Reader Q&A

Q: You frequently refer to an article from some past newsletter and I can’t ever seem to find it. How about an index to all this stuff?

A: OK. I’d be happy to do that. Unfortunately, that index would be for the MS Word versions of all these newsletters and would be updated, say, every 10 issues. To attach an updated index to each issue, referring back to all the previous issues, would make every issue huge. I am not sure how many of you are actually keeping these (or even reading them). So, how about those of you who want an index, send me a note with your vote. And tell me, do you want an index only of article titles (an alphabetical Contents) or a standard book-style index of keywords (e.g., Aspergillus niger, Issue 99, page 3, Issue 101, pages, 5-7)?

Q: In issue 51, you said: “How pathetic and fragile are those systems of thought that dare not expose their followers to any dissenting view or alternative explanation.” Does that mean you believe that public schools should teach creationism along with evolution?

A: I had promised earlier that I would try to keep religion out of these newsletters, and I intend to hold to that, but I suspect this query goes deeper than the simply stated question. As in, “Am I biased in any area?” Well, let’s start with the question as stated. No, I don’t believe creationism should be taught in public schools, for the reasons that 1) the science teacher who hands out the theory of evolution probably isn’t qualified to teach “intelligent design” and 2) if the school board demands the science teacher teach something s/he doesn’t even believe in, you know there would be a very biased skew to that lesson. So, as a more general statement, what I would suggest, whether we are talking about science versus religion or allopathic doctors versus naturopathic doctors, is that both sides of the issue merely acknowledge that there is another possibility. I do not believe anyone should teach, proscribe, or prescribe for an area that is not within his/her knowledge base. I do believe that MDs, if seeing that s/he cannot fix the problem, or that an herb might be a better solution, might wisely suggest his patient go see an herbalist. When the family doctor sees you have a screwed up leg, s/he refers you to an orthopedic specialist, so why not with those problems for which they admit “there is no known cause or cure”? But now that you’ve got an appointment with the village wise woman, what are the odds that she, like the MD, also does not know anything about fungi and mycotoxins? Sadly, that is the case here. Some of the best dieticians in the country are still recommending foods that are harmful (or have the potential to be) simply because they exist within this all-mighty food pyramid. Some of the best herbalists and naturopaths hand you an infusion of something that has no chance to defeat mycotoxins. Some of them know about this stuff, but not very many. That is the purpose of this newsletter: to teach you to know, so whichever choice you make as to who to see, you will go armed with knowledge and can make decisions for yourself. Or, even better, perhaps you can educate your MD or ND. Now for a similar question with a different answer.

Q: You seem to be very open-minded at times and quite biased at others. Which is it?

A: I am not open-minded. Is that a surprise? Let me explain. A person who is totally open-minded is a person who has absolutely nothing in his/her brain. Oh, many of us like to think we are open-minded, but the fact is, we all have formed opinions about the things in our lives, and often we defend those opinions to the max, regardless of the facts. This is one of the reasons why most doctors refuse to believe in what we are teaching here. They spent many years in school being told what is and what is not and they honestly believe that. Now we come along and try to force contradictory data in the cracks of their minds and what is the natural reaction? Yeah, resistance. Sometimes extreme vehement resistance.

However, the question was about me and my open-mindedness (or lack thereof). I contend that I am always open to alternatives. What I claim to know as truth today (i.e., my beliefs), can be modified by new data, if that data meets the tests as suggested by the scientific processes described in Issue 51. I do not hold to any of the fringe quack ideas because they cannot withstand those tests. Even though I do believe in the power of prayer, I also cannot rely on “divine intervention” as a regular healing tool, perhaps because of my belief that God will not do for man that which She perceives that man must do for himself. That is, you must assume the responsibility for your own life and not expect someone else, whether that is God or your doctor, to fix all your mistakes for you. We are attempting to give you sufficient data that you will be able to do that.

Q: In the last issue, you put in that article about the pillows being full of fungi and mites. Well isn’t that just great! Now we not only can’t eat anything, we need to replace our pillows every few months. Some of mine are quite old, and though I have sometimes thought about those dust mites, who would have ever thought they were eating the fungus, which we had no idea was there, but they are also pooping out food for it. Geez, maybe we’re supposed to have some forms of fungus around to keep us healthy. It’s obviously everywhere!

A: Yes, it is everywhere, and some of it is OK. The question that one might find in her frustrated comment here is, “Because it is everywhere, why is this only such a huge health problem today?” The answer is simply that man has screwed up this planet and the demands of our large population for better, faster, and easier ways of doing things means that we can never return our planet to the way it was back during the time of the hunter-gatherer societies when our physical tolerance for all this fungi was higher. Not only were we immuno-compromised by antibiotics and bad diet, but the over-use of antibiotics, antiseptics, antimicrobials, etc., have also produced mutated bacteria, mutated viruses, and mutated fungi, capable of withstanding whatever we throw at them today.

Not only have we fed ourselves a bad diet, but our cheapest (most cost effective) storage systems have introduced mycotoxins to food that used to be safe and healthy. On top of that, we have polluted our environment to the point where most people must suffer with contaminated/toxic air and water. The garbage we pour into our rivers and oceans has even toxified the fish to the point where some of them are too dangerous to eat. We have over-planted our fields and under-nourished them, to the point where our crops suffer and we produce an inferior product, so we fix that by adding chemicals, either to the product before harvest, or to the food as it is being manufactured after harvest. The chemical corporations make the same promises to the farmer as the pharmaceutical corporations make to the doctors: we’ve got a new breakthrough chemical (or shot or pill, pick one) that will fix all that is wrong. Or Monsanto and gang will just make a genetically engineered crop that will grow where Mother Nature’s plants can no longer survive.

There is also a topic I haven’t introduced here (because it is not about diet and toxins): that is the electro-magnetic side of our physiology. It might have been vaguely hinted at in the anatomy issues (1-5), but your nervous system works by electrical impulses. All electrical movements create magnetic fields around the wires (nerves in this case). If those fields are disturbed by larger magnetic fields, they create an interference pattern (inductive reactance) that alters the intended characteristics of the original signal, which is then likely to be sending the wrong signal (my major career field was electrical/electronic 1974-1999). Is your wobbliness due to old age, or is it because you have so many electronic labor-saving devices in your home that you can no longer walk a straight line because the signals from your brain to your feet are messed up?

We have shown that the advent of those huge cross-country power transmission lines (you’ve all seen these) did increase the incidence of thunderstorms in their vicinity and the severity of thunderstorms in areas that didn’t use to have such storms. Yes, man has changed the weather. (see The Body Electric: Electromagnetism and the Foundation of Life, Robert O. Becker, MD, and Gary Selden, ©1985.) So what are all those appliances in your home doing to your body? You do know that all the claims that these things are absolutely safe has the same reasoning as the FDA’s approval of “safe and effective” drugs that end up killing people: Money! When someone wants to sell you something, they will find a way to make it appear to be safe. And, we consumers are only too happy to buy such toys because it means less work for us.

Can I ask you to change your life to the point where you don’t have all those toys? No. I wouldn’t even try. It’s like all the bad food in the supermarkets (90% of it is processed with added chemicals). Can I ask you to not eat any of that stuff? No. The only thing I can do about any of this is to educate and inform. Your life is yours and you must make your own decisions about which risks you are willing to accept. Do the best you can with what you’ve got.

EPA’s Final Risk Assessment of Aspergillus niger (February 1997)

I have pulled selected sections from the complete document. If you want to see the whole thing, click on: http://www.epa.gov/opptintr/biotech/fra/fra006.htm Not only have I added commentary in green, but I have underlined or bold-faced some of their text (they wouldn’t dream of adding such emphasis).

Aspergillus niger is a member of the genus Aspergillus, which includes a set of fungi that are generally considered asexual, although perfect forms (forms that reproduce sexually) have been found. Aspergilli are ubiquitous (def: seeming to be everywhere at the same time; omnipresent) in nature. They are geographically widely distributed, and have been observed in a broad range of habitats because they can colonize a wide variety of substrates. A. niger is commonly found as a saprophyte growing on dead leaves, stored grain, compost piles, and other decaying vegetation. The spores are widespread, and are often associated with organic materials and soil.

The primary uses of A. niger are for the production of enzymes and organic acids by fermentation. While the foods, for which some of the enzymes may be used in preparation, are not subject to TSCA (this acronym means Toxic Substances Control Act), these enzymes may have multiple uses, many of which are not regulated except under TSCA. Fermentations to produce these enzymes may be carried out in vessels as large as 100,000 liters (Finkelstein et al., 1989). A. niger is also used to produce organic acids such as citric acid and gluconic acid. (Which is in bunches of the processed foods you eat and drink)

The history of safe use (note this because I’ll rant about it in a few paragraphs) for A. niger comes primarily from its use in the food industry for the production of many enzymes such as amylase, amyloglucosidase, cellulases, lactase, invertase, pectinases, and acid proteases (Bennett, 1985a; Ward, 1989). In addition, the annual production of citric acid by fermentation is now approximately 350,000 tons, using either A. niger or Candida yeast as the producing organisms. Citric acid fermentation using A. niger is carried out commercially in both surface culture and in submerged processes (Berry et al., 1977; Kubicek and Rohr, 1986; Ward, 1989).

Human Health Hazards

The growth of the fungus Aspergillus in human tissue or within air-containing spaces of the body, such as bronchus or pulmonary cavity, is termed aspergillosis (Bennett, 1979a). Exposure to Aspergillus must be nearly universal but disease is rare. (That is an assumption based solely on the fact that no fungal diseases relating to it are reported by doctors (who don’t believe in it) to the CDC – and, of course, such reporting is voluntary.) The physiological condition of the exposed individual thus appears to be of paramount importance. Patients exhibiting aspergillosis are generally immuno-compromised, and thus susceptible to otherwise common and usually harmless microorganisms. (As I have said in past issues, you became immuno-compromised the minute you had your very first antibiotic shot or pill.) Factors that may lead to immuno-suppression include an underlying debilitating disease (e.g., chronic granulomatous diseases of childhood), chemotherapy, and the use of supraphysiological doses of adrenal corticosteroids (Bennett, 1980). And, because they refuse to believe the pure mycotoxin antibiotics hurt anyone – denying all those other articles that prove they are – they insist the definition of immuno-compromised or immuno-suppression can only be from these three items.

Pulmonary aspergillosis is the most common clinical manifestation of aspergillosis. The most common symptoms of pulmonary aspergillosis are a chronic productive cough and hemoptysis (coughing up blood). According to a standard medical textbook, “Aspergillus can colonize ectatic bronchi, cysts (thereby creating a “cancer” if they’d just open their eyes), or cavities in the lung. Colonization is usually a sequel of a chronic inflammatory process, such as tuberculosis, bronchiectasis, histoplasmosis, or sarcoidosis. A ball of hyphae may form within an air-containing space, particularly in the upper lobes, and is termed an aspergilloma. The fungus rarely invades the wall of the cavity, cyst, or bronchus in such patients” (Bennett, 1979a). It is not clear what role Aspergillus plays in non-invasive lung disease. Plugs of hyphae may obstruct bronchi. Perhaps allergic or toxic reaction to Aspergillus antigens could cause bronchial constriction and damage (Bennett, 1980). Isn’t this final admission a contradiction to what was said just above it?

Both the severity of aspergillosis and the patient’s prognosis are dependent on the physiologic status of the patient. Invasion of lung tissue in aspergillosis is almost entirely confined to immunosuppressive patients (Bennett, 1980). (Almost? Then are they admitting that it can hurt people who are not immuno-suppressed?) Roughly 90 percent of invasive pulmonary case patients will have two of these three conditions: severe immuno-suppression (less than 500 granulocytes per cubic millimeter of peripheral blood), supraphysiological doses of adrenal corticosteroids, and a history of taking cytotoxic drugs such as azathioprine (Bennett,1980). In addition, the type of disease produced affects the patient’s chances for recovery. For example, simple colonization is treatable, but if the simple colonization becomes chronic or invades neighboring tissues, the infection becomes more difficult to treat (McGinnis, 1980). Surgical excision has been used successfully to treat invasive aspergillosis of the paranasal sinus as well as non-invasive sinus colonization. Intravenous amphotericin B has resulted in arrest or cure of invasive aspergillosis when immuno-suppression is not severe (Bennett, 1980). Pleural aspergillosis often responds well to surgical drainage alone (Bennett, 1979b).

Although Aspergillus fumigatus is the usual cause of aspergillosis (Bennett, 1979b), there have been several recent case reports of pulmonary aspergillosis caused by A. niger. For example, Kierownik (1990) described a 66-year-old man who was admitted to the hospital with pulmonary lesions and cavitation of his lung. Fungi were cultured and the sputum contained fungal forms typical for A. niger, complicating a pulmonary abscess in the course of a pneumonia. Korzeniowska, Kosela, et al. (1990) also describe a pulmonary aspergilloma caused by A. niger. Medina et al. (1989) reported on cases of bilateral maxillary sinusitis and a right pansinusitis.

A. niger was implicated in a case described by Louthrenoo et al. (1990), in which an amputation of the right foot had to be performed on a malnourished 70-year-old man who presented with a painful black “gangrenous appearing” mass on the right foot. Tissue samples showed not only branching hyphae, but dark pigmented fungal fruiting heads with double sterigmata in which Aspergillus niger was identified. Ah, so this does affect other parts of the body besides those bronchio-pulmonary areas cited in the first paragraph of this section.

Although Aspergillus niger is regarded as an opportunistic pathogen (Padhye, 1982; Walsh and Pizzo, 1988), (The American Heritage Dictionary says a pathogen is: an agent that causes disease, especially a living microorganism such as a bacterium or fungus – gee, do you suppose the dictionary knows more than most doctors who rarely admit fungus does anything?) an earlier report said that it can cause otomycosis in healthy, uncompromised persons who have no underlying disease (Austwick, 1965). Otomycosis is the name given to the growth of Aspergillus, often A. niger, on ceruman and desquamated debris in the external auditory canal. The condition is benign. Of 159 suspected cases of otomycosis in Nigeria, 36 were specifically confirmed on the basis of demonstrating microscopically fungal structures in epithelial debris plugs and a positive culture (Gugnani et al., 1989). Another 31 cases gave positive cultures but were negative microscopically, and thus were considered of doubtful fungal pathology. Again, A. niger was predominant.

Allergic Reactions to Aspergillus niger

Allergens produced by A. niger can produce allergic reactions in humans. When inhaled, A. niger can cause hypersensitivity reactions such as asthma (If they know this much, then why, damn it, does the medical community continue to claim they need more donations to find the cause of asthma?) and allergic alveolitis (Edwards and AlZubaidy, 1977). However, only a few instances of asthma induced by A. niger have been reported. (Only a few? Oh, have been “reported.” And of course we aren’t going to report anything contrary to our continued source of income, are we?) One such instance involved a manufacturing plant in which a specially selected strain of A. niger was being used to ferment molasses to produce citric acid. (Remember, folks, we drink and eat this crap every day!!!) Both stirred tank and surface methods were being used. Eighteen workers were diagnosed as having occupational asthma; half had IgE antibody to A. niger based on skin and RAST tests (this acronym means: Radio-Allergo-Sorbent Test, a blood test for allergies). As determined by RAST inhibition experiments using a commercial extract of A. niger, the antigen that caused the sensitization appeared to be peculiar to the A. niger strain used for the fermentation (Topping et al., 1985).

In studies on 30 of 83 patients who showed symptoms of bronchial asthma, it was found that skin hypersensitivity to Aspergillus antigens with a high serum IgE to these antigens is indicative of Aspergillus sensitivity. Excuse me for changing the subject just a tad bit, but 30 of 83 patients is a statistical result of 36%. Why don’t they think this is huge when the medical community boasts “breakthroughs” at rates as low as 2-5%?

Massive inhalation of Aspergillus spores by normal persons can lead to an acute, diffuse, self-limiting pneumonitis. Spontaneous recovery taking several weeks is the usual course (Bennett, 1980). For example, Dykewicz et al. (1988) described the case of a 28-year-old man who developed fevers, cough, shortness of breath and other symptoms several hours after cutting live oak and maple trees. Fungal cultures of the wood chips yielded A. niger along with other Aspergillus species, three species of Penicillium, Paecilomyces sp., and Rhizopus sp.

Toxin Production by A. niger

Aspergillus niger can produce a variety of fungal metabolites, termed mycotoxins, depending upon growth conditions and the strain of the organisms. The mycotoxins include oxalic acid crystals, kojic acid, and cyclic pentapeptides called malformins. The mycotoxins range from moderately to highly toxic in terms of acute toxicity.

A. niger produces oxalic acid and kojic acid abundantly. These two products have only a slight acute toxicity. Oxalic acid has an intraperitoneal LD50 of 150 mg/kg in rats and kojic acid has an intraperitoneal LD50 of 250 mg/kg in mice (Ueno and Ueno, 1978).

Malformins produced by A. niger are more potent toxins, at least by the intraperitoneal route of administration. Malformin A has an intraperitoneal LD50 as low as 3.1 mg/kg in mice (Kobbe et al., 1977.) Pathologic signs accompanying fatality included dilatation with hemorrhage of the gastrointestinal tract and changes in the liver and kidney. Death occurred within four days.

I am convinced that this is what killed my Tennessee Walking Horse. He ate a bale of hay containing black mold (Aspergillus niger) and died in 3 ½ days. The molds severely depleted his body’s calcium levels and caused a creeping paralysis from which he had no hope of recovery. Never let your horse get to moldy hay.

In 1976, Anderegg et al. (1976) reported that a strain of A. niger collected from mold-damaged rice produced a highly toxic metabolite, Malformin C, which they established as the disulfide of cycloDcysteinylDcysteinylLvalylDleucylL-leucyl. When grown on white wheat in a fermentative process, malformin C was highly toxic to newborn rats (LD50 0.9 mg/kg; i.p.) and exhibited antibacterial activity against both gram-positive and gram-negative bacteria (Ciegler and Vesonder, 1987). Malformin C appears to have more mammalian toxicity than malformin A (Moss, 1977). Meaning that this mold is capable of taking over the places in the body that are normally occupied by bacteria, whether “good” or “bad.”

The production of malformins is related to the composition of the growth substrate and usually occurs in stationary phase cultures. While not always true, mycotoxins are generally produced on solid substrates with high carbon/nitrogen solid content (Ciegler and Kurtzman, 1970; Anderegg et al., 1976). For example, malformins are produced when A. niger is grown on onion bulbs (Curtis et al., 1974) and on fermenting grains (Kobbe et al.,1977). A strain of A. niger recovered from mold-damaged rice produced malformin A. A survey to define the number of strains in nature that are malformin producers appears not to have been made.

The loci involved in mycotoxin biosynthesis have not been genetically mapped at present due to the difficulty of working with an asexual microorganism such as A. niger. Does that mean that, because it’s hard, we aren’t going to do it?

Conclusions

A. niger is not a significant human pathogen. (You butt heads gotta be kidding me! What the heck do they consider significant? If it gave 36% of the people exposed a disease, then just what is significant? Oh, and it killed your mice and my horse. You use mice in all the lab experiments on any drug which is directed toward human consumption because they are so similar in reaction to humans, so why is their death by mold not significant?) Throughout years of use and widespread exposure to A. niger in the environment, there are only several reports of aspergillosis with A. niger, and in Nigeria, one report of a number of cases of otomycosis. There have been only several reports of allergic reactions, which are not uncommon for aspergilli in general, and not unique to A. niger. A. niger is capable of producing several mycotoxins. However, mycotoxin production appears to be controlled by the conditions of fermentation.

Environmental Hazards

Hazards to Animals

Livestock ingesting A. niger contaminated feed have been shown to be adversely affected by mycotoxins. Calcium depletion and other physiological abnormalities including death can result from ingestion of A. niger-colonized feed due to the fungal production of oxalic acid or malformins (Austwick, 1965). Chicks and mice were killed after being fed with moldy soybeans and mice died after eating contaminated wheat containing isolates of A. niger (Semeniuk, et al., 1971). The cause of death was assumed to be toxicosis, but pathogenicity was observed in some cases. Some of the malformins are currently under development for use as insecticidal compounds (Wicklow, 1991). Now let me get this straight. You admit it kills livestock and mice and chicks, and you want to make an insecticide out of it because you’re sure it will kill them, but you still think this can’t harm human beings?

Hazards to Plants

A. niger has been isolated from 37 genera of plants (Farr et al., 1989). Often these reports involve coisolation with other perhaps more destructive microorganisms or isolation from a stored plant product (yeah, like all our grains). There are reports of A. niger being a plant pathogen in peanuts (Jackson, 1962) (But, the FDA only looks for Aflatoxins in that area, so they apparently don’t care about this particular killer.). Apparently, A. niger can induce a crown rot of peanuts due to A. niger-infected seed under specific hot, humid growth conditions. The mycotoxins described above, namely oxalic acid, malformin A, and malformin C, have been shown to cause significant growth effects such as root curling and top deformation in plants (Anderegg et al., 1976).

A. niger can cause the rotting of numerous fruits, vegetables, and other food products, thus causing substantial economic losses due to spoilage. For example, black rot of onions associated with A. niger is responsible for serious losses of onion bulbs in the field and in storage. There are also reports of A. niger-induced spoilage of mangos (Prakash and Raoof, 1989), grapes (Sharma and Vir, 1986), and tomatoes (Sinha and Saxena, 1987).

Other Ecological Concerns

Members of the Aspergillus genus are well known as biodeteriogens (organisms that cause deterioration of materials). For example, A. niger causes discoloration and softening of the surface layers of wood, even in the presence of wood preservatives. A. niger also causes damage to raw cotton fibers and other cellulose-containing materials, as well as to tanning liquors used in the tanning of hides and leather. It can also attack plastics and polymers such as cellulose nitrate, polyvinyl acetate and polyester-type polyurethanes (Thomas, 1977). A. niger is also the major spoilage isolate on bakery products such as English style crumpets (Smith et al., 1988).

Conclusions

One set of major concerns for environmental hazard is, like that for human hazard, associated with mycotoxin production. Toxins from A. niger may affect other vertebrates and plants as well. There is one early report of crown rot of peanuts by A. niger under specific growth conditions. However, it is not a significant pathogen in the environment. In addition, A. niger is one of many commonplace spoilage-associated fungi, which can cause severe economic effects.

These folks have me baffled. If, as they say, it is not a significant pathogen in the environment, then how can the next sentence be true? They did use the word “severe” regarding the economic effects, didn’t they. And how is that not “significant”?

Aspergilli are among the fungi most frequently isolated from soils and have been found to rapidly colonize and degrade easily available organic matter. The abundant asexual spores produced within the conidiophores are resistant to many environmental stresses which enables the organism to survive during inactive periods (Atlas and Bartha, 1981). Although no specific data comparing the survivability of industrial and wild type strains were available in the literature, the above characteristics indicate that released strains are likely to survive outside of containment (Versar, 1992).

Um, excuse me EPA folks, but what do you think your body is, if not “organic matter”? This stuff is in the dirt and on plants all over the world. Now you nice folks reading this from other countries (Hey Europe!), listen up. This is not just a problem with the United States government, researchers, chemists, and doctors having their heads up their butts. I was gleaning info from the DSM site yesterday (a large food products manufacturer in Europe, whose acronym is not defined anywhere in their corporate site) and they seem to think that the Aspergillus species remain the most significant fungus for commercial enzyme production and particularly Aspergillus niger is the main microorganism used within DSM Food Specialties.” Um, don’t think you’re immune – it’s in your food too. And no matter how much official denial we get, this and other fungi are killing people.

Curry Spice Appears to Shut Down a Protein

Active in the Spread of Breast Cancer

Curcumin, the main ingredient of turmeric and the compound that gives curry its mustard-yellow color, inhibits metastasis to the lungs of mice with breast cancer, report researchers at The University of Texas M. D. Anderson Cancer Center.

The study, to be published in the Oct. 15 issue of the journal Clinical Cancer Research, reports that the spice appears to shut down a protein active in the spread of breast cancer to a major target for metastasis.

Though the study results are early, researchers found that the non-toxic natural substance not only repelled progression of the disease to the lungs, but also appeared to reverse the effects of paclitaxel (Taxol), a commonly prescribed chemotherapy for breast cancer that may trigger spread of the disease with use over a long period of time.

Now, stop a moment and think about what was just said here. Curcumin is non-toxic. It repels the progression of a cancer and reverses the effects of Taxol. Why can’t they figure out the simple part here? Taxol is a product made with mycotoxins, cancer is probably a fungal sac, and curcumin is an antifungal. Gee, wasn’t that easy to figure out? Instead we go on with the rest of their excuses…

Because Taxol is so toxic, it activates a protein that produces an inflammatory response that induces metastasis. Curcumin suppresses this response, making it impossible for the cancer to spread. In fact, researchers found that adding curcumin to Taxol actually enhances its effect. Curcumin breaks down the dose, making the therapy less toxic and just as powerful while delivering the same level of efficacy. Most inflammations are caused by mycotoxins, so isn’t it simple logic that taking an antifungal will help?

“We are excited about the results of the study and the possible implications for taking the findings into the clinic in the next several years,” says Bharat Aggarwal, Ph.D., professor of cancer medicine in M. D. Anderson’s Department of Experimental Therapeutics. “At this time, advanced breast cancer is a difficult foe to fight with few proven treatments available after surgery, chemotherapy and radiation therapy.” I love that sentence. According to the rule book for doctors, there are only three possible treatments for cancer: surgery, chemotherapy, and/or radiation treatment. Both chemo and radiation are “known carcinogens.” Two of the three things they use to fight cancer are also things which cause more cancer. And now they are excited about adding an antifungal to the chemo-poisons. Why don’t they just try this non-toxic natural product all by itself?

Taxol is currently used as the front-line chemotherapeutic agent in breast cancers, but because the drug frequently induces drug resistance after prolonged use, it is not effective in treating metastatic breast cancer, says Aggarwal.

Researchers studied 60 mice with breast cancer, which were randomly assigned to one of four groups: control group, Taxol only, curcumin only and the combination of Taxol and curcumin. After the tumors grew to 10 mm (about the size of a pea), they were surgically removed, and the mice were fed a powdered curcumin diet.

Macroscopic lung metastasis, or metastasis that is visible to the naked eye, was seen in 96 percent of the mice in the control group. Treatment using Taxol alone only “modestly reduced” the incidence of metastases, while the group using curcumin alone and curcumin plus Taxol “significantly reduced” both the incidence and numbers of visible lung metastases.

Microscopic metastasis, or metastasis that is visible only when using a microscope, was found in the lungs of 28 percent of mice treated with the combination of curcumin and Taxol, and there was no macroscopic disease present. The micrometastases present consisted of only a few cells, suggesting that the combination inhibited the growth of breast cancer tumor cells that were in the lung before the tumors were removed.

In a previous study published in the Aug. 15 issue of the journal Cancer, M. D. Anderson researchers found that when the nuclear factor-kappa B (NF-kB) (a powerful protein known to promote the inflammatory response necessary to cause breast cancer to spread) is shut down, cancer strains are unable to grow and cells are pushed to commit suicide.

The mechanism in this curcumin study works the same way. Taxol activated the NF-kB in breast cancer cells, while curcumin stopped this activation by blocking the protein known as “IKK” that switched on the NF-kB, demonstrating how curcumin and Taxol work against one another. Taxol produced the inflammatory response, triggering metastasis, and curcumin suppressed it, causing cell death.

Extracted from the roots of the curcuma longa plant, curcumin is a member of the ginger family. While it is not used in conventional medicine, it is widely prescribed in Indian medicine as a potent remedy for liver disorders, rheumatism, diabetic wounds, runny nose, cough and sinusitis. Traditional Chinese medicine uses curcumin as a treatment for diseases associated with abdominal pain, and it is used in ancient Hindu medicine as a treatment for sprains and swelling. (Gee, do you suppose all those ailments might be caused by fungi or mycotoxins?)

According to the American Cancer Society, the chance of a woman having invasive breast cancer sometime during her life is one in eight. About 211,240 women in the United States will be diagnosed with invasive breast cancer in 2005, and approximately 40,410 women will die from the disease this year.