Is it
Healing or Curing? Some of the words here are paraphrased from Women’s Bodies, Women’s Wisdom by Christiane Northrup, M.D. She didn’t say it this way, but that’s where I got the idea.
External treatments do not address the factors that
contributed to the problem in the first place. Healing
goes deeper than curing and must always come from within (e.g., the decision
to become healthy or the decision to change your lifestyle). The healing process addresses
the imbalance that caused the symptoms. Healing also brings together the hidden aspects of
your life as they relate to your illness (one of the reasons I suggested those writing
activities). Healing is different from curing, though curing and the restoration of
physical function often accompanies or precedes the healing. When you have become cured
of an illness, that is only the first step to getting totally over that condition or state
of being. In order to be healed, however, you must change your field of intentions and put
the old state of being behind you. Vow never to return to that state and be willing to do
whatever it takes to move forward. Midwest
Grain, Milk Tested for Toxin by Scott Kilman A friend and reader of this newsletter scanned the following from a
newspaper and sent it to us. I figured it had enough interesting admissions that you folks
might want to read this. I have highlighted some areas for those of you who choose just to
speed-read/scan through it. Of course, I also can’t resist adding a few comments as
footnotes. J The Midwest drought is triggering an outbreak of poisonous aflatoxin at thousands of corn farms, spurring regulators and food companies to greatly expand testing of grains and milk. Grain elevators are rejecting newly harvested corn from many of these farms, adding to the woes of growers already bruised by drought-depressed yields and crop prices still hurt by Hurricane Katrina’s disruption of grain-exporting facilities around New Orleans. “It’s a nightmare,” said Daryl Sywassink, a feed specialist in Muscatine, Iowa, which has found worrisome levels of aflatoxin in about 20% of the corn that farmers were peddling.[1] The managers of some 13 grain elevators operated by River Valley Cooperative, Clarence, Iowa, are rejecting as much as 10% of the newly harvested crop. Aflatoxin is excreted by the common soil fungus Aspergillus flavus under drought-like conditions[2] in crops such as corn, peanuts and cotton. The substance is so toxic that it is one of 19 contaminants[3] – along with mercury and DDT – for which the Food and drug Administration imposes strict tolerance levels in food, with only trace amounts allowed. The FDA considers it unsafe for humans to consume corn containing more than 20 parts per billion of aflatoxin,[4] high levels of which can cause acute liver damage.[5] Low-level consumption of aflatoxin is suspected of increasing the chances of liver cancer.[6] The FDA isn’t aware of any human outbreaks in the U.S., but human cases are hard to diagnose.[7] FDA rules forbid dairy cows from consuming corn containing more than 20 parts per billion of aflatoxin,[8] but farmers are allowed to feed corn containing higher levels to some farm animals. The Midwest outbreak is concentrated in eastern Iowa and far western Illinois, about the worst place possible for the food industry. While other parts of the Farm Belt mostly raise corn for feeding livestock, much of the corn produced in the affected region is used to make food ingredients and is also bought by grain-processing giants such as Archer-Daniels-Midland Co. and Cargill, Inc. for shipment down the Mississippi River to overseas customers. Although the scope of the outbreak won’t be clear until the corn harvest ends in several weeks, some government officials and scientists estimate that between 10% and 30% of the corn being harvested in eastern Iowa – the nation’s biggest corn-producing state – is unfit for human consumption. Federal authorities also have received reports of spotty outbreaks in Indiana and Ohio, in addition to Iowa, Illinois, and Missouri. While aflatoxin is a chronic problem on Southern farms,[9] the last big Midwest outbreak occurred during the drought of 1988, when regulators were overwhelmed with trying to police a faint, yet potent, toxin appearing randomly across millions of acres of farm land.[10] Many dairies were forced to dump milk[11] after cows consumed contaminated corn; foreign customers complained of receiving infested grain. In 1990, the U.S. Department of Agriculture began screening all corn bound for overseas markets. Testing technology has rapidly advanced since the 1988 outbreak, when many Midwest grain elevators relied on black lights to look for kernels emitting a greenish-yellow glow – an indication of the fungus. Now, rapid-test kits based on antibody technology[12] are widely available from companies such as Vicam L.P., Watertown, Mass., which said orders from Iowa for its aflatoxin screening kits are double what they were last year. Officials at the FDA
said U.S. consumers shouldn’t be alarmed by the Midwest outbreak, even though one
sample of corn tested by Illinois regulators contained 3,000 parts per billion of
aflatoxin.[13] While the FDA
doesn’t require mandatory screening of corn before processing into food, it
has alerted Midwest food companies to increase their surveillance.[14] At the Quaker Oats breakfast cereal plant in Cedar Rapids, Iowa, for example, every truckload of corn is being screened, said Patti Jo Sinopoli, a spokeswoman for the Quaker unit of PepsiCo, Inc. The plant hasn’t rejected any corn for aflatoxin.[15] Earlier this month, Iowa officials grew concerned that diary cows might be consuming contaminated corn. They began weekly testing of the milk from each of the 750 dairy farms located in 26 eastern counties, as well as milk tankers coming into Iowa from Illinois or Missouri. Any tanker of milk that contains more than 0.5 parts per billion of aflatoxin will be discarded.11 Since adult beef cattle are allowed to consume some aflatoxin, up to 300 parts per billion, contaminated grain can still be sold.8 But farmers are receiving only about 75 cents a bushel for contaminated corn, less than half what many eastern Iowa farmers are receiving for aflatoxin-free corn, and far less than their costs of growing it. “It is a very confusing situation,” said Kortney Kotz, a 43-year-old farmer in Mechanicsville, Iowa, who had one truckload of his corn rejected by a grain dealer and worries that more aflatoxin is in his fields. Now, besides all my little rants in the footnotes, I must ask this question: Don’t doctors read the newspapers? And, if a doctor read that article, would he simply say, “That’s an agricultural problem, not something affecting my patients.”? Why can’t these supposedly intelligent people put the pieces of the puzzle together? Or do we, once again, have to fall back on the old money-trail excuse? Sigh…
[1]
They found it in only 20% of the corn, but that doesn’t mean it isn’t in more
– even the FDA admits that not all shipments get tested. [2]
This statement is very misleading, perhaps because the reporter only wrote what he was
told. Drought conditions will cause the Aspergillus mold to die and, in so doing, secrete
their defense mechanism, which is the metabolite aflatoxin. This is not the only condition
where these crops are subject to aflatoxin contamination. Storage at high temperature and
humidity also creates abundant growth of Aspergillus, which in turn, creates
aflatoxin-infested grains. Because almost no corn or peanuts ever goes directly from field
to grocery shelves, all corn and peanuts are considered “universally contaminated”
and all other grains should be considered as “suspect.” [3]
Here is an admission that the FDA tests for only 19 of a couple hundred mycotoxins, all of
which can and do cause illness in humans. [4]
20 ppb is the official cutoff line. I guess they have to draw a line somewhere, but does
that mean it is safe for you to consume a product with only 19 ppb? Given that fungi and
their metabolites have been shown to be cumulative in your body – that is, it could
take you many many years to build up to a deadly level, I consider that any level
detectable should be considered as unfit for consumption. [5]
Isn’t that interesting? What else do you know of that causes liver damage? Alcohol?
Hard alcohol is full of mycotoxins! Beer and wine are full of yeast, which also produce
mycotoxins. And how about high cholesterol? LDL is produced by fungi! Starting to see a
picture here? [6]
They just keep on shooting themselves in the foot with this article. Liver cancer is
caused by aflatoxins? Wow! Such an admission could put the Run for the Cure nuts out of business. The
American Cancer Institute (and friends) will just dry up and blow away if the public
actually discovers that cancer is produced by
fungi! [7]
Human cases are hard to diagnose because no doctor will perform a test for fungal causes.
It is strictly against their teaching and the directives from above. Fungus is the
cause of cancer, but they refuse to admit it because it would put them out of business. [8]
Here we have an admission that the aflatoxins that go into the cow do come out in the
milk, so when are they going to wise up enough to see that it also goes into the rest of
the animal? See highlighted line about beef cattle farther down this article. [9]
What is the difference between Midwest and Southern farms? Humidity. Now this article
started out saying that drought caused the aflatoxins in the corn. Now they are admitting
that corn grown in areas of high humidity is also subject. Hot and humid conditions foster
Aspergillus formation, which in turn, causes aflatoxin contamination. See also Note 2. [10]
And they are trying to do all that work with far too few testing agents, which means,
without doubt, that some of those contaminated crops get through the net. [11]
Weren’t some of you asking us why we thought milk was not a good thing? These dairies
don’t dump an expensive product without a direct order to do so, therefore it seems
wise to assume the FDA order is because they know what harm can be done to you by
consuming contaminated milk – and that level is only 0.5 ppb instead of 20 ppb. [12]
Interesting, isn’t it, that the technology to detect aflatoxin is an “antibody”
test? Is this another admission that antibiotics are just as dangerous as this fungal
toxin? [13]
We shouldn’t be worried? Gee, that’s typical authoritarian speak. If one sample
was 3,000 ppb when the line-in-the-sand is 20 ppb, and that sample might have slipped
through as one of the many that fail to get tested at all, I’d damn well worry. This
is almost like your doctor saying, “You’ve got cancer, but don’t worry, we’ll
just cut your arm off.” [14]
And will they do it? Given that they have already bought the product, contaminated or not,
they are likely to use it. I have worked for companies (thankfully, not food producers)
who have deliberately shipped faulty products in the hopes that the customer wouldn’t
notice. They could tolerate a service call at a later date, but they couldn’t
tolerate a failure to ship a certain quantity on schedule. [15]
Notice that they did not say they had not found any aflatoxins. They said they had not
rejected any corn. And, um, why are they putting corn in Quaker Oats?
How to
Make Sense of Technical Medical or Scientific Documents Below is a short piece of technical blather that most people cannot
understand unless they have spent six or 10 years in the medical research environment. I
am going to attempt to show you how you can
wade through those types of documents and, even if still not perfectly clear, at least
they will become a bit more comprehensible. Here’s the sample: ULTRASTRUCTURAL APPEARANCE OF SQUAMOUS CELL CARCINOMAS Squamous cell carcinomas are tumors that are derived from squamous cells. These cells exist in the skin and squamous mucosas such as those in the mouth, pharynx, cervix, and vagina. In some instances these tumors derive from an epithelium that has undergone metaplasia such as those that occur in the respiratory tract and bladder. Squamous cells reside on a basement membrane and are attached to each other by desmosomes which exist among their interdigitating cell membranes called intercellular bridges. Each desmosome consists of an electron dense area (2) on the membrane that is separated on the two opposing cell membranes by a gap, normally about 300 nm in width. Within the squamous cells, one can observe tonofilaments that converge on the desmosomal structures. The tonofilaments are part of the cytoskeleton of the squamous cells which consists of intermediate filaments called cytokeratins. The cells within the well-differentiated squamous cell carcinomas, gradually undergo apoptosis This process is associated with progressive increase in keratinization of the cells, which ultimately leads to the formation of the keratin pearls. Depending on the amount of this keratinization, the squamous cell carcinomas are divided into the well-differentiated, moderately-differentiated and poorly-differentiated squamous cell carcinomas. The well-differentiated tumors possess large numbers of keratinization and kertain pearl formation. On the other hand, the poorly differentiated tumors rarely exhibit these features. Therefore, the pathognomonic ultrastructural features of squamous cell carcinomas consist of basement membrane, desmosomes and tonofilaments. OK, the first step is to get out the dictionary. If you have a newer
version of MS Word, you can simply highlight a word and hit the Research button, which
gives you the definition or an encyclopedia entry. Otherwise, you either search the web or
get out the hardbound books. So, pick out every word from the above paragraph that you don’t
understand and get a definition of each word. Go ahead. Highlight this and try it before
reading the next paragraph. Squamous cell (consisting of, or resembling scales or thin plates of the type that make up the covering of fish, reptiles, and some mammals) carcinomas (a malignant tumor that starts in the surface layer) are tumors that are derived from squamous cells. These cells exist in the skin and squamous mucosas (having to do with a mucous membrane) such as those in the mouth, pharynx, cervix, and vagina. In some instances these tumors derive from an epithelium (a thin layer of tightly packed cells lining internal cavities, ducts, and organs of animals and covering exposed bodily surfaces, especially in healing wounds) that has undergone metaplasia (the transformation of one kind of tissue into another) such as those that occur in the respiratory tract and bladder. Squamous cells reside on a basement membrane (a structure that supports an overlying epithelium, which is a thin layer of tightly packed cells lining internal cavities, ducts, and organs of animals and covering exposed bodily surfaces, especially in healing wounds) or endothelium (a layer of cells that lines the inside of certain body cavities, for example, blood vessels). and are attached to each other by desmosomes (junctional complexes that form among opposing plasma membranes) which exist among their interdigitating (to fit together like the fingers of clasped hands or to place or hold objects together in such a pattern) cell membranes called intercellular bridges. Each desmosome consists of an electron dense area on the membrane that is separated on the two opposing cell membranes by a gap, normally about 300 nm (a really tiny measurement) in width. Within the squamous cells, one can observe tonofilaments (filamentous structures and are part of the cytoskeleton of cells) that converge on the desmosomal structures. The tonofilaments are part of the cytoskeleton (the internal network of protein filaments and microtubules in an animal or plant cell that controls the cell’s shape and movement) of the squamous cells which consists of intermediate filaments called cytokeratins. The cells within the well-differentiated squamous cell carcinomas, gradually undergo apoptosis (a form of cell death necessary to make way for new cells and to remove cells whose DNA has been damaged to the point at which cancerous change is liable to occur). This process is associated with progressive increase in keratinization of the cells, which ultimately leads to the formation of the keratin pearls (a fibrous insoluble protein that is the main structural element in hair, nails, feathers, and hooves). Depending on the amount of this keratinization, the squamous cell carcinomas are divided into the well-differentiated, moderately-differentiated and poorly-differentiated squamous cell carcinomas. The well-differentiated tumors possess large numbers of keratinization and kertain pearl formation. On the other hand, the poorly differentiated tumors rarely exhibit these features. Therefore, the pathognomonic ultrastructural features of squamous cell carcinomas consist of basement membrane, desmosomes and tonofilaments. Now that you have inserted the definitions next to each $25 word, if
that still doesn’t help you, you can then replace their big words with the definition
phrases. It might look like this: Scale-like cells that can become malignant are just tumors derived from those scale-like cells. These cells exist in the skin and the mucous layers of the mouth, pharynx, cervix, and vagina. In some instances, these tumors derive from a thin layer of tightly packed cells lining internal organs that have undergone the transformation of one kind of tissue into another. These scale-like cells reside on a structure that supports an overlying thin layer of tightly packed cells or a layer of cells that lines the inside of certain body cavities and are attached to each other by junctional complexes that form among opposing plasma membranes, which exist among cells that fit together like the fingers of clasped hands that we call intercellular bridges. Each of these consists of an electron-dense area on the membrane that is separated on the two opposing cell membranes by a gap, normally about 0.000000037 inch in width. Within these scale-like cells, you can observe filament-like elements that converge on the junctional complexes. These are part of the internal network of protein filaments of the scale-like cells, which consists of intermediate filaments we call cytokeratins. The cells within the well-differentiated malignant scale-like cells gradually undergo a form of cell death necessary to make way for new cells and to remove cells whose DNA has been damaged to the point at which cancerous change is possible. This process is associated with progressive increase in the deposition of keratin on the cells, which ultimately leads to the formation of a fibrous insoluble protein. Depending on the amount of this deposition, the malignant scale-like cells are divided into classes called well-differentiated, moderately-differentiated and poorly-differentiated. The well-differentiated tumors possess large numbers of keratin deposition and kertain pearl formation. On the other hand, the poorly differentiated tumors rarely exhibit these features. Therefore, the diagnosis of this as a disease made up of minute structural features of possibly malignant scale-like cells consist of three really big words we like to use so you won’t understand a damn thing we are talking about.. Summary in Even More Plain
English These cell membranes they are talking about attract things to them if
they have the right conditions. They then bind them, either by chemical chain formation or
with those cellular fingers. The more this occurs, the greater the chance of a hard lump
(like hair or bone) occurring. Because cell wall damage allows DNA strands to be broken or
altered in some way, this might produce mutated growth rates, therefore this attraction
process can become accelerated, meaning that the lumps will grow and/or spread rapidly. They really are only trying to define the playing field and the
interaction of the players. So, did you guys get something similar out of all that? What’s Not in
Their Article Our belief, although this article does not so state, is that fungal invaders are the mechanism of cell damage and
DNA mutation that starts the abnormal growth. Your body’s natural response is to
gather those enemies and encase them in something that will prevent them from passing on
that mutation – the keratin forms a “stone” around the damaged cells. Lots
of mutated cells makes lots of stones, which eventually get stuck together into a lump big
enough to be detected and/or felt (as in, when you perform your routine breast exam by
rubbing, or when you find a weird hard spot on your skin, etc.). While these can be cut
out, the only “cure” is to remove the source of whatever caused the mutations in
the first place. That is the part the medical people do not agree with. We say we know the
cause. They say the cause is not known, so we must be full of caca. Clearly, they
can analyze what happens, but not what caused it in the first place. Is That Your Final Answer? by David Holland, M.D. The following is copied from the book The Fungus Link 2, Tracking the Cause, by Doug A.
Kaufmann with David Holland, M.D. Reprinted here with permission of the authors. Since becoming aware that cancer is often misdiagnosed in patients who actually suffer from fungal infections, I’ve often wanted to ask my fellow doctors, ‘‘Are you sure your patient really has cancer?” I can only imagine the frustration that nutrition experts such as Patrick Quillin, Ph.D., RD, CNS must experience. They have to face cancer patients on a daily basis, knowing modern medicine may be approaching their symptoms from entirely the wrong angle. Automatic diagnoses of cancer, the theory that infections are caused by either a bacteria or a virus, and practices such as the knee-jerk prescription of antibiotics are all considered acceptable norms in medicine today. In contrast, most doctors would laugh at the idea of prescribing antifungal therapy for a disease that has resisted antibiotics. You see, despite fungi’s role as a leading, hospital-acquired infection, 1 most doctors continue to believe that such infections occur relatively rarely. On top of this, a lot of clinicians hesitate to take too much time in diagnosing cancer. They dread the possibility that, were they to step back and make sure their diagnosis is correct, they might endanger the patient by delaying lifesaving treatments such as chemotherapy, radiation and surgery. J Doug and I once consulted with a very nice, middle-aged woman who had been diagnosed with lymphoma. She told us that a chest CT (x-ray) had revealed that a mass measuring five inches across had engulfed her aorta. Having given up on conventional therapy, she sought our advice on how to enhance her own immune system, hoping to give her body the best opportunity to fight off her disease. A trial treatment including the Initial Phase Diet (what we have been Calling Phase I) and antifungal therapy with Diflucan and nystatin yielded astounding results. Three weeks into the program, we suggested she repeat the CT scan just in case other, potentially more beneficial therapies might be indicated. She reported that her mass had reduced in size to a nodule less than an inch across! Sadly, the therapies recommended by previous doctors had exacerbated her heart condition. She died within a few weeks after the second test. The above woman’s response to fungal therapy resembles several cases in Germany. Doctors reported seeing remission in leukemia patients who had been treated with antifungals for what were thought to be secondary fungal infections.2 Excerpts from Clinical Mycology (Kibbler, C.C., Ed.) and Report No. 116 from the Council for Agricultural Science and Technology (CAST), as well as Dr. Costantini’s Fungalbionics series, will no doubt astound doctors with their insights into not only how fungi can be confused with cancer, but also as to how cancer itself is actually caused by fungal mycotoxins. Doug’s book, The Germ that Causes Cancer, continues to blow away the medical field with knowledge never offered in medical school. Some of the most powerful mycotoxins that CAST discusses are the aflatoxin group, a series of toxins produced by Aspergillus molds. Other, common toxins include ochratoxin and the trichothecenes group. All are believed to cause cancer of the liver, intestines, bladder, kidneys, adrenals, uterus, ovaries, brain, and other organs, as well as leukemia. Another, familiar carcinogen produced by yeasts is alcohol, the reason for DWI, MADD and sometimes DOA, not to mention cirrhosis of the liver. In analyzing cancerous growths themselves, we must distinguish whether the bump, the mass, or the spot is really a cancer – in which case Doug and I believe it is likely caused by one of the mycotoxins mentioned above – or if it is an infection or growth from another source. In the Medscape.com article mentioned above, John Rex is right when he says clinicians are not trained to look for fungal organisms. Neither Dr. Rex nor I were trained in med school or during our internships and residencies to consider fungi as a possible cause of disease. Even if we had been trained, a reliable test to accurately verify the presence of fungi has yet to be devised. So, negative results for the inadequate tests presently available do not necessarily mean that fungi are not a part of the equation for a given disease. Attitudes toward bacteria vs. those toward fungi continue to be a study in contrasts. For example, in candidemia, the spread of the Candida albicans yeast in the blood stream, only half of the blood cultures performed generate positive results. The same is true for bacterial sepsis cases. In other words, in half of all such cases, evidence supports the use of neither an antibiotic nor an antifungal. And yet, although doctors are quite willing to make a working diagnosis that bacteria lie behind sepsis-like symptoms, they hesitate to make the same kind of judgment when different symptoms point to Candida albicans. In addition, fungi are sometimes missed when clinicians use the wrong stains to prepare slides. In the textbook, Clinical Mycology, referred to above, C.C. Kibbler maintains that fungi should be included in every differential diagnosis where cancer is a possibility. That’s because, in bone diseases, x-rays of bones infected with fungi can be mistakenly interpreted as metastatic cancer, tuberculosis, sarcoidosis, rheumatoid arthritis, or eosinophilic granulomas. Kibbler tells us that distinguishing x-rays of blastomycoses bone diseases from those of cancer is particularly difficult. Some 30 percent of patients who suffer from cancers of the bloodstream also test positive for infection by fungi. As Doug mentioned earlier, while mainstream physicians insist that the drug-and-disease weakened immune systems of such patients are what allowed fungi in, we believe that the fungal toxins or the fungi themselves caused the leukemia or the lymphoma in the first place. If the above-mentioned German case reports of cancer remissions achieved after administration of antifungals are true, all the information needed for an answer has already been presented. If patients improve after they take an antifungal drug, then fungi likely caused the disease in question to begin with. Lung infections are worth taking a look at here. Cases of blastomycosis – caused by the mold, Blastomyces dermatitidis – are often confused with either primary or metastatic cancer. The infection can be present in a healthy person and spread to the prostate or to the skin, finally mimicking prostate metastases or skin cancer. In a lung biopsy, as well, patients’ cellular reaction to blastomycosis can resemble lung cancer. There is more. In the intestines, histoplasmosis can lead to growths or ulcers that mimic cancer. Zygomycosis in the stomach can cause an area of hardness and grow through various tissues, which in turn feels like a cancer upon examination. In one case, nine of ten patients were thought to have cancer until endoscopy or biopsy was performed, revealing the presence of fungi. 3 Prevention is key here. You should eat foods not heavily contaminated with molds or their toxins, and you should avoid sugar. Have a look at the antifungal program outlined toward the back of this book for more information. (We gave that to you in previous issues) Also, be sure to include in your diet foods that neutralize mycotoxins, such as broccoli and other vegetables. You have also got to exercise. If I were diagnosed with cancer, I’d look not only at my life-style, but I would also take my biopsy sample to a lab that is adept at looking for fungi. I would refuse to accept “cancer” as the final answer until I failed to prove otherwise. 1.
4/23/00 Medscape.com: “Managing fungal infections in the new millennium,”
John Rex, M.D. 2.
Treatment of fungal infections led to leukemia remissions. The Medical Tribune .Johns Hopkins Medical
Center. 29 Sept. 1999. 3.
Thompson, et. al. 1991. |