Mad Cow Disease

Many people seem frightened by the recent discovery of a downed cow diagnosed as having Mad Cow Disease (bovine spongiform encephalopathy [BSE]).  The authorities are saying that there is no cure for it or the human form, called new variant Creutzfeldt-Jakob Disease (CJD).  Some people with the genitic requirements get CJD without eating bad meat.

Many cattle were fed the same feed, but not all of them came down with mad cow disease.

This seems to imply that cattle do not invariably  become sick from being exposed to the prion that is the supposed cause.

Britain had the first case of mad cow disease in late 1986 and the first case in a human was identified in 1995, and controls were put in place.  So far only 139 people have become infected or died from the disease.  Are we to believe that only 139 people ate beef in England during those years?

It is thought that it requires a particular genetic characteristic to be susceptible to CJD.  It is estimated that only 1 in 1 to 2 million people have this characteristic.  Since there are 300 million people in the U.S., only 150 to 300 people could get it from eating BSE contaminated meat.

And even it a person is at risk, there is no guarantee that he/she will get it.  No one knows the amount of exposure required to set off the disease.  Does it take a single molecule, one bite, one pound or one cow?  No one knows.

No one knows if well-done meat has had the protein be broken down.  No one knows if the amount of stomach acid makes a difference.  Since proteins normally get digested in the stomach, there is reason to believe that the protein thought to cause CJD may be digested as well.

Most likely, there is a variation depending on the person's heath at the time of exposure, as there is in all other diseases.  Eating a healthy diet, and perhaps taking vitamin and mineral supplements, may slow or even prevent the disease in those people who are susceptible.  (1) (2) (3) (4)

CJD is so rare that no scientific investigation of it in humans has been possible.

And there is the possibility that the prion disease is a result of a mineral imbalance.  Too much manganese in the presence of organophospate insecticides seems to be implicated.  There is quite a bit of evidence supporting this theory.

Mad Cows Are Back  Full Text 

Mark Purdey's website

Update 2004 [UK Department of Health Monthly CJD Statistics 1/5/04]  The total number of definite or probable cases of new variant Creutzfeldt-Jakob disease (vCJD) is 145, including 6 patients who are still alive and 139 who have died. Of the 139 who died, 103 were confirmed vCJD and 34 did not have neuropathologic confirmation. 

The initial report of deaths was 3 in 1995; this subsequently increased to a peak of 28 in 2000 and decreased to 18 in 2003. 

Cases of vCJD in the United Kingdom, 1995-2003
Year  vCJD 
1995  3
1996 10
1997 10
1998 18
1999 15
2000 28
2001 20
2002 17
2003 18
Total 139

(1) Van Everbroeck B, Dobbeleir I, De Waele M, De Leenheir E, Lubke U, Martin JJ, Cras P.    Extracellular protein deposition correlates with glial activation and oxidative stress in Creutzfeldt-Jakob and Alzheimer's disease.   Acta Neuropathol (Berl). 2004 Jun 19  Abstract

(2)  Castellani RJ, Perry G, Smith MA.  Prion disease and Alzheimer's disease: pathogenic overlap. Acta Neurobiol Exp (Wars). 2004; 64(1): 11-7. Abstract

(3)  Arlt S, Kontush A, Zerr I, Buhmann C, Jacobi C, Schroter A, Poser S, Beisiegel U. Increased lipid peroxidation in cerebrospinal fluid and plasma from patients with Creutzfeldt-Jakob disease.  Neurobiol Dis. 2002 Jul; 10(2): 150-6.  Abstract

(4)  Nishida Y.  Elucidation of endemic neurodegenerative diseases--a commentary.
Z Naturforsch [C]. 2003 Sep-Oct;58(9-10):752-8.  Abstract

(5)   'vCJD Timebomb' Fears Discounted   1/11/05 Full Text

See the Medscape article.

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