Mad Cow Disease - Alternative Causes and Treatments




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Purdey: foreign cation substitution creates prion TSE? Feb 2000

From: (jean hudon)
Date:      26 Jan 2001
Subject:  Re: Mad Cow disease

Hello Jean,
Perhaps you would like to read these articles to expand your view on BSE. I agree fully with you that organic farming is the only way into a healthy future. Let us bring the informations out to the people all the best.   

Med Hypotheses 2000 Feb;54(2):278-306
Ecosystems supporting clusters of sporadic TSEs demonstrate excesses of the radical - generating divalent cation manganese and deficiencies of antioxidant co factors Cu, Se, Fe, Zn. Does a foreign cation substitution at prion protein's Cu domain initiate TSE? 
Purdey M
High Barn Farm, Elworthy, Taunton, UK.

Analyses of food chains supporting isolated clusters of sporadic TSEs (CWD in N Colorado, scrapie in Iceland, CJD in Slovakia) demonstrate a consistent 2 1/2+ fold greater concentration of the pro-oxidant divalent cation, manganese (Mn), in relation to normal levels recorded in adjoining TSE-free localities. Deficiencies of the antioxidant co factors Cu/Se/Zn/Fe and Mg, P and Na were also consistently recorded in TSE foodchains. Similarities between the clinical/pathological profile of TSEs and Mn delayed psycho-neurotoxicity in miners are cited, and a novel theory generated which suggests that sporadic TSE results from early life dependence of TSE susceptible genotypes on ecosystems characterised by this specific pattern of mineral imbalance. Low Cu/Fe induces an excessive absorption of Mn in ruminants and an increased oxidation of Mn2+ into its pro oxidant species, Mn3+, which accumulates in mitochondria of CNS astrocytes in Mn SOD deficient genotypes. Deficiencies of scavenger co-factors Cu/Zn/Se/Fe in the CNS permits Mn3+ initiated chain reactions of auto-oxidant mediated neuronal degeneration to proliferate, which, in turn, up-regulates the expression of the Cu-metalloprotein, prion protein (PrP). Once the rate of PrP turnover and its demand for Cu exceeds the already depleted supply of Cu within the CNS, PrP can no longer bind sufficient Cu to maintain its conformation. Mn3+ substitutes at the vacated Cu domain on PrP, thus priming up a latent capacity for lethal auto-oxidative activity to be carried along with PrP like a 'trojan horse'; where Mn 3+ serves as the integral 'infectious' transmissible component of the misfolded PrP-cation complex. The Mn overactivation of concanavalin A binding to glycoprotein and Mn-initiated autoxidation results in a diverse pathological profile involving receptor capping, aggregation / modification of CNS membrane / cytoskeletal proteins.   TSE ensues. The BSE/nv CJD strain entails a 'synthetic' induction of the same CNS mineral disturbance, where 'in utero' exposure to Cu-chelating insecticides/Mn supplements accelerates the onset of a more virulent 'strain' of adolescent TSE. 
Copyright 2000 Harcourt Publishers Ltd. Publication Types: Review    Review, academic PMID: 10790765, UI: 20253832
Med Hypotheses 1998 Feb;50(2):91-111
High-dose exposure to systemic phosmet insecticide modifies the phosphatidylinositol anchor on the prion protein: the origins of new variant transmissible spongiform encephalopathies?
Purdey M
High Barn Farm, Elworthy, Taunton, Somerset, UK.

Compulsory exposure of the UK bovine to exclusively high biannual doses of a 'systemic' pour-on formulation of an organo-phthalimido-phosphorus warblecide, phosmet, during the 1980s (combined with exposure to the lipid-bound residues of 'bioconcentrated' phosmet recycled back via the intensive feeding of meat and bone meal), initiated the 'new strain' modification of the CNS prion protein (PrP) causing the UK's bovine spongiform encephalopathy (BSE) epidemic. A lipophilic solution of phosmet was poured along the bovine's spinal column, whence it penetrated and concentrated in phospholipids of the CNS membranes, covalently modifying endogenous phosphorylation sites on phosphatidylinositols (PIs) etc., forming a 'toxic membrane bank' of abnormally modified lipids that 'infect' any membrane proteins (such as PrP) that are programmed to conjugate onto them for anchorage to the membrane. Thus, phosmet invokes a primary covalent modification on PrP's PI anchor which, in turn, invokes an overall diverse disturbance upon CNS phosphoinositide second messenger feed back cycle, calcium homeostasis and essential free radicals; thus initiating a self-perpetuating cascade of abnormally phosphorylated PI-PrP that invokes a secondary electrostatic and allosteric disturbance on the main body of PrP impairing tertiary folding. Chaperone stress proteins conjugate onto misfolded PrP blocking its sites of proteolytic cleavage. Fresh epidemiological evidence is presented and experimental evidence referenced that adds support to a multifactorial hypothesis which proposes that BSE is a hitherto unrecognized and previously unmanifested class of subtle chronic phosmet-induced delayed neuro - excitotoxicity in the susceptible bovine.
Publication Types: Review  Review, academic
PMID: 9572563, UI: 98232276

Purdey M.
Ecosystems supporting clusters of sporadic TSEs demonstrate excesses of the radical-generating divalent cation manganese and deficiencies of antioxidant co-factors Cu, Se, Fe, Zn. Does a foreign cation substitution at prion protein's Cu domain initiate TSE?
Med Hypotheses. 2000 Feb;54(2):278-306. Review.
PMID: 10790765; UI: 20253832

Purdey M.
High-dose exposure to systemic phosmet insecticide modifies the phosphatidylinositol anchor on the prion protein: the origins of new variant transmissible spongiform encephalopathies?
Med Hypotheses. 1998 Feb;50(2):91-111. Review.
PMID: 9572563; UI: 98232276

Purdey M.
The UK epidemic of BSE: slow virus or chronic pesticide-initiated modification of the prion protein?
Part 2: An epidemiological perspective.
Med Hypotheses. 1996 May;46(5):445-54.
PMID: 8735882; UI: 96330947

Purdey M.
The UK epidemic of BSE: slow virus or chronic pesticide-initiated modification of the prion protein? Part 1: Mechanisms for a chemically induced pathogenesis / transmissibility.
Med Hypotheses. 1996 May;46(5):429-43.
PMID: 8735881; UI: 96330946
Purdey, M.
Are organophosphate pesticides involved in the causation of bovine spongiform encephalopathy (BSE)? Hypothesis based upon a literature review and limited trials on BSE cattle.
Journal of Nutritional Medicine
1994 , Vol. 4 , No. 1 , pp. 43-82  UK , En , 229 ref.
High Barn Farm, Elworthy, Lydeard St Lawrence,
Taunton, Somerset TA4 3PX, UK.

This paper questions the view that spongiform encephalopathies, particularly bovine spongiform encephalopathy, are solely due to infection with an ultrafilterable protein called a prion. The literature is reviewed and date and circumstantial evidence presented to support the hypothesis that the BSE epidemic in the UK was initiated as a result of a combination of factors. These factors, it is suggested, were genetic, nutritional and chronic exposure to mutagenic organophosphate pesticides which disrupt the genetic pathway of prion protein synthesis. Possible mechanisms are discussed and the broader implications of modern farming practices examined.
Organophosphate Madness?   by   Si Mitchell

When a cluster of new variant (nv) CJD victims were discovered in and around the Leicestershire village of Queniborough in June, fingers began to point at local butchers and school meal caterers. The government line has always been that Mad Cow Disease came about by feeding scrapie infected meat and bone meal to cows. However there is a different theory. One that the authorities and the pesticide producers have gone to great lengths to silence. Si Mitchell unveils the other elements at work in the Leicestershire countryside.

Since 1982 British farmers have been forced by law to treat their cows for warble fly with a pour-on systemic organophosphate called phosmet1 - originally formulated as a weapon by Nazi chemists during World War II[2]. The money men were soon to realise its profit potential and after the war it was exclusively marketed as an agricultural pesticide by ICI, and later their renamed subdivision Zeneca[3].

One farmer, Mark Purdey, refused to treat his Somerset herd with the nervous system - attacking toxin after observing how his own organically reared cows never developed BSE, but phosmet-treated cattle brought onto the farm did. In 1984 the Ministry of Agriculture, Fisheries and Food (MAFF) took him to the High Court, but a judicial review found in his favour, ruling that the government couldn't enforce treatment as it was neither a vaccine or serum.[4]

"Before 1982 farmers could treat warbles with an organic ground-up root compound called derris. This was outlawed, so they could sell more organophosphates," said Purdey. "You can pick warbles out by hand, they don't really harm the cows, just make skin holes which the leather industry don't like."

Organophosphates (OPs), used to treat headlice in school children, have been identified as one potential cause of Gulf War Syndrome[5] (Purdey managed to allieviate symptoms in a BSE infected cow by injecting oxime, an antidote to pesticide poisoning. The cure was never completed as MAFF turned up and destroyed the cow). For years schools advised parents to treat lice with malthion (an OP similar to phosmet) - since the Queniborough Mad Cow Disease cluster's exposure, the local authority have been questioning parents. However whether lice treatment appears on their questionnaire is not known - the document is being kept under wraps. Phosmet also contains thalimide[6], the chemical base of thalidomide, a drug which caused severe birth defects in the 1960s.


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Unconvinced by the accepted cause of Transmissible Spongiform Encephalopathy (TSEs -- the kind of brain disease that includes BSE and CJD), Purdey set about studying the epidemiology of these diseases and how their clustering reflected OP usage.

He found Britain, the only country enforcing phosmet use, to have the highest rate of TSEs. Ireland had some BSE, but OP use was voluntary, and given at a lower dose (6mg/kg annually, compared to Britain's twice yearly 20mg/kg-- British phosmet is also produced at a higher initial concentrate). Brittany began to develop BSE following an enforced phosmet trial, after which the disease began to appear across France, reflecting the spread of OP use too. Purdey also found nvCJD in people to be clustered in the Weald Valley in Kent, where hop and top fruit growth attract a hundred-fold levels of systemic OP spraying[7].

Similarly meat and bone meal feed is peddled all over the world, including the Middle East where there hasn't been a single case of Mad Cow Disease, and US scientists have been force-feeding scrapie-infected gunk to cows for years without managing to give them BSE.

Agitated by Purdey's discoveries, the pesticide industry hit back. The dubiously named National Office of Animal Health (NOAH), a lobby group representing the UK animal medicine industry (whose membership reads like a White House dinner party invite list[8] - includes Bayer, Monsanto, Novartis, Pfizer, Roche, Schering-Plough, Intervet) published documents discrediting Purdey's work[9]. In a briefing paper to Lord Philips' BSE inquiry[10] -- who were due to publish a year ago, but are still taking statements - NOAH said Purdey's facts "do not add up". They said: "Many independent experts [have said] a relationship between OPs and BSE does not exist." To back it up NOAH claimed that warble treatment took place in Jersey but not Guernsey, yet there was five times the BSE in Guernsey than Jersey. They wrote to science editors explaining that phosmet was licensed in New Zealand and Australia, yet no cases of BSE had occurred there. Purdey dismisses their argument: "They twist the facts - phosmet was used in Guernsey, but as a lice treatment. And the stuff used in Australia and New Zealand was non-systemic (ie it doesn't penetrate the skin and subsequently every organ) as it was dissolved in water, not oil as in Britain."

NOAH's independent expert, Dr David Ray, turned out to be receiving funding from Zeneca for his Medical Research Council toxicology unit[11].

"I don't think this affected my judgement," says Ray. "You may not believe it, but I didn't realise Zeneca produced phosmet at the time."

Ray chose not to test with phosmet, but with another organophosphate, DFP. He also used synthetic brain proteins, which Purdey believes would have reacted differently to their natural counterparts.

In January Ray was appointed to the Veterinary Products Committee (VPC), a quango of academics and farmers, whose job is to scrutinise the safety of animal medicines before licences are issued (and review existing-licences, like phosmet's).

Ray said that the interests he has with pesticide producers will not affect his judgement on the VPC. He admitted that Astra (now merged with Zeneca) still fund a research post in his unit, as does the pharmaceutical company Bayer. Neither of these corporate links are listed in Ray's declared interests.[12] "There are two ways to get bad pesticides off the market: ban them, or get the companies to develop better pesticides," he says.

Food Safety Minister Baroness Hayman, reportedly told the committee that she recognised the need for 'experts' with links to industry. Less than a quarter of VPC members have no declared financial interest in the pharmaceutical industry. Professor Karl Linklater, for example, holds commercial consultancies with pharmaceutical producers including Intervet, Novartis, Roche and Shering-Plough[13] (when approached about their funding sources, the Scottish Agricultural College-- of whom Linklater is Principal and Chief Executive-- refused to co-operate, citing 'commercial confidentiality'). Pfizer has two consultants on the committee as does Grampian Pharmaceuticals.

Hoechst, SmithKline Beecham, the Wellcome Trust and Merck, are all represented in the declarations of interests of VPC members. A similar picture is painted by the declarations of the Spongiform Encephalopathy Advisory Committee (SEAC), which advise the government on CJD and BSE, and the other committees set up under the Medicines Act to ensure pharmaceutical safety.

According to Richard Young of the Soil Association, the Thatcher government's withdrawal of state funding for research into medicines that were nearing a marketable state left only industry-funded research, or no research at all: "There are very few academics who aren't in some way beholden to industry," he says. During the 1980's, when the academic / industry grip was weaker, a VPC sub-committee attempted to scrutinise the merit of antibiotic livestock feed additives. When hindered by the VPC, the committee's chair James Howie wrote to the then MAFF Minister, Peter Walker, who immediately disbanded the committee.

In March 1996 - one week before the UK government admitted to a link between BSE and nvCJD - Zeneca 'sold' the phosmet (trade name Imidan) patent to a previously unheard of PO Box company in the Arizona desert called Gowan[14]. As Ray says: "Zeneca are not keen to be sued."

In her submission to the BSE inquiry, dairy farmer Joanna Wheatley says: "The initial epidemiological study carried out in 1988 that identified meat and bonemeal as the cause of BSE was flawed. It recorded 68 per cent of farms affected by the disease had not used chemicals or weed killers. This could not possibly be the case." Wheatley points out that OP treatment was enforced on all farms and organic farming was rare and viewed with suspicion by the majority of farmers in the 1980s.

Taking his research overseas Purdey discovered clusters of CJD downwind of large ferromanganese and glass factories in Slovakia; around a missile production plant in Tucson; and around the scene of the Seveso disaster in Milan-- where a pesticide factory exploded in 1976. Similar scrapie clusters appeared in sheep in certain volcanic areas of Iceland. Soil, water and plant samples in all these areas showed high levels of manganese and low levels of copper.

Intrigued by Purdey's findings, a Cambridge University chemist, Dr David Brown, carried out tests which found that not only could manganese replace copper in the brain proteins, but it transformed them into the protease resistant isoforms that are found in TSE diseased brains[15]. Purdey reckons that phosmet prevents the brain proteins bonding with the copper, which is subsequently replaced by manganese - readily available to cows in high dose mineral licks. The CJD and BSE symptoms also mirror 'manganese madness', an irreversible fatal neuro-psychiatric degenerative syndrome that plagued manganese miners in the first half of the last century[16].

Queniborough has an agricultural college and experimental farm nearby[17]. It is situated on an outfold of pre-cambrian manganese-heavy rock that is being quarried locally, and a chemical distribution company, Omnichem, is based in the area. None of these activities have been mentioned in reports.

"If phosmet is proven to have caused BSE, the worldwide use of organo - phosphates could be put into jeopardy, costing the chemical industry billions. The government know more than they're letting on. They've stuck to the scrapie theory to placate people and give the impression they've got it under control," says Purdey.

Whether Purdey is a genius or a paranoiac, MAFF's continued reluctance to explore the OP link to BSE is significant. According to a spokesman: "Anyone with a suitable proposal [concerning the cause of BSE] can approach MAFF for funding." However Brown could not continue his research as he couldn't get more funding, and another chemist, Steven Whatley, had to stop similar tests a year ago for the same reasons.

Richard Young, of the Soil Association, says: "If it could be established that BSE was caused by OPs it would be a major liability issue for both the government and manufacturers."

More sinister is the attention that Purdey, and those who have taken up his theory, have received. Purdey's house was mysteriously burnt down and a structurally sound barn collapsed onto the caravan that housed his science library. He's been shot at[18] (another anti OP campaigner's husband had his fingers broken), and following the publication of an Independent newspaper article in 1993, he awoke to find his telephone lines cut-- preventing him receiving follow-up media calls. He says strangers with in-depth knowledge of his movements appear on his farm freaking out his wife, and when he travels to talk about his theory he is constantly tailed. The solicitor who defended his High Court action died when his car went inexplicably out of control. Purdey's vet (who said Purdey's theory should be taken seriously) was killed in what the local paper described as: 'Mystery Vet Death Riddle' when his car was "magnetised" into the front of an oncoming lorry on a clear straight road.

"I'm easier to marginalise as a crank," said Purdey, "but these people were professionals."

Anyone familiar with the start of the anti-nuclear movement, may recall the discrediting of Alice Stewart who discovered the link between radiation and cancer. Scientists who aligned themselves with her had their cars rammed off the road.19 In 1978 four children belonging to anti-herbicide activist Carol Van Strum were killed in a house fire in Five Rivers, USA. In 1993, also in America, a couple who filed a suit against Merck - claiming contamination from their plant had caused the death of their unborn baby - had their house broken into eleven times and a doctor who was helping them had his dog's throat cut.20

Officials from MAFF met with Purdey in the spring, to 'help' him apply for funding to further his research, though a promised meeting with the Food Safety Minister never materialised.

The MRC's David Ray says he is interested in identifying OP toxicity and that all new scientific theories should be tested. Except for Purdey's which is "implausible". "I'm not the only scientist around," says Ray. Though, of course, uncovering their own complicity in a killer disease is not the sort of research that chemical companies flock to fund. In February of this year the US Environmental Protection Agency began reassessing phosmet as a health hazard to farm workers. Sources within MAFF say they are about to take the possibility of linking OPs and BSE seriously - but whether they wish to take the issue up in order to discredit it, remains to be seen.

Mark Purdey is funding his research (testing /labs/travel to cluster sites) himself (no corporate backing on his side of the fence)-- any donations to his research fund will help him carry on. Send to: Mark Purdey Research Fund, High Barn Farm, Elworthy, Nr Taunton, Somerset TA4 3PX

[1] MAFF Warble Fly Order 1982
[2] IG Farben developed organophosphate sarin as chemical nerve agent weapon for the Nazis.
[3] Extonet - Extension Toxicology Network-- pesticide information profiles June 1996
[4] Mark Purdey statement to BSE Inquiry 23.3.98
[5] Sarin gas (organophosphate) used by Saddam Hussein during Gulf War-- in the frame as a possible cause of Gulf War Syndrome.
[6] Claire Gilbert, Blazing Tattles, New Theory, New Intrigue and the Mad Cows, June 3, 1996
[7] Mark Purdey Journal of Medical Hypotheses February 2000
[8] NOAH corporate membership list
[9] NOAH briefing notes to editors April and September 1998
[10] NOAH statement to BSE Inquiry
[11] David Ray statement to BSE Inquiry June 1998
[12] Medicines Act Advisory Bodies, Annual Report 1998
[13] Medicines Act Advisory Bodies, Annual Report 1998
[14] Department of Pesticide Regulation Branch, Notice of Proposal and Final Decisions and Directors Findings
[15] David Brown, Embojournal Spring 2000
[16] Manganese: a review of occupational and environmental toxicology--
V Benko and M Cikrt, Journal of Hygeiene, Epidemiology, Microbiology and Immunology 28(2)1984. Manganese exposure in steel smelters a health hazard to the nervous system -- A Wennberg, Scandinavian Journal of Work, Environment and Health August 1991
[17] Brooksby Agricultural College
[18] The Independent 11.3.97
[19] The Woman Who Knew Too Much, Alice Stewart and the Secrets of Radiation -- Gayle Green, University of Michigan Press
[20] Green Backlash - Andrew Rowell, Routledge
BSE INQUIRY      Statement of Mark Purdey (23 March 1998)

I am a dairy farmer currently farming at High Barn Farm, Elworthy, Taunton, Somerset. I was educated at Forres School, Swanage and then was admitted to the scholarship form at Haileybury College, Hertford. In 1972 I declined a university place to study zoology and psychology, in order to start a pioneering organic farming community in the west of Ireland. I have been farming ever since. I am also an independent scientist involved in the aetiology of TSEs, investigating for environmental factors in isolated clusters of TSE all over the world and have published five articles on the BSE/Organo phosphorus theory in peer-reviewed science journals with one article shortly to be published.

[Murray: This document gives extensive details of  Mark Purdey's experiences, research, and discoveries.]

Issued on behalf of the witness by:
The BSE Inquiry Press Office
6th  Floor Hercules House
Hercules Road
London SE1 7DU
Tel: 0171 261 8383 / 8385 / 8377
Fax: 0171 803 0893

Rich Murray, MA    Room For All
1943 Otowi Road   Santa Fe, New Mexico  87505 USA


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