Brain tumors and conventional medicine
The National Cancer Institute (NCI) and the American Cancer Society (ACS) estimate that 22,020 primary malignant brain tumors will be diagnosed in 2010 (Porter KR et al 2010). The American Brain Tumor Association, since they count both malignant and benign brain tumors, predicts twice as many cases (Jemel A et al 2008). Secondary brain tumors, which originate elsewhere in the body, outnumber primary tumors four-to-one, so add another 100,000 cases a year to get an idea of the total number of people who will be diagnosed with brain cancer each year (Davis FG et al 2001).
The medical treatment of primary brain tumors typically consists of two steps: surgical excision followed by combined radiation and chemotherapy. For advanced or high-grade tumors, the benefit of these therapies seems small. “After conventional treatments, the survival rate for patients with astrocytomas or glioblastomas is about 50% at 1 year, 25% at 2 years, and 10 to 15% at 5 years” (Online Merck Manual, accessed Oct, 2010). Thus, many patients wisely seek complementary therapies hoping to improve their odds.
The risk factors for brain tumor are almost unknown, though there are hints that suggest early exposure to certain chemicals might play a role.
In 2010, the Fred Hutchinson Cancer Research Center in Seattle reported that children who develop brain tumors are likely both to have been exposed to higher than average amounts of pesticides and to have been born with a reduced ability to detoxify these chemicals (Barrett JR 2010, Nielsen SS et al 2010).
Other studies also point to chemical exposure as a potential risk factor. The children of women who had high exposure to beauty-products are at increased risk for brain tumors (Efird JT et al 2005). Personal hair dye use increased risk in one study. Using brown hair dye for 20 years, for example, almost quadrupled risk of glioma in women (Bluhm EC et al 2007). Individuals who engage in a hobby that involves using glue are at 18 times the average risk (Spinelli V et al 2010).
A 2009 review found that people who used cell phones for at least 10 years had a 2.4-fold greater risk of developing an acoustic neuroma in the ear to which they routinely held their phone, but had no change in risk for other types of cancer (Han YY et al 2009).
The idea that nitrosamines in processed meats may increase the risk of glioma has been circulating for several decades (Michaud DS et al 2009), yet a July 2010 paper found only a modest increase in risk in people who ate large amounts of nitrosamines compared to those who ate very little (Dubrow R et al 2010).
There are no tests to predict risk of brain cancer, or steps we can take to prevent it. Our focus is on preventing recurrence, or at least slowing down the disease.
Brain Tumor Nutritional Protocol
Hormones and Brain Tumors
Vitamin D: Vitamin D deficiency that occurred before birth may have set the stage for brain tumor formation later in life. Vitamin D deficiency during gestation causes long-term effects on brain development (Levenson CW et al 2008).
Vitamin D remains important after birth, as it activates chemical pathways, in particular the sphingomyelin pathway, which kills glioblastoma cells (Magrassi L et al 1998). Vitamin D3, the chemical form of vitamin D made in the skin and sold as a nutritional supplement, calcitriol (1,25-dihydroxy vitamin D), the active form of vitamin D, and various chemical analogs and metabolites of vitamin D, have all been shown to inhibit growth and trigger apoptosis in neuroblastoma and glioma cells (Naveilhan P et al 1994, Baudet C et al 1996, Elias J et al 2003, van Ginkel PR et al 2007).
A 2009 report on brain tumor death statistics from Finland alludes to the benefit of vitamin D. Mortality from brain tumors is highest in patients who were diagnosed and underwent surgery during the late winter, particularly from February to March. This is the time of year when vitamin D levels are at their lowest (Hakko H et al 2009). Similar seasonal variations in cancer survival rates are seen for lung (Porojnicu AC et al 2007), breast (Stajner I et al 2010), and colon cancer (Robinson D 2010). The explanation tendered in all these studies is that in the winter people have lower vitamin D levels and are less capable of fighting the cancer.
Another data analysis from Spain revealed a direct correlation between latitude and brain cancer incidence. The higher the latitude, that is the further from the equator someone lives, the greater their risk for brain cancer (Grant WB et al 2007). The further people live from the equator, the lower their vitamin D levels (Genuis SJ et al 2009).
Melatonin: Melatonin is often suggested for treating various forms of cancer, particularly breast, lung and colorectal cancers. Lissoni has conducted repeated studies demonstrating that patients with advanced cancers given melatonin survive longer than patients receiving a placebo (Lissoni P et al 2007).
There is growing evidence suggesting melatonin may be useful in treating primary brain tumors. An in vitro experiment showed that melatonin, at physiologic concentrations, inhibits growth of neuroblastoma cells (Cos S et al 1996). A 2006 paper published in Cancer Research reported that melatonin stopped the growth of gliomas that had been implanted into rats (Martín V et al 2006). As a result, some researchers suggest melatonin might be useful in treating glioma (Wion D et al 2006).
The strongest evidence for the use of melatonin in brain cancer is in treating pituitary tumors. Melatonin given to rats inhibits the chemical-induced formation of pituitary tumors (Gao L 2001). Giving melatonin to rats with pituitary tumors halts tumor growth and triggers apoptosis, especially if the tumor secretes prolactin (Yang QH et al 2006).
Vitamins and Minerals
Folic Acid and 5-MTHF: To be of use in the body, natural folate from food and folic acid from supplements must be converted into the active form, 5-MTHF (5-methyltetrahydrofolate), by the enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR). In certain people the gene that codes for this enzyme produces a less effective enzyme. In some studies, the risk for glioma in these people is increased by about 23% while meningioma risk is more than doubled (Sirachainan N et al 2008, Bethke L et al 2008, Kafadar AM et al 2006).
People can compensate for this genetic problem by taking a supplement of active 5-MTHF and bypassing the need for the MTHFR enzyme.
A German study compared survival times of patients with glioblastoma multiforme with their MTHFR gene variants. Those patients who were best able to convert folate into its active form survived for about 13 months. Those with the less effective MTHFR genes survived for only seven months (Linnebank M et al 2008). This suggests that supplementing with the active form of folate might be helpful.
Selenium: Selenium is another antioxidant that patients with brain tumors should consider. Many oncologists fear that any nutritional supplement classified as an antioxidant will interfere with the ability of radiation or chemotherapy to kill cancer cells. Though this theory sounds logical, there is little published evidence to support it.
In the case of selenium, a 2004 paper in the journal Anticancer Research, reports a “radiosensitizing effect” on glioma cells (Schueller P et al 2004). Exposing brain cancer cells to selenium makes them more sensitive to, and more likely to die after, radiation therapy.
Selenium also inhibits growth and invasion, and induces apoptosis in various types of brain tumor cells, including malignant cell lines (Sundaram N et al 2000, Rooprai HK et al 2007).
Vitamin E: Vitamin E is another antioxidant of particular interest in connection with brain cancer. According to a 2005 study, alpha-tocopherol-succinate enhances chemotherapy treatment of drug resistant glioblastoma cells, increasing effectiveness (Kang YH et al 2005).
A researcher from Tufts University described the use of vitamin E in treating glioblastoma multiforme in a 2004 article in the Journal of Nutrition. “Glioblastoma multiforme is the most common and aggressive brain cancer in humans and resists all forms of therapy. Vitamin E (succinate) induces apoptosis in glioblastoma cells in a dose-related manner; we find that a 48-h exposure to 50 micromol/L vitamin E results in a 15% increase in apoptosis in the glioblastoma cells over control. Pretreatment with vitamin E may have a potential role in sensitizing glioblastoma to radiotherapy” (Borek C 2004).