A Cure for Mad Cow Disease
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    "A Cure For Mad Cow Disease"

    A Cure For Mad Cow Disease
    On January 10th, 2005, the third case of "Mad Cow" disease in Canada was made public, about a month after the discovery of the 2nd case of "Mad Cow" disease in Alberta, Canada.

    At the time, at least one expert was quoted by the news as saying that we should get used to it, that "Mad Cow" disease will be with us from now on.



    This, in my view, is the height of an irresponsibility so great it staggers the mind. The reason is that "Mad Cow" disease, or to give it its proper name, Bovine Spongiform Encephalopathy (BSE) can readily become genetic. Creutzfeldt-Jacob disease is a closely related disease in humans - indeed the human form of BSE is called vCreutzfeldt-Jacob disease, where the "v" stands for "variant" - which has become hereditary a long time ago. It is in the genes of certain populations where inbreeding is a matter of religious doctrine. And the whole cattle industry is deeply and profoundly inbred for optimum meat or milk production.

    For these and other reasons, which we will outline below, it is guaranteed, and only a matter of time that "Mad Cow" disease will become genetic, if nothing is done to eradicate it. And this would be the height of an irresponsibility so great it staggers the mind - not only for allowing BSE to penetrate and spread into the genes of our deeply inbred cattle industry, but also for exposing millions of people to the high risk of vCreutzfeld-Jacob disease, the deadly human form of Mad Cow Disease.

    The deadly irony is that BSE should be easily preventable, and perhaps even curable. The simple fact is that BSE is a brand new disease, which appeared all of a sudden and for the first time in 1986 in the UK. So, something triggered it, there is a cause, and once we know the cause it can be prevented and, perhaps even cured.

    At present, the cause of BSE is thought to be in fodder which contains the malformed proteins called "prions" typical of BSE in cattle, and/or similar prions in sheep afflicted with the closely related "scrapie" disease. Consequently, it has been forbidden to include brain, nervous, endocrine and eye tissue from cattle and sheep in cattle fodder. This is a very prudent measure to be sure, but it leaves the root cause unrecognized.

    You see, scrapie has existed in the US since 1947, and scrapie infected sheep byproducts have long been included in cattle fodder. So, why did "Mad Cow" disease not appear in Canada until May 2003, and in US not until December 2003 (in a cow imported from Canada), fully 56 years after the first instance of scrapie in the US?

    And why hasn't "Mad Cow" disease not arisen independently in the US to this date, despite their cattle being fed scrapie infected fodder for more than half a century?

    So, for 56 years, both Canadian and US cattle have been immune to scrapie transmitted BSE and, apparently, US cattle still is.

    Further, and while scrapie has been known in Europe and elsewhere for about 250 years, all European cattle had been immune to scrapie infected fodder, and to BSE, until the first case appeared, all of a sudden, in 1986 in the UK. So, European cattle have been immune to scrapie infected fodder for around 250 years.

    And miraculously perhaps, Dr. Stephen Dealler, author of "Lethal Legacy", and one of the original investigators of "Mad Cow" disease, states in his book that scrapie infected sheep shipped to Australia there recovered from the disease. To date, Australia and New Zealand remain the only countries free of scrapie. Dealler also states in his book that scrapie was confined to certain farms in the UK, while other farm were completely untroubled by this deadly disease. Indeed, when the infected sheep were replaced by healthy sheep on the infected farms, the new flocks promptly came down with the disease.

    Similarly, there is the tantalizing mention in Dealler's book that many small farms in the UK remained free of "Mad Cow" disease. Why is this so? Why are only the large farms, and not the small farms affected by BSE? This, in my view, is a very important clue.

    Meanwhile, the ultimate cause of scrapie remains unknown. The original notion that scrapie is caused by the larvae of flesh flies has now been supplanted by the recognition that flesh flies are only a vector, that prions are simply transmitted by prion-infected flesh fly larvae.

    This though is known. All cases of TSE (Transmittable Spongiform Encephalopathy) are characterized by the presence of a ubiquitous normal protein which has become misfolded. This misfolded protein is called a "prion", short for proteinaceous infectious particle, because it can infect normal tissue both in the host and in other organisms - as in the well documented transmission of "Mad Cow" disease to humans. These prions then aggregate in the brain and kill adjacent brain cells which leaves holes in the brain, causing the typical "spongy" appearance for which the TSE's have been named.

    The TSE family of diseases includes bovine spongiform encephalopathy (BSE - or "mad cow" disease) which affects cattle; scrapie which affects sheep and goats; transmissible mink encephalopathy; feline spongiform encephalopathy (FSE) of cats in Europe; chronic wasting disease (CWD) of deer and elk (also a new disease first documented in 1981 in Larimer County in Colorado); and five rare human variants; kuru, both classical and variant Creutzfeldt-Jakob disease (nvCJD), Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia. TSEs have also been reported in Europe in captive wild ruminants in the bovid family, cats, and monkeys. The occurrence of TSEs in captive wild animals is believed to have resulted from prion-contaminated feed.


    normal protein malformed protein - prion
    images curtesy of University of Leicester


    Here, it is clearly apparent that some spirals in the normal protein, have failed to form from the flat amino acid ribbons in the misfolded protein.

    We now have two questions on our hands; what causes normal proteins to misfold; and how do prions infect normal proteins? We'll consider first what causes normal proteins to misfold.


    The Cause of Malfolded Protein

    All proteins are assembled in our cells from ribbons of amino acids. In every case, these ribbons are then folded into highly and precisely specific configurations - according to the electromagnetic charges and potentials of the component elements, according to the blueprint in the DNA - in order to carry out their specific functions. In most cases, an atom of a specific trace metal lies at the nexus of every fold and turn. It is our contention that a missing trace element is the cause of the misfolding of this natural protein. The following is a conceptual illustration of the cause of misfolding.


    normal protein

    normal protein
    misfolded protein

    proteinD - prion


    Here, a certain trace element which is crucial for the proper folding of the protein as in the "B" example, is missing and not available when the protein was assembled, resulting in the misfolding of the protein into the malformed "D" example. Obviously, the ability of the malformed protein to perform its normal function is sabotaged.

    Here then, we have the cause of prions, and the cure and prevention of prion caused diseases.


    The Cure of Prion Caused Diseases

  • Fact #1: All of nature operates with the complete natural range of the 72 trace elements.

  • FacT #2: Our modern agriculture knows of and maintains only 8 (eight) trace elements in its soils, feed and fodder.

    Due to this 150 year long ignorance and neglect, about 64 natural trace elements have become either severely deficient or exhausted in all chemically farmed soils, feed, fodder and food. This massive trace element deficiency is the cause of a great many diseases (see SUPREME HEALTH in these pages), among them "Mad Cow" disease and the other TSE's.

    This would explain many factors, among them the de novo, spontaneous and independent appearance of "Mad Cow" disease; the freedom from "Mad Cow" disease of the small farms in the UK, which would be more inclined to return all life wastes to the soils, and so maintain a high level of the 72 natural trace elements; the same applies to those farms which remain free of scrapie; the quick reinfection of healthy stock on scrapie prone farms; the centuries long immunity of cattle to scrapie infected fodder; and finally, the freedom from scrapie, and the 'miraculous' recovery of scrapie infected sheep in Australia, where modern agriculture was introduced only fairly recently, and where the levels of the 72 natural trace elements in the soil, and hence in feed and fodder, would be naturally high.

    The recovery of scrapie infected sheep in Australia also offers much promise that the TSE's - when not of genetic origin - could be curable.

    We now also have a remedy for "Mad Cow" disease, as well as for scrapie; and perhaps, for people infected with "Mad Cow" disease. The most readily and immediately available natural source of the 72 trace elements comes from the sea in such resources as kelp meal, seaweed meal and fish meal (both as fertilizer for soils, and as feed additives for livestock), and in a daily serving of seafood for people (all as described in these pages).

    Since sea resources are insufficient by far to supply all of modern agriculture and animal husbandry with sources of the 72 natural trace elements, the only long term solution is the extraction of a 72 trace element fertilizer from sea water. This can be easily accomplished (see SUPREME HEALTH in these pages).


    The Method by Which Prions Infect Normal Cells

    As we have seen in the "B" and "D" conceptual illustration, the malformed protein, or prion, lacks a crucial trace element. This represents a lower available state of energy, which is powerfully attractive to higher energy proteins.

    With the sole exception of Gravitation which seeks its higher available state of energy, this is a fundamental law of physics, as well as of chemistry, that all matter seeks its lowest available state of energy. Consequently, when a normal, higher state of energy protein finds itself adjacent to a lower state of energy protein, there exists a powerful force to transit to the lower state of energy - and in effect, turn into a prion. This then is the method and driving force by which the prion 'infects' other proteins within is radius of influence.

    We may well ask then why does the normal protein exist at all, if a lower state of energy - the prion state - is readily available.

    First of all, the normal protein is constructed according to the blueprint in the responsible gene. This state is a certain and exquisitely specific "stratum of Complexity" in which the normal protein is the lowest available stat of energy.

    However, when a certain trace element is not available when the normal protein is being assembled, this results in a lower stratum of Complexity, in which the malformed protein - ie. the prion - is the lowest available state of energy. To illustrate:


    strata of progressive complexity


    Strata of Progressive Complexity constitute their own specific and intrinsic Strata of Stability (see COMPLEXITY in these pages), all of which is energy-determined. Each Stratum of Progressive Complexity/Stability accommodates its own specific range of maximal and minimal energy, and when these maximal or minimal levels of energy are exceeded, a quantum phase shift occurs to either the next higher, or next lower Stratum of Complexity/Stability, determined by whether there is an influx or loss of energy.

    The crux of the matter, and the great danger here is that the lower ("D" - or prion) level of complexity becomes the universally preferred level - driven by the universal law that matter seeks its lowest available state of energy - the law that also governs the folding of proteins.





  • Mad Cow, Mad Humans?






     






















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