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If you're from Japan, you're probably wondering why I've listed PSK under alternative therapies. In Japan, PSK is an approved anti-cancer drug with 20 years of research behind it. PSK sales in Japan account for hundreds of millions dollars worth of sales each year. But in the US, PSK is little known, is not used by mainstream doctors, and until recently nothing like it was readily available. Now a nutritional supplement designed to be identical to PSK is available in the US, but very few mainstream doctors, and actually not many alternative practitioners are aware of it. So in the US, PSK has the status of a little known nutritional supplement or alternative therapy. Which is too bad in light of its proven benefits, easy administration, and lack of toxicity. Before I start sounding too much more like an advertisement, let me confess. I really am excited about it, but I have no financial interest in it; I'm not selling it.

Over many centuries, Frankincense oil has been found to have medicinal benefits. Now, an enriched extract of the Somalian Frankincense herb (Boswellia carteri) has been shown to kill off bladder cancer cells growing in culure. Research presented in the journal BMC Complementary and Alternative Medicine demonstrates that this herb has the potential to become an alternative therapy for bladder cancer.

Grant WB, Holick MF. Benefits and requirements of vitamin D for optimal health: a review. Altern Med Rev. 2005 Jun;10(2):94-111. Review. PMID: 15989379 [PubMed - indexed for MEDLINE]

Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease. Kidd P. Altern Med Rev. 2003 Aug;8(3):223-46. Review. PMID: 12946237 Th1 pathways typically produce activation of cytotoxic T lymphocytes (Tc), NK cells, macrophages, and monocytes, all of which can attack cancer cells and generally defend against tumors.55 IFN-gamma and other Th1 cytokines are typically lower in advanced cancer patients, while the Th2 marker IL-4 can be higher or unchanged

Mainstream medical treatment of cancer revolves around surgery, chemotherapy, and radiation therapy, used either alone or in combination (Isobe T et al 2005; Ostoros G et al 2005). Chemotherapy and radiation therapy cannot discriminate between cancer cells and healthy cells; thus, they damage both types of cells and cause serious and often debilitating side effects, frequently forcing patients to abandon treatment (Ettinger DS 2005; Giraud P et al 2004; Munden RF et al 2005). Therefore, it is not surprising that many cancer patients now opt to complement conventional treatments with alternative therapies that may not only temper the adverse side effects of conventional cancer therapy, but also improve its effectiveness via independent anti-cancer effects.

Complementary and alternative medicine (CAM) and complementary and integrative medicine (CIM) are therapies of proven or unproven efficacy that have been used to promote wellness, to manage symptoms associated with cancer and its treatment or to treat cancer. When properly combined with standard cancer treatments, some complementary therapies can enhance wellness and quality of life, but others may be harmful during or after treatment for cancer. Most, but not all, are natural products.

Lerner, Michael, 1943 - Choices in healing : integrating the best of conventional and complementary approaches to cancer / Michael Lerner. p. cm. Includes bibliographical references and index. ISBN 0-262-12180-8 1. Cancer--Treatment. 2. Cancer--Alternative treatment. 3. Cancer--Popular works. I. Title. RC270.8.L47 1994 616.99é406--dc20 93-39913 CIP

Deciding upon a course of treatment for cancer is a personal decision that shouldn't be reached lightly.

Simultaneously Blocking Glycolysis and Fat Metabolism Can the use of DCA and a fatty acid metabolism blocker together force more cancer cells into using aerobic metabolism? Tim McGough used green tea extract, which contains EGCG, in his fantastic response. DCA works by reactivating mitochondria and shifts metabolism from glycolysis to glucose oxidation. Hopefully the cancer cell will then undergo apoptosis. However, cancer cells have an alternate energy source: fat metabolism. This page explores to possibility of blocking fat metabolism to help force the cell into apoptosis. Oral squamous cell carcinoma is a cancer that does not respond well to DCA. This study, Head and Neck Cancer Cell Lines Are Resistant to Mitochondrial-Depolarization-Induced Apoptosis states: "Results: ΔΨm in head and neck cell lines started to show slight loss of ΔΨm, while HL-60 showed significant loss of ΔΨm after 30 min of treatment. All cell lines demonstrated complete mitochondrial depolarization within 24 h, however, only the control cell line HL-60 underwent apoptosis. In addition, HNSCC cell lines did not demonstrate cytoplasmic cytochrome c release despite significant mitochondrial membrane depolarization, while HL-60 cell initiated apoptosis and cytochcrome c release after 24 h of treatment. Conclusions: Head and neck cancer cell lines exhibit defects in mitochondrial-membrane-depolarization-induced apoptosis as well as impaired release of cytochrome c despite significant mitochondrial membrane depolarization. Proximal defects in the mitochondrial apoptosis pathway are a feature of HNSCC.(head and neck squamous cell carcinoma)" Note that although the cell lines were depolarized, apoptosis did not occur. So I checked to see if fatty acid metabolism is used by squamous cell carcinoma.

Frankincense oil derived from Boswellia carteri induces tumor cell specific cytotoxicity. Frank MB, Yang Q, Osban J, Azzarello JT, Saban MR, Saban R, Ashley RA, Welter JC, Fung KM, Lin HK. BMC Complement Altern Med. 2009 Mar 18;9(1):6. [Epub ahead of print] PMID: 19296830 doi:10.1186/1472-6882-9-6

Ginger inhibits cell growth and modulates angiogenic factors in ovarian cancer cells. Rhode J, Fogoros S, Zick S, Wahl H, Griffith KA, Huang J, Liu JR. BMC Complement Altern Med. 2007 Dec 20;7:44. PMID: 18096028 doi:10.1186/1472-6882-7-44

Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator. Pereira CV, Machado NG, Oliveira PJ. Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3. PMID: 18599498 doi: 10.1124/jpet.107.128017 The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study. Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs. In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.

Other compounds to consider

When doctors discovered a tumor on Steve Jobs's pancreas, he chose nine months of alternative therapies before undergoing surgery. Did he make the right decision?