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Whittling Words:

Jacob Schor ND, FABNO

September 27, 2010

I’ve been working on a long article, a survey of supplements that might be useful in treating brain tumors, that hopefully will get published. My first drafts were far too long and I’ve been slowly chopping away at it, whittling away sentence by sentence. Before it becomes a toothpick of the original, and incomprehensible, I thought I would post it online.

 

Brain Tumor Protocol

Introduction

Brain tumors are classified in several different ways. The simplest division is between primary or secondary tumors. Primary brain tumors originate in the brain while secondary tumors originate elsewhere in the body and metastasize to the brain.

Another division is between benign and malignant. Slow growing cancers are classified as benign; fast growing as malignant. Benign tumors still take up space, compressing the brain, causing symptoms that can still prove fatal.

The classification system used by doctors and oncologists is more complex. In it brain tumors are classified by the tissue or cell type from which they have originated or by their location. According to the National Brain Tumor Society, there are 120 different types of brain cancer.

The nervous system is made up of two types of cells, the neurons, which send and receive nerve impulses, and ‘glial cells’ that surround the neurons, supporting them and providing nourishment.

Brain tumors that originate from glial cells are called gliomas. Gliomas account for about one third of all primary brain and nervous system tumors. Gliomas are further subdivided by the type of cell they originated from. The most common gliomas come from astrocyte cells so are called an astrocytomas; they are the most common type of primary brain tumors. The highest grade or fastest growing, astrocytomas are called glioblastomas.

How common are brain tumors?

The number of brain cancers diagnosed in the United States each year seems to vary with whom you ask. The National Cancer Institute (NCI) and the American Cancer Society (ACS) reports there are 22,020 brain tumors diagnosed in the United States each year; they are only reporting cases of primary malignant tumors The American Brain Tumor Association gives a number more than twice as high, reporting 52,000 new brain tumors a year because they count both malignant and benign tumors. There are about four times as many secondary tumors as primary tumors, so actually an additional 100,000 more brain tumors should be added to these other counts. There’s another way to look at these statistics.

During 2000, about 359,000 people were alive in the United States who had at some point been diagnosed with a primary brain tumor; about 81,000 of them with a malignant tumor, about 267,000 persons with a benign tumor, and another 10,000 with undefined tumor type s. So about 75% have benign tumors, 23% have malignant tumors, and 2% with mystery tumor types.

The Bad Numbers:
There has been a slight improvement in brain tumor survival in recent years. Five year survival rates for malignant brain tumors in the 1970’s were 21%, in the 1980’s 27%, and in the 1990’s 31%. Ten year survival for all types of brain cancer is still below 50%; for the more aggressive types of brain cancer such as glioblastoma multiforme, the numbers are far worse. Those with these types of cancer survive an average of 12 months. The rare 3-5% who survive three years are called, ‘long term survivors.’ These numbers are with treatment.

It is reasonable for people diagnosed with brain tumors, especially the more malignant higher-grade cancers to do everything they can to fight the cancer, both the therapies advised by their medical oncologist along with complementary and nutritional therapies of the sort as will be outlined in this document.

 

What Causes Brain Tumors?
It is unclear what causes most brain tumors. In rare instances, specific causes like hereditary, radiation or immune-suppression are to blame, but these instances account for only a small percentage of the total. Without a clear understanding of etiology, we nevertheless try to make sense of a hodgepodge of data.

There is some indication that something very early in life contributes to these cancers. First, brain cancer is relatively common in children. Second, risk of getting brain cancer varies by the month, in which someone is born. People born in the late fall to early spring are at higher risk of getting glioma; those born in October are at highest risk of getting meduloblastoma.

The explanation put forward to explain this is that vitamin D is protective against cancer and so gestational deficiency may increase risk. Other plausible explanations are possible. In some studies, risk for brain tumors increases if either the pregnant mother or infant was in contact with farm animals. Early exposure to animals lowers risk for allergies. Having allergies or autoimmune disease decreases risk for gliomas by about half. A late spring or summer birth may trigger allergies in the infant and confer protection.

Being left handed changes risk. A 2003 paper reported that, “Persons who described themselves as left-handed or ambidextrous appeared to be at reduced risk of glioma relative to those who described themselves as right-handed.” Their risk of brain tumors was about 30% lower. Unless of course they are left handed and born in October, in which case, risk for glioma is higher than if they were right handed.

Being left or right handed is a trait one is born with and so assumed to be determined while still in the womb, regulated by gestational exposures, perhaps to hormones.

Much attention has been devoted to seeking links between environmental chemicals and brain tumor risk. Research conducted by the Fred Hutchinson Cancer Research Center in Seattle tells us that children who develop brain tumors are likely to have both been exposed to higher than average pesticide levels and also been born with reduced abilities to detoxify these chemicals.

Children born of women who had high exposure to beauty-products are at increased risk for brain tumors. Personal hair dye use increases risk, but in the user. In one study, using brown hair dye for 20 years almost quadrupled risk of glioma in women. Other studies have not produced consistent results.

A February 2010 German report found no correlation between brain cancer risk and occupation, suggesting that disease development was not solely chemical exposure.

Cell Phones, EMFs, Hobbies and Hot Dogs:

Whether cell phone use causes brain cancer is controversial and too large a subject to review adequately in this article. Suffice to say that a 2009 meta-analysis 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 they routinely held their phone to but had no change in risk for other types of cancer.

EMFs etc.
It has been theorized that electromagnetic fields (EMFs) cause an alteration in cellular reactive oxygen levels. This might, “… play a causal role in cancer development.” Though a recurring worry, to date, no strong evidence has actually linked EMFs with brain cancer. Curiously, a February 2010 study tells us that living near a cell phone tower actually lowers risk of brain tumors by about half.

Individuals who engage in a hobby that involves using glue appear to be in serious trouble; their risk of brain tumors is almost 18 times normal.

Nitrosamines found in processed meats have long been suspected of increasing brain cancer risk but recent research isn’t telling us that it is a significant worry. A July 2010 paper found only a modest increase in risk, about 59% in people who ate large amounts of nitrosamines compared to those who ate very little. Interestingly, the same study found that high fruit and vegetable intake caused a 42% increase in risk. The authors concluded that processed meat didn’t increase risk and vegetables and fruit didn’t decrease risk. A 2009 study also found no increased glioma risk among people who ate large amounts of processed meat.

Socio-demographics plays a confusing role in brain tumor risk. Higher household income increased risk for low-grade glioma, meningioma, and acoustic neuroma, but not for high-grade glioma. Higher levels of education also increased risk for low-grade glioma and acoustic neuroma, but not for high-grade glioma or meningioma. Being Jewish increases risk for meningioma by 4 times.

This information taken together, though somewhat confusing, suggests that if we want to lower rates of brain tumors, our efforts should focus on reducing chemical exposure during pregnancy, keeping pregnant women and young children away from farm animals and most important, avoiding glue fumes.

Knowledge of these risk factors is perhaps of intellectual interest but it does not offer any clear suggestions for effective treatment once someone has a brain tumor. We can’t change our birthdays, make ourselves allergic or which hand we write with. We can’t reverse the damage caused by glue fumes.

 

 

Brain Tumor Nutritional Protocol:

A Disclaimer:
The brevity of this review prevents adequate detail for it to serve as a guide for self-treatment; it is written to give examples of potential therapies to consider. Seek out a practitioner experienced in therapies such as these. Do not self-treat brain cancer.

These protocol examples are not meant to replace the standard medical therapies, but rather to complement them. Brevity also forces this list to omit many therapies worthy of consideration.

Readers should understand that scientific research is ongoing and opinions based on today’s knowledge may shift with the publication of new studies. Readers should seek consul from practitioners who strive to stay current with these shifts in understanding.

Hormones:

Vitamin D:
There is more research supporting the anti-cancer effect of vitamin D than any other nutrient. The path to brain cancer may start in the womb. Couple that with the fact that vitamin D deficiency during gestation causes long-term effects on brain development. Vitamin D deficiency, which occurred before birth, may have set the stage for brain tumor formation.

Vitamin D remains important after birth as it activates chemical pathways that kill glioblastoma cells. Both vitamin D-3, the chemical form of vitamin D made in the skin and sold as nutritional supplements, calcitriol, 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. Apoptosis is cellular suicide. Apoptosis is how the body prunes away cancer cells.

A 2009 paper on brain tumor death statistics from Finland hints 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. Similar seasonal variations in cancer survival rates are seen for lung, breast and colon cancer. The explanation tendered in all these studies is that low winter vitamin D levels lowers the chance of survival.

Analysis of data from Spain found a direct correlation between latitude and brain cancer incidence. The higher the latitude, that is further from the equator and less ultraviolet light exposure, the lower the vitamin D and the greater the risk for brain cancer.

Not all studies support this idea. A 2006 study done in the United States, although it found an inverse relationship between ultraviolet exposure and other cancers, did not find a correlation with brain cancer.

We supplement vitamin D to raise our patients’ serum 25(OH)D-3 levels above midrange normal, > 65 ng/ml.

Melatonin:
Melatonin might be considered complementary to vitamin D. Where D is the ‘sun hormone,’ melatonin is the ‘night hormone.’ The pituitary gland in the brain secretes melatonin when the lights go out. Melatonin is often suggested for treating cancer, particularly breast, lung and colorectal cancers. Lissoni has repeatedly published studies demonstrating that patients with advanced cancers given melatonin survive longer.

Some practitioners consider using high dose melatonin with brain tumors as well. The research is mixed. In a 2007 clinical trial melatonin did not help patients with secondary brain tumors, which had metastasized from elsewhere in the body, who were also treated with radiation. There is evidence suggesting melatonin may be useful for primary brain tumors. An in vitro experiment showed that melatonin, when given at physiologic concentrations, inhibits growth of neuroblastoma cells. Melatonin was also shown to stop the growth of gliomas that had been implanted into rats. As a result some researchers suggest melatonin might be useful in treating glioma.

Melatonin is made in the pituitary gland and the strongest evidence for use in brain cancer is in treating pituitary tumors. Melatonin given to rats inhibits the formation of pituitary tumors when chemicals are administered known to trigger tumor formation. Treating rats with pituitary tumors with melatonin halts tumor growth and triggers apoptosis especially if the tumor secretes prolactin. Cancer or radiation treatment can damage the pituitary gland and disrupt sleep. Melatonin may help maintain a normal circadian rhythm.

Vitamins and Minerals:

MTHFR:
One known risk factor that may offer a possible treatment option involves folic acid. To be of use in the body, folate from food must be converted into its active form by the enzyne 5,10-methylenetetrahydrofolate reductase (MTHFR). In certain people the gene that codes for this enzyme produces a less effective enzyme. In some, but not all studies, the risk for glioma in these people is increased by about 23% while meningioma risk is more than doubled.

People can compensate for this genetic problem by taking a supplement of active 5-methyl folate and bypassing the need for the MTHFR enzyme. The role of folate in cancer treatment though is still uncertain. For some cancers, folate actually increases the risk while MTHFR mutations lower risk. An example is acute lymphoblastic leukemia. Less effective variations of the MTHFR gene may also protect against colon cancer. We cannot make generalizations if these mutations are good or bad for cancer.

A German paper from 2008, compared survival times for patients with glioblastoma multiforme with their MTHFR gene variants. Those patients who were best able to convert folate into its active form survived about 13 months. Those with the less effective MTHFR genes survived only seven months. This suggests that supplementing with the active forms of folate might be helpful, but this is a single paper and far from conclusive.

Selenium is a supplement that patients with brain tumors should be taking. Selenium inhibits growth and invasion and induces apoptosis in various types of brain tumor cells.

Though many radiation oncologists will [have a cow over] advise against this suggestion, patients with brain tumors should take selenium during radiation treatment. Many oncologists fear that any nutritional supplement classified as an antioxidant will interfere, stopping radiation therapy from killing cancer cells. This theory sounds logical, but there is little published evidence to support it. Our preference is to consider each supplement on a case-by-case basis, examining whether research supports potential benefit.

In the case of selenium, a 2004 paper in the journal Anticancer Research, reports a,“radiosensitizing effect” on glioma cells. Exposing brain cancer cells to selenium makes them more sensitive to and more likely to die after being treated with radiation therapy.

There are a number of different forms of selenium on the market. Some appear to have stronger or weaker anticancer effect varying with tumor type. It will be important over the coming years to follow the research closely in order to decide which form of selenium offers the most benefit.

 

Vitamin E is the supplement we hear oncologists objecting to patients using the most often because it is an antioxidant. Yet there is no evidence that it interferes with radiation therapy. There is decent evidence that it will help. We use the succinate form of vitamin E, alpha-tocopherol-succinate, with cancer. This form of vitamin E enhances chemotherapy treatment of drug resistant glioblastoma cells, increasing effectiveness. In other types of cancer vitamin E succinate makes the cancer cells more sensitive to radiation treatment. The same may apply to glioblastoma. Vitamin E succinate triggers reactive oxygen species (ROS) generation in glioblastoma cells.

In 2004, Carmia Borek of Tufts University described the use of vitamin E in treating glioblastoma multiforme 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.”

 

 

Botanical or Herbal Extracts:

Berberine: Berberine is a yellow colored alkaloid common in herbal medicine. It is found in several medicinal herbs; the most popular is Golden seal (Hydrastis Canadensis), but also in Oregon grape (Berberis aquifolium)
and Chinese Isatis (Isatis tinctoria). Berberine should be considered for all brain tumors.

Berberine increases the benefit of chemotherapy. In one study testing both various glioma cell cultures and also rodents implanted with tumors, the tumor killing effect of berberine was compared to the chemotherapy drug BCNU (Carmustine) and to a combination of berberine and BCNU. Berberine used alone produced a 91% kill rate in cell cultures, compared to 43% for BCNU. Combining berberine with BCNU yielded a kill rate of 97%.

Berberine increases the benefit of radiation treatment, making glioblastoma cells more sensitive to radiation damage without effecting healthy brain cells. [A similar effect is seen in lung cancer; berberine sensitizes lung tumor cells to radiation. ]

Berberine inhibits growth and expansion of cancer. It inhibits nasopharyngeal carcinoma, decreasing motility. Berberine inhibits gene expression and enzyme activity necessary for gliolbastoma and astrocytoma growth.

Berberine enhances laser effects: A1994 paper described in vitro experiments using berberine alone or in combination with laser treatments on glioma cells: the combination was especially effective suggesting, “…the possibility of berberine as a photosensitive agent.”

Mechanisms of action: A description of action was published in 2007, suggesting berberine acts, “… through several ways such as regulating apoptotic gene expression, …And Ber[berine] still could inhibit tumor metastasis through suppressing the formation of tumor angiogenesis, blocking signal transduction pathway…” An April 2008 study, explained that berberine triggers apoptosis in glioblastoma cells through the mitochondrial/caspases pathway. As of 2009, Berberine kills glioma cells through several mechanisms. “cytotoxicity … is attributable to apoptosis mainly through induced G2/M-arrested cells, in an ER-dependent manner, via a mitochondria-dependent caspase pathway regulated by Bax and Bcl-2.” In 2010, explanations for action expanded to include inhibition of NF KappaB and reduction of a chemical called survivin.

Beyond brain tumors: several hundred published papers suggest that berberine is effective against a range of cancers. In the last few months, interesting papers have been published: Berberine prevents cell growth and induces apoptosis in breast cancer cells. Berberine is cytotoxic to cervical cancer cells. Berberine inhibits cell growth in pancreatic cancer cells by inducing DNA damage. And it triggers cellular suicide in tongue cancer.


[Berberine also protects against radiation induced intestinal injury in both mice but more importantly in human subjects. At the same time it enhances the anticancer effect of radiation therapy against liver cancer cells. ]

Doses: 300 mg several times a day are used.

Boswelia:
The resin from the Asian plant, Boswellia serrata, called frankincense, also has an important role in treating brain cancer. Boswellia is commonly used for treating inflammation. Frankincense is an nfKappaB inhibitor, it is neuroprotective, anti-inflammatory, and reduces anxiety: An important use is treatment of traumatic brain injuries: Boswellia “… inhibited hippocampal neurodegeneration and exerted a beneficial effect on functional outcome after CHI [closed head injury], indicated by reduced neurological severity scores and improved cognitive ability in an object recognition test.” Boswellia decreases the brain swelling from glioblastoma allowing a decrease in the use of prednisone and the resulting side effects. A 2006 paper reports that the resins, “of Boswellia serrata, are gaining more and more importance in the treatment of peritumoural oedema and chronic inflammatory diseases. They may be even considered as alternative drugs to corticosteroids in reducing cerebral peritumoural oedema. An important focus for drugs acting in the central nervous system is achieving a high extent of brain penetration” We like to use Boswellia for any patient taking steroids to decrease brain swelling.

Boswellia is also useful for treating secondary brain tumors. In 2007, Dana Flavin published a report in the Journal of Neuro-Oncology about using Boswellia to treat a patient with breast cancer metastasis to the brain.

Finding ways to replace steroids in the treatment of brain tumors is important. Steroids interfere with glioma cell apoptosis. According to a 2000 paper in Neuroscience, “Since glucocorticoids are often used in the treatment of gliomas to relieve cerebral oedema, the inhibition of apoptosis by these compounds could potentially interfere with the efficacy of chemotherapeutic drugs.” Steroids also block the cancer killing action of camptothecin, a chemotherapy drug used in treating glioma. While steroids may protect glioma cells, Boswellia kills glioblastoma cells in a dose dependent manner.

Curcumin:
If we were to make a list of desirable attributes or actions that we would want in a supplement for use in cancer treatment, then curcumin is close to ideal. Curcumin is safe; it is extracted from turmeric root (Curcuma longa) a plant that has been eaten without harm for thousands of years. Clinical trials tell us that curcumin can be taken in high doses without serious mishap. A significant body of research supports the use of curcumin against cancer. As of this writing, the National Institute of Health’s website, PubMed, lists 1335 published papers on curcumin in the peer reviewed scientific literature. A growing number focus on brain cancers.

Curcumin slows or inhibits tumor growth: It suppresses growth of glioblastoma.
Curcumin triggers apoptotic pathways that destroy glioblastoma cells. It turns off the signals in the cells that protect glioblastoma cells from apoptosis, allowing the suicide process to destroy the cancer cells. Curcumin has a similar action against other brain tumor types, including meduloblastoma cells and pituitary cancers. Curcumin inhibits pituitary cancer from forming. It also slows growth of pituitary tumors and inhibits production of excess pituitary hormones by tumors.

Curcumin’s mechanisms of action are complex. It doesn’t act via a single pathway but through multiple pathways, interferring with cancer growth and stimulating cancer destruction via apotosis. It also acts as an angiogenesis inhibitor

Curcumin crosses the blood brain barrier. Not all nutrients are able to do this. We know that it reaches the brain and the tumor cells.

Curcumin decreases Glial cell line-derived neurotrophic factor (GDNF) a chemical that promotes tumor migration and invasion.

Curcumin prevents development of chemoresistance. In other words, the chemotherapy drugs keep working; the cancer cells don’t become drug resistant.

Curcumin sensitizes brain tumor cells to both the chemotherapy agents used in treating these tumors and also to radiation therapy: “Curcumin sensitized glioma cells to several clinically utilized chemotherapeutic agents (cisplatin, etoposide, camptothecin, and doxorubicin) and radiation … These findings support a role for curcumin as an adjunct to traditional chemotherapy and radiation in the treatment of brain cancer.”

Curcumin is not well absorbed from the digestive tract. The old trick to improve absorption was to blend curcumin with fat, for example, coconut cream, peanut butter, fish oil or avocado, and then eat this mixture on an empty stomach. New curcumin products are manufactured with phosphatidyl serine and form small microscopic liposomal spheres that are far better absorbed.

 


“curcumin effectively blocks brain tumor formation and also eliminates brain tumor cells.”

Other plants:
There other plant extracts that we consider when treating brain cancer. Research supporting their use is weaker than with curcumin, berberine or Boswellia, yet we often still use green tea, quercetin, resveratrol and sulforaphane with brain cancers. The evidence supporting these substances with cancer in general is solid so we assume, in time, data supporting utilization in brain cancers will be published.

These supplements may work better when taken together; a number of studies report synergistic action when used in combination.

Quercetin is commonly used to treat allergies though in the last year or so several studies report it also useful in improving exercise performance by increasing cellular mitochondria. Quercetin enhances glioma cell death. While killing cancer cells, quercetin protects healthy brain cells.

Quercetin has a synergistic effect with resveratrol. Resveratrol also strongly inhibits brain tumor cells. Quercetin and resveratrol when taken together, stop the tumor cells from growing as if they were slowed by old age: “Most important, resveratrol and quercetin chronically administered presented a strong synergism in inducing senescence-like growth arrest. These results suggest that the combination of polyphenols can potentialize their antitumoral activity, thereby reducing the therapeutic concentration needed for glioma treatment.”

Green Tea: A 2006 study informed us that the EGCG in green tea reduces the radio-resistance of glioblastoma cells potentially increasing the benefit of the standard radiation and chemotherapy treatment of this cancer.

Sulforaphane is one of the active chemicals in cruciferous vegetables, especially broccoli, responsible for its anti-cancer action. Sulforaphane activates, “multiple molecular mechanisms for apoptosis in glioblastoma cells following treatment ...” Resveratrol and sulforaphane act synergistically against brain tumor cells. A 2010 article states that “… combination treatment with resveratrol and sulforaphane inhibits cell proliferation and migration, reduces cell viability, …. resveratrol and sulforaphane, may be a viable approach for the treatment of glioma.”

 

Homeopathy:
Although homeopathic remedies are typically selected based on a patient’s unique symptoms and presentation, it has become common to use a standard homeopathic protocol for brain tumors. This is inspired by a paper published in 2003 in the International Journal of Oncology written by researchers at MD Anderson. The paper recounted a series of experiments and clinical trials using homeopathic Ruta graveolens in combination with the cell salt, calcarea phosphorica. In particular the authors describe a small clinical trial in which, “…6 of the 7 glioma patients showed complete regression of tumors.” The Ruta is used in a 6c potency and the calc.-phos. in a 3x.

 

 

A Diet for Brain Cancer

There are two specific diets that should be considered for treating brain tumors either separately or in combination.

The Ketogenic Diet: has been the subject of several interesting papers over the last few years. This is a very high fat, high protein, and extremely low carbohydrate diet. When there are not enough carbohydrates to produce glucose, the preferred ‘food’ for cells, the body starts making and using ketones to feed the cells instead. This diet is typically used to treat epilepsy.

Healthy brain cells can metabolize either glucose or ketones. Brain tumor cells can only metabolize glucose. If the body shifts to a ketone metabolism, brain cancer cells go hungry.

A 2007 study tested this theory on mice with malignant brain tumors. Some of the mice were fed a high fat and protein drink designed to cause ketosis in children with epilepsy and some of the mice were allowed to eat all they wanted of a standard high carbohydrate diet. The ketone producing diet decreased growth of the brain tumors from 35 to 65% depending on the tumor line, significantly enhanced health and survival compared to the control group who were on the low fat high carbohydrate diet.

In April 2010, the first case report was published describing a patient treated for glioblastoma multiforme with a ketogenic diet. The patient did well until she stopped the diet. The tumor returned ten weeks later.

At this point the theory supporting the metabolic management of brain cancer through a ketogenic diet is so strong and the risks so minimal that there seems little reason to argue against trying it.

Caloric Restriction also appears to slow brain tumor growth. A 2002 paper by Mukherjee et al from Boston College reported on experiments with mice with brain tumors. Compared to mice who had been fed all they wanted, the brain tumors in mice on a calorie restricted diet grew slower, were less dense, and there was less angiogenesis (building new blood vessels to feed the tumor). The tumor cells in the hungry mice were more likely to undergo apoptosis.

A July 2010 paper confirmed the benefit but this time in mice with glioblastoma multiforme; caloric restriction, “… can be effective in reducing malignant brain tumour growth and invasion.”

Caloric restriction, although it may put the body into ketosis, is thought to act differently than the ketogenic diet. Hunger puts a stress on the body; mild stress is hypothesized to create a hormetic reaction awakening protective mechanisms within the body, stimulating the individual cells to fight the cancer.

Caloric restriction means just what it sounds like; one restricts the amount of calories consumed in a day, typically about 40% less than what is required to maintain weight. Obviously following this diet forever may cause significant weight loss. It has been hypothesized that a less stringent method, alternate day caloric restriction, will make chemotherapy and radiation treatment of cancer more effective, but at this time is still untested on brain tumors.

Researchers at Boston College are now investigating using both of these dietary strategies simultaneously, using a caloric restricted ketogenic diet against brain cancer.

Conclusion:
We acknowledge that the data cited in this article are not always obtained through the rigorous clinical trials that the modern medical world prefers to see prior to adopting new protocols. On the other hand, the history of use, the current studies, and clinical experience, all suggest these suggested therapies will not cause harm or interfere with other medical treatments. The evidence is also certainly adequate to suggest the possibility that implementation may slow brain tumor growth. Given the inadequacy of standard medical treatment at controlling high-grade malignant brain tumors, this approach of co-treating brain tumors with nutritional supplementation in addition to the medical oncology standard of care can by summarized simply as, “It can’t hurt, but it might help.”


Antidepressants and brain tumors
People with brain tumors should not take antidepressants or use supplements that increase serotonin.

There is a chemical made in the brain called glial cell line derived neurotrophic factor (GDNF). As the name suggests, GDNF is made by glial cells. This protein typically aids neurons to survive after injury. The problem is that it also help brain tumor cells survive, in particular gliomas, and not just to survive but to migrate and invade surrounding brain tissue.

A potential problem with antidepressants is that they increase GDNF. A 2007 paper reported, “… that amitriptyline, a tricyclic antidepressant,” did so. Serotonin itself increases GDNF. Thus, antidepressants classified as selective serotonin reuptake inhibitors (SSRIs) may increase GDNF, increasing tumor survival and helping it spread further into the brain.

Exception to the rule:
The antidepressant Comipramine may be an exception to this rule; it triggers apoptosis in glioma cells encouraging them to commit suicide. In addition, steroids appear to enhance its anticancer effect. If this research in confirmed, it may be actually advisable for brain tumor patients to take Comipramine while using steroid treatment. [I can’t believe I’m encouraging steroid and antidepressant use, but I’m simply following the science here. Obviously you may want to cut out this part]

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Steroids are a ‘Catch 22’

Almost all patients who undergo surgery or radiation treatment will be prescribed steroid medications like prednisone or dexamethasone as part of their treatment. These drugs are needed to reduce brain swelling. The catch is that, dexamethasone inhibits apoptosis in glioma cells, it keeps the cancer cells alive. A 2000 paper summarized this: “Since glucocorticoids are often used in the treatment of gliomas to relieve cerebral edema, the inhibition of apoptosis by these compounds could potentially interfere with the efficacy of chemotherapeutic drugs.” Steroids also block the chemo drug, camptothecin from killing glioma cells.

Patients should use these drugs for the least possible time and at the lowest doses. Concomitant doses of curcumin and Boswellia act to reduce inflammation reducing the necessity for steroids.
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Online Resources:

www.OncANP.org The Oncology Association of Naturopathic Physicians. Lists of naturopathic physicians who specialize in naturopathic oncology as well as naturopathic physicians who have been board certified in naturopathic oncology are found on this website.

Essential Guide to Brain Tumors

http://www.braintumor.org/patients-family-friends/about-brain-tumors/publications/essentialguide.pdf


Primer of Brain Tumors

http://www.abta.org/index.cfm?contentid=170

 

References:

http://www.braintumor.org/

Porter KR, McCarthy BJ, Freels S, Kim Y, Davis FG. Prevalence estimates for primary brain tumors in the United States by age, gender, behavior, and histology.  Neuro Oncol. 2010 Jun;12(6):520-7.

National Cancer Institutue: http://www.cancer.gov/cancertopics/types/brain

Jemel A, Siegel, R, Ward, E. Murray, T, et al. Cancer Statistics, 2008. CA: A Cancer Journal for Clinicians. American Cancer Society. Vol. 58, No. 2, pp. 71-96.

CBTRUS 2007-2008. Primary Brain Tumors in the United States Statistical Report 2000-2004. Central Brain Tumor Registry of the United States

Davis FG, Kupelian V, Freels S, McCarthy B, Surawicz T. Prevalence estimates for primary brain tumors in the United States by behavior and major histology groups. Neuro Oncol. 2001 Jul;3(3):152-8.

Jemel A, Siegel, R, Ward, E. Murray, T, et al. Cancer Statistics, 2008. CA: A Cancer Journal for Clinicians. American Cancer Society. Vol. 58, No. 2, pp. 71-96.

Sundeep, D, Lynch, C. Trends in brain cancer incidence and survival in the United States: Surveillance, Epidemiology, and End Results Program, 1973 to 2001. Neurosurgical Focus 20 (4):E1, 2006

Krex D, Klink B, Hartmann C, von Deimling A, Pietsch T, Simon M, et al. Long-term survival with glioblastoma multiforme.  Brain. 2007 Oct;130(Pt 10):2596-606.

Brenner AV, Linet MS, Shapiro WR, Selker RG, Fine HA, Black PM, Inskip PD. Season of birth and risk of brain tumors in adults.  Neurology. 2004 Jul 27;63(2):276-81.

Hoffman S, Schellinger KA, Propp JM, McCarthy BJ, Campbell RT, Davis FG. Seasonal variation in incidence of pediatric medulloblastoma in the United States, 1995-2001. Neuroepidemiology. 2007;29(1-2):89-95.

Yeni-Komshian H, Holly EA. Childhood brain tumours and exposure to animals and farm life: a review. Paediatr Perinat Epidemiol. 2000 Jul;14(3):248-56.

Ménégoz F, Little J, Colonna M, Arslan A, Preston-Martin S, Schlehofer B, et al. Contacts with animals and humans as risk factors for adult brain tumours. An international case-control study. Eur J Cancer. 2002 Mar;38(5):696-704.

Efird JT, Holly EA, Preston-Martin S, Mueller BA, Lubin F, Filippini G, et al. Farm-related exposures and childhood brain tumours in seven countries: results from the SEARCH International Brain Tumour Study. Paediatr Perinat Epidemiol. 2003 Apr;17(2):201-11.

von Mutius E. 99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: farm lifestyles and the hygiene hypothesis. Clin Exp Immunol. 2010 Apr;160(1):130-5.

Brenner AV, Linet MS, Fine HA, Shapiro WR, Selker RG, Black PM, Inskip PD. History of allergies and autoimmune diseases and risk of brain tumors in adults. Int J Cancer. 2002 May 10;99(2):252-9.

Schwartzbaum J, Jonsson F, Ahlbom A, Preston-Martin S, Lönn S, Söderberg KC, Feychting M. Cohort studies of association between self-reported allergic conditions, immune-related diagnoses and glioma and meningioma risk. Int J Cancer. 2003 Sep 1;106(3):423-8.

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