The Media & Mad Cows

The anti-Trump Fake News blitz by the legacy media has invoked memories of the Mad Cow Disease epidemic amongst several new media commentators.

Although these references are deployed for humorous effect it’s worth remembering that Mad Cow Disease is deadly serious.

Bovine spongiform encephalopathy (BSE), commonly known as mad cow disease, is a transmissible spongiform encephalopathy and fatal neurodegenerative disease in cattle that causes a spongiform degeneration of the brain and spinal cord.

The disease may be most frequently transmitted to humans by eating food contaminated with the brain, spinal cord, or digestive tract of infected carcasses.

However, the infectious agent, although most highly concentrated in nervous tissue, can be found in virtually all tissues throughout the body, including blood.

When it has been transmitted to humans, it is known as new variant Creutzfeldt–Jakob disease (vCJD or nvCJD), and by June 2014 it had killed 177 people in the United Kingdom, and 52 elsewhere, primarily in western Europe in countries supplied with beef or beef products from the UK.

Mad Cow Disease can also be used as a metaphor for the legacy media which habitually assigns inconvenient stories to the memory hole.

The infectious agent in BSE is a specific type of misfolded protein called a prion.

In the brain, these proteins cause native cellular prion protein to deform into the infectious state, which then goes on to deform further prion protein in an exponential cascade.

This results in protein aggregates, which then form dense plaque fibers leading to the microscopic appearance of “holes” in the brain, degeneration of physical and mental abilities, and ultimately death.

Therefore, it’s worth reviewing the status of Mad Cow Disease and Creutzfeldt–Jakob Disease just in case an inconvenient story has slipped down the memory hole.

In the United Kingdom there is good and bad news about Mad Cow Disease.

The good news is that the Mad Cow Disease epidemic is officially over.

According to the World Animal Health Organization (OIE) through the end of 2006, 190,129 diagnosed cases of BSE (including domestic and imported animals) have been recorded worldwide. Of these, 97 percent or 184,484 cases occurred in the United Kingdom.

BSE cases in the U.K. have declined from a peak of 37,280 cases in 1992 to 114 cases in 2006.

BSEinfo – BSE Incidence/Cases

The first confirmed instance in which an animal fell ill with the disease occurred in 1986 in the United Kingdom, and lab tests the following year indicated the presence of BSE; by November 1987, the British Ministry of Agriculture accepted it had a new disease on its hands.

The BSE crisis led to the European Union banning exports of British beef with effect from March 1996; the ban lasted for 10 years before it was finally lifted on 1 May 2006 despite attempts in May 1996 by British prime minister John Major to get the ban lifted.

The bad news is that Mad Cow Disease hasn’t gone away.

The problem being that Mad Cow Disease has an incubation period of 2.5 to 5 years.

BSE has a long incubation period, of 2.5 to 5 years, usually affecting adult cattle at a peak age onset of four to five years

Therefore, when the United Kingdom introduced their Over Thirty Months Rule [whereby cattle could not be sold for food if they were aged over 30 months] it meant infected animals were slaughtered for human consumption before they developed Mad Cow Disease.

Because the majority of cattle were slaughtered for human consumption at 18-24 months, before they could develop clinical disease, there were infected animals that were neither detected nor detectable by test methods used in the past 20 years.

BSEinfo – BSE Incidence/Cases

There have been three main BSE Controls:

Animal feed that contained animal protein thought to have spread BSE is banned.
This is called the Feed Ban.

The parts of an animal most likely to contain BSE are removed when an animal is slaughtered, and they do not go into our food.
This is called the Specified Risk Material Control and removes almost all the risk (over 99%) that could be present if any animal has BSE.

Until November 2005, cattle could not be sold for food if they were aged over 30 months, as BSE does not develop fully in cattle until they are older.
This was called the Over Thirty Months Rule.

An additional control was also introduced banning the process of recovering meat mechanically from the bones of cattle.

Food Standards Agency – BSE and Beef: New Controls Explained – 2005

The system of BSE testing healthy slaughtered cattle aged over 30 months was introduced on 7 November 2005. Between then and the end of 2011, over 2.4 million healthy cattle slaughtered for human consumption were tested for BSE.

There were ten cases of BSE detected, of which two were less than 72 months of age (one in 2006 and one in 2008), and eight were over 72 months of age.

Impact Assessment of change to BSE Testing – 2011

Mad Cow Disease returns to the UK after dead cow tests positive for BSE

But only one case of BSE was identified in animals last year – following three cases in 2013.

The Mirror – Richard Smith and David Ottewell – 1 Oct 2015

The other bad news is that the official origin of Mad Cow Disease “will probably never be known with certainty” because it “originated from a novel source”.

By the end of 1987 Mr John Wilesmith, the Head of the CVL Epidemiology Department, had concluded that the cause of the reported cases of BSE was the consumption of meat and bone meal (MBM), which was made from animal carcasses and incorporated in cattle feed.

This conclusion was correct. It had been reached with commendable speed.

BSE probably originated from a novel source early in the 1970s, possibly a cow or other animal that developed disease as a consequence of a gene mutation.

The origin of the disease will probably never be known with certainty.

The BSE Inquiry – Executive Summary

A U.K. review of BSE origins noted it seems likely that from 1970 to the 1980s when MBM was widely used in cattle feed, an unusual linkage of events occurred.

The diet of calves, in particular a high proportion of dairy calves, was changed so that MBM was included in their starter rations.

Infected cattle carcasses were rendered into MBM, increasing the levels of the cattle-adapted scrapie agent in the protein supplement and eventually causing a full-scale BSE epidemic.

BSEinfo – BSE Origin

The practice in the UK of recycling animal protein as an ingredient of animal feed dates back to at least 1926.

The theory that BSE was caused by a reaction to the use of organophosphorus compounds (OPs) poured on cattle as systemic pesticides cannot be reconciled with the epidemiology and is not supported by research.

One experiment has, however, given some limited support to the possibility that the OP phosmet might modify the susceptibility of cells to the prion disease agent.”)

When it comes to Creutzfeldt–Jakob Disease there is also good and bad news.

Creutzfeldt–Jakob disease (CJD) is an incurable, and universally fatal neurodegenerative disease.

CJD is at times called the human form of mad cow disease (bovine spongiform encephalopathy or BSE) but only Variant Creutzfeldt–Jakob disease (vCJD) is acquired from BSE.

Rapid mental deterioration will spiral within months and worsen over time, leading to coma in most cases.

The disease will invariably lead to death within one or two years, with a 1-year survival rate of just 10%. Direct causes of death include heart failure, respiratory failure, pneumonia and other infections.–Jakob_disease

The good news is that the epidemic of variant Creutzfeldt–Jakob Disease is officially over.

variant (vCJD) (acquired from Bovine spongiform encephalopathy), caused by consuming food contaminated with prions

familial (fCJD), caused by an inherited mutation in the prion-protein gene.

iatrogenic CJD, caused by contamination with tissue from an infected person, usually as the result of a medical procedure.–Jakob_disease

For many of the vCJD patients, direct evidence exists that they had consumed tainted beef, and this is assumed to be the mechanism by which all affected individuals contracted it.

As of August 2005, 150 deaths from vCJD had been reported in the United Kingdom, at a median age of 28.

U.S. Beef Industry Faces New Policies And Testing For Mad Cow Disease – Kate O’Neill – Oct–Dec 2005

The UK death toll from BSE stands at 177 since teenager Stephen Churchill died of a fatal brain condition linked to mad cow disease in 1995.

The Mirror – Richard Smith and David Ottewell – 1 Oct 2015

The bad news is that an epidemic of sporadic Creutzfeldt–Jakob Disease has developed.

sporadic (sCJD), caused by the spontaneous misfolding of prion-protein in an individual.

This accounts for 85% of cases of CJD.

The sporadic Creutzfeldt–Jakob Disease epidemic has been developing since [at least] 1970.

And sporadic Creutzfeldt–Jakob Disease “may” be linked to Mad Cow Disease [aka BSE aka Bovine Spongiform Encephalopathy].

In a BBC News article published in 2004 entitled BSE link to different CJD types it states:

“Eating BSE-infected meat could lead to people developing different types of CJD, researchers have suggested.

Until now, it had been thought that BSE was only linked to the variant form of Creutzfeldt – Jakob disease, but Medical Research Council experts say BSE may also manifest itself as sporadic CJD, or a new form of the disease not yet seen in humans.

The study, in Science, raises the possibility that more people than previously thought may be at risk.”

BSE ‘link to different CJD types – BBC News – 12 Nov 2004

So, I’m wondering if there could be a possibility of a misdiagnosis, mistaking CJD for Alzheimer’s, which appears to be on the increase.

The BSE Outbreak in the UK and Cases of Creutzfeldt–Jakob Disease Observed Now – Philip Oldfield – 28 Aug 2015

For females, the death rates from heart disease and stroke have halved since 2001, whereas the death rate from dementia and Alzheimer’s disease has doubled

Public Health England – Major Causes Of Death And How They Have Changed

In other words:

Mad Cow Disease and Creutzfeldt–Jakob Disease never went away.

I guess it’s another inconvenient story that’s been stuffed down the memory hole.

For some perspective here are some United Kingdom Measles Death statistics.

Gallery | This entry was posted in Medicine. Bookmark the permalink.

9 Responses to The Media & Mad Cows

  1. TimE. says:

    From “Mad Cows” to “some very peculiar signals” – The Mass Media is on a BLITZKREIG:

    ‘Strange’ signals that appear to be coming from a star close to Earth may have been sent by ALIENS, scientists say

    Astronomers picked up the communications in May and have refused to rule out the possibility they were sent by extraterrestrials

  2. TimE. says:


    The U.S. Department of Agriculture has confirmed an “atypical” case of bovine spongiform encephalopothy (BSE), commonly known as mad cow disease, in an 11-year old beef cow in Alabama but emphasized that the animal never entered the slaughterhouse and “at no time presented a risk to food supply or to human health.”

    According to a news release from the Alabama Department of Agriculture and Industries, the sick animal was discovered during routine surveillance at an Alabama livestock market. The animal died at the market before entering the slaughter channels and samples were sent to a USDA lab in Iowa for confirmation.

    The department referred to this case as “atypical,” and “a rare and spontaneous incident.”

  3. Thx1138 says:

    “I’M APPALLED by the unfounded assumptions of ‘experts’ about the hyper-infectious nature of the BSE/CJD agent (Mail). Basic evidence suggests variant CJD didn’t arise from eating BSE-affected cattle. Third World countries imported even greater quantities of the incriminated British meat than we consumed here, but no cases of vCJD have occurred in those countries. I’ve travelled worldwide carrying out analyses of areas with prion diseases, of which vCJD is one. These diseases increase only in areas with a high manganese/low copper imbalance. Experiments at Cambridge and Case Western, Cleveland, universities confirmed my findings that misshapen prions develop whenever brain cells are exposed to this imbalance.
    I found one organophosphate — poured on cows to counteract warble fly and on humans for headlice — which bonded with copper in the brain, starving the prion protein of its copper partner. When this happens, foreign metals, such as manganese, are more likely to bond with prions, which can have devastating consequences. Manganese is increasing in the environment due to its use as a fertiliser and fungicide, a lead substitute in petrol, and emission from factories. It was fed to UK cattle in calf milk replacement powder (at levels up to 1,000 times higher than in normal cow’s milk) and as supplements for bone growth. Manganese is also fed to humans (in health food supplements), deer (for antler growth) and cats —and all have had prion disease. The totalitarian mindset about the origins of prion diseases betrays an agenda. It’s more about global profitys for the GM soya protein empires than about the illusory health risks of animal proteins to humans. MARK PURDEY. Taunton.”

    A prion is nothing more than a poisonous protein. To speak of being infected with it is tantamount to saying that you can be “infected” with arsenic, lead or cadmium. That’s just crazy talk.

    • malagabay says:

      A prion is nothing more than a poisonous protein. To speak of being infected with it is tantamount to saying that you can be “infected” with arsenic, lead or cadmium. That’s just crazy talk.

      The problem with dismissing this as “just crazy talk” is that:

      1) The pathology of Creutzfeldt–Jakob Disease is not fully understood.
      2) Creutzfeldt–Jakob Disease is associated with an incubation period.

      They have also proposed that individuals having contracted CJD in the early 1990s represent a distinct genetic subpopulation, with unusually short incubation periods for bovine spongiform encephalopathy (BSE).

      This means that there may be many more vCJD patients with longer incubation periods, which may surface many years later.

      Prions are infectious agents composed entirely of a protein material that can fold in multiple, structurally abstract ways, at least one of which is transmissible to other prion proteins, leading to disease in a manner that is epidemiologically comparable to the spread of viral infection.

      Virtually indestructible, the prions that cause prion disease are resistant to heat, radiation, and other techniques that are commonly used for sterilization.

      About Prions
      Department of Chemical Engineering – University of California, Berkeley

      Kuru, for example, is another “abnormally folded prion proteins” disease associated with an “incubation period” that ranges “from 10 to over 50 years”.

      Incubation period is the time elapsed between exposure to a pathogenic organism, a chemical, or radiation, and when symptoms and signs are first apparent.

      Kuru is a very rare, incurable neurodegenerative disorder that was formerly common among the Fore people of Papua New Guinea.

      Kuru is caused by the transmission of abnormally folded prion proteins, which leads to symptoms such as tremors, loss of coordination, and neurodegeneration.

      While the Fore people stopped eating human meat half a century ago, the disease lingered due to kuru’s long incubation period of anywhere from 10 to over 50 years.

  4. Thx1138 says:

    Could the Scientists Be Wrong on Madcow Disease?

    By Elizabeth Piper

    SOMERSET, England (Reuters)—Mark Purdey still eats beef, even “junk’’ in pies and hamburgers, and he has no fear that he or his wife or six children will be struck down by the deadly human form of mad cow disease. “It’s an absolute myth,’’ the 48-year-old organic farmer says, banging his fist on a large wooden table to underline his argument that much of the accepted logic on bovine spongiform encephalopathy, or BSE (news—web sites ), is wrong.
    His story unfolds—a 16-year campaign to explore the effect of organophosphates, the chemicals he believes are behind the spread of the brain-wasting disease in cattle and in people. Purdey says we should distance ourselves from “the men in bow-ties’’ who have what he calls a monopoly on thought. Forget the role of tainted animal feed in spreading BSE among cattle or infected meat in passing the disease to humans as new variant Creutzfeldt-Jakob Disease (news—web sites) (vCJD). Look instead at the use of systemic organophosphates, derived from military nerve gas, which the UK agriculture ministry told farmers to pour along the spine of their cattle in the early 1980s to kill a parasite called the warble fly. And those used in sprays used in Britain’s countryside.
    “I have been hammering the establishment theory, the so-called meat-and-bone meal theory, since 1988 or 1989. Even then I had identified that meat and bone meal had been sold all over the world, particularly the Middle East,’’ he says. “If you’re blaming this stuff and you’re sending it all over the world, why on earth aren’t you getting more BSE?’’
    He agrees that other scientists would argue it has yet to appear because of the long incubation period of disease, believed to be caused by a mutated prion protein in the brain. But Purdey argues there is little logic in the theory. He also disputes the argument that BSE is passed to humans via infected beef.
    “If it was to do with eating beef we’d have lots of cases in towns, where most burger bars are, but 60 percent of cases are in rural areas,’’ he said. “Most victims live by fields, where crops are sprayed.’’
    Self-Taught Scientist A self-taught scientist, Purdey says he acted first on ‘‘intuition,’’ refusing to treat his 60 cows with the organophosphate, called phosmet, and going on to win a court battle with the agriculture ministry to make his point. When BSE was first detected in a British herd in 1986, he immediately thought phosmet was the problem—a theory which after years of unpaid research has now won respect from senior scientists, public figures and politicians.
    “Like most things it was instinct. Being a farmer, I was horrified when I was approached by a ministry official to treat a cow for warble fly by pouring this chemical along the spinal cord and the base of the head,’’ he said. “It was an oil designed to seep through the skin and to change the entire internal environment of the cow into a poisonous medium to kill off the parasites.’’
    Purdey began to trawl through books and do field research. He looked at the clusters of BSE in Britain, clusters of deer and elk in the United States with a similar illness called chronic wasting disease, and villages where many people were dying of the more common Creutzfeldt-Jakob disease (news—web sites). “I went on the road,’’ he said, describing trips to the United States, Slovakia, Calabria in Italy and Iceland. “To me it was clearly something in the environment that was igniting these illnesses. But what was this factor?’’ He found one common factor—high levels of manganese, a metal given to cattle in high doses via the organophosphate. “What I found in the environment was supported by the laboratory,’’ he said, describing tests by David Brown, a neurobiologist at Cambridge University. Purdey explains the prion would normally bond with copper and carry it around the brain to destroy free radicals. But if lacking copper, the prion bonds with another metal—manganese, which stops the prion from folding properly. He did soil analysis on the areas near clusters of vCJD in Britain and found high levels of manganese from crop spraying. He concluded the doses of manganese intensifies the traditional illness, giving vCJD the potency to kill younger people. Funding Required Now all he wants is funding for more research—something that Agriculture Minister Nick Brown says may be ready in May after a scientist has reviewed all work into the origins of BSE. “In the BSE inquiry there is a caveat that it is not clear whether organophosphates could have been a contributory factor…it leaves the door open on organophosphates,’’ Brown told Reuters. But Purdey is worried that the funding may never come. “No one’s prepared to admit it because it would involve massive compensation,’’ he said. “By keeping the causal agent as something mystified, no one’s to blame.’’

    A causal relationship with organophosphates has not been disproven.

  5. Thx1138 says:

    Mark Purdey BSE & CJD: the chemical connection
    Mark Purdey and the Mad Cows

    By Claire W. Gilbert, Ph.D.
    Copyright 1996
    On May 5, 1996, I conducted a long distance telephone interview with Mark Purdey of Somerset, England. Purdey has published scientific papers on Mad Cow Disease and he has appeared on British television regarding the same. It was his TV appearance last year which prompted the November, 1995 cover of Blazing Tattles. His views are not mainstream because he sees an “intervening variable” of chemicals between the healthy cow and the mad cow. I had assumed incorrectly that the “prion protein” was a figment of scientific imagination, but according to Purdey there is such a thing. The question is how the prion protein becomes “incorrectly folded.” Now, before the reader says “Whoa!,” let me backtrack.
    Of recent years, a disease has been observed among cattle. A sick cow drools, wobbles as if drunk, and has difficulty using its hind legs (if I have that right). Then one day it falls over dead. [The US version may be the “downer cow.”] It has been found upon autopsy that their brains are not normal, and the disease is caused from an infectious agent. It was widely believed to be a slow incubating virus, but now some scientists believe it is caused from an almost indestructible protein molecule called a “prion.” It was assumed humans could not catch this disease. It is an incorrectly folded prion protein molecule, according to Purdey. These incor- rectly folded molecules have an abnormal electrical charge which facilitate the neighboring prions to become incorrectly folded. These proteins are not destroyed by ordinary cooking and there is also no known remedy for the disease. Over a period of years, this process continues, until the cow falls ill.
    Purdey believes that the cause of the problem is that a chemical gets into the brain and binds with the normal prions to produce abnormal ones. He believes it is a specific chemical called “phosmet” which does this. Phosmet is a combination of an organophosphate pesticide (OP) and thalimide (base of thalidomide) which is used against the warble fly in cattle. The phosmet is applied on the skin in an oily base, with the intent of it being taken into the skin, into the cow’s body where the fly burrows in. According to Purdey, the warble fly actually lives in the cow nine months of the year. The OP plus thalimide initiates the prion change. Once changed, its electrical charge can trigger normal prion protein into abnormal form.
    Purdey controls the warble fly with “derris root powder.” It kills the warble fly and does not harm the cow — it is not necessary to use phosmet to kill the warble fly.
    It seems researchers in many fields who get onto something regarding toxic chemicals have bad things happen. Purdey’s re- search that was contracted out to the Medical Research Council was intercepted by the government, and one trial was cancelled while the other was mysteriously changed. The chemical he designated for the experiment was altered and diluted. The results therefrom were weakened, although still was found a slight bond with the OG and the prion protein.

    A big issue today is whether the mad cow disease could cross the species barrier and be transmitted to humans or between other animal species. There is an emerging view, based on a variety of correlations, that this is possible.
    With respect to humans, there is a disease known as “CJD” which resembles Mad Cow Disease in that it has a long incubation period and when a fatality is autopsied, the human brain shows minuscule holes as does the cow’s. The British believe it is caused from eating contaminated beef. CJD is an extremely rare illness and normally strikes only older people. More recently a second strain has emerged in which younger people have been affected.
    But Purdey says that human cases can be caused from chemicals. He says there was a cluster of CJD in Kent, England. There were four cases in four small villages. These villages are ten miles downwind of a factory which manufactures phosmet. In 1986 they had a leak and the chemical went all around the countryside. The incubation period is ten years. He says there is another cluster of this very rare disease in Teeside, where another plant is located. His conclusion is that the second strain is caused from chemicals.
    There’s been another ominous story going around about hay mites infecting minks. Purdey says the mite prion which infected the minks was itself affected by the chemical.

    I asked Purdey if it is true that both his veterinarian and his lawyer were killed in car crashes, and he confirmed this. His lawyer was run off the road by another car and died as a result of the accident. His new lawyer also had a car crash, but he survived. Purdey’s house was burned down.
    Purdey related that the scientist, Dr. C. Bruton died in a car crash. He had just produced a paper on a new strain of CJD. Bruton was a CJD specialist. Posthumously, his work was announced to the public. It is likely or at least possible that Bruton knew more than what was in the paper, said Purdey.
    I asked Purdey if he thought the arrest and firing from his research position of the distinguished, US resident, Nobel Award CJD specialist, Dr. D.C. Gajdusek was also related to this mad cow situation. Purdey said that weeks before the arrest of Gajdusek Purdey was told by Ray Bradly of the Ministry of Agriculture that Gajdusek was seeking alternative hypotheses and specifically requested all of Purdey’s papers. They were faxed to Gajdusek.

  6. Copper will enter the body when handling pennies….

    Oh yes, they are too valuable a metal to remain in circulation! INFLATION!

    Bankers, killing us in billions of ways!

    THX1138 are you Stephen? Thanks for that bit about Purdey!

  7. Pingback: Fear Porn Friday: Tuberculosis | MalagaBay

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