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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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Mad cows, Bretons
and manganese George Monbiot - Guardian - Thursday November 23, 2000 The most interesting aspect of France's BSE scandal is that it makes no sense at all. Britain stopped exporting contaminated cattle feed to Europe in 1991 (though we continued sending it to the third world until 1996). In most other EU countries cases have already peaked and declined, as expected. But in France, the number of infected animals has doubled in the last year. It is impossible to see how this pattern could result from the export of British bone meal. The simple fact is that the transmission of BSE has never been satisfactorily explained by the prevailing theory. The consumption of meat and bone meal from infected cows has doubtless had an important role to play. Yet this explanation alone fails to account for the huge numbers of cattle in Britain which continued to become infected after most contaminated feed had been removed from the food chain. The latest research on the human form of the disease, nvCJD, published three weeks ago, failed to find any link with the consumption of infected beef. You might have imagined that when its theory isn't working, a government would wish to test the alternatives. But the British administration has, so far, sought only to attack a hypothesis which does appear to fit the facts. Since 1988, a Somerset farmer called Mark Purdey has been arguing that scientists have overlooked the root causes of BSE. Self-taught and self- financed, he has mastered the brain's complex biochemical pathways and this year published a groundbreaking paper in a respected medical journal. His reward is to have been reviled, misrepresented and physically attacked. Prions, the brain proteins whose alteration seems to be responsible for BSE, are designed to protect the brain from the oxidising properties of chemicals activated by dangerous agents such as ultra- violet light, Purdey argues. When, he suggests, the prion proteins are exposed to too little copper and too much manganese, the manganese takes the place of the copper the prion normally binds to. This means that the protein becomes distorted and loses its function. BSE arose in British herds during the 1980s, Mark Purdey asserts, because the Ministry of Agriculture started forcing all cattle farmers to treat their animals with an organophosphate pesticide called phosmet, at far higher doses than are used elsewhere in the world. The pesticide had to be poured along the line of the spinal cord. Phosmet, Purdey has shown, captures copper. At the same time, cattle feed was being supplemented with chicken manure, from birds dosed with manganese to increase their egg yield. The prion proteins in the cows' brains were both deprived of copper and dosed with manganese. In France, the use of phosmet first became mandatory in Brittany. Twenty of the country's initial 28 cases of BSE emerged there. BSE's subsequent spread, Purdey maintains, mirrors the use of the pesticide. Poisoning by similar means may explain the distribution of the human form of the disease. Of the two main clusters in Britain one, in Kent, is in the middle of a fruit and hop growing area where huge quantities of both organophosphates and manganese-based fungicides are used. The other is in Queniborough in Leicestershire, whose dyeworks (until they caught fire a few years ago, spraying chemicals over the village) used to dump some of their residues into the sewage system, Purdey alleges. The sewage was spread over the fields. Dyeworks use shedloads of manganese. Purdey has tested his theory on BSE and CJD clusters in Iceland, Colorado, Slovakia and Sardinia. He found that people and animals had been exposed to deficiencies of copper and surfeits of manganese. Most of the clusters, intriguingly, are in mountainous areas, where levels of ultraviolet light are high. But the most compelling evidence in support of his hypothesis comes from a paper published by a team of biochemists at Cambridge this year. They found that when copper was substituted by manganese in prion proteins, the prions adopted precisely the distinguishing features which identify the infective agent in BSE. If Purdey is right, he deserves a Nobel Prize for medicine. Instead he has been shot at, his phone lines have been cut and his house has been burnt down. The Ministry of Agriculture, which for 50 years has enjoyed a dangerously close relationship with the agrochemical industry, has repeatedly sought to discredit him. Suddenly, however, its tone has changed, and it has now promised to start funding his research. The families of the French victims of CJD are threatening to sue the British government, and it desperately needs an alternative transmission theory. With funding on its way, and new evidence accumulating every month, a self-educated Somerset dairy farmer could be about to overturn the entire body of scientific research on the biggest public health scandal of modern times. |
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