The main listed author of the appalling drivel in “Herb Drug Interactions in Oncology” is none other than the notorious “quackwatcher” Barrie Cassileth PhD. Cassileth is not a physician but a “psychosocial oncologist” who runs the Goebbels like anti-herb propaganda unit at SKMCC. For many years she was on the American Cancer Society’s “Questionable Methods Committee”. The original name of this group, which was founded in the 1950s was the “Committee on Quackery” whose techniques were directly derived from McCarthy-esque approach of blacklisting “unamerican” alternative treatments and the people associated with them, while promoting cytotoxic chemotherapy.

Cassileth was for a longtime a controversial figure, a blatant quackbuster determined to rubbish any and every non-mainstream therapy. HERBLOG readers interested in the background could check out an archive of Ralph Moss’s Cancer Chronicles from 1993 entitled ACS OFFICIAL CONTINUES ON OAM BOARD: CASSILETH, CLAIMING “GOOFS, REFUSES TO RESIGN.

In today’s environment, with the enormous public interest in alternatives to mainstream medicine in all areas, but especially cancer treatment, Cassileth the crude quackbuster has dropped the “Witchfinder general” approach and retooled as Cassileth the patient advocate for Integrative Medicine. Her bio on the SKCC integrative medicine services pages unbelievably states proudly that she is “an outspoken critic of quack therapies and unproven remedies”.

How come Cassileth can now be Chief of the Integrative Medicine Services at SKMCC? How can white be black? Easy.

“CAM” is divided by Cassileth into Good ( Complementary) and Bad (Alternative). The bad guys are still out there, - herbal medicines and dietary supplements. These nasty “alternative” things prevent toxic chemotherapy from curing cancer, and (just like the old days) falsely claim to be treatments. Meanwhile, patients undergoing conventional chemo and radiation treatments are likely to experience pain, and a horrendous variety of side effects. That’s where Complementary (good) therapies come in, massage, music therapy, guided visualization, acupuncture, art therapy and (very clever) even the odd herb as long as it is treated like a drug ( ginger for nausea) . In other words, complemntary therapies that do not directly interfere with physiology and pharmacology can be used to address “emotional, social, and spiritual needs of patients and families” - also known as side-effects?.

Here is a link to SKCC’s clear statement on the distinction between nice (ineffective) and nasty (effective) forms of CAM which is directly based on Cassileth’s formulations. The nasty ones are “unproved, expensive and harmful” The front of such statements is so brazen that presumably many readers do not even think about it and draw the intended conclusion that chemotherapy is cheap, harmless, and proven?
The whole “integrative medicine” phenomenon is an obvious attempt to shore up the extraordinary deficiences of biomedicine. All over the country, medical schools are establishing such departments, and medical students are demanding them. However, while there are no doubt variations it is the case that such departments are staffed entirely by biomedical people and are a little more than a desperate rearguard action in response to a situation perceived to be increasingly out of control of the AMA. With SKMCC the quackbusting credentials of integrative medicine are not even cosmetically concealed.

BY the end of January the appeal to the herbal community for donations to the AHG Herbalist Medical Trust for Michael Moore exceeded $15,000.00. Michael and Donna sent a message of thanks and requested that from now on, further donations should remain in the Medical Trust Fund to be distributed to others in need in future. Their message and a brief health update are on the appeal web page (sidebar link) which will be taken down at the end of his month. (more…)

As Amazon Books figured out with their “see inside this book feature” , you can tell a lot about a book by checking the contents page. In the SKMCC “Herb Drug Interactions In Oncology” - its gruesome …
Firstly, there is not a single chapter describing or defining what an interaction is, or in what context they may arise. Well, OK, perhaps they don’t know, or perhaps they think everyone knows? Are there different kinds of interaction? Are there any good ones? Useful ones? Bad ones? Dangerous ones? Benign Ones? Do they vary depending on the situation? How do you prove an interaction? Well there are a lot of unanswered questions there. Trouble is, providing even a tentative answer to these questions would imply understanding something about the topic, which these people have no interest in at all. Their real agenda is bashing non-conventional cancer treatments, including herbs, as well as a motley array of dietary supplements.

Over one third ( 35%) of the topics in the book contents relate to entirely non herbal remedies or miscellaneous alternative therapies of varying provenance, ranging from the wild and whacky to merely unproven. A brief sample will indicate their obvious “quackwatch” agenda - the very first topic is 714X. Other chapters cover Bioresonance, CanCell, DiBella Multitherapy, Gerson, Hydrazine sulfate, Magnet therapy, Metabolic therapies, MICOM, Oxygen therapies, Livingston Wheeler Therapy, Sun Soup, etc. etc Of course none of these are herbs or even herbal therapies.

A number of micronutrients including a weirdly random selection of vitamins are covered, for example only B6 from the B group, obviously none of which herbs, together with quite a few non herbal dietary supplements ranging from well studied accessory nutrients such as CoQ10 SAMe, carnitine, and glutamine through to materials that are entirely unavailable to the public such as Phenylbutyrate, or Ukrain (the latter actually contains a pharmaceutical).
The agenda is clear, this so called herb-drug interactions in oncology book contains no general discussion of interactions in the oncology setting between herbs and drugs, and sets out to rubbish a wide range of so called alternative therapies which have nothing to do with herbs.

Next time we will look at some of the herbs they actually do cover and expose the rubbish that passes for “scientific information on botanicals from SKMCC Integrative Medicine Service.

By modulating androgen receptor coactivators, daidzein may act as a phytoandrogen: Chen JJ, Chang HC Prostate. 2007 Jan 24;

BACKGROUND: To identify the phytoandrogen from phytohormone, we established an assay to assess the androgenicity of phytoestrogens by using androgen receptor (AR) cofactors to modulate the AR transcriptional activity. METHODS: A Dual-luciferase reporter assay was used to evaluate the transcriptional activity of AR stimulated by the phytoestrogen daidzein. RESULTS: The Dual luciferase data showed that daidzein can enhance androgenic effects in AR negative PC-3 cells cotransfected with AR and AR cofactors. In AR and ARA70 positive LNCaP cells, daidzein can enhance ARA55-mediated induction of AR transcriptional activity. With increasing amounts of transfected ARA55, AR transcriptional activity was enhanced by daidzein in a dose-dependent manner. CONCLUSIONS: Although daidzein is a phytoestrogen, it can create androgenic effects when cells are cotransfected with AR cofactors. When screening for phytoandrogens, the modulating effects of AR cofactors with AR should be considered in the assay system. Prostate (c) 2007 Wiley-Liss, Inc.

PMID: 17252558 [PubMed - as supplied by publisher]

Phytoestrogens activate estrogen receptor beta1 and estrogenic responses in human breast and bone cancer cell lines.: Chrzan BG, Bradford PG: Mol Nutr Food Res. 2007 Feb 1;51(2):171-177

Plant-derived phytoestrogens and estrogens in hormone replacement therapies have overlapping yet sometimes divergent effects on the incidence of breast cancer and osteoporosis. Using human MCF-7 breast carcinoma and G-292 osteosarcoma cell lines, it was investigated whether the phytoestrogens genistein and daidzein affect reporter gene transcription via the estrogen receptors (ERs) ERalpha and ERbeta1 as well as whether they affect the expression of estrogen-responsive genes in MCF-7 cells and the secretion of the cytokine IL-6 from G-292 cells. The results showed that genistein and daidzein potently trigger transactivation with ERbeta1 from estrogen response element-reporter genes (EC50s of 1.7-16 nM) although they were 400- to 600-fold less potent than 17beta-estradiol (E2) (EC50 of 0.02-0.04 nM). E2 was the only potent activator of ERalpha (EC50 of 0.1-0.4 nM). The rank order potency (E2 > genistein > daidzein) is maintained in MCF-7 cells as well as G-292 cells with both receptor subtypes, with a strong receptor selectivity of the phytoestrogens for ERbeta1 over ERalpha. Genistein and daidzein increased the expression of estrogen-responsive genes in MCF-7 cells. Daidzein, like E2, inhibited IL-1beta- and hormone-mediated IL-6 secretion from G-292 cells. The results provide a basis for understanding how dietary phytoestrogens protect bone without increasing the risks for breast cancer.

PMID: 17266178 [PubMed - as supplied by publisher]

Effects of the phytoestrogen genistein on hot flushes, endometrium, and vaginal epithelium in postmenopausal women: a 1-year randomized, double-blind, placebo-controlled study.
D’Anna R, Cannata ML, Atteritano M, Cancellieri F, Corrado F, Baviera G, Triolo O, Antico F, Gaudio A, Frisina N, Bitto A, Polito F, Minutoli L, Altavilla D, Marini H, Squadrito F : Menopause. 2007 Jan 23;

OBJECTIVE:: To evaluate in a 12-month, prospective, randomized, double-blind, placebo-controlled study whether pure administration of the phytoestrogen genistein (54 mg/d) might reduce the number and severity of hot flushes in postmenopausal women with no adverse effect on the endometrium. DESIGN:: A total of 389 participants met the main study criteria and were randomly assigned to receive the phytoestrogen genistein (n = 198) or placebo (n = 191). About 40% of participants in both groups did not suffer from hot flushes, and the evaluation was performed in a subgroup of 247 participants (genistein, n = 125; placebo, n = 122). Reductions from baseline in the frequency and severity of hot flushes were the principal criteria of efficacy. Endometrial thickness was evaluated by ultrasonography. The maturation value was also used to determine hormonal action on the vaginal cells. RESULTS:: There were no significant differences in age, time since menopause, body mass index, and vasomotor symptoms between groups at baseline (4.4 +/- 0.33 hot flushes per day in the genistein group and 4.2 +/- 0.35 hot flushes per day in the control group). The effect was already evident in the first month and reached its peak after 12 months of genistein therapy (-56.4% reduction in the mean number of hot flushes). Furthermore, there was a significant difference between the two groups at each evaluation time (1, 3, 6, and 12 months). No significant difference was found in mean endometrial thickness and maturation value score between the two groups, either at baseline or after 12 months. CONCLUSIONS:: The phytoestrogen genistein has been shown to be effective on vasomotor symptoms without an adverse effect on endometrium.

PMID: 17251874 [PubMed - as supplied by publisher]

Disruption of the female reproductive system by the phytoestrogen genistein.:
Jefferson WN, Padilla-Banks E, Newbold RR .Reprod Toxicol. 2006 Dec 9;

Studies in our laboratory have shown that developmental exposure to genistein causes deleterious effects on the reproductive system. Oral exposure to genistin (25mg/kg) increases uterine weight at 5 days of age similar to subcutaneous injection of genistein (20mg/kg) suggesting that subcutaneous injection of genistein is a suitable model for oral exposure to genistin. Mice treated neonatally by subcutaneous injection of genistein (0.5-50mg/kg) exhibit altered ovarian differentiation leading to multi-oocyte follicles (MOFs). Ovarian function and estrous cyclicity were disrupted in genistein treated mice with increasing severity over time. Reduced fertility was observed in mice treated with genistein (0.5, 5, or 25mg/kg) and infertility was observed at 50mg/kg. Females generated from genistein 25mg/kg females bred to control males have increased MOFs suggesting these effects can be transmitted to subsequent generations. Thus, neonatal treatment with genistein at environmentally relevant doses caused adverse consequences on reproduction in adulthood.

PMID: 17250991 [PubMed - as supplied by publisher]

Of course we would rather no-one did tamoxifen, but this is relevant to those that find themselves in that situation

The combination of green tea and tamoxifen is effective against breast cancer. Sartippour MR, Pietras R, Marquez-Garban DC, Chen HW, Heber D, Henning SM, Sartippour G, Zhang L, Lu M, Weinberg O, Rao JY, Brooks MN; Carcinogenesis. 2006 Dec;27(12):2424-33

Epidemiologic data have suggested that green tea may prevent breast cancer. Studies in our laboratory have provided evidence that green tea extract inhibits breast cancer growth by a direct anti-proliferative effect on the tumor cells, as well as by indirect suppressive effects on the tumor-associated endothelial cells. In this study, we asked whether concurrent administration of green tea may add to the anti-tumor effects of standard breast cancer therapy. We observed that green tea increased the inhibitory effect of tamoxifen on the proliferation of the ER (estrogen receptor)-positive MCF-7, ZR75, T47D human breast cancer cells in vitro. This combination regimen was also more potent than either agent alone at increasing cell apoptosis. In animal experiments, mice treated with both green tea and tamoxifen had the smallest MCF-7 xenograft tumor size, and the highest levels of apoptosis in tumor tissue, as compared with either agent administered alone. Moreover, the suppression of angiogenesis in vivo correlated with larger areas of necrosis and lower tumor blood vessel density in treated xenografts. Green tea decreased levels of ER-alpha in tumors both in vitro and in vivo. We also observed that green tea blocked ER-dependent transcription, as well as estradiol-induced phosphorylation and nuclear localization of mitogen-activated protein kinase. To our knowledge, this study is the first to show the interaction of green tea with the ER pathway, as well as provide mechanistic evidence that the combination of green tea and tamoxifen is more potent than either agent alone in suppressing breast cancer growth. These results may lead to future improvements in breast cancer treatment and prevention.

PMID: 16785249 [PubMed - indexed for MEDLINE]

Ginkgo is an important renal protective and can help restore impaired renal function. Animal data suggests benefit in platinum induced nephrotoxicity, but this study relates to adriamycin which causes damage through a different mechanism - oxidative stress.

Ginkgo biloba leaf extract (EGb 761) diminishes adriamycin-induced hyperlipidaemic nephrotoxicity in rats: association with nitric oxide production. Abd-Ellah MF, Mariee AD.Biotechnol Appl Biochem. 2007 Jan;46(Pt 1):35-40

The aim of this experimental study was to investigate the effect of a standardized preparation of Ginkgo biloba extract (EGb 761) on the hyperlipidaemic nephrotoxicity and oxidative stress induced by a single intravenous injection (5 mg/kg) of adriamycin. EGb 761 was received daily thereafter by a gavage at the dose of 100 mg/kg for 35 consecutive days. EGb 761 administration significantly attenuated adriamycin-induced renal dysfunction, as assessed by measuring serum lipid profile, serum total protein, serum urea and Ccr (creatinine clearance). Furthermore, urinary excretions of protein and NAG (N-acetyl-beta-D-glucosaminidase; a marker of renal tubular injury) were significantly inhibited following EGb 761 administration. EGb 761 supplementation significantly prevented the generation of TBARS (thiobarbituric acid-reacting substances) with a marked improvement in terms of GSH content and activity of antioxidant enzymes in the kidney homogenate. Moreover, EGb 761 treatment significantly reduced both renal-tissue and urine total NO (nitric oxide) levels. The results suggest that the protective potential of EGb 761 in the prevention of adriamycin-induced hyperlipidaemic nephrotoxicity in rats was associated with the decrease in the oxidative stress and the total NO levels of renal tissues. Likewise, the present study demonstrates the ability of EGb 761 to reduce the hyperlipidaemia and proteinuria associated with this nephropathy, which might be beneficial to enhance the therapeutic index of adriamycin.

PMID: 16848766 [PubMed - indexed for MEDLINE]

A simple and eloquent statement in this abstract ( my emphasis added - see below ) should qualify these guys for a Nobel peace prize or equivalent. Free full text on PLos….

Willow Leaves’ Extracts Contain Anti-Tumor Agents Effective against Three Cell Types. El-Shemy HA, Aboul-Enein AM, Aboul-Enein KM, Fujita K: PLoS ONE. 2007;2:e178

Many higher plants contain novel metabolites with antimicrobial and antiviral properties. However, in the developed world almost all clinically used chemotherapeutics have been produced by in vitro chemical synthesis. Exceptions, like taxol and vincristine, were structurally complex metabolites that were difficult to synthesize in vitro. Many non-natural, synthetic drugs cause severe side effects that were not acceptable except as treatments of last resort for terminal diseases such as cancer. The metabolites discovered in medicinal plants may avoid the side effect of synthetic drugs, because they must accumulate within living cells. (DUH!! YEAH!!) The aim here was to test an aqueous extract from the young developing leaves of willow (Salix safsaf, Salicaceae) trees for activity against human carcinoma cells in vivo and in vitro. In vivo Ehrlich Ascites Carcinoma Cells (EACC) were injected into the intraperitoneal cavity of mice. The willow extract was fed via stomach tube. The (EACC) derived tumor growth was reduced by the willow extract and death was delayed (for 35 days). In vitro the willow extract could kill the majority (75%-80%) of abnormal cells among primary cells harvested from seven patients with acute lymphoblastic leukemia (ALL) and 13 with AML (acute myeloid leukemia). DNA fragmentation patterns within treated cells inferred targeted cell death by apoptosis had occurred. The metabolites within the willow extract may act as tumor inhibitors that promote apoptosis, cause DNA damage, and affect cell membranes and/or denature proteins.

PMID: 17264881 [PubMed - in process]

Marigold is active against colon CA, melanoma and leukemia. Oh yes. We love kalendoola.

Anti-inflammatory, anti-tumor-promoting, and cytotoxic activities of constituents of marigold (Calendula officinalis) flowers.: Ukiya M, Akihisa T, Yasukawa K, Tokuda H, Suzuki T, Kimura Y: J Nat Prod. 2006 Dec;69(12):1692-6

Ten oleanane-type triterpene glycosides, 1-10, including four new compounds, calendulaglycoside A 6′-O-methyl ester (2), calendulaglycoside A 6′-O-n-butyl ester (3), calendulaglycoside B 6′-O-n-butyl ester (5), and calendulaglycoside C 6′-O-n-butyl ester (8), along with five known flavonol glycosides, 11-15, were isolated from the flowers of marigold (Calendula officinalis). Upon evaluation of compounds 1-9 for inhibitory activity against 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced inflammation (1 microg/ear) in mice, all of the compounds, except for 1, exhibited marked anti-inflammatory activity, with ID50 values of 0.05-0.20 mg per ear. In addition, when 1-15 were evaluated against the Epstein-Barr virus early antigen (EBV-EA) activation induced by TPA, compounds 1-10 exhibited moderate inhibitory effects (IC50 values of 471-487 mol ratio/32 pmol TPA). Furthermore, upon evaluation of the cytotoxic activity against human cancer cell lines in vitro in the NCI Developmental Therapeutics Program, two triterpene glycosides, 9 and 10, exhibited their most potent cytotoxic effects against colon cancer, leukemia, and melanoma cells.

PMID: 17190444 [PubMed - indexed for MEDLINE]

Prospective patients at our clinic are clearly advised before they make an initial appointment that botanical medicine and clinical nutrition strategies for malignancy do not have support from RCT evidence. The reason for this is the blindingly obvious fact that there are NO TRIALS….for the obvious reason that RCTs are driven by drug companies who have no interest in unpatentable botanicals and non-conventional approaches. So what’s new? Well nothing, except that Ernst, once again,.cranks out yet another paper concluding that there is no evidence for CAM in breast cancer.

Someone needs to systematically review Ernst’s salary and performance. The man is an jackass.

Complementary/Alternative therapies for the treatment of breast cancer. A systematic review of randomized clinical trials and a critique of current terminology.: Ernst E, Schmidt K, Baum M Breast J. 2006 Nov-Dec;12(6):526-30

The objectives of this study was to evaluate and critically analyze all randomized clinical trials (RCTs) of ”alternative cancer cures” (ACCs) for breast cancer. The electronic databases Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, Allied and Complementary Medicine, Scirus, BIOSIS, CancerLit and CINAHL and for ongoing trials the MetaRegister at http://www.controlled-trials.com/ and the National Research Register at http://www.update-software.com/national/ were searched from their inception. Bibliographies of located studies were scanned. Unpublished or ongoing trials were identified through correspondence with experts in the field. Our own files were hand searched for further RCTs. Review methods included a systematic review of RCTs involving breast cancer patients treated with ACCs, survival, parameters indicative of tumor burden, disease progression, cancer recurrence, and cancer cure. Results were tabulated and summarized. Thirteen RCTs met the inclusion criteria. In most cases their methodological quality is low, with only two RCTs scoring ”4” and four RCTs scoring ”3” out of 5 possible points for methodological quality. The treatments tested included various methods of psychosocial support such as group support therapy, cognitive behavioral therapy cognitive existential group therapy, a combination of muscle relaxation training and guided imagery, the Chinese herbal remedy Shi Quan Da Bu Tang, thymus extract, transfer factor, melatonin, and factor AF2. Encouraging but not fully convincing results emerged for melatonin.

PMID: 17238981 [PubMed - in process]