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La strana storia di Mark Purdey e la mucca pazza

Sin dal 1988, Mark Purdey, un allevatore del Somerset, ha sostenuto l'ipotesi che gli scienziati non abbiano studiato a fondo le cause della BSE. Autodidatta e senza finanziatori ha indagato sui complessi meccanismi biochimici del cervello, arrivando a pubblicare un rivoluzionario e documentato studio su un'autorevole rivista medica, ottenendone però soltanto attacchi, verbali e fisici. Lo studio di Purdey inizia con l'esame delle funzioni dei prioni, le proteine cerebrali la cui alterazione sembra essere responsabile della BSE. I prioni hanno il compito di proteggere il cervello dalle proprietà ossidanti di alcune sostanze chimiche attivate da agenti esterni come i raggi ultravioletti. La sua ipotesi è che quando i prioni sono esposti a una carenza di rame e un eccesso di manganese, il manganese prende il posto del rame cui normalmente il prione si lega. In tal modo, la proteina perde la propria funzione. La prima insorgenza della BSE in Gran Bretagna, ricorda Purdey, si ebbe negli anni '80, quando il Ministero dell'Agricoltura impose a tutti gli allevatori il trattamento degli animali con un pesticida a base di organofosfati chiamato Phosmet, impiegato a dosi molto più alte che nel resto del mondo. Il pesticida veniva versato lungo la colonna vertebrale degli animali. La ricerca di Purdey mostra che il Phosmet cattura il rame. In quegli stessi anni il mangime degli animali veniva arricchito con sterco di polli proveniente da allevamenti dove gli animali erano nutriti con manganese per aumentare la quantità di uova prodotte. I prioni contenuti nel cervello dei bovini, in tal modo, venivano contemporaneamente privati di rame e intossicati dal manganese. In Francia, l'impiego del Phosmet divenne obbligatorio inizialmente in Bretagna. 20 dei 28 casi di BSE vennero alla luce proprio in quella regione. Sempre secondo le ricerche di Purdey, la diffusione della malattia coincide con quella del pesticida. Un analogo tipo di avvelenamento potrebbe spiegare la distribuzione della versione umana della malattia. Dei due principali ceppi di vCJD in Gran Bretagna, uno, nel Kent si trova nel pieno di un'area con coltivazioni nelle quali vengono usate ingenti quantità di fungicidi a base di organofosfati e manganese. L'altro ceppo è a Queniborough, nel Leicestershire, dove una fabbrica di vernici (distrutta da un incendio alcuni anni fa, con grave inquinamento chimico sul paese) ha per anni riversato parte degli scarti di lavorazione nel sistema di canalizzazioni usate per irrigare i campi. Nella produzione di vernici viene usato il manganese. Ma Purdey non si è limitato a queste indagini, andando a verificare sul campo la propria teoria sui ceppi di BSE e CJD in Islanda, Colorado, Slovacchia e Sardegna. Ovunque vi siano ceppi di queste malattie, egli ha riscontrato esposizione degli animali e degli esseri umani a carenze di rame e eccessi di manganese. La maggioranza dei ceppi, inoltre, si trovano in aree montane, nelle quali i livelli di luce ultravioletta sono alti. Ma la prova più concreta a sostegno della sua ipotesi viene da uno studio pubblicato da un'équipe di biochimici all'università di Cambridge quest'anno. Questi hanno scoperto che quando il rame viene sostituito dal manganese nei prioni, i prioni adottano precisamente i comportamenti che identificano l'agente infettivo della BSE.

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• ALTERNATE HYPOTHESES FOR THE ORIGIN OF BSE

Mark Purdey and the Mad Cows 

By Claire W. Gilbert, Ph.D. Copyright 1996 

On May 5, 1996, I conducted a long distance telephone interview with Mark Purdey of Somerset, England. 
Purdey has published scientific papers on Mad Cow Disease and he has appeared on British television regarding the same. It was his TV appearance last year which prompted the November, 1995 cover of Blazing Tattles. 
His views are not mainstream because he sees an "intervening variable" of chemicals between the healthy cow and the mad cow. I had assumed incorrectly that the "prion protein" was a figment of scientific imagination, but according to Purdey there is such a thing. The question is how the prion protein becomes "incorrectly folded." Now, before the reader says "Whoa!," let me backtrack. 

Of recent years, a disease has been observed among cattle. A sick cow drools, wobbles as if drunk, and has difficulty using its hind legs (if I have that right). Then one day it falls over dead. [The US version may be the "downer cow."]
It has been found upon autopsy that their brains are not normal, and the disease is caused from an infectious agent. It was widely believed to be a slow incubating virus, but now some scientists believe it is caused from an almost indestructible protein molecule called a "prion." It was assumed humans could not catch this disease. It is an incorrectly folded prion protein molecule, according to Purdey. 
These incorrectly folded molecules have an abnormal electrical charge which facilitate the neighboring prions to become incorrectly folded. These proteins are not destroyed by ordinary cooking and there is also no known remedy for the disease. Over a period of years, this process continues, until the cow falls ill. Purdey believes that the cause of the problem is that a chemical gets into the brain and binds with the normal prions to produce abnormal ones. He believes it is a specific chemical called "phosmet" which does this. 
Phosmet is a combination of an organophosphate pesticide (OP) and thalimide (base of thalidomide) which is used against the warble fly in cattle. The phosmet is applied on the skin in an oily base, with the intent of it being taken into the skin, into the cow's body where the fly burrows in. 
According to Purdey, the warble fly actually lives in the cow nine months of the year. The OP plus thalimide initiates the prion change. Once changed, its electrical charge can trigger normal prion protein into abnormal form. Purdey controls the warble fly with "derris root powder." It kills the warble fly and does not harm the cow -- it is not necessary to use phosmet to kill the warble fly. 
It seems researchers in many fields who get onto something regarding toxic chemicals have bad things happen. Purdey's research that was contracted out to the Medical Research Council was intercepted by the government, and one trial was cancelled while the other was mysteriously changed. The chemical he designated for the experiment was altered and diluted. The results therefrom were weakened, although still was found a slight bond with the OG and the prion protein. 

CROSSING THE SPECIES BARRIER 

A big issue today is whether the mad cow disease could cross the species barrier and be transmitted to humans or between other animal species. There is an emerging view, based on a variety of correlations, that this is possible. With respect to humans, there is a disease known as "CJD" which resembles Mad Cow Disease in that it has a long incubation period and when a fatality is autopsied, the human brain shows minuscule holes as does the cow's. 
The British believe it is caused from eating contaminated beef. CJD is an extremely rare illness and normally strikes only older people. More recently a second strain has emerged in which younger people have been affected. But Purdey says that human cases can be caused from chemicals. He says there was a cluster of CJD in Kent, England. There were four cases in four small villages. These villages are ten miles downwind of a factory which manufactures phosmet. In 1986 they had a leak and the chemical went all around the countryside. The incubation period is ten years. He says there is another cluster of this very rare disease in Teeside, where another plant is located. His conclusion is that the second strain is caused from chemicals. There's been another ominous story going around about hay mites infecting minks. Purdey says the mite prion which infected the minks was itself affected by the chemical. 

COINCIDENCE OR CONSPIRACY? 

I asked Purdey if it is true that both his veterinarian and his lawyer were killed in car crashes, and he confirmed this. His lawyer was run off the road by another car and died as a result of the accident. His new lawyer also had a car crash, but he survived. 
Purdey's house was burned down. Purdey related that the scientist, Dr. C. Bruton died in a car crash. He had just produced a paper on a new strain of CJD. Bruton was a CJD specialist. Posthumously, his work was announced to the public. It is likely or at least possible that Bruton knew more than what was in the paper, said Purdey. I asked Purdey if he thought the arrest and firing from his research position of the distinguished, US resident, Nobel Award CJD specialist, Dr. D.C. Gajdusek was also related to this mad cow situation. Purdey said that weeks before the arrest of Gajdusek Purdey was told by Ray Bradly of the Ministry of Agriculture that Gajdusek was seeking alternative hypotheses and specifically requested all of Purdey's papers. They were faxed to Gajdusek.