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Common Diseases > Creutzfeld Jakob Disease (& Mad Cow Disease) BSE is the bovine version of a larger class of diseases called "transmissible spongiform encephalopathies," (TSEs) that can afflict most mammals including humans. The symptoms of TSEs are the same in all species, an infection leads to the progressive destruction of brain cells, dementia and death. A New Variant In Britain where the most severe BSE outbreaks occurred, citizens began to die of a new disease, called "new variant of Creutzfeld-Jakob disease" or NVCJD. CJD (Creutzfeld-Jakob disease) had been recognized for a long time and occurs occasionally in different countries but it almost never occurs in people younger than 30, but the NVCJD affects people as young as 13 and research published late in 1999 showed that NVCJD is a human form of mad cow disease proving that the species barrier cannot protect humans from this deadly bovine affliction. Causes of CJD The cause of CJD is not clear and many believe that it is because cattle have been fed animal products or that BSE and CJD May be Due to Environmental Contamination with Manganese Compounds and Organophosphates. For years the British establishment has largely ignored a hypothesis proposed by Mark Purdey (a Somerset farmer and biochemist) who links BSE and CJD to oil soluble organophosphates and high levels of manganese oxide. Evidence in support of Purdey's hypothesis continues to mount. It is outlined briefly below. A more detailed summary of the hypothesis, recently published in "Medical Hypothesis" is also available. The essence of Purdey's research is that certain proteins in the brain owe their structural stability to the presence of copper ions. Cattle or humans can be contaminated with oil soluble organophosphates that effectively remove those copper ions. At the same time there can be high uptakes of manganese salts in the animal or human. This can occur due to high manganese levels in the soil; in growth enhancing chicken feed (chicken manure is later incorporated into cattle feed); or manganese formulated into fungicides. Either way the manganese ion can be absorbed by the body and bind to the proteins in the brain instead of copper. Conformational changes occur that result in the formation of proteins called prions that are resistant to the body's natural enzymes. Spongiform encephalophathy (BSE in cattle or CJDnv in humans) develops. Purdey's hypothesis (backed up by work by David Brown at Cambridge University) explains many puzzling events that at first glance are unrelated. It explains: why BSE occurred in UK cattle and not in Australian cattle (Phosmet, an oil based organophosphate was compulsorily used in the UK to control Warble Fly in cattle why life long vegetarians have developed CJDnv and why CJDnv cases are higher for market gardeners (contamination occurred from organonophosphates and manganese containing fungicides)why some U.S. deer are infected with a wasting disease (pine needles that they feed on are high in manganese)why there are hot spots for CJD around the world (high manganese in the soil) why manganese mine workers in South America had similar symptoms to CJD. To date there has been considerable opposition to Purdey's hypothesis and research. There needs to be a more open mind on the cause of CJD and Purdey's explanation for the disease should be researched, not shunned. Does the contaminant manganese cause the displacement of copper in glycoproteins (prions) leading to CJD and BSE? Ecosystems supporting clusters of sporadic TSEs (transmittable Spongiform Encephalophathy) demonstrate excesses of the pro-oxidant manganese cation and deficiencies of antioxidant co factors; copper, selenium, iron, zinc. Mark Purdey, Medical Hypotheses, (2000), 54(2). The current theory on transmittable Spongiform Encephalophathy (TSE) is that it is transmitted via micro quantities of a yet to be identified "slow viral" agent found in animal feeds containing central nervous tissue. However, this explanation does not account for many of the cases of "new variant" Creutzfeld Jakob Disease (nvCJD) found around the world. In "Medical Hypotheses", (2000), 54(2), Purdey proposes that transmittable spongiform encephalopathy (TSE) can be initiated in humans or animals by a combination of the following: low levels of copper and high levels of the contaminant manganese in the diet, low levels of antioxidant cofactors, selenium, iron and zinc in the body, higher levels of estrogenic compounds that enhance the uptake of manganese, and presence of organophosphates that remove copper from the body. In the body, manganese will replace copper in glycoproteins (called prions), resulting in conformational changes and free radical cascading reactions throughout the body leading to TSE diseases such as BSE and CJD. Prions Purdey suggests that in the development of TSEs, prions (metalloglycoprotiens), can become depleted of their copper cation. Depletion of copper in the body can either occur through copper complexing with organophosphates that have been introduced, or due to the presence of manganese compounds and excessive calcium. Manganese (or nickel) can replace the copper ion within the prion while calcium can impair the uptake of copper. As a result, the prion can misfold into an abnormal protease resistant protein. This abnormal prion can infect otherwise normal systems in the body, leading to diseases such as CJD and BSE. Source of manganese Manganese (manganese sulphate, manganese oxide etc) used to be added to poultry feed to promote egg and broiler production and rearing. Considerable quantities (95%) ended up in the chicken manure. The manure was incorporated into cattle feed as both a binder and source of protein. Manganese also entered the cattle’s food chain from other by-products such as rice bran. Manganese is found in some fungicides such as "Maneb". Maneb is used in a few countries on crops/fruit post harvest to prolong shelf life. The mining of manganese particularly in South America has lead to a disease in miners with marked similarities to CJD and BSE. Manganese is shown to be 2.5 times higher in regions around the world where CJD/BSE is prevalent. Manganese is considered to be more efficiently absorbed in ruminants (cattle, sheep, goats) compared to monogastric species (pigs and poultry). This may explain why pigs and poultry are relatively free of TSE. Manganese is rendered less available in some food sources eg after drought or protracted sunlight, but it can accumulate considerably in other food sources eg pine needles (feed for deer). Manganese and its action In environments low in the antioxidant cofactors: copper, iron, zinc and selenium, manganese 2+ can be oxidised to Mn3+ and beyond, becoming a lethal pro oxidant. This pro oxidant can catalyze free radical reactions involving the auto oxidation of dopamine, serotonin and other catecholamines (chemical transmitters in the body). Higher valency states of Mn are not only more reactive, Mn3+ complexes to transferrin and crosses cell membranes. Manganese is considered to accumulate more readily in early life when the homeostatic mechanisms controlling and balancing absorption/excretion are less developed. The conformational change in the prion is only the beginning of a series of changes in the body. This is supported by the fact that manganese chelating agents are only effective in the primary stages of TSEs and not secondary stages. The presence of free radical chain reactions that result later may explain the incubation period before pathological changes are seen. There are various biochemical reactions that manganese can disrupt Manganese can disrupt the structural stabilisation and activation of glutamine synthesaze, leading to accumulation for the neurotoxic glutamate instead of glutamine. In the body there are glycosaminoglycans that bind to glycoproteins and protect the glycoprotein from bonding with abnormal prions. However, manganese can cause the overactivation of Lectins in the body. A lectin, concanavalin A, is known to bind to glycosaminoglycans impairing its normal protective function against abnormal prions. Estrogen Individuals low in copper or iron show a marked increase in the absorption of manganese. Estrogen also mediates a dramatic increase in absorption of Manganese, while suppressing copper absorption. A proportionately large number of body builders & gymnasts have contracted nvCJD (due to the hormone therapies?) Organophosphates Phosmet, a systemic insecticide (i.e. oil based, to ensure skin penetration), was compulsorily used in the UK to control warble fly on cattle in the 1980s. It is proposed that this organophosphate complexed out the copper from the glycoproteins. (It is understood Australia has used Phosmet, but only in the aqueous form where there was little risk of skin penetration.) CJD clusters Purdey looked at 3 TSE clusters: chronic wasting disease in deer in N. central Colorado, sheep scrapie in N. Iceland, and CJD in Slovakia. Purdey was able to show that compared to control areas, these regions were higher in manganese and low in copper. Purdey also noted that Guernsey, which has the highest incidence of BSE in the world and Brittany, which has 20 of the 28 BSE cases in France, both have soils deficient in copper. Weald district in Kent, England has a high incidence cluster of CJD. This is an area of hop farming where the manganese fungicide Maneb is used in conjunction with systemic organophosphates. A paper in the Lancet demonstrated a high incidence rate of sporadic CJD amongst market gardeners and farmers in Australia where 83 out of 241 confirmed cases were involved. Was this due to use of organophosphates? Included in the TV documentary were interviews with human CJD sufferers/ caregivers and the symptoms were sever. What was lacking was any discussion on treating patients with supplements of copper and other trace minerals. This may also work with livestock if the pathology involving manganese is similar. Mark Purdey's website can be visited at http://www.purdeyenvironment.com. More information can also be found at www.mad-cow.org. |
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