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Mark Purdey

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Comment - BSE Press Release - 2nd September 2005

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1994-2001 - Mark Purdey - Lectures

 

 

Mark Purdey - Biography

I was born on December 25, 1953 in the village of Much Hadham in the UK. I am a descendent of the globally renowned "Purdey shotgun" family and was educated at Haileybury College private school,  and then accepted into London University to study Zoology and psychology.

In my mid twenties, I pioneered an organic dairy farm on which I bred up a herd of pedigree Jersey cattle. 

Breeding was designed to produce cattle that demonstrated longevity and an ability to produce milk from a self-sufficient arable/legume-grass rotational system with minimal reliance upon purchased in concentrate feed. Semen was introduced from New Zealand, Danish and Canadian blood lines in an attempt to breed a high fat, high yielding, pasture fed, robust and ideal conformation jersey cow. One of our home bred cows turned out to be the highest yielding jersey cow in the UK in 1997 (10,150 litre lactation), after she had been sold onto a conventionally managed dairy farm.

I initiated research into the environmental prerequisites of transmissible spongiform encephalopathies after BSE erupted in four cows that I had purchased onto my farm. None of my farm bred cows ever contracted BSE. My early research and observations demonstrated that both sporadic and new variant forms of TSE (BSE, vCJD) are unlikely to be infectious through either animal to animal, or animal > environment > animal contact.

I designed and embarked upon my own self funded pilot field studies which involved a total eco-analyses of several noted TSE cluster and TSE-free zones around the world. The results suggested that a combination of high manganese/ low copper and high environmental oxidizing agents (such as ultra violet radiation) could initiate a self-perpetuating free radical mediated neurodegenerative disease process (e.g., a TSE) in susceptible genotypes.

Follow up research at Cambridge University confirmed my published hypotheses, that manganese would bond to the vacated copper domain on prion protein and form the misfolded prion protein - the protease resistant isoform that is a central hallmark of the spongiform diseased brain. Neuropathological surveillance of CJD brain tissue at Case Western University, Cleveland, Ohio, recorded a ten-fold increase in manganese and 50 percent reduction in copper in CJD brain tissue in relation to control brains.

Kobe University in Japan ran experiments where they beamed manganese prion cell cultures with ultra violet radiation. The prions subsequently aggregated into the fibril formation, which is the key characteristic tombstone feature of the TSE diseased brain.

Although not accepted, as yet, by the conventional scientific establishment, my work has been widely debated in Europe and I have lectured around the world. 

My investigative journey into the origins of TSEs has been featured on several UK television documentary films, and I have been invited to address many UK government scientific advisory committees and the BSE Phillips Inquiry, as well as meet to discuss with HRH Prince of Wales and the former UK Minister of Defense, Lord Tom King.

Bibliography (click on the leaf to the left of the titles to view/download those available on the site

1: Purdey M. Related Articles, Links 
Auburn university research substantiates the hypothesis that metal microcrystal nucleators initiate the pathogenesis of TSEs.
Med Hypotheses. 2005 Oct 12; [Epub ahead of print] No abstract available. 
PMID: 16226390 [PubMed - as supplied by publisher]

2: Purdey M. Related Articles, Links 
Metal microcrystal pollutants; the heat resistant, transmissible nucleating agents that initiate the pathogenesis of TSEs?
Med Hypotheses. 2005;65(3):448-77. 
PMID: 15908137 [PubMed - in process] 

3: Purdey M. Related Articles, Links 
The pathogenesis of Machado Joseph Disease: a high manganese/low magnesium initiated CAG expansion mutation in susceptible genotypes?
J Am Coll Nutr. 2004 Dec;23(6):715S-29S. Review. 
PMID: 15637221 [PubMed - indexed for MEDLINE] 

4: Purdey M. Related Articles, Links 
Elevated levels of ferrimagnetic metals in foodchains supporting the Guam cluster of neurodegeneration: do metal nucleated crystal contaminents evoke magnetic fields that initiate the progressive pathogenesis of neurodegeneration?
Med Hypotheses. 2004;63(5):793-809. 
PMID: 15488650 [PubMed - indexed for MEDLINE] 

5: Purdey M. Related Articles, Links 
Elevated silver, barium and strontium in antlers, vegetation and soils sourced from CWD cluster areas: do Ag/Ba/Sr piezoelectric crystals represent the transmissible pathogenic agent in TSEs?
Med Hypotheses. 2004;63(2):211-25. 
PMID: 15236778 [PubMed - indexed for MEDLINE] 

6: Purdey M. Related Articles, Links 
Chronic barium intoxication disrupts sulphated proteoglycan synthesis: a hypothesis for the origins of multiple sclerosis.
Med Hypotheses. 2004;62(5):746-54. 
PMID: 15082100 [PubMed - indexed for MEDLINE] 

7: Purdey M. Related Articles, Links 
Does an infrasonic acoustic shock wave resonance of the manganese 3+ loaded/copper depleted prion protein initiate the pathogenesis of TSE?
Med Hypotheses. 2003 Jun;60(6):797-820. 
PMID: 12699706 [PubMed - indexed for MEDLINE] 

8: Bounias M, Purdey M. Related Articles, Links 
Transmissible spongiform encephalopathies: a family of etiologically complex diseases--a review.
Sci Total Environ. 2002 Oct 7;297(1-3):1-19. Review. 
PMID: 12389776 [PubMed - indexed for MEDLINE] 

9: Purdey M. Related Articles, Links 
Does an ultra violet photooxidation of the manganese-loaded/copper-depleted prion protein in the retina initiate the pathogenesis of TSE?
Med Hypotheses. 2001 Jul;57(1):29-45. Review. 
PMID: 11421622 [PubMed - indexed for MEDLINE] 

10: Purdey M. Related Articles, Links 
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 [PubMed - indexed for MEDLINE] 

11: Purdey M. Related Articles, Links 
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 [PubMed - indexed for MEDLINE] 

12: Purdey M. Related Articles, Links 
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 [PubMed - indexed for MEDLINE] 

13: Purdey M. Related Articles, Links 
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 [PubMed - indexed for MEDLINE] 

____________

Purdey M, Mad Cows and Warble Flies.  Ecologist 1994 24 (3) 100-104.

Purdey M, Degenerative Nervous Diseases and chemical Pollution. Ecologist 1994 24 (3) 100-104.

Purdey M, BSE, Ecologist 2002 32 (9) 33-37.

Purdey M, The manganese loaded/Copper depleted bovine brain fails to neutralise incoming shockbursts of low frequency infrasound; The Origins of BSE?
Journal of Cattle Practice ( J of British Cattle Veterinary Association ) 2002 October, Vol 10 (4) p 311-335.

Bounias M, Purdey M, An epidemiological evaluation of a possible link between BSE and systemic warblecide treatments in France.  Under peer review.

Bounias M, Purdey M, TSEs; a family of etiologically complex diseases.
 "The Science of the Total Environment." 2002 297 (1-3) pages 1-19 

AWARDS.

Acres USA; - Eco Agriculture Annual Achievement Award 2001.

Weston A Price Foundation; - Integrity in Science Annual Award 2002.

Key Lectures/Presentations - 1994-2001 - 2002 - 2003 - 2004 - 2005


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