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From the Townsend Letter
August/September 2006


by Jule Klotter

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Alkylglycerols have increased survival times and prevented metastasis in human
and animal cancer studies. These ether lipids, normally made by bone marrow, decrease inflammation and increase natural killer cell and macrophage activity. Alkylglycerols are also believed to inhibit the activation of protein kinase C, an enzyme used in cancer cell reproduction. When used as an adjuvant cancer treatment, alkylglycerols lessen the side effects of chemotherapy and radiation treatment. The compounds also help prevent cancer.

Two Japanese scientists discovered alkylglycerols in shark liver oil in the 1920s, but the compounds' benefits remained obscure for years. Then, in 1958, Astrid Brohult, MD, reported that a bone marrow formula helped children with leukemia. Further research attributed the formula's benefit to alkylglycerols, the same compounds found in shark liver oil. Brohult and her husband Sven Brohult, PhD, found that shark-derived alkylglycerols produced positive effects in their 1970 study with cancer patients. Their 1986 study reported higher survival rates among cervical cancer patients who received alkylglycerols along with radiation treatment. A 2004 animal study by French researchers, published in
Nutrition and Cancer, further supports alkylglycerols' cancer-fighting effects. In that study, mice with Lewis Lung carcinoma tumors received pure alkylglycerols, shark liver oil, or acted as a control. The incidence of metastasis was 64+/-8% lower in those receiving pure alkylglycerols than in those in the control group. Metastasis in the shark liver oil group was 30+/-9% less than in the control group.

O'Brien C. Alkylglycerols: Mysterious immune stimulators from the deep. Available at: Accessed January 30, 2006.

Pedrono F, Martin B, Leduc C, et al. Natural alkylglycerols restrain growth and metastasis of grafted tumors in mice. (Abstract)
Nutr Cancer. 2004;48(1):64-9. Available at: (Note: Once at that page, search "natural alkylglycerols restrain growth" without the quotation marks.) Accessed on May 16, 2006.

Burzynski's Antineoplaston Therapy
For 40 years, Stanislaw Burzynski, MD, PhD, has identified and investigated antineoplastons, cancer-fighting peptides found in the blood of healthy people. People with cancer excrete these peptides in their urine; antineoplastons do not appear in their blood. Dr. Burzynski has isolated and synthesized 20 different antineoplastons. Some target specific cancers. Others affect a variety of cancers. Because antineoplastons do not harm healthy cells, Burzynski's therapy has very low toxicity. Four of these peptides have been studied in FDA-supervised clinical trials, involving brain stem glioma, childhood cerebral astrocytoma (a type of brain tumor), malignant lymphoma, colon cancer, melanoma, prostate cancer, breast cancer, and others.

In September 2004, antineoplastons A10 and AS2-1 gained orphan drug status from the FDA to treat brain stem glioma. Orphan drug status is given to treatments for diseases that affect less than 200,000 people in the US each year and that show "a significant therapeutic advantage over existing treatments." Orphan drug status entitles a product's developers to clinical research funding, tax credits on clinical research and development expenses, guidance in navigating the regulatory approval process, and other perks.

Conventional chemotherapy has had little effect on glioblastoma multiforme (a type of brain cancer); it produces a partial response in about five percent of patients and increases survival time by two to five months. Antineoplaston therapy has a significantly higher response rate. One trial followed 80 people whose tumors had persisted or returned despite undergoing conventional treatment. After receiving antineoplaston therapy, 15 of the 80 (18.75%) had a complete or more than 50 % reduction in tumor size. Five of the 15 lived for over seven years. Twenty-four of the 80 (30%) remained stable, showing no progression and less than 50% reduction in tumor size. The cancer progressed in 41 of the 80, just over 50%.

Antineoplaston therapy must be given gradually over a period of two to eight months via pumps that patients wear continuously. Patients sicken if cancer cells die off too quickly. "We've noticed that people who get antineoplastons for cancer treatment," Dr. Burzynski said in an interview with Terri Mitchell, "receive other benefits as well – for example, they are resistant to common viral infections. Their blood cholesterol is normalized and they are less susceptible to breast cancer and enlargement of the prostate. Their skin is healthier, they are less depressed, and they have more energy."

Burzynski Research Institute Receives Orphan Drug Designation for Antineoplastons A10 and AS2-1 for Treatment of Brain Stem Glioma. Available at: Accessed May 16, 2006.

Mitchell T. Unlocking the Mystery of Antineoplastons.
LE Magazine. May 2004. Available at: Accessed on May 16, 2006. (8/16/06: Link no longer working.

Aspartame & Cancer Risk
A long-term bioassay on aspartame, conducted by The Cesare Maltoni Cancer Research Center (CMCRC) of the European Ramazzini Foundation, found that the artificial sweetener produced cancer in mice at a daily dose of 20 mg/kg of body weight (bw) (Environmental Health Perspectives; March 2006). The acceptable daily intake for humans is 40 mg/kg bw in Europe and 50 mg/kg bw in the US. Humans, other primates, and rodents break down aspartame into three components: aspartic acid, phenylalanine, and methanol. The body metabolizes phenylalanine methanol into formaldehyde and, then, into formic acid. CMCRC undertook this bioassay because of the increasingly widespread use of aspartame in industrialized countries and the critical view in those countries of earlier studies that found no link between aspartame and cancer.

CMCRC's study divided eight-week-old Sprague-Dawley rats into groups (100-150/sex) that received food-grade aspartame in their feed throughout their lives at one of seven concentrations: 100,000, 50,000, 10,000, 2,000, 400, 80, or 0 ppm. These concentrations simulate a daily intake by humans of 5,000, 2,500, 500, 100, 20, 4, or 0 mg/kg bw. Rats consuming as little as 400 ppm (20 mg/kg bw) showed a significant increase in lymphomas/leukemias compared to controls. Female rats also showed a statistically significant increase in dysplastic lesions and carcinomas of the renal pelvis and ureter (combined). The researchers also found malignant schwannomas of peripheral nerves (72% originated in cranial nerves), preneoplastic and neoplastic lesions of the olfactory epithelium, and malignant brain tumors. Overall, they found "no substantial difference in survival" among the treated and control groups.

A 1981 FDA study also used Sprague-Dawley rats but did not find carcinogenic effects. The authors of the CMCRC point out that their study had a greater number of animals per sex per groups than the 1981 study, "allowing a more thorough and reliable statistical analysis." Also, the 1981 experiment ended when the rats reached 110 weeks old instead of waiting for the animals to die a natural death, cutting aspartame's effect short. CMCRC researchers explain, "Had we stopped the experiments at 110 weeks of age, we would most likely never have demonstrated the carcinogenicity of important industrial compounds such as xylenes, mancozab, vinyl acetate monomer, and toluene."

Aspartame is used in over 6,000 products, including soft drinks, powdered drinks, hot chocolate, chewing gum, candy, desserts, yogurt, and some pharmaceutical products, such as vitamins and sugar-free cough drops. One packet of Equal® contains 33 mg of aspartame; one can of Diet Coke® (355 ml) contains 131 mg of aspartame; and one-half cup of Jello-Light® contains 40 mg of aspartame, according to the Canadian Diabetes Association. A 44 pound (20 kg) child would have to consume 400 mg, about the equivalent of three Diet cokes per day, to reach the carcinogenic 20 mg/kg bodyweight dose.

Canadian Diabetes Association. Sugar Substitute Content. Available at: Accessed May 22, 2006.

Soffritti M, Belpoggi F, Esposti DD, Lambertini L, et al. First experimental demonstration of the multipotential carcinogenic effects of aspartame administered in the feed to sprague-dawley rats.
Environmental Health Perspectives. March 2006; 114(3). Available at: Accessed May 15, 2006.

Aneuploidy-Cancer Theory
In January 2004, 70 cancer researchers met in Oakland to discuss clinical and experimental evidence for the aneuploidy-cancer theory. Unlike the oncogene/tumor suppression gene hypothesis that has dominated research for over 20 years, the aneuploidy theory focuses on the gain or loss of chromosomes or chromosome segments (and the genes they carry). This change in chromosome distribution (aneuploidy) results from exposure to carcinogens or arises spontaneously. It is not inherited. Carcinogens such as asbestos, tobacco smoke, benzene, etc. do not damage genes, but they do cause aneuploidy.

Most cells with abnormal chromosomes die, but some of these random chromosome combinations thrive. Surviving cells produce abnormal protein teams, responsible for repairing and synthesizing DNA. Without properly functioning repair teams, gene mutations result. The more severe the aneuploidy, the greater the genetic instability.
Aneuploidy may explain some of the puzzles that the genetic mutation theory cannot. In the mutant-gene theory of cancer, researchers propose that people inherit cancer genes and these mutant genes produce tumors. When researchers have introduced hypothetical cancer genes into a line of transgenic mice, "the individual cancer-risks of these mice are only marginally higher or even the same as that of controls," according to an article in
Cell Cycle (June 2004). In actuality, cells in most tumors display a startling diversity, and not all cells in the tumor have the same cancer-causing power. Muhammad Al-Hajj of the University of Michigan (Ann Arbor) and colleagues reported in April 2003 that just 100 human breast cancer cells with specific markings quickly produced cancer in mice without immune systems, yet thousands of cells taken from the same breast tumors (but lacking the markings) produced no cancer in the animals. Researchers have yet to identify a set of genetic mutations that reliably occurs in every case of a specific type of cancer, according to Scientific American (July 20, 2003).

However, researchers at the aneuploidy conference have found evidence that specific chromosome reassortments (missing or swapped chromosome segments) provide cancer cells with resistance to cancer drugs. Some doctors in European countries are using aneuploidy to determine treatment and prognosis. Evidence at the conference supports the view that, for the most part, malignancy is directly proportional to the degree of aneuploidy. Because aneuploidy is not inherited, cancer prevention may involve testing foods, drugs, and chemicals to identify substances that cause aneuploidy and removing the culprits from the environment.

A booklet of abstracts and shorts papers written by the participants of 1st Conference on Aneuploidy and Cancer: Clinical and Experimental Aspects (January 23-26, 2004) is available at
The Scientist published an independent meeting report in its March 15, 2004 issue.

Duesberg P, Li R, Rasnick D. Aneuploidy approaching a perfect score in predicting and preventing cancer – highlights from a conference held in Oakland in January 2004.
Cell Cycle. 3:6, 823-828; June 2004. Available at: Accessed May 14, 2006.

Gibbs WW. Roots of Cancer.
Scientific American (July 2003) Available at Accessed May 14, 2006.

Mercola J, Duesberg P. What if everything we thought we knew about cancer was wrong? April 21, 2001. Available at: Accessed May 15, 2006.

Melanoma & Electromagnetic Waves
The rising incidence of melanoma in Sweden and some other countries has a stronger association with FM radio broadcasting at full-body resonant frequencies than with Ultraviolet (UV) radiation from sun exposure, according to Swedish researchers Örjan Hallberg and Olle Johansson. Melanoma is the fastest rising cancer in Sweden. In their 2004 study, the researchers looked at Swedish statistics for charter traveling to sunny vacation areas as well as at melanoma death rates, beginning in the 1950s. Melanoma deaths jumped sharply in 1955, the same year that FM broadcasting to the Swedish population began. Travel to sunny vacation areas did not become popular until about seven years later. After that initial spike in melanoma mortalities in 1955, the number of deaths slowed while the number of people diagnosed with melanoma gradually increased. FM broadcasting reached most of Sweden during the 1970s. The incidence of new cases began to level out around 1980. Hallberg and Johansson hypothesize that FM broadcasting at the 100 MHz frequency range may interfere with cell repair mechanisms. They suggest that the sharp increase in deaths among melanoma patients in 1955, when FM broadcasting was introduced to Sweden, was due to patients' abrupt exposure to frequencies that inhibit cellular repair.

No animal studies have investigated low-level resonant electromagnetic field (EMF) exposure and skin cancer, according to the authors. Several studies, however, have found a link between electromagnetic fields and cellular changes. A 1994 study by T. Haider, et al. reported, "Radiofrequency radiation in the immediate vicinity of broadcasting antennae yields moderate but statistically significant clastrogenicity [disintegration/breaking of chromosomes]" [
Mutation Research Letters. 1994;324: 65-68]. A 1996 study by Z. Balode found that cows pastured near radio transmitters had 0.6 micronuclei/1000 erythrocytes (red blood cells) compared to 0.1/1000 cells in cows, acting as controls who were pastured farther away [Sci Total Environ. 1996; 189: 81-85]. A 2001 study by P. Boscolo, et al. reported that high-frequency electromagnetic fields from radio/television towers affected immune response by reducing "cytotoxic activity in the peripheral blood of women without a dose-response effect" [Sci Total Environ. 2001; 273: 1-10].

Hallberg O, Johansson O. Malignant melanoma of the skin – not a sunshine story!
Med Sci Monit. 2004; 10(7): CR336-340.

Heat Treatments for Cancer
Researchers are experimenting with various ways to use heat, created by radio frequency waves, to destroy tumors. Some oncologists use radio-frequency ablation, involving surgical implantation of probes into cancerous tissue that are then heated with radio waves. Researchers are also using hyperthermia (heat therapy) to deliver chemotherapy more effectively. Heat opens channels on the cell surface so that chemotherapy drugs can enter more easily. Duke University researchers have developed tiny bubbles of water mixed with doxorubicin (a chemo drug), encapsulated with fat. These liposomes remain stable at body temperature but burst open when heated with radio waves. The technique allows doctors to direct more chemotherapy to cancer sites.

Treating cancerous tissue with radio waves also makes radiation therapy more effective. Radiation requires oxygen to destroy cancer cell DNA. Heat brings more blood to poorly oxygenated cancerous areas. The combination of radio waves with chemotherapy or radiation has improved local control of melanoma and cancers of the esophagus, cervix, neck, brain, and breast cancers that have spread to the chest wall in several studies.

John Kanzius began experimenting with yet another way to use radio waves to heat and kill cancer cells while he was undergoing treatment for lymphoma. In May 2004, he filed a patent for a technique that involves injecting patients with a substance that would accumulate in tumors, providing a target for heat generated by radio waves. His technique is being investigated by Dr. Steven A. Curley and colleagues at M.D. Anderson Cancer Center (Houston, Texas). Curley believes that carbon nanoparticles can be charged and then drawn to key areas of a tumor with the help of magnets. His team is testing the technique on animals.

Using nanoparticles may have unexpected side effects. Eva Oberdorster at Duke University discovered that fullerness, a "highly praised nanoparticle" consisting of 60 carbon atoms, caused oxidative damage in brains of fish living in a tank of water to which a solution of fullerness had been added. These particles bypassed the protective blood-brain barrier by traveling up nerve cells into the brain, according to a Project Censored report. Another study, led by Anna A. Shevedova at the National Institute of Safety and Health, showed that "carbon nanotubes generated dangerous free radicals in cultures of human skin cells…[causing]oxidative damage that triggered the deaths of cells" (Project Censored). It will be interesting to see how the use of radio waves and nanoparticles plays out.

Foreman J. Wielding heat as a weapon.
Los Angeles Times. March 20, 2006. Available at:,15969616.column?coll=la-headlines-health. Accessed May 15, 2006. (8/16/06: Link is no longer viable. Abstract of story is available in its archives. Full story is available for a fee.)

Monastersky R. The dark side of small. September 10, 2004. Available at: Accessed on May15, 2006.

Panepento P. Sparks of genius.
Reader's Digest. May 2006;132-138.

Lantus Cancer Risk?
Concerns have been raised that long-term use of Lantus, a genetically-engineered insulin, may cause cancer. The FDA approved Lantus, made by Aventis S. A., in 2000. Drug manufacturers are promoting Lantus and similar analogues as replacements for animal-based insulin and human insulin. Ernst Chantelau, MD, a professor at Diabetesambulanz MNR-Klinik in Dusseldorf, Germany, and other doctors are concerned about a study headed by Peter Kurtzhals, published in Diabetes, June 2000. This study found Lantus to be highly mitogenic during in vitro testing with human osteosarcoma cells. Chantelau wants these findings to be explored further.

The study headed by Peter Kurtzhals looked at several analogues of human insulin. The researchers compared the analogues' IGF-1 receptor binding properties, metabolic potencies, and ability to stimulate growth in cultured human cancer cells. The Danish researchers reported that Lantus, unlike the other analogues, showed "a six to eightfold increased IGF-1 [insulin-like growth factor 1] receptor affinity and mitogenic potency compared with human insulin." Other research studies have shown links between circulating IGF-1 levels and increased risk of colorectal cancer and of breast cancer among premenopausal women.

Although this in vitro cell study indicates that Lantus is more attracted to IGF-1 receptor sites than human insulin is, the manufacturer does not believe that it actually increases cancer risk in humans. Aventis S.A. says, "The extensive preclinical safety data and clinical post-marketing data collected by Sanofi-Aventis indicate there is no carcinogenic safety risk with the use of Lantus."

Kurtzhals P, Schaffer L, Sorensen A, et al. Correlations of receptor binding and metabolic and mitogenic potencies of insulin analogs designed for clinical use (Abstract).
Diabetes. 2000 Jun;49(6):999-1005. Available at: Accessed on May 30, 2006. (Once on that page, search for "Kurtzhals correlations receptor binding" without the quotation marks.)

Trecroci D. And then there were some.
Diabetes Health. February 2006. Available at:,1048,4504,1.html. Accessed on May 22, 2006.

Trecroci D. Can insulin cause cancer?.
Diabetes Health. February 2006. Available at:,1048,4508.html. Accessed on May 22, 2006.

Medicaid Troubles
In February 2006, the US Congress passed a Medicaid reform bill that addresses some concerns expressed by states' governors. States are responsible for growing shares of the health insurance program's costs. The bill lets state governments increase the amount that Medicaid patients pay for prescription drug and hospital visits. It also changes the formula used to calculate the baseline price that states pay for drugs given to Medicaid patients and requires drug manufacturers to provide states with more information about the prices they charge. In addition, the bill lets states apply a penalty period to seniors who have given away their assets within five years before asking Medicaid to cover their nursing home costs. About two-thirds of nursing home patients are on Medicaid. Overall, the program covers more than 53 million poor Americans.

Even with these reforms, states' Medicaid costs will continue to rise. State Medicaid officials blame increasing health care costs, enrollment growth, and prescription drug costs for the ongoing increases, according to the Kaiser Foundation. As costs rise and federal support decreases, some states (required by their state constitutions to maintain a balanced budget) have restricted Medicaid eligibly and required participants to make higher co-payments. Missouri, for example, lowered its Medicaid eligibility threshold from 75% to 22% of the federal poverty level in 2005, according to
The Wall Street Journal. Before this cut, a family of three needed to make less than $12, 067 per year to qualify. Now, the same family must earn less than $3,505 a year. Missouri may be an extreme case. A July-August 2005 survey by the Kaiser Commission on Medicaid and the Uninsured and the Center on Budget and Policy Priorities found signs that "states are coming out of their fiscal crisis." As of July 2005, children in most states are eligible for Medicaid even if their family income is twice the federal poverty level, according to Kaiser Family Foundation.

In addition to restricting eligibility, states are simplifying procedures as a means of cutting Medicaid costs. Some are saving by outsourcing claims processing and other administrative services to private companies. Other states are searching for more innovative ways to cut costs. Florida, for example, has set up a plan in which Medicaid recipients get a fixed amount of money for health care through a managed care organization.

The Missouri Legislature voted to end Medicaid in 2008 and is actively seeking alternatives. Some possibilities include encouraging small businesses to offer health insurance via tax credits and incentives to encourage people to buy nursing home insurance. These measures do little to help those with the least income. Forty percent of the nation's Medicaid costs support elderly or disabled persons, who are also eligible for Medicare. Medicare covers basic physical and hospital care. Medicaid pays for Medicare premiums, long-term care, and other benefits not covered by Medicare. These dual-eligible recipients live on less than $10,000 per year and tend to have the poorest health.

Kaiser Commission on Medicaid and the Uninsured. Summary of Findings. Available at: Accessed on April 12, 2006

Kaiser Commission on Medicaid Facts. Dual Eligibles: Medicaid's Role for Low-Income Medicare Beneficiaries. February 2006. Available at: Accessed April12, 2006

Solomon D. Wrestling with medicaid cuts.
The Wall Street Journal. February 16, 2006; A4.

Vock DC. Medicaid cuts, welfare reform target poor. February 2, 2006. Available at Accessed on March 1, 2006
(8/16/06: Link no longer viable. Access story here.)

Trace Metals & Prostate Tumors
Turkish researchers measured trace metal concentrations in 11 cancerous and six benign prostate samples. Unexpectedly, the malignant samples contained higher levels of beneficial metals – iron, copper, zinc, magnesium, and calcium – than the benign samples did. While iron and copper are essential for health, high concentrations cause oxidative DNA damage, which may lead to cancer. (Iron deficiency also promotes oxidative DNA damage.) The study's authors found the higher levels of zinc in the malignant samples puzzling. Zinc deficiency has been viewed as a cancer risk factor, and the prostate gland normally contains higher levels of zinc than other organs in the body, according to literature data. The authors suggest that the difference may be due to the part of the prostate sampled (Zn is higher in the lateral lobe than anterior lobe) and/or measurement differences (wet tissue vs. dry weight basis). Although the authors have no comment about the higher magnesium content of the malignant samples, they were intrigued by the distribution of calcium. Calcium levels in the malignant samples were two times higher than calcium levels found in the benign ones. The authors suggest that functional disturbances in the malignant cells may be preventing calcium from leaving the cell. They believe that investigation of this phenomenon may provide further understanding of how cancer cells work.

Yaman M, Atici D, Bakirdere S, Akdeniz I. Comparison of trace metal concentrations in malign and benign human prostate.
J. Med. Chem. 2005; 48:630-634.

Oleic Acid & Breast Cancer
Oleic acid, a monounsaturated fatty acid found in olive oil, suppresses Her-2/neu over-expression, according to an Annals of Oncology article. At least one-fifth of breast cancer cases display over-expression by the oncogene Her-2/neu (also known as erbB-2). Her-2/neu over-expression is linked to highly aggressive tumors and is the target of trastuzumab (Herceptin™) immunotherapy.

Studies of women living in the Mediterranean have indicated a link between olive oil and reduced breast cancer risk, but researchers debated whether the effect was due to oleic acid or to other components. Using breast cancer cell lines BT-474 and SKBr-3 (lines that exhibit Her-2/neu over-expression), J. A. Menendez and colleagues found that oleic acid reduces the oncogene's expression up to 46%. It also increases trastuzumab's effectiveness. The authors state, "This previously unrecognized property of [oleic acid] offers a novel molecular mechanism by which individual fatty acids may regulate the malignant behavior of breast cancer cells and therefore be helpful in the design of future epidemiological study and, eventually, dietary counseling."

How Olive Oil Fights Breast Cancer. January 10, 2005. Available at: Accessed October 5, 2005.
(8/16/06: Link no longer viable.)

Menendez JA, Vellon L, Colomer R, et al. Oleic acid, the main monounsaturated fatty acid of olive oil, suppresses Her-2/neu (erbB-2) expression and synergistically enhances the growth inhibitory effects of trastuzumab (Herceptin™) in breast cancer cells with Her-2/neu oncogene amplification (Abstract).
Annals of Oncology 2005 16(3):359-371; doi:10.1093/annonc/mdi090. Available at Accessed May 15, 2006. (8/16/06: Use this direct link to full text article.)


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