[HealthPillarWell] Insecticide Causes Mad Cow Disease

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Misty L. Trepke

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Insecticide Causes Mad Cow Disease

Taken from:

http://www.mercola.com/2000/dec/17/bovine_spongiform_disease.htm

 

DR. MERCOLA'S COMMENT:

 

Fascinating information about the truly horrible things that

pesticides can do and the travesty of Mad Cow Disease.

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Do Not Use Systemic Organophosphate Insecticides

 

Do NOT treat children with OP head lice products - they may cause

CJD and Alzheimer's

 

Do NOT treat your pets with OP anti-flea products

 

Do NOT treat cattle or animals with OP products - they may cause BSE

 

Do NOT give manganese to cattle previously dosed with a systemic OP

 

The relative availability of the metals copper and manganese in you

local environment is a major factor in BSE & CJD

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Insecticide Causes Mad Cow Disease

by Fintan Dunne

Research by Kathy McMahon

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Pharmaceutical interests in the UK are ignoring new scientific

research that shows the insecticide used in the UK government's own

warble-fly campaigns triggered the UK surge of 'Mad Cow' disease.

 

Latest experiments by Cambridge University prion specialist, David

R. Brown, have shown that manganese bonds with prions. Other

researchers work shows that prions in the bovine spine -- along

which insecticides are applied -- can be damaged by ICI's Phosmet

organophosphate(OP) insecticide -causing the disease.

 

British scientists have led the current theory that an infectious

prion in bonemeal fed to cattle causes bovine spongiform disease

(BSE).

 

Infectious prions are also claimed to cause new variant Creutzfeld-

Jakob Disease (CJD) in humans -from ingesting beef. But the

infectious prion theory serves to obscure a tragic chemical

poisoning scandal behind the majority of BSE cases.

 

The new work proves that the prions can bond with manganese in

animal feeds or mineral licks. These manganese prions cause the

neurological degeneration seen in BSE. By a similar process, prions

in human brains are damaged by lice lotions containing

organophosphate. This can result in neurological diseases like CJD

and Alzheimers -later in life.

 

Many might be surprised to hear that organophosphates were developed

by Nazi chemists during the course World War Two, as a chemical

weapon nerve agent. One formulation of the insecticide -

- Maneb, or Mancozeb -- actually contains manganese in addition to

organophosphate.

 

The marginalized research has devestating financial implications for

ICI. It would provide a firm basis for litigants -who could include

CJD sufferers, farmers across the world and families of the many

British farmers who committed suicide during this BSE debacle.

 

Phosmet organophosphate has been used at high doses in British

warble fly campaigns. In 1996, ICI subsidiary Zeneca sold the

phosmet patent to a PO Box company in Arizona called Gowan -just one

week before the UK government admitted to a link between BSE and

nvCJD.

 

The politically well-connected British pharmaceuticals group, ICI

has the financial and political clout to block research into any

cause other than the infective model. Indeed no substantive

alternative research has been done. British BSE disease management

and research bodies have taken decisions that do not seem guided by

spirited scientific enquiry. Mysterious prions that jump species is

the preferred research arena.

 

Scientist and organic farmer, Mark Purdey gave evidence to the UK

BSE inquiry, that warble fly insecticide was the cause of the

disease. The scientist wheeled out to rubbish Purdy's evidence -Dr.

David Ray, later turned out to have been receiving funding from the

insecticide manufacturer ICI.

 

A lobby group that includes Bayer, Monsanto, Novartis, Pfizer, Roche

and Schering-Plough was behind the effort to discredit Purdey. In

December 1999, the same David Ray was appointed to the UK Veterinary

Products Committee (VPC) -a government body that licences animal

medicines.

 

Purdey has been consistently denied even exploratory funding to

extend his privately supported research. Yet the Purdey/Brown

chemical poisoning model matches with the epidermiological spread of

CJD clusters in humans. It also predicts the incidence of BSE-type

diseases in animals. The accepted infectious model fits neither.

 

The pharmaceutical industry is all the more determined to hide the

chemical source of BSE and CJD, because a spotlight on chemicals

would expose the role the insecticides in Alzheimer's -- another

neurodegenerative disease -- that might lead to claims which would

dwarf those from BSE and CJD litigants. In fact, two leading brain

researchers into CJD and Alzheimers have died in suspicious

circumstances in recent years.

 

In the United States, the Environmental Protection Agency is already

reviewing Phosmet's safety. The Centers for Disease Control in the

US has recently conducted experiments on mice that confirm the

organophosphate risk.

 

Not only is the EC beef slaughter campaign futile -because BSE

disease is mostly non-infectious, but unless the underlying chemical

cause is addressed, BSE will simply reappear from chemical causes. A

new warble fly campaign is already underway in France using the

organophosphate insecticide.

 

Of greater concern is that some lotions for scabies and head lice

are now priming children and adults, for CJD and Alzheimers in later

life.

 

Bonding The Prion

 

Cambridge University prion biochemist, David R. Brown is dismissive

of the science behind the infectious model of BSE. He terms it " a

very limited amount of science by a few assumed- reputable

scientists. " He insists there is " no evidence an infectious agent is

present in either meat or milk. "

 

" Simple tests on udder walls of cows -- which could easily detect an

infectious prion -- have not been done, why I don't understand. "

 

A number of researchers have found that organophosphate(OP) in

systemic warble fly insecticide can deform the prion molecule,

rendering it ineffective at buffering free radical effects in the

body. Worse still, the prion is then partial to bond with manganese

and become a 'rogue' prion. A chain reaction whereby rogue prions

turn others to rogues also, can explain the bovine spongiform

disease mechanism.

 

Brown showed how prion protein bonds benignly with copper, but

lethally with manganese. Even natural variations in relative

environmental availability of manganese versus copper can trigger

prion degradation.

 

The CJD and BSE symptoms mirror 'manganese madness', an irreversible

fatal neuro-psychiatric degenerative syndrome that plagued manganese

miners in the first half of the last century

 

 

Shining a Light on Spongiform

 

Organic dairy farmer and peer-review-published independent

scientist, Mark Purdey, says the accepted theory of transmission

from BSE-infected cattle to human CJD -by bonemeal or meat, is

dependent on a mutant prion that has never been isolated under the

scientific protocol called Koch's postulates.

 

Purdey's insistence on sticking to the letter of this scientific law

earned him the condemnation of UK officialdom when he first mooted

his theory. But Purdey pointed to CJD clusters downwind of a British

Phosmet production plant to back his case.

 

He gave evidence to the UK Government BSE inquiry and was supported

by Conservative MP, Thessa Gorman. His views were discounted, but

his subsequent research and the new Cambridge prion work have

confirmed the alternative theory. Despite this, and the backing of a

British peer, he is denied even exploratory funding.

 

Speaking from his rural English Somerset farm yesterday -as plans

forge ahead for the European cattle cull, he asks:

 

" Why does CJD degeneration in humans begin in the retina, and why

are CJD disease clusters found in high altitude locations? "

 

The question is rhetorical, and Purdey has an eye-opening answer. He

argues that the prion molecule has a known natural role as a shock

adsorber of damaging energy from ultraviolet rays and other

oxidizing agents.

 

Once this prion defence system is rendered ineffective by

organophosphates - for example in human head lice lotions, these

oxidizing effects have an unmediated impact on tissues. Eventually,

UV radiation damages the retina and oxidative stress destroys the

brain tissues of CJD patients. This theory would expect to find

higher CJD incidence in mountain regions -where UV radiation levels

are elevated. That prediction holds true.

 

A similar but accelerated mechanism could be driving BSE. ICI's

Phosmet organophosphate warble fly insecticide -applied on the backs

of animals along the spinal column, similarly degrades

prions. " Systemic versions of the insecticide are designed to make

the entire cow carcass toxic to warble fly, " explains

Purdey. " Unfortunately it's toxic to prions too -especially those

prions located just millimeters from the point of application. "

 

The damaged prions are then ready to react with manganese in animal

feed, or manganese sprayed on land or in mineral licks -to become

the driving force of BSE neurodegeneration. Purdey says manganese-

tipped prions set off lethal chain reactions that neurologically

burn through the animal.

 

Chickens notoriously excrete most of the supplements fed to them -

including manganese. And their manganese-rich excreta have been

blended into cattle feed in the UK. Natural variations in the

relative environmental availability of copper and manganese can also

spur prion degeneration says Purdey.

 

From this research, any prudent person would conclude there is a

significant risk attaching to the use of organophosphate in humans.

Preparations for head lice and scabies are known to be overused in

practice and might be priming users for CJ disease.

 

Purdey believes his bias for field work is the key to his success.

He bemoans the " reductionism " of much lab-centered science. " I have

traveled the world to investigate known clusters of spongiform

disease -something mainstream researchers don't seem remotely

interested in doing. "

 

Since first postulating an environmental -rather than infectious-

theory of spongiform diseases, Purdey has built evidence from around

the world that explains and predicts the incidence in humans and

animals: a cluster of CJD in Slovakia, Eastern Europe -around a

manganese plant; Rocky Mountain deer with Chronic Wasting Disease

(CWD), who were found to be eating pine needles rich in manganese;

the futile slaughter of sheep in Cyprus -only for BSE to reemerge

within years.

 

" The reappearance of BSE in Cyprus obviously points to an

environmental cause, " says Purdey, who is sanguine when reflecting

on the condemnation of him by mainstream scientists.

 

" I suppose they have mortgages and kids who need to go to

university, " he muses. " Privately, some were agreeing with me, but

then they would denounce me publicly. It was quite strange really. "

 

The Money Trail

 

Critical scientists like Purdey are unlikely to prevail. The

pharmaceutical industry holds most research purse strings, and would

hardly energetically explore an avenue of research that could expose

them to litigation for causing BSE. The official theory is lavishly

funded, alternative theories rarely, if at all.

 

There are more explosive implications to his -and other's latest

research. Purdey says similar organophosphate-induced protein

deformation could also underlie Alzheimer's disease. If that were

true, the litigation fallout would destroy some pharmaceutical

giants, and a lot of very influential noses would be out of joint.

 

Disturbingly, Purdey and other brain researchers seem to have had an

undue share of unfortunate accidents. Purdey's house was burned down

and his lawyer who was working with him on Mad Cow Disease was

driven

off the road by another vehicle and subsequently died. The

veterinarian on the case also died in a car crash -locally reported

as: 'Mystery Vet Death Riddle.'

 

Dr. C. Bruton, a CJD specialist -- who had just produced a paper on

a new strain of CJD -- was killed in a car crash before his work was

announced to the public. Purdey speculates that Bruton might have

known more than what was revealed in his last scientific paper.

 

In 1996, leading Alzheimer's researcher Tsunao Saitoh, 46 and his

13 -year-old daughter were killed in La Jolla, California, in what a

Reuters report described as a " very professionally done " shooting.

 

What Alzheimer's Disease, Mad Cow Disease, and CJ Disease have in

common, is abnormal brain proteins and a putative link to

organophosphates. Even Gulf War syndrome among returning veterans

has been attributed, in part to the insecticide. But the sidelined

scientists' suspicions are still largely ignored.

 

In their favour at the moment, is a growing unease on the part of

the public. As BSE forges on and Governments panic, Science may be

out to lunch on BSE, compromised by bovine spongythinking myopathy.