Beta-Glucan Shows Treatment Promise
b1,3-glucan, a long-chain polysaccharide, is one of the compounds that stimulates the body's antibacterial and antitumor responses. Found in mushrooms, yeast, and cereal grains, this compound increases macrophage, neutrophil, and natural killer (NK) cell activity as well as cytokine production. (Cytokines are proteins that coordinate antibody and T cell immune interactions and amplify immune reactivity.)
A 2002 pilot study conducted by Vaclav Vetvicka, PhD, and colleagues showed that a commercial, yeast-derived b1,3-glucan product (Imucell WGP Beta Glucan, Biopolymer Engineering Inc., Eagan, Minnesota) protects mice against anthrax infection and cancer. To investigate beta-glucan's ability to fight infection, 20 mice received 7 days of oral treatment with beta-glucan. Ten received 0.2 mg of beta-glucan/kg of body weight per day, and 10 got 20 mg/kg. At the end of treatment, researchers gave these mice and 10 untreated controls a subcutaneous injection of anthrax spores. All of the beta-glucan subjects survived anthrax infection. Only 5 of the 10 untreated control mice lived.
For the cancer investigation, another group of mice received 28.4 mg of beta-glucan per kilogram of body weight daily for 21 days. Researchers then injected tumor cells into treated mice and untreated controls. Twenty-one days later, the mice were killed and the tumors removed. Tumors taken from the treated mice weighed less than those from the control: 0.52 ± 0.06 grams vs. 0.66 ± 0.06 grams in control mice. Moreover, the control mice clearly felt worse: "… the control animals were observed to be inactive and crouching, and had reduced body temperature in comparison to the WGP Beta Glucan-treated animals." Cytokine levels in spleen cells taken from treated mice and control mice also differed. Interleukin-2, which increases T lymphocytes and natural killer cells, was 2.3-fold higher in cells from the treated mice than those from controls. Interferon-g, which activates macrophages, increases B cell differentiation and NK cell activity, and decreases tumor growth, was 4.4-fold higher in cells from the beta-glucan mice; and tumor necrosis factor-a, which increases cytokines and inflammatory and immune responses, was 2.2-fold higher.
Russell L. Blaylock, MD, who wrote an editorial commentary about this study, says: "The use of b1,3-glucan is of special interest in the cancer patient undergoing chemotherapy and/or radiation treatment, since b-glucans have shown a remarkable ability to accelerate hematopoietic recovery [normal blood cell development] in both sub-lethally and lethally irradiated mice, even when given after the radiation dose. It can also stimulate recovery of the bone marrow following chemotherapy, something vital to restricting tumor growth and preventing infectious complications during treatment."
Since not all beta-glucan products are alike, Vaclav Vetvicka and Jana Vetvickova evaluated and compared the immunological effects of seven commercial b1,3-glucan products in a 2007 study. The glucans in these products came from different sources: yeast, mushrooms, and cereals. The researchers looked at interleukin-2 production, phagocyte activity, surface markers on splenocytes, and antibody response. The glucans that produced the greatest response in mice were Transfer Point's Glucan #300, NOW Beta Glucan, and Maitake Gold 404. The glucan's purity affects results more than the source of the glucan, the researchers say. Vetvicka and Vetvickova encourage practitioners and consumers to use glucan products "from a solid vendor who is able to back the claims with solid scientific data." Some of the products tested in their study had "surprisingly low activity." This study is available at www.ana-jana.org/members/journals/JANAvol10no12007.pdf. (4.41MB)
Blaylock RL. Yeast b1,3-glucan and its use against anthrax infection and in the treatment of cancer. JANA. Spring 2002;5(2):3–4. Available at: www.ana-jana.org/Journal/journals/JANAVol52.pdf. (4.41MB) Accessed June 23, 2010.
Lanigan AJ. The immune response enhanced by beta-1,3-D glucan [press release]. Available at: www.bakersyeastbetaglucan.com/ImmuneResponseEnhancedbyBetaGlucan.htm. Accessed June 24, 2010.
Vetvicka V. A daily dose could save your life. Health+News. 11(10):1,4.
Vetvicka F, Terayama K, Mandeville R, Brousseau P, et al. Pilot study: orally-administered yeast b1,3-glucan prophylactically protects against anthrax infection and cancer in mice. JANA. Spring 2002;5(2):5–9. Available at: www.ana-jana.org/Journal/journals/JANAVol52.pdf. (987KB) Accessed June 23, 2010.
Vetvicka V, Vetvickova J. An evaluation of the immunological activities of commercially available b1,3-glucans. JANA. 2007;10(1);25–31. Available at www.ana-jana.org/members/journals/JANAvol10no12007.pdf. (4.41MB) Accessed June 23, 2010.
Film Documents Cancer 'Warriors' Survival
Cancer Survivors USA – a road trip, and an open letter to Senator Tom Harkin is a compelling 90-minute DVD that consists of interviews with eight cancer "warriors." The interviewees, ranging in age from 40 to 75, were diagnosed with a variety of stage III or IV metastatic cancers, including melanoma, breast cancer, lymphoma, and esophageal-stomach cancer that spread to the pancreas. Most of the eight had surgery to remove tumors. A few also had some chemotherapy before recurrence pushed them to find alternative treatment at CHIPSA Medical Center in Mexico. At that clinic, these patients were given injections of Coley's fluids (a.k.a. Coley's toxins) in addition to following the Gerson cancer protocol. Gerson's protocol helps the body detoxify and heal.
Gar and Christeene Hildenbrand of Gerson Research Organization (www.gerson-research.org) produced the DVD to revive interest in Coley's fluids and to lobby for research that would lead to its use in the US. Coley's fluids, based on the research of William B. Coley, MD, is a bacterial endotoxin that produces a high fever. Coley (1862–1936) discovered that high temperatures that do not affect normal cells will kill cancer cells. This early 20th-century treatment was accepted by medical practitioners and is still used in other countries. The FDA's failure to grandfather the treatment as acceptable led to its decline in the US. The fluid used by the Mexican clinic where these eight people received treatment is made in Canada. Injections of Coley's fluid produce a flulike reaction with intense chills (fever) sometimes accompanied by vomiting, diarrhea, and hallucinations. The patients report that the intensity of the reaction tends to decrease with succeeding injections.
The interviewees reported three difficulties with their treatment. First, following the Gerson diet and juicing guidelines, which is necessary for healing, is time-consuming. The program requires the patient's commitment and the help of a caregiver. Second, their treatment was not covered by insurance – even though it produced very positive results. Another difficulty was limited access to medical care. Travel to Mexico to receive treatment was difficult for some. Finding a physician who was willing to monitor their health after returning from Mexico was particularly problematic. Most oncologists, in the interviewees' experiences, wanted nothing to do with the patients after they chose alternative treatment. At least one, however, had the support of a family doctor who requested scans to monitor changes and dealt with an emergency when a secondary tumor to the pancreas "bled to death."
Cancer Survivors USA is a powerful film. It is posted at www.youtube.com/garhildenbrand in short segments and well worth watching. Spread the word. There are alternatives to chemotherapy and radiation that do work, even in end-stage cancers.
Gc-MAF Injections May Support Immune Defense
Gc-MAF injections appear to be an effective way to overcome one of the tactics that cancer cells use to block the body's immune function. Cancer cells secrete an enzyme called NaGalase (alpha-N-acetylgalactosaminidase). This enzyme prevents a glycol protein found in blood serum (called Gc protein or vitamin D binding protein) from converting into Gc macrophage activating factor (Gc-MAC; macrophages identify and gobble up foreign matter, including cancer cells). By blocking the conversion of Gc protein to Gc-MAF, cancer cells reduce macrophage function, limiting the body's ability to detect and destroy malignant cells and leaving it susceptible to infection.
For almost 20 years, Nobuto Yamamoto, director of the Division of Cancer Immunology and Molecular Biology at Socrates Institute for Therapeutic Immunology (Philadelphia, Pennsylvania), has been studying the effect of directly administering GcMAF to cancer patients, thereby bypassing the malignant cells' NaGalase defense. Yamamoto has used Gc-MAF injections (100 nanograms once a week) "on a variety of cancers … [including] prostate, breast, colon, stomach, liver, lung, kidney, bladder, uterus, ovary, head/neck, melanoma, and fibrosarcoma." Undifferentiated tumor cells, such as breast and prostate adenocarcinomas, respond more quickly to Gc-MAC injections than well-differentiated cancer cells, such as those found in squamous carcinomas. In a 2008 study with 16 breast cancer patients, NaGalase enzyme fell to levels found in healthy people after 16 to 22 weekly doses of Gc-MAC. In contrast, it took over 75 weekly doses before NaGalase reached healthy levels in people with well-differentiated head/neck tumors. Treatment appears to be long lasting. A 2008 study with 16 prostate cancer patients found no increase in serum NaGalase during the seven years of observation after Gc-MAC treatment. Annual computed tomographic scans also found no evidence of prostate cancer in these men.
A PubMed search locates numerous studies involving vitamin D binding protein-macrophage activating factor (DBP-maf) and Gc-macrophage activating factor. In an animal study performed by Oliver Kisker et al., DBP-maf was isolated from a human pancreatic cancer cell line. (It appears that the tumor uses DBP-maf to prevent secondary tumors.) DBP-maf may have antiangiogenic properties in addition to macrophage activating properties, according Kisker and colleagues. Yamamoto and colleagues treated purified Gc protein with immobilized b-galactosidase and sialidase to make the Gc-MAF used in their studies. Their manufacturing process is patent protected. Gc-MAF itself is not patentable because it is a natural compound. Despite the positive studies, Bill Sardi and Timothy Hubbell report: "There is no evidence of any current effort to commercialize this therapy or put it into practice."
Kisker O, Onizuka S, Becker CM, Fannon M, et al. Vitamin D binding protein-macrophage activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice. Neoplasia. January 2003;5(1):32–40. Available at: www.ncbi.nlm.nih.gov/pmc/articles/PMC1502120/pdf/neo0501_0032.pdf. (3.42MB) Accessed June 16, 2010.
Sardi B, Hubbell T. Real help for cancer? [Web article]. LewRockwell.com. May 22, 2008. http://www.lewrockwell.com/sardi/sardi84.html. Accessed June 16, 2010.
Yamamoto N, Suyma H, Yamamoto N. Immunotherapy for prostate cancer with Gc protein-derived macrophage-activating factor, GcMAF. Transl Oncol. June 2008:1(2):65–72. Available at: www.transonc.com/pdf/manuscript/v01i02/neo08106.pdf. Accessed June 16, 2010.
Homeopathic Treatment Helps Some Cancers
A February 2010 study in the International Journal of Oncology reports that four specific homeopathic remedies had "cytotoxic effects" on two types of breast cancer cells but not on normal breast tissue. Researchers at the University of Texas M. D. Anderson Cancer Center (Houston) conducted this laboratory study using Carcinosin, Phytolacca, Conium, and Thuja. Thesehomeopathics are often given to cancer patients in India. In this study, cancer cells exposed to the remedies displayed "cell cycle delay/arrest and apoptosis." The researchers call for more studies of these remedies using additional cell lines and animal models
The protocol for using homeopathics to treat cancer patients may be as important as the remedies used. Holistic veterinarian Joe Demers recommends the approach of Dr. A. U. Ramakrishnan of India. "I have had much better results using Ramakrishnan's method than I ever had using the standard classical homeopathic approach of using low potencies, LM potencies, or high potencies then waiting," he writes. Although trained in classical homeopathy, Ramakrishnan began trying different protocols when cancer patients failed to respond. His protocol alternates an organ specific homeopathic remedy with a nosode (usually Carcinosin or, if the tumor is hard, Scirrhinum)on a weekly schedule.The protocol and list of remedies are found in the book A Homeopathic Approach to Cancer, which Ramakrishnancoauthored with Catherine T. Coulter.
Ramakrishnan does not claim that his protocol is a cure for all cancers. Since he began using it in 1994, he has observed "particularly good results in patients with breast cancer, prostate cancer, and esophageal cancer." He estimates about an 80% cure rate in his patients with these cancers. Ramakrishnan advocates an integrative approach that includes surgery and the use of modern diagnostic technology but shuns chemotherapy and radiation therapy because of their toxicity. He collaborates with oncologists throughout the world. "It's a question of mind," he says. "If you have an open mind, you can work together."
Demers J. A holistic approach for the treatment of cancer. J Am Holist Vet Med Assoc. January 2005; 23(4):31–39. Available at: http://cancer.landofpuregold.com/the-pdfs/holistic.pdf. Accessed August 4, 2008.
Frenkel M, Mishra BM, Sen S, Yang, P, et al. Cytotoxic effects of ultra-diluted remedies on breast cancer cells [abstract]. Int J Oncol. February 2010;36(2):395–403. Available at: www.ncbi.nlm.nih.gov/pubmed/20043074. Accessed May 19, 2010.
Guess G. A Homeopathic Approach to Cancer [book review]. J Am Inst Homeopath. Autumn 2001;94(3). Available at: www.minimum.com/reviews/homeopathic-cancer.htm. Accessed May 19, 2010.
Ridley K. Using homeopathy to treat cancer. Ode. Jan/Feb 2006. Available at: http://www.odemagazine.com/doc/30/using_homeopathy_to_treat_cancer. Accessed May 19, 2010.
Light, Cancer, and Fritz-Albert Popp
What makes some substances carcinogenic and others benign, even though they are chemically similar? In 1970, Fritz-Albert Popp, a German theoretical biophysicist, discovered that benzo[a]pyrene, a potent carcinogen, absorbs ultraviolet light at one wavelength and emits it at another. Yet, benzo[e]pyrene, a benign compound that is nearly identical to benzo[a]pyrene, absorbs and reemits the same light at its original wavelength. Popp tested 37 different chemicals. The carcinogens "scrambled" light with a wavelength of 380 nanometers. The benign chemicals did not. That finding in itself is fascinating. Using ultraviolet light, the EPA could target which of the thousands of chemicals used by industry are most likely to be carcinogenic. However, Popp's work with light and carcinogens led to momentous findings about cancer and about light's role in biology, as Lynn McTaggart explains in her book The Field.
During his work with chemicals, Popp learned that 380 nanometers, the wavelength altered by carcinogens, is also the wavelength that cells prefer to use to repair themselves. After exposure to intense UV light, cells quickly self-repair when they are exposed to very weak UV light, particularly that with a wavelength of 380 nanometers. Popp hypothesized that cancer results from a disruption of cells' photorepair system. His hypothesis raised a question: what in the body produced this very weak light that powered the repair system? Popp and his student Bernard Ruth found that all living systems store light energy (photons) acquired from the sun and from plants consumed as food (photosynthesis), in DNA. This stored light is released as very weak, extremely coherent biophotons. "Photons switch on the body's processes like a conductor launching each individual instrument into the collective sound," explains McTaggart. "At different frequencies they perform different functions."
Over the years, Popp found that biophoton emissions from healthy humans display rhythmic patterns. He also observed that the coherence of the emissions, the intensity, and the rhythmic patterns varied in people with different illnesses. People with multiple sclerosis, for example, absorb too much light and their photon emissions display too much order. Biophoton emissions from cancer patients lack coherence and fail to follow natural rhythmic patterns. Also, tumors emit high amounts of photons: an average of 300 ± 90 photons/cm per minute compared with normal tissue that emits an average of 22 ± 6 photons/cm per minute. Popp and colleagues at the International Institute of Biophysics have discovered that surface tumors and tumors excised during surgery respond to remedies with changes in photon emissions. Most possible treatments have no effect on the tumor's high emission rate. However, when the tumor responds to a nontoxic remedy with decreased emissions, the agent will likely improve the patient's condition and may even promote a cure. Rather than killing tumor cells, the beneficial agent appears to stimulate the normal cells to overcome the cancerous ones.
McTaggart L. Beings of light. In: The Field. New York: HarperCollins; 2002:39–55.
Musumeci F. Tumor tissues [Web article]. www.lifescientists.de/ib1003e4.htm. Accessed May 19, 2010.
International Institute of Biophysics. Basic theory of cancer development and defense [Web article]. http://www.lifescientists.de/publication/pub2002-05.htm. Accessed May 19, 2010.
Book Offers Guidance on Nutriton and Supplements in Treatment
All too often, oncologists give cancer patients little guidance on ways to use nutrition and supplements to aid their recovery and prevent recurrence. The book I Have Cancer: What Should I Do? by Michael J. González, DSc, PhD; Jorge R. Miranda-Massari, PharmD; and Andrew W. Saul, PhD, fills this gap. González and Miranda-Massari are members of RECNAC II at the University of Puerto Rico. RECNAC II is a research initiative that was inspired by Dr. Hugh Riordan's RECNAC project at the Center for the Improvement of Human Functioning (Wichita, Kansas). Saul is assistant editor of the Journal of Orthomolecular Medicine and author of Fire Your Doctor! and Doctor Yourself.
I Have Cancer: What Should I Do? gives readers the basics about nutrition, supplements, and lifestyle that can be used with conventional cancer treatment. It explains the orthomolecular (high-dose supplement) program that the authors themselves would follow if diagnosed with cancer. It is also the program that Saul uses to prevent cancer.
"Cancer is a multifactorial disease that requires a multifactorial treatment plan: medical, nutritional, and lifestyle changes as well as mental, emotional, social, and spiritual support," assert the authors. "You cannot just take some pills and not change your diet, or change the diet and ignore important emotional or spiritual issues in your life, and then expect that everything will be fine. Any effective approach for cancer must be truly integrated." Keeping that in mind, the authors explain why nutrition is such an important part of any treatment plan. Food choices can reduce toxic effects of oncology treatments, strengthen the immune response, and aid recovery. The dietary guidelines are the basics: a whole-food diet that includes pulses (beans and lentils), whole grains (particularly sprouted grains), nuts, and an abundance of fresh vegetables and fruits. The authors recommend limiting red meat and salt and avoiding sugar and dairy foods altogether, particularly if the cancer is hormone related. Fresh air, exercise, and drinking plenty of pure water are strongly encouraged. The book also discusses dietary supplements that reinforce and augment the benefits of this diet plan.
In his foreword for I Have Cancer: What Should I Do? the late Dr. Abram Hoffer wrote: "Oncologists have to learn not to destroy hope. It is essential that patients not be deprived of hope even with what appears to be terminal cases. I have seen too many of these so-called hopeless cases recover." He tells of a middle-aged woman with kidney cancer that had spread to her back and aorta. Conventional oncologists had no treatment for her, so she entered hospice care. She also consulted Hoffer about orthomolecular treatment. Two years later, hospice discharged her because she was too healthy to die. Six years after consulting Hoffer, the woman was "still well." "Should you be afraid that it might be too late for you," Saul writes, "remember this: some 98 percent of the atoms in your body are replaced every year. … And every one of those atoms can only come from what you breathe, drink, and eat."
I Have Cancer: What Should I Do? is well worth the $18.95 cost. The book teaches people self-care and gives much-needed words of hope. It is published by Basic Health Publications.
Overdiagnosis Poses Challenges
The debate about cancer overdiagnosis continues. Cancer overdiagnosis refers to the detection of slow-growing tumors that in themselves will not cause harm; but people who undergo treatment for them are exposed to possible complications and potential harm from the treatment itself. As more people obtain screening and the screening devices become more sensitive to finding abnormalities, cancer diagnoses have also risen. At this point, however, medical science cannot distinguish between cancers that are dangerous and those that are harmless. For this reason, some researchers are suggesting that practitioners and patients take a little time to see if a tumor is actually growing before jumping into potentially harmful treatment.
Even though diagnoses have increased over the past 30 years, mortality rates for five cancers have changed very little, according to radiologist William Black, MD, and physician-researcher H. Gilbert Welch, MD. This observation has made the Dartmouth-Hitchcock Medical Center researchers take a close look at overdiagnosis. Recently, Welch and Black reviewed data from large randomized screening trials to estimate the extent of overdiagnosis. Their article appears in the Journal of the National Cancer Institute (April 22, 2010; this journal is published by Oxford University Press and is not affiliated with the National Cancer Institute.) The doctors estimate that overdiagnosis is present in 25% of breast cancers detected on mammograms, 50% of lung cancers detected with chest X-rays and sputum tests, and 60% of prostate cancers detected with prostate-specific antigen (PSA) tests. By definition, patients who are overdiagnosed (that is, who have slow-growing, nonlethal tumors) are going to have long survival rates – whether or not they receive treatment. The inclusion of overdiagnosed patients in clinical trials, says Black in an article by Jennifer Durgin, can make a treatment seem more effective than it actually is.
Neither Black nor Welch is advocating the abandonment of cancer screening, particularly if a patient has a higher risk of getting the disease; however, they and other physicians, including Lisa Schwartz, MD, and Steven Woloshin, MD, do criticize the ubiquitous scare tactics and peer pressure messages that promote universal screening. These messages cause unnecessary anxiety, ignore personal preference, and prevent dialog that leads to informed consent. "Our main point," says Black, "is that there are pros and cons and none of them, none of the screening tests, is a slam dunk in terms of producing a lot more good than harm." Schwartz, who codirects the VA Outcomes Group with Welch, says that overdiagnosis is a factor in any disease associated with early screening, including heart disease and osteoporosis.
Durgin J. Are we hunting too hard? Dartmouth Medicine. Summer 2005. Available at: http://dartmed.dartmouth.edu/summer05/print/hunting.php. Accessed October 23, 2006.
Magnitude of overdiagnosis in cancer indicates need for strategies to address the problem [press release]. Science Daily. April 22, 2010. Available at: www.sciencedaily.com/releases/2010/04/100422170145.htm. Accessed May 19, 2010.
Surgery and Cancer Metastasis
Cancer surgery can be a double-edged sword. On the one hand, removing tumors appears to increase the likelihood of disease-free survival. On the other, surgery incites changes in the body that can stimulate metastasis. These changes include immune function suppression, increased angiogenesis and cancer cell adhesion, and inflammation. "Since metastatic disease is often deadlier than the original tumor," writes Steven Nemeroff, ND, "it is important to utilize preventive strategies to prevent cancer metastasis." Nemeroff offers several adjunctive treatments in his informative article "Preventing Surgery-Induced Cancer Metastasis."
Surgery for any reason, not just surgery for cancer, depresses the immune system. The type of anesthesia is one factor. General anesthesia depresses NK cell activity, part of the body's innate defense against cancer: NK cells locate and destroy cancer cells. Regional anesthesia (which affects local areas instead of rendering patients unconscious) does not have the same depressive effect on NK cells. Using regional anesthesia with a reduced amount of general anesthesia (or without general anesthesia altogether) keeps NK cell activity from plummeting. In addition, surgery patients who forego general anesthesia are far less likely to require morphine to control pain after surgery. Like general anesthesia, morphine depresses NK cell activity.
Certain nutraceuticals and pharmaceuticals, taken before and after surgery, help mitigate negative effects to NK cell activity. PSK (protein-bound polysaccharide K), extracted from the mushroom Coriolus versicolor, increases NK cell activity. It decreased the number of deaths in a five-year period among lung cancer patients undergoing radiation therapy (Cancer Detect Prev. 1997;21[1]:71–77). Mistletoe extract also lessens NK cell activity depression caused by general anesthesia, according to German research. The nutraceuticals garlic, glutamine, IP6 (inositol hexaphosphate), and AHCC (active hexose correlated compound) and the pharmaceuticals interferon-alpha and granulocyte-macrophage colony-stimulating factor also stimulate NK cell activity.
Beyond the effect of anesthesia, the actual surgery promotes metastasis in several ways. First, some large tumors secrete compounds that keep secondary tumors from growing or forming. Removing these primary tumors gives the secondary tumors permission to grow. In addition, cancer cells may be freed from the excised tumor during surgery and enter the bloodstream. Surgical incisions also stimulate the body's healing response. Some aspects of the healing response, such as the production of blood vessels (angiogenesis) and production of inflammatory proteins that increase cyclooxygenase-2 (COX-2) activity, encourage cancer proliferation. COX-2 inhibitors such as Celebrex, and nonsteroidal anti-inflammatory drugs (aspirin and ibuprofen) have been linked to decreased risk of cancer and increased survival time for cancer patients. Several nutritional and herbal supplements also inhibit COX-2, including curcumin (in turmeric), resveratrol (found in red grape skins and made from Japanese knotweed), vitamin E, genistein (a soy isoflavone), epigallocatechin gallate (EGCG, found in green tea), quercetin, fish oil, garlic, feverfew, and silymarin (milk thistle). Nutraceuticals like resveratrol, genistein, EGCG, and curcumin also reduce angiogenesis.
Another effect of cancer surgery is an increase in cancer cell adhesion (ability to attach to one another and to body tissue). Modified citrus pectin (MCP) is one nutraceutical that reduces cancer cell adhesion. MCP attaches to the galectin-3 adhesion molecules on a cancer cell's surface, which prevents the cell from attaching to other cancer cells. The heartburn-alleviating drug cimetidine also inhibits cancer cell adhesion. This drug blocks the adhesion molecule E-selectin. A 1994 study performed by W. J. Adams and D. L. Morris found that 93% of colorectal cancer patients who received cimetidine for seven days around their surgery survived three years compared with a 59% survival rate in the control group.
"Taken together, it is evident that the perioperative period harbors many risks," write Israeli researchers Y. Goldfarb and S. Ben-Eliyahu in their 2006–2007 article; "however, it is also the ideal time for battling [minimal residual disease] to reduce recurrence and future metastases. …" They are not talking about more chemotherapy to kill off remaining cancer cells; rather, they recommend making choices that lessen cell-mediated immunity suppression due to surgery. The use of appropriate nutraceuticals or drugs around the time of surgery can bring great benefits with little risk to patients.
Goldfarb Y, Ben-Eliyahu S. Surgery as a risk factor for breast cancer recurrence and metastasis: mediating mechanisms and clinical prophylactic approaches. Breast Dis. 2006-7;26:99–114.
Kohn D. Cancer surgery concerns. Baltimore Sun. May 26, 2006. Available at: http://articles.baltimoresun.com/2006-05-26/news/0605260081_1_breast-cancer-tumors-cancer-research-surgery.
Nemeroff S. Preventing surgery-induced cancer metastasis. Life Extension. December 2009;57–69. |
