucositis and Their Impact on Quality of Life in Cancer Patients: An Umbrella Review, Pain Res Manag 2026 (8 przegladow systematycznych, 257 badan pierwotnych; PMID 41647299): europepmc.org ↗
4. [4] Radiation-induced oral side effects in head and neck cancer: a scoping review and interdisciplinary recommendations, BMC Oral Health 2026 (151 badan; prochnica, suchosc, martwica popromienna kosci; PMID 41862928): europepmc.org ↗
5. [5] Nutritional and Supplemental Interventions for Prevention and Treatment of Oral Mucositis in Pediatric Oncology, Nutrients 2025 (PMID 41305573): europepmc.org ↗

WHAT IT IS AND WHY PATIENTS TAKE IT

Ashwagandha (Withania somnifera) is an Ayurvedic herb sold over the counter as a dietary supplement. Cancer patients most often take it on their own hoping to reduce anxiety, stress and fatigue, improve sleep and — less commonly — ease joint pain.

WHAT THE EVIDENCE SHOWS

Clinical data are limited and come from few, small studies. Memorial Sloan Kettering notes reports of reduced chemotherapy-induced fatigue in breast cancer patients, and of improved sleep quality and reduced anxiety. This is not a basis for a recommendation: there are no large randomised trials, no independent confirmation, and the endpoints are subjective.

WHAT ASHWAGANDHA DOES NOT DO

Laboratory studies have shown slowed growth of cancer cells, but — as MSKCC states explicitly — this effect has not been observed in humans. Ashwagandha is not anticancer treatment and does not replace any therapy.

SAFETY — THIS IS THE MAIN ISSUE. Commonly reported adverse effects are drowsiness, nausea, headache, stomach upset and diarrhoea. Serious events have also been reported:

• liver injury associated with use of ashwagandha supplements,
• thyrotoxicosis,
• kidney transplant rejection.

SPECIFIC WARNINGS

• Pregnancy: do not use — the herb may increase the risk of miscarriage.
• Hormone-sensitive prostate cancer: discuss with the treating physician, because ashwagandha may raise testosterone levels.
• Autoimmune disease: the herb may trigger or exacerbate it.
• Liver disease or abnormal liver tests: discuss with the treating physician before considering use.

INTERACTIONS WITH CANCER TREATMENT

• CYP3A4: ashwagandha is a moderate inducer of this enzyme. Many oncology drugs (including kinase inhibitors) are metabolised by it, and induction may lower their blood levels.
• CYP2B6: inhibition shown in vitro.
• Sedatives and antiepileptics (benzodiazepines, barbiturates): ashwagandha has sedative, GABAergic properties; additive effects are possible.
• Thyroid medication: thyroxine levels may rise.
• Digoxin: may cause falsely elevated immunoassay results.

MSKCC notes that the clinical relevance of several of these interactions is yet to be determined — which means they have not been measured, not that they are unimportant.

BOTTOM LINE

The quality of evidence for benefit is limited, while the list of documented hazards — including liver injury and CYP3A4 induction — is concrete. Any supplement use during cancer treatment is a decision for the treating physician, who knows the patient's full medication list.

WHAT IT IS AND WHY PATIENTS TAKE IT

Berberine is an alkaloid found in several medicinal plants (including barberry and goldenseal). It is sold as a dietary supplement. Patients most often take it for reasons unrelated to cancer: type 2 diabetes, raised cholesterol, digestive complaints, and under the banner of "cleansing".

WHAT THE EVIDENCE SHOWS

Memorial Sloan Kettering summarises that several studies and meta-analyses suggest benefit from berberine, but better-designed studies are needed and the effect may be small. Diabetes studies are described as of limited quality. In hyperlipidaemia, improvement in the lipid profile has been reported in people who cannot or will not take statins.

THE ONE ONCOLOGY FINDING

A reduced rate of recurrence of colorectal adenomas has been reported in people after adenoma removal. This is prevention of recurrence of BENIGN lesions with malignant potential, not treatment of colorectal cancer — and it should be read that way. There are no data showing that berberine treats any malignancy.

ADVERSE EFFECTS

Reported as mild: appetite loss, upset stomach, diarrhoea, constipation, rash.

SPECIFIC WARNINGS

• Pregnancy and breastfeeding: do not use — berberine may worsen neonatal jaundice.
• Bosutinib: do not use together (see interactions).
• Immunosuppressants (tacrolimus, ciclosporin): avoid.

INTERACTIONS WITH CANCER AND SUPPORTIVE TREATMENT

• CYP2D6, CYP2C9, CYP3A4: berberine reduces the activity of these enzymes, which can alter levels of many drugs cleared by them — in oncology this includes kinase inhibitors.
• Bosutinib: simulations predict a 1.3-fold increase in drug exposure; MSKCC advises against combining them.
• Tacrolimus and ciclosporin: berberine raises their blood levels — relevant after transplantation and in graft-versus-host disease.
• Sulfonylureas: additive blood-glucose-lowering effect is possible.

BOTTOM LINE

Berberine is not anticancer therapy and there is no basis for treating it as an adjunct to cancer treatment. It does, however, have a concrete documented interaction profile that can change the levels of drugs a patient is already taking. Any supplement use during cancer treatment is a decision for the treating physician, who knows the patient's full medication list.

WHY PATIENTS REACH FOR IT

Ginkgo biloba is marketed to improve circulation, enhance memory and treat tinnitus ^[1]. In oncology it is taken mainly by people left with problems of concentration, memory and mental speed after chemotherapy — a real and burdensome complaint for which no treatment of proven efficacy exists. That gap is what drives sales of the supplement.

WHAT THE TRIALS SHOWED

Memorial Sloan Kettering Cancer Center summarises the evidence without ambiguity: ginkgo was INEFFECTIVE in preventing chemotherapy-associated cognitive dysfunction in breast cancer patients ^[1]. Large randomised trials, notably the Ginkgo Evaluation of Memory (GEM) study, generally show that supplementation does not improve cognitive performance or prevent Alzheimer's disease or dementia ^[1]. Cancer incidence data from GEM do not support using ginkgo to reduce cancer risk ^[1].

ADVERSE EFFECTS — WHERE THE MAIN RISK LIES. Spontaneous bleeding has been documented, including haematomas and brain haemorrhages ^[1]. Also reported: low blood sodium, seizures in susceptible individuals, and acute haemolytic anaemia in people with glucose-6-phosphate dehydrogenase (G6PD) deficiency ^[1]. In oncology this list carries more weight than in the general population: chemotherapy-induced thrombocytopenia, surgery and biopsies are settings in which a prolonged bleeding time stops being theoretical.

INTERACTIONS WITH CANCER TREATMENT

• Anticoagulants and antiplatelet drugs: ginkgo may induce or prolong bleeding time, creating a serious haemorrhage risk when combined with warfarin or similar agents ^[1].
• CYP450 enzymes: ginkgo both inhibits and induces multiple pathways (CYP3A4, CYP2D6, CYP2B6), potentially altering drug metabolism ^[1]. A large share of anticancer drugs, including kinase inhibitors, is metabolised through CYP3A4, and shifting their concentration in either direction is undesirable.
• Drugs that lower the seizure threshold: combined use increases seizure risk ^[1].
• Reduced effectiveness of efavirenz, midazolam and insulin has also been reported ^[1].

CONTRAINDICATIONS. Avoid during pregnancy, especially near childbirth, because of antiplatelet properties that prolong bleeding time ^[1].

STRENGTH OF EVIDENCE

Moderate — and pointing towards absence of benefit. This grade reflects the fact that the conclusions of ineffectiveness come from randomised trials, including the large GEM study, rather than from observation ^[1]. The harm evidence is of a different kind: it rests on case reports and interaction data, so it does not allow the frequency of complications to be estimated — but it does establish that they are possible and serious.

WHAT THIS ENTRY DOES NOT SAY

It neither recommends nor advises against anything for any individual, and gives no doses. It states what the trials showed and which interactions are documented. The decision to take or stop any supplement before surgery, during chemotherapy or while on anticoagulation belongs to the treating physician, who knows the full list of medicines taken.

SOURCES.

• ^[1] Memorial Sloan Kettering Cancer Center, About Herbs: Ginkgo

Sources

1. [1] Memorial Sloan Kettering Cancer Center — About Herbs: Ginkgo: mskcc.org ↗

WHY PATIENTS REACH FOR IT

Echinacea is among the most widely bought herbal products, marketed for colds, flu, wound healing and "immune support" ^[1]. In oncology it is taken mainly by people whose white cell counts have been lowered by chemotherapy — precisely the situation in which the promise of "boosting the immune system" sounds most convincing. That intuition, rather than the herb itself, is the problem here.

WHAT THE EFFICACY TRIALS SHOWED

The evidence is mixed and limited. Memorial Sloan Kettering Cancer Center reports that echinacea was INEFFECTIVE in preventing the common cold caused by rhinoviruses ^[1]. On the other hand, one influenza trial found it as effective as oseltamivir, with fewer adverse events ^[1]. Neither line of evidence concerns cancer patients, and neither shows that the supplement repairs immunity damaged by chemotherapy — no such evidence exists.

WHY THIS IS NOT A NEUTRAL SUPPLEMENT IN ONCOLOGY.

• Some studies suggest echinacea could decrease plasma drug levels, affect therapeutic efficacy, or cause adverse effects with some anticancer drugs ^[1].
• Profound thrombocytopenia was reported in a lung cancer patient receiving cisplatin and etoposide, attributed to echinacea use ^[1].
• In laboratory studies echinacea inhibits CYP3A4 and CYP2C8 ^[1]. The thrombocytopenia seen with etoposide was thought likely to be due to CYP3A4 inhibition ^[1].
• The same mechanism works in the opposite direction: in vitro there is a risk of subtherapeutic systemic exposure of prodrugs such as tamoxifen, which must be metabolised to become active ^[1].
• Echinacea may antagonise the effects of immunosuppressants ^[1].

ADVERSE EFFECTS

Reported effects include headache, dizziness, nausea, constipation, gastrointestinal upset and rash ^[1]. More rarely: thrombotic thrombocytopenic purpura, acute hepatitis, acute liver failure, leukopenia and exacerbation of pemphigus vulgaris ^[1].

CONTRAINDICATIONS. Memorial Sloan Kettering lists: chemotherapy, autoimmune and allergic conditions, immunosuppression, and pregnancy or breastfeeding ^[1]. Note the apparent contradiction that is in fact consistent: a product said to stimulate the immune response is unsuitable both when the immune system attacks the body's own tissues and when it is being deliberately suppressed by drugs.

STRENGTH OF EVIDENCE

Limited. The efficacy trials concern respiratory infections in generally healthy people, give conflicting results, and do not transfer to a patient undergoing cancer treatment. The harm evidence rests on case reports and laboratory work on drug metabolism ^[1] — it does not allow the frequency of complications to be estimated, but it does establish that they are possible and involve drugs used in everyday oncology practice.

WHAT THIS ENTRY DOES NOT SAY

It neither recommends nor advises against anything for any individual, and gives no doses. It states what the trials showed and which interactions are documented. The decision to take or stop any supplement during chemotherapy belongs to the treating physician, who knows the full list of medicines taken.

SOURCES.

• ^[1] Memorial Sloan Kettering Cancer Center, About Herbs: Echinacea

Sources

1. [1] Memorial Sloan Kettering Cancer Center — About Herbs: Echinacea: mskcc.org ↗

WHERE THE IDEA CAME FROM

Pomegranate (Punica granatum) is a rich source of polyphenols, and laboratory work showed effects on prostate cancer cell proliferation and apoptosis. In 2006 the first clinical trial in men with rising PSA after prostatectomy or radiotherapy was published: a phase II study with no control group, in which mean PSA doubling time increased from 15 months to 54 months ^[1]. The authors stated explicitly that the result warranted testing in a placebo-controlled study ^[1] — yet it is precisely the "15 to 54 months" figure that still circulates today.

WHAT THE CONTROLLED TRIAL SHOWED

A multi-institutional, double-blind, placebo-controlled study enrolled 183 men with rising PSA after primary therapy, randomly assigned 2:1 (extract 102, placebo 64, juice 17) ^[2]. The primary endpoint was change in PSA doubling time. The authors' conclusion is unambiguous: compared with placebo, pomegranate extract did NOT significantly prolong PSA doubling time ^[2].

WHY THE EARLIER RESULT WAS MISLEADING

In the placebo-controlled study, PSA doubling time lengthened significantly in BOTH arms — in the placebo group the median rose from 11.1 months at baseline to 15.6 months ^[2]. This shows that a lengthening of PSA doubling time during follow-up does not by itself demonstrate that a preparation works. The 2006 phase II study had no control group and so could not tell the two apart. It is a textbook illustration of why an uncontrolled result is not enough.

A GENETIC SUBGROUP — WHAT MUST NOT BE READ INTO IT: In an exploratory analysis, men with the manganese superoxide dismutase (MnSOD) AA genotype taking the extract had a change in median PSA doubling time from 13.6 to 25.6 months ^[2]. The authors themselves note that this observation requires prospective hypothesis testing and validation ^[2]. A subgroup identified after the fact is not a basis for using the preparation.

INTERACTIONS WITH CANCER TREATMENT

• CYP3A: in rat studies pomegranate juice inhibited CYP3A activity similarly to grapefruit juice, but human clinical trials did NOT show clinically relevant inhibition ^[3]. Equating pomegranate with grapefruit is therefore unwarranted.
• CYP2C9: inhibition was shown in rats (increased tolbutamide bioavailability); in humans no effect on CYP2C9 activity was found ^[3].
• warfarin: a case report suggests that pomegranate juice may interact with warfarin ^[3].
• metformin: in a rat model, prior administration of the juice reduced metformin efficacy; clinical relevance remains undetermined ^[3].

TOLERABILITY: Pomegranate is generally well tolerated; daily consumption of about 240 ml of juice for over two years produced no significant adverse effects ^[3]. Mild effects reported included nausea, constipation and decreased appetite, with diarrhoea at higher doses in some patients ^[3].

WHAT FOLLOWS

Pomegranate as a fruit and juice is a dietary component with a good safety profile. There is, however, no controlled-trial evidence that pomegranate extract slows the rise of PSA after treatment for prostate cancer. Decisions about management of a rising PSA are made by the treating physician; a supplement replaces neither surveillance nor treatment.

Sources

1. [1] Pantuck AJ i wsp., Phase II study of pomegranate juice for men with rising PSA following surgery or radiation for prostate cancer, Clin Cancer Res 2006: pubmed.ncbi.nlm.nih.gov ↗
2. [2] Pantuck AJ i wsp., A randomized, double-blind, placebo-controlled study of the effects of pomegranate extract on rising PSA levels in men following primary therapy for prostate cancer, Prostate Cancer Prostatic Dis 2015;18(3):242-8: pubmed.ncbi.nlm.nih.gov ↗
3. [3] Memorial Sloan Kettering Cancer Center, About Herbs: Pomegranate (interakcje i tolerancja): mskcc.org ↗

WHY PATIENTS REACH FOR ALOE

Aloe gel is among the most common home remedies applied to the skin during radiotherapy — it is cheap, available without prescription and associated with soothing burns. Radiation dermatitis affects a large proportion of irradiated patients, and the expectation that a "burn" preparation will help here too is intuitive. Clinical evidence does not clearly bear that intuition out.

WHAT THE BREAST CANCER TRIAL SHOWED

A three-arm randomised phase III trial enrolled 248 patients with breast cancer assigned to powder, aloe cream or placebo cream; acute skin toxicity was scored weekly on a modified 10-point Catterall scale and patients rated their own symptom severity ^[1]. The aloe formulation did NOT reduce acute skin toxicity or symptom severity ^[1]. The authors found no evidence supporting prophylactic use of aloe and stated that their results support a dry powder skin care regimen ^[1]. They also noted that both study creams were associated with a greater skin reaction than the dry powder regimen ^[1].

WHAT THE HEAD AND NECK TRIAL SHOWED

A multicentre, randomised, double-blind, placebo-controlled trial enrolled 120 patients with head and neck cancer receiving concurrent chemoradiation; skin reaction was assessed with the RISRAS scale ^[2]. In the main comparison, median RISRAS values from week 1 to week 8 did NOT differ significantly between groups ^[2]. Differences appeared in individual weeks: moderate to severe erythema occurred in week 5 in 13.6% of patients using aloe versus 27.8% on placebo (p=0.05), and in week 6 in 24.1% versus 42.6% (p=0.038) ^[2].

HOW TO READ THE TWO TOGETHER

The two randomised trials give an inconsistent picture, and in both the main comparison showed no significant difference. A favourable result in individual weeks of follow-up is weaker ground than a result in the planned comparison across the treatment period. The honest conclusion is therefore: there is no high-quality evidence that aloe gel prevents radiation dermatitis or reduces its severity. This is not evidence that the gel is harmful on the skin — it is an absence of confirmed benefit.

ORAL MUCOSITIS

Preliminary findings suggest a benefit of aloe in preventing chemotherapy-induced oral mucositis in adults, and studies in children report a similar benefit ^[3]. These are preliminary data, not established practice.

THE KEY WARNING — GEL IS NOT JUICE: Aloe gel must not be confused with aloe juice or aloe latex; both contain anthraquinone, a cathartic laxative ^[3]. Internal use of aloe should be discouraged because of possible adverse effects ^[3]. Reported effects include stomach pain, nausea, vomiting, seizures, low potassium and liver dysfunction ^[3]. Low potassium matters particularly in cancer patients, who often receive drugs affecting electrolyte balance.

INTERACTIONS WITH CANCER TREATMENT

• liver enzymes: aloe juice inhibited CYP3A4 and CYP2D6, which may affect intracellular concentrations of drugs metabolised by these enzymes ^[3] — this concerns many anticancer drugs;
• surgery: excessive intraoperative bleeding was reported in a patient taking oral aloe vera tablets, under sevoflurane anaesthesia ^[3];
• practical conclusion: information about taking aloe orally should reach the treating team before a planned procedure and when systemic treatment is being decided. The decision rests with the treating physician.

Sources

1. [1] Hoopfer D i wsp., Three-Arm Randomized Phase III Trial: Quality Aloe and Placebo Cream Versus Powder as Skin Treatment During Breast Cancer Radiation Therapy, Clin Breast Cancer 2015: pubmed.ncbi.nlm.nih.gov ↗
2. [2] Reduction in severity of radiation-induced dermatitis in head and neck cancer patients treated with topical aloe vera gel: a randomized multicenter double-blind placebo-controlled trial, Eur J Oncol Nurs 2022: pubmed.ncbi.nlm.nih.gov ↗
3. [3] Memorial Sloan Kettering Cancer Center, About Herbs: Aloe Vera (zapalenie blony sluzowej, ostrzezenia, interakcje): mskcc.org ↗

WHAT IT IS

EGCG (epigallocatechin gallate) is the principal polyphenol of green tea. Two things that are often conflated must be kept apart: an infusion of green tea leaves, and a supplement containing an extract in which the EGCG dose is many times higher. The safety concerns described below apply to extracts, not to tea drunk in ordinary amounts ^[4].

THE MOST IMPORTANT WARNING — BORTEZOMIB (MULTIPLE MYELOMA). Bortezomib carries a boronic acid group. EGCG forms a stable chemical adduct with it, so the drug no longer binds the proteasome — that is, it stops doing what it is given for. In myeloma and glioma cell lines the antitumour effect of bortezomib was blocked, and in a mouse model it was abolished completely ^[2]. The NCI PDQ database describes this mechanism explicitly and notes that human studies have not been performed ^[3]. Memorial Sloan Kettering lists the interaction among its patient warnings ^[4].

• Level of evidence: laboratory and animal studies plus a defined chemical mechanism — there are no clinical data.
• Why it is nevertheless taken seriously: the mechanism is direct and requires no assumption beyond the chemistry of the two molecules.

OTHER DOCUMENTED INTERACTIONS

• Irinotecan — in models, higher plasma drug levels and reduced biliary excretion of the active metabolite SN-38, meaning a risk of increased toxicity ^[4].
• Kinase inhibitors (erlotinib, lapatinib, sunitinib, palbociclib) — reduced oral bioavailability in animal models; a single human case has been reported with sunitinib ^[4].
• Statins — increased exposure to atorvastatin and a marked decrease in exposure to rosuvastatin ^[4].
• Nadolol — the extract inhibits the OATP1A2 transporter and reduces drug absorption ^[4].

WHAT HUMAN STUDIES HAVE NOT SHOWN

• Prostate cancer: a double-blind randomised trial in 97 men with precancerous lesions (HGPIN/ASAP), 400 mg EGCG daily for one year. Cancer was diagnosed in 5 of 49 men on the preparation and 9 of 48 on placebo; p=0.25. The primary endpoint was not met ^[1].
• Oral precancerous lesions: a randomised phase 2 trial showed a clinical response in 50% (n=28) versus 18.2% on placebo (n=11), p=0.09 — not statistically significant ^[6].
• Chronic lymphocytic leukaemia: a single-arm phase 2 study (n=42) reported a response in 69% of patients, but measured by a surrogate marker (fall in lymphocyte count, reduction of nodal masses), not by survival or time to treatment ^[7].
• Neither the NCI nor Memorial Sloan Kettering recommends green tea or EGCG for cancer prevention or treatment; the FDA has approved no such indication ^[8].

SAFETY OF EXTRACTS

The European Food Safety Authority concluded that catechins from a traditional infusion are generally safe, whereas doses from supplements of 800 mg EGCG per day and above produced a statistically significant rise in transaminase activity; the panel was unable to identify a safe dose for extracts ^[5]. The NIH LiverTox registry assigns green tea extracts its highest likelihood category for liver injury, describing more than a hundred cases including acute liver failure requiring transplantation; the injury is idiosyncratic and typically appears after one to six months of use ^[9].

WHAT TO DISCUSS WITH THE TREATING PHYSICIAN

Every supplement being taken — and particularly so during treatment with bortezomib, irinotecan or a kinase inhibitor. The decision to stop or continue a preparation rests with the specialist who knows the patient's full medication list; this page describes the state of knowledge, not a recommendation for any individual.

Sources

1. [1] Kumar NB i wsp. Randomized, placebo-controlled trial of green tea catechins for prostate cancer prevention. Cancer Prev Res 2015: pmc.ncbi.nlm.nih.gov ↗
2. [2] Golden EB i wsp. Green tea polyphenols block the anticancer effects of bortezomib. Blood 2009;113(23):5927-37: pubmed.ncbi.nlm.nih.gov ↗
3. [3] NCI PDQ — Cancer Therapy Interactions With Foods and Dietary Supplements (Health Professional Version): cancer.gov ↗
4. [4] Memorial Sloan Kettering Cancer Center — About Herbs: Green Tea: mskcc.org ↗
5. [5] EFSA — Scientific opinion on the safety of green tea catechins (2018): efsa.europa.eu ↗
6. [6] Tsao AS i wsp. Phase II randomized trial of green tea extract in oral premalignant lesions. Cancer Prev Res 2009: pubmed.ncbi.nlm.nih.gov ↗
7. [7] Shanafelt TD i wsp. Phase 2 trial of daily oral Polyphenon E in patients with CLL. Cancer 2013: pubmed.ncbi.nlm.nih.gov ↗
8. [8] NCI PDQ — Prostate Cancer, Nutrition, and Dietary Supplements (Patient Version): cancer.gov ↗
9. [9] NIH LiverTox — Green Tea (Camellia sinensis): ncbi.nlm.nih.gov ↗

WHAT THE EVIDENCE SHOWS

The National Cancer Institute lists St John's wort among supplements that must be discussed with the treating team, stating plainly: "St. John's [wort], which some people use for depression, may cause certain cancer drugs to not work as well as they should ^[1]." A review of herb–chemotherapy interactions in Frontiers in Oncology (2019) names St John's wort among six herbal products with interactions demonstrated in humans rather than only in the laboratory, mediated by inhibition or induction of drug-metabolising enzymes ^[2].

HOW IT WORKS

St John's wort induces the CYP3A4 isoenzyme of the cytochrome P450 system and P-glycoprotein — the very pathways by which the body breaks down and clears a large share of anticancer drugs, particularly oral ones ^[2]. The effect is the opposite of what the patient intends: the drug is cleared faster, blood levels fall, and treatment may lose effectiveness even though the full prescribed dose is being taken ^[1][2].

THE SCOPE OF WHAT WE STATE HERE

We deliberately do not quote by how many per cent the levels of specific drugs fall. Publications reporting such figures exist, but we could not confirm them in the reference-class sources available to us — and an unverified number is worse than no number. For a patient's decision the direction of the effect is enough, and it is not disputed: St John's wort WEAKENS the action of some anticancer drugs.

WHO SHOULD PAY PARTICULAR ATTENTION

Anyone on systemic treatment, especially oral targeted agents and oral chemotherapy, and anyone reaching for St John's wort because of low mood during cancer treatment — precisely the situation in which the interaction risk is highest. St John's wort is also an ingredient in herbal blends and calming preparations, so the composition is worth checking, not just the brand name.

WHAT TO DO

Every supplement taken, including herbal and over-the-counter products, should be reported to the treating physician and clinical pharmacist BEFORE treatment starts ^[1]. Antidepressants should never be stopped or replaced with St John's wort on one's own; low mood during cancer is a medical problem with treatment that can be chosen with interactions in mind.

Sources

1. National Cancer Institute — Complementary and Alternative Medicine (CAM), cancer.gov 2024: cancer.gov ↗
2. Fasinu PS, Rapp GK — Herbal Interaction With Chemotherapeutic Drugs — A Focus on Clinically Significant Findings, Frontiers in Oncology 2019 (PMID 31850232): europepmc.org ↗

WHAT THE EVIDENCE SAYS The broadest appraisal is a 2025 systematic review (European Journal of Clinical Pharmacology) covering 34 randomised trials and 2,580 patients undergoing cancer treatment ^[1]. Patients most often had head and neck cancers, followed by breast, prostate and colorectal cancer; curcumin was given topically or systemically ^[1]. Results for oral and skin symptoms, pain, body weight, body composition, survival and disease progression were heterogeneous ^[1]. The authors recorded significant findings only for oral mucositis and weight loss ^[1].

STRENGTH OF EVIDENCE — WEAK The authors state plainly that all included studies had a moderate to high risk of bias, and that because of heterogeneous results and methodological limitations no clear statement about the effectiveness of curcumin in cancer patients can be made ^[1]. Higher-quality research is needed ^[1]. A harm was also recorded: in one trial vomiting was significantly more frequent in the curcumin group ^[1].

INTERACTIONS WITH CANCER TREATMENT This is the most important part of this entry. In a 2019 study (Cancers), in breast cancer patients taking tamoxifen, adding curcumin (1,200 mg three times daily) reduced the area under the curve for endoxifen by 7.7% (95% CI: −15.4 to 0.7%; p=0.07), and curcumin with piperine by 12.4% (95% CI: −21.9 to −1.9%; p=0.02) ^[2]. Endoxifen is the active metabolite of tamoxifen — the form of the drug that does the work ^[2]. The authors conclude that co-treatment with curcumin could lower endoxifen concentrations below the threshold for efficacy, in their estimate potentially in 20–40% of patients, especially in extensive CYP2D6 metabolisers ^[2]. Note that piperine, added to supplements precisely to improve curcumin absorption, made the unfavourable effect LARGER in this study ^[2].

The National Cancer Institute states the general rule: “Tell your doctor if you're taking any dietary supplements, even vitamins, no matter how safe you think they are”, noting that some such products can change how cancer treatment works ^[3].

THE SCOPE OF WHAT WE WRITE HERE We give no figures for interactions between curcumin and cytotoxic drugs or kinase inhibitors, because we could not confirm them in accessible reference-class sources — the only clinically confirmed interaction in patients is the tamoxifen interaction described above. We also found no clinical data on perioperative bleeding risk in cancer patients taking curcumin. A missing number here is information, not an oversight: an unverified number would be worse than none.

This page describes the state of knowledge. It is not advice for any individual and not a recommendation to take or stop any preparation.

Sources

1. Gutsche et al. — Curcumin as a complementary treatment in oncological therapy: a systematic review, European Journal of Clinical Pharmacology 2025: europepmc.org ↗
2. Hussaarts et al. — Impact of Curcumin (with or without Piperine) on the Pharmacokinetics of Tamoxifen, Cancers 2019: europepmc.org ↗
3. National Cancer Institute — Complementary and Alternative Medicine (CAM): cancer.gov ↗

WHAT THIS ENTRY COVERS

This concerns cancer-related fatigue — exhaustion out of proportion to exertion and not relieved by rest, the most commonly reported symptom during cancer treatment. The entry covers one specific botanical: the root of American ginseng (Panax quinquefolius). It does NOT cover Asian ginseng (Panax ginseng) or Korean red ginseng — different species with a different ginsenoside profile, and the recommendation cited below was formulated for the American species only.

WHAT THE EVIDENCE SHOWS

The principal evidence is a multicentre, double-blind, placebo-controlled randomised trial, NCCTG N07C2 (JNCI, 2013; PMID 23853057): 364 patients from 40 institutions, 2,000 mg of ground root daily for 8 weeks.

• primary endpoint (general subscale of the MFSI-SF) at 8 weeks: change score 20.0 (SD 27) with ginseng versus 10.3 (SD 26.1) with placebo, p = .003
• the difference was NOT significant at 4 weeks — the effect emerged only with longer use

The ASCO/Society for Integrative Oncology guideline on the management of cancer-related fatigue lists American ginseng among options that "may be recommended in adults undergoing cancer treatment", while stating that certainty and quality of evidence for fatigue interventions are low to moderate. This is conditional wording ("may be"), not a strong recommendation.

A smaller, more recent placebo-controlled randomised trial in Supportive Care in Cancer (2026; PMID 41838185) in 65 survivors of gastrointestinal cancer reported improved fatigue scores at 4 weeks (3.99 ± 0.86 vs 5.37 ± 1.27; p < .001), but it used a Panax ginseng extract at 250 mg — a different species and dose from N07C2, so the two results should not be read as confirming one another.

WHAT THESE RESULTS DO NOT SAY

They do not say that ginseng affects the course of the cancer — the endpoint measured was how patients feel, not survival or treatment response. Nor do they make it a first-line measure: in the same guideline the best-documented interventions for fatigue are physical activity and psychological approaches, not oral products. Finally, it is unknown whether the effect persists after stopping, or whether it applies to fatigue that continues long after treatment ends.

INTERACTIONS WITH CANCER TREATMENT — MANDATORY SECTION.

• WARFARIN and other vitamin K antagonists: ginseng has been described as potentially lowering INR, i.e. weakening anticoagulation. In cancer patients, in whom thrombosis is a frequent complication, this matters practically.
• DRUGS METABOLISED BY CYP3A4, including tyrosine kinase inhibitors (e.g. imatinib): liver injury has been reported with concurrent ginseng use. The interaction mechanism is the same as for St John's wort, though its direction and magnitude are less well documented.
• ANTIDIABETIC DRUGS: ginseng may lower blood glucose, so the effect adds to glucose-lowering therapy.
• OESTROGEN-LIKE ACTIVITY: ginsenosides show oestrogenic activity in vitro, and ethanol-extracted preparations contain more of them. N07C2 deliberately used pure ground root rather than an ethanol extract. In hormone-dependent cancers this is a reason for caution, although clinical evidence of harm is lacking.

THE DECISION BELONGS TO THE PHYSICIAN

Cancer-related fatigue has reversible causes that must be excluded first — anaemia, hypothyroidism, pain, sleep disturbance, depression, drug effects. A supplement does not replace that work-up. Introducing any botanical product during chemotherapy, targeted therapy or anticoagulation requires agreement with the treating physician and clinical pharmacist.